Commonly Treated Illnesses
If you have an allergy, your immune system reacts to something that doesn’t bother most other people. People with seasonal allergies (also called hay fever or allergic rhinitis) react to pollen from plants. Symptoms may include sneezing, coughing, a runny or stuffy nose, and itching in the eyes, nose, mouth, and throat.
This page discusses complementary health approaches for allergic rhinitis. Another page on the NCCIH Web site has information on complementary approaches for asthma.
The most common culprit for fall allergies is ragweed, a plant that grows wild almost everywhere, but especially on the East Coast and in the Midwest. Ragweed blooms and releases pollen from August to November. In many areas of the country, ragweed pollen levels are highest in early to mid-September.
Other plants that trigger fall allergies include:
- Burning bush
- Sagebrush and mugwort
- Tumbleweed and Russian thistle
While the timing and severity of an allergy season vary across the country, the following climate factors also can influence how bad your symptoms might be:
- Tree, grass and ragweed pollens thrive during cool nights and warm days.
- Molds grow quickly in heat and high humidity.
- Pollen levels tend to peak in the morning hours.
- Rain washes pollen away, but pollen counts can soar after rainfall.
- On a day with no wind, airborne allergens are grounded.
- When the day is windy and warm, pollen counts surge.
- Moving to another climate to avoid allergies is usually not successful — allergens are virtually everywhere.
Allergy Management and Treatment
If you feel like you’re always getting sick, with a cough or head congestion, it’s time to see an allergist. You may think you’re sure pollen is causing your suffering, but other substances may be involved as well. More than two-thirds of spring allergy sufferers actually have year-round symptoms. Your best resource for finding what’s causing your suffering and stopping it, not just treating the symptoms, is an allergist.
Work together with your allergist to devise strategies to avoid your triggers:
- Monitor pollen and mold counts. Weather reports in newspapers and on radio and television often include this information during allergy seasons.
- Keep windows and doors shut at home and in your car during allergy season.
- To avoid pollen, know which pollens you are sensitive to and then check pollen counts. In spring and summer, during tree and grass pollen season, levels are highest in the evening. In late summer and early fall, during ragweed pollen season, levels are highest in the morning.
- Take a shower, wash your hair and change your clothes after you’ve been working or playing outdoors.
- Wear a NIOSH-rated 95 filter mask when mowing the lawn or doing other chores outdoors, and take appropriate medication beforehand.
Your allergist may also recommend one or more medications to control symptoms. Some of the most widely recommended drugs are available without a prescription (over the counter); others, including some nose drops, require a prescription.
If you have a history of prior seasonal problems, allergists recommend starting medications to alleviate symptoms two weeks before they are expected to begin.
One of the most effective ways to treat seasonal allergies linked to pollen is immunotherapy (allergy shots). These injections expose you over time to gradual increments of your allergen, so you learn to tolerate it rather than reacting with sneezing, a stuffy nose or itchy, watery eyes.
Seasonally Related Triggers
While the term “seasonal allergies” generally refers to grass, pollen and mold, there is a different group of triggers that are closely tied to particular seasons. Among them:
- Smoke (campfires in summer, fireplaces in winter)
- Insect bites and stings (usually in spring and summer)
- Chlorine in indoor and outdoor swimming pools
- Candy ingredients (Halloween, Christmas, Valentine’s Day, Easter)
- Pine trees and wreaths (Thanksgiving to Christmas))
What the Science Says
Many complementary health approaches have been studied for allergic rhinitis. There’s some evidence that a few may be helpful.
Mind and Body Practices
A 2015 evaluation of 13 studies of acupuncture for allergic rhinitis, involving a total of 2,365 participants, found evidence that this approach may be helpful.
Rinsing the sinuses with a neti pot (a device that comes from the Ayurvedic tradition) or with other devices, such as nebulizers or spray, pump, or squirt bottles, may be a useful addition to conventional treatment for allergic rhinitis.
A 2007 evaluation of six studies of the herb butterbur for allergic rhinitis, involving a total of 720 participants, indicated that butterbur may be helpful.
Researchers have been investigating probiotics (live microorganisms that may have health benefits) for diseases of the immune system, including allergies. Although some studies have had promising results, the overall evidence on probiotics and allergic rhinitis is inconsistent. It’s possible that some types of probiotics might be helpful but that others are not.
It’s been thought that eating honey might help to relieve pollen allergies because honey contains small amounts of pollen and might help people build up a tolerance to it. Another possibility is that honey could act as an antihistamine or anti-inflammatory agent. Only a few studies have examined the effects of honey in people with seasonal allergies, and their results have been inconsistent.
Many other natural products have been studied for allergic rhinitis, including astragalus, capsaicin, grape seed extract, omega-3 fatty acids, Pycnogenol (French maritime pine bark extract), quercetin, spirulina, stinging nettle, and an herb used in Ayurvedic medicine called tinospora or guduchi. In all instances, the evidence is either inconsistent or too limited to show whether these products are helpful.
Side Effects and Risks
- People can get infections if they use neti pots or other nasal rinsing devices improperly. The U.S. Food and Drug Administration (FDA) has information on how to rinse your sinuses safely.
- Most important is the source of water that is used with nasal rinsing devices. According to the FDA, tap water that is not filtered, treated, or processed in specific ways is not safe for use as a nasal rinse. Sterile water is safe; over-the-counter nasal rinsing products that contain sterile saline (salt water) are available.
- Some tap water contains low levels of organisms, such as bacteria and protozoa, including amoebas, which may be safe to swallow because stomach acid kills them. But these organisms can stay alive in nasal passages and cause potentially serious infections. Improper use of neti pots may have caused two deaths in 2011 in Louisiana from a rare brain infection that the state health department linked to tap water contaminated with an amoeba called Naegleria fowleri.
- Acupuncture is generally considered safe when performed by an experienced practitioner using sterile needles. Improperly performed acupuncture can cause potentially serious side effects.
- Raw butterbur extracts contain pyrrolizidine alkaloids, which can cause liver damage and cancer. Extracts of butterbur that are almost completely free from these alkaloids are available. However, no studies have proven that the long-term use of butterbur products, including the reduced-alkaloid products, is safe.
- In healthy people, probiotics usually have only minor side effects, if any. However, in people with underlying health problems (for example, weakened immune systems), serious complications such as infections have occasionally been reported.
- Be cautious about using herbs or bee products for any purpose. Some herbs, such as chamomile and echinacea, may cause allergic reactions in people who are allergic to related plants. Also, people with pollen allergies may have allergic reactions to bee products, such as bee pollen, honey, royal jelly, and propolis (a hive sealant made by bees from plant resins). Children under 1 year of age should not eat honey.
- Talk to your health care provider about the best way to manage your seasonal allergies, especially if you’re considering or using a dietary supplement. Be aware that some supplements may interact with medications or other supplements or have side effects of their own. Keep in mind that most dietary supplements have not been tested in pregnant women, nursing mothers, or children.
Alzheimer’s Disease & Memory Disorders Diagnosis
Alzheimer’s disease is the most common cause of dementia among older adults. MILD COGNITIVE impairment (MCI) is conceptualized as a boundary or transitional state between aging and dementia. Memory deficit is both the usual complaint in MCI and the cardinal feature of Alzheimer disease (AD). The major focus of MCI research has been to distinguish individuals who will progress to AD from those who will not. Interest in MCI has been stimulated by the hope that pharmacologic intervention at this stage may delay or prevent progression to AD.10 Multicenter trials of cholinesterase inhibitor drugs and other agents with putative benefit for AD already are being conducted in individuals with MCI.
The diagnosis of MCI is established by (1) evidence of memory impairment, (2) preservation of general cognitive and functional abilities, and (3) absence of diagnosed dementia. Mild cognitive impairment is staged clinically at the 0.5 level on the Clinical Dementia Rating (CDR) scale. The perceptions of a knowledgeable informant regarding an individual’s cognitive abilities in everyday functioning, on the other hand, have been shown to be sensitive and reliable for early dementia detection.
Psychaitry Department at the Alabama Clinics offer hopes through screening programs; early diagnosis; delaying progression by treating memory, cognitive problems and behavioral disturbances at an early stage; supporting and providing education to the caregivers and the public; and in conducting cutting-edge research. Alabama Clinics multidisciplinary approach incorporates neurology, psychiatry, geriatrics, diagnostic imaging, counseling, social support and referral to appropriate community resources to develop successful and effective treatment options for Alzheimer’s disease and other forms of dementia and memory disorders.
Overdependence on cognitive test performance and underutilization of knowledgeable informants may result in failure to detect very mild dementia in many individuals who nominally meet MCI criteria. Progression of patients with MCI to “diagnosable AD” may be confounded because the threshold for dementia diagnosis. Therefore, the early diagnosis of MCI is a complex process, and here, our specialist psychiatrist Dr. Meghani comes with over 20 years of experience when it comes treating and diagnosing patients with memory disorders, and Alzheimer’s.
Why is Early Diagnosis an Excellent Idea?
Alzheimer’s disease is just one of a number of potential reasons an individual may experience memory loss. Side effects of medications, depression and anxiety, endocrine problems, stroke, vision or hearing loss, cardiac or pulmonary disorders or vitamin deficiencies can also trigger memory problems. An early diagnosis can prevent the person from vulnerability to be prone to AD, MCI or Memory Problems.
Alabama Clinics team includes psychiatrists, neurologists, a neurophysiologist, a geriatric psychiatrist and other clinicians who are experts in the diagnosis and treatment of the following conditions:
- Alzheimer’s disease
- Frontotemporal dementia
- Lewy Body dementia
- Vascular dementia
- Cognitive effects of stroke
- Mild cognitive impairment
- Age-related memory loss
Alabama Clinics have carefully designed a program for the early diagnosis of AD, and memory related problem that includes:
- Repeat questions
- Misplace possessions
- Are at a loss for words
- Forget recent events, conversations and names of friends or relatives
- Confuse sense of direction and time and become lost in familiar places
- Have difficulty performing chores or using appliances and tools
- Have difficulty handling finances
- Show changes in mood and/or personality
It is therefore a great idea for person aged 49 or more to have a screening to suspend the impact of age-related memory problem.
A group screening or program can also be designed for critical-nature businesses. Please contact the Alabama Clinics for the special arrangements. All the data and results are kept strictly confidential.
Anemia is a condition in which you don't have enough healthy red blood cells to carry adequate oxygen to the body's tissues. Having anemia may make you feel tired and weak.
There are many forms of anemia, each with its own cause. Anemia can be temporary or long term, and it can range from mild to severe. See your doctor if you suspect you have anemia because it can be a warning sign of serious illness.
Treatments for anemia range from taking supplements to undergoing medical procedures. You may be able to prevent some types of anemia by eating a healthy, varied diet.
Anemia signs and symptoms vary depending on the cause of your anemia. They may include:
- Pale or yellowish skin
- Irregular heartbeats
- Shortness of breath
- Dizziness or lightheadedness
- Chest pain
- Cold hands and feet
At first anemia can be so mild that it goes unnoticed. But symptoms worsen as anemia worsens.
When to see a doctor
Make an appointment with your doctor if you're feeling fatigued for unexplained reasons. Some anemias, such as iron deficiency anemia or vitamin B-12 deficiency, are common.
Fatigue has many causes besides anemia, so don't assume that if you're tired you must be anemic. Some people learn that their hemoglobin is low, which indicates anemia, when they go to donate blood. If you're told that you can't donate blood because of low hemoglobin, make an appointment with your doctor.
Anemia occurs when your blood doesn't have enough red blood cells. This can happen if:
- Your body doesn't make enough red blood cells
- Bleeding causes you to lose red blood cells more quickly than they can be replaced
- Your body destroys red blood cells
What red blood cells do
Your body makes three types of blood cells — white blood cells to fight infection, platelets to help your blood clot and red blood cells to carry oxygen throughout your body.
Red blood cells contain hemoglobin — an iron-rich protein that gives blood its red color. Hemoglobin enables red blood cells to carry oxygen from your lungs to all parts of your body and to carry carbon dioxide from other parts of the body to your lungs so that it can be exhaled.
Most blood cells, including red blood cells, are produced regularly in your bone marrow — a spongy material found within the cavities of many of your large bones. To produce hemoglobin and red blood cells, your body needs iron, vitamin B-12, folate and other nutrients from the foods you eat.
Causes of anemia
Different types of anemia and their causes include:
- Iron deficiency anemia. This is the most common type of anemia worldwide. Iron deficiency anemia is caused by a shortage of iron in your body. Your bone marrow needs iron to make hemoglobin. Without adequate iron, your body can't produce enough hemoglobin for red blood cells. Without iron supplementation, this type of anemia occurs in many pregnant women. It is also caused by blood loss, such as from heavy menstrual bleeding, an ulcer, cancer and regular use of some over-the-counter pain relievers, especially aspirin.
- Vitamin deficiency anemia. In addition to iron, your body needs folate and vitamin B-12 to produce enough healthy red blood cells. A diet lacking in these and other key nutrients can cause decreased red blood cell production. Additionally, some people may consume enough B-12, but their bodies aren't able to process the vitamin. This can lead to vitamin deficiency anemia, also known as pernicious anemia.
- Anemia of chronic disease. Certain diseases — such as cancer, HIV/AIDS, rheumatoid arthritis, kidney disease, Crohn's disease and other chronic inflammatory diseases — can interfere with the production of red blood cells.
- Aplastic anemia. This rare, life-threatening anemia occurs when your body doesn't produce enough red blood cells. Causes of aplastic anemia include infections, certain medicines, autoimmune diseases and exposure to toxic chemicals.
- Anemias associated with bone marrow disease. A variety of diseases, such as leukemia and myelofibrosis, can cause anemia by affecting blood production in your bone marrow. The effects of these types of cancer and cancer-like disorders vary from mild to life-threatening.
- Hemolytic anemias. This group of anemias develops when red blood cells are destroyed faster than bone marrow can replace them. Certain blood diseases increase red blood cell destruction. You can inherit a hemolytic anemia, or you can develop it later in life.
- Sickle cell anemia. This inherited and sometimes serious condition is an inherited hemolytic anemia. It's caused by a defective form of hemoglobin that forces red blood cells to assume an abnormal crescent (sickle) shape. These irregular blood cells die prematurely, resulting in a chronic shortage of red blood cells.
- Other anemias. There are several other forms of anemia, such as thalassemia and malarial anemia.
These factors place you at increased risk of anemia:
- A diet lacking in certain vitamins. Having a diet that is consistently low in iron, vitamin B-12 and folate increases your risk of anemia.
- Intestinal disorders. Having an intestinal disorder that affects the absorption of nutrients in your small intestine — such as Crohn's disease and celiac disease — puts you at risk of anemia.
- Menstruation. In general, women who haven't experienced menopause have a greater risk of iron deficiency anemia than do men and postmenopausal women. That's because menstruation causes the loss of red blood cells.
- Pregnancy. If you're pregnant and aren't taking a multivitamin with folic acid, you're at an increased risk of anemia.
- Chronic conditions. If you have cancer, kidney failure or another chronic condition, you may be at risk of anemia of chronic disease. These conditions can lead to a shortage of red blood cells. Slow, chronic blood loss from an ulcer or other source within your body can deplete your body's store of iron, leading to iron deficiency anemia.
- Family history. If your family has a history of an inherited anemia, such as sickle cell anemia, you also may be at increased risk of the condition.
- Other factors. A history of certain infections, blood diseases and autoimmune disorders, alcoholism, exposure to toxic chemicals, and the use of some medications can affect red blood cell production and lead to anemia.
- Age. People over age 65 are at increased risk of anemia.
Left untreated, anemia can cause many health problems, such as:
- Severe fatigue. When anemia is severe enough, you may be so tired that you can't complete everyday tasks.
- Pregnancy complications. Pregnant women with folate deficiency anemia may be more likely to experience complications, such as premature birth.
- Heart problems. Anemia can lead to a rapid or irregular heartbeat (arrhythmia). When you're anemic your heart must pump more blood to compensate for the lack of oxygen in the blood. This can lead to an enlarged heart or heart failure.
- Death. Some inherited anemias, such as sickle cell anemia, can be serious and lead to life-threatening complications. Losing a lot of blood quickly results in acute, severe anemia and can be fatal.
Eat a vitamin-rich diet
Many types of anemia can't be prevented. But iron deficiency anemia and vitamin deficiency anemias can be avoided by having a diet that includes a variety of vitamins and nutrients, including:
- Iron. Iron-rich foods include beef and other meats, beans, lentils, iron-fortified cereals, dark green leafy vegetables, and dried fruit.
- Folate. This nutrient, and its synthetic form folic acid, can be found in fruits and fruit juices, dark green leafy vegetables, green peas, kidney beans, peanuts, and enriched grain products, such as bread, cereal, pasta and rice.
- Vitamin B-12. Foods rich in vitamin B-12 include meat, dairy products, and fortified cereal and soy products.
- Vitamin C. Foods rich in vitamin C include citrus fruits and juices, peppers, broccoli, tomatoes, melons and strawberries. These items help increase iron absorption.
Consider a multivitamin
If you're concerned about getting enough vitamins from the food you eat, ask your doctor whether a multivitamin may be right for you.
Consider genetic counseling
If you have a family history of an inherited anemia, such as sickle cell anemia or thalassemia, talk to your doctor and possibly a genetic counselor about your risk and what risks you may pass on to your children.
Anemia can be a complication of malaria. If you plan on traveling to a place where malaria is common, talk with your doctor beforehand about taking preventive drugs. In areas where malaria is common, prevention involves reducing exposure to mosquitoes, for example, by using bed nets treated with insecticide.
To diagnose anemia, your doctor may ask you about your medical and family history, perform a physical exam, and run the following tests:
- Complete blood count (CBC). A CBC is used to count the number of blood cells in a sample of your blood. For anemia your doctor will be interested in the levels of the red blood cells contained in the blood (hematocrit) and the hemoglobin in your blood. Normal adult hematocrit values vary from one medical practice to another but are generally between 40 and 52 percent for men and 35 and 47 percent for women. Normal adult hemoglobin values are generally 14 to 18 grams per deciliter for men and 12 to 16 grams per deciliter for women.
- A test to determine the size and shape of your red blood cells. Some of your red blood cells may also be examined for unusual size, shape and color.
Additional diagnostic tests
If you receive a diagnosis of anemia, your doctor may order additional tests to determine the underlying cause. For example, iron deficiency anemia can result from chronic bleeding of ulcers, benign polyps in the colon, colon cancer, tumors or kidney problems.
Occasionally, it may be necessary to study a sample of your bone marrow to diagnose anemia.
Anemia treatment depends on the cause.
- Iron deficiency anemia. Treatment for this form of anemia usually involves taking iron supplements and making changes to your diet. If the underlying cause of iron deficiency is loss of blood — other than from menstruation — the source of the bleeding must be located and stopped. This may involve surgery.
- Vitamin deficiency anemias. Treatment for folic acid and B-12 deficiency involves dietary supplements and increasing these nutrients in your diet. If your digestive system has trouble absorbing vitamin B-12 from the food you eat, you may need vitamin B-12 shots. At first, you may receive the shots every other day. Eventually, you'll need shots just once a month, which may continue for life, depending on your situation.
- Anemia of chronic disease. There's no specific treatment for this type of anemia. Doctors focus on treating the underlying disease. If symptoms become severe, a blood transfusion or injections of synthetic erythropoietin, a hormone normally produced by your kidneys, may help stimulate red blood cell production and ease fatigue.
- Aplastic anemia. Treatment for this anemia may include blood transfusions to boost levels of red blood cells. You may need a bone marrow transplant if your bone marrow is diseased and can't make healthy blood cells.
- Anemias associated with bone marrow disease. Treatment of these various diseases can include medication, chemotherapy or bone marrow transplantation.
- Hemolytic anemias. Managing hemolytic anemias includes avoiding suspect medications, treating related infections and taking drugs that suppress your immune system, which may be attacking your red blood cells. Depending on the severity of your anemia, a blood transfusion or plasmapheresis may be necessary. Plasmapheresis is a type of blood-filtering procedure. In certain cases, removal of the spleen can be helpful.
- Sickle cell anemia. Treatment for this anemia may include the administration of oxygen, pain-relieving drugs, and oral and intravenous fluids to reduce pain and prevent complications. Doctors also may recommend blood transfusions, folic acid supplements and antibiotics. A bone marrow transplant may be an effective treatment in some circumstances. A cancer drug called hydroxyurea (Droxia, Hydrea) also is used to treat sickle cell anemia.
- Thalassemia. This anemia may be treated with blood transfusions, folic acid supplements, medication, removal of the spleen (splenectomy), or a blood and bone marrow stem cell transplant.
Preparing for your appointment
Make an appointment with your primary care doctor if you have prolonged fatigue or other signs or symptoms that worry you. He or she may refer you to a doctor who specializes in treating blood disorders (hematologist), the heart (cardiologist) or the digestive system (gastroenterologist).
Here's some information to help you get ready for your appointment.
What you can do
Before your appointment make a list of:
- Symptoms you've been having and for how long
- Key personal information, including any major stresses, implanted medical devices, exposure to toxins or chemicals, and recent life changes
- All medications, vitamins and supplements you take, including the doses
- Questions to ask your doctor
For anemia, some basic questions to ask your doctor include:
- What's the most likely cause of my symptoms?
- Are there other possible causes?
- Do I need any tests?
- Is my anemia likely temporary or long lasting?
- What treatments are available, and which do you recommend?
- What side effects can I expect from treatment?
- I have these other health conditions. How can I best manage them together?
- Do I need to follow any dietary restrictions?
- Do I need to add any foods to my diet? How often do I need to eat these foods?
- Do you have any brochures or other printed materials I can take with me? What websites do you recommend?
What to expect from your doctor
Your doctor is likely to ask you a number of questions, such as:
- When did you begin having these symptoms?
- Do your symptoms come and go or are they constant?
- How severe are your symptoms?
- Does anything seem to improve your symptoms?
- What, if anything, appears to worsen your symptoms?
- Are you a vegetarian?
- How many servings of fruits and vegetables do you usually eat in a day?
- Do you drink alcohol? If so, how often, and how many drinks do you usually have?
- Are you a smoker?
- Have you recently donated blood more than once?
Asthma Attack Immediate Treatment
An asthma attack can be a terrifying experience. It can feel as if someone is sitting on your chest or there’s a cloud in your lungs. You struggle to draw in a full breath. Your chest tightens. Your breathing quickens. It feels, as one asthma sufferer put it, “like you’re drowning in air.”
Asthma (also called bronchial asthma) is an inflammation and obstruction of the bronchial tubes — the passages that allow air to enter and leave the lungs. During an asthma attack, the muscles that surround the bronchial tubes constrict, narrowing the air passages and making it extremely difficult to breathe. Other common symptoms are wheezing and a rattling sound in the chest.
The duration of an attack can vary, depending on what caused it and how long the airways have been inflamed. Mild episodes may last only a few minutes; more severe ones can last from hours to days. Mild attacks can resolve spontaneously or may require medication, typically a quick-acting inhaler. More severe asthma attacks can be shortened with appropriate treatment.
An asthma attack can be triggered by exposure to an allergen, such as tree, grass or weed pollen, dust mites, cockroaches or animal dander. Other common triggers are irritants in the air, such as smoke or chemical fumes, and strong odors, such as perfume.
Certain illnesses — particularly the flu, sinusitis or an upper respiratory infection — may also trigger an asthma attack, as can strenuous exercise, extreme weather conditions and strong emotions that change normal breathing patterns.
Warning signs of a potential asthma attack can include an increase in your need for rescue medication (especially albuterol), a worsening cough, shortness of breath (particularly if it wakes you up at night) and diminished tolerance for exercise.
All of these factors — bronchospasm, inflammation, and mucus production — cause symptoms of an asthma attack such as difficulty breathing, wheezing, coughing, shortness of breath, and difficulty performing normal daily activities. Other symptoms of an asthma attack may include:
- Severe wheezing when breathing both in and out
- Coughing that won’t stop
- Very rapid breathing
- Chest tightness or pressure
- Tightened neck and chest muscles, called retractions
- Difficulty talking
- Feelings of anxiety or panic
- Pale, sweaty face
- Blue lips or fingernails
- Or worsening symptoms despite use of your medications
Prime Med of Ozark provides immediate treatment during the Asthma attack. However, if the attack occurs outside the clinic working schedule, or you think that all the above symptoms are very severe then call 911.
If you are experiencing some of the above symptoms then it’s better to see the doctor for the diagnosis of the asthma.
Dealing with an acute attack. In general, it is important to stay calm and use the medications your allergist has prescribed.
Quick-relief medications — often administered via an inhaler — are used to treat asthma attacks as needed. They include short-acting, rapid-onset beta2-agonist and/or anticholinergic bronchodilators (which relax airway muscles) and systemic corticosteroids (which reduce airway inflammation). If symptoms persist, see your allergist.
Panic can prevent a person with asthma from relaxing and following instructions, which is essential during an attack. Scientists have found that rapid breathing associated with strong emotions, like panic, can cause bronchial tubes to constrict.
Seek immediate medical treatment if coughing or shortness of breath persists or seems to be worsening.
Triggers in Children
Asthma affects as many as 10% to 12% of children in the United States and is the leading cause of chronic illness in children. Some triggers particularly affect children with asthma and can make the inflammation in their lungs even worse. The common cold is one of the most frequent triggers for asthma attacks in very young children. Others include:
- Exposure to allergens (such as animal dander, dust mites or pollen)
- Strong smells (perfumes or other odors)
- Changes in weather; cold air
- Running or playing hard
- Crying or laughing
If your child has asthma, your family care doctor will help you discover the triggers that bring on or worsen the symptoms. The first step to controlling symptoms is to stay away from whatever makes your child cough or wheeze.
Know About Unusual Asthma Symptoms
Not everyone with asthma has the usual symptoms of cough, wheezing, and shortness of breath. Sometimes individuals have unusual asthma symptoms that may not appear to be related to asthma. Some “unusual” asthma symptoms may include the following:
- rapid breathing
- inability to exercise properly (called exercise-induced asthma)
- difficulty sleeping or nighttime asthma
- difficulty concentrating
- chronic cough without wheezing
Also, asthma symptoms can be mimicked by other conditions such as bronchitis, vocal cord dysfunction, and even heart failure. It is better that you consult a doctor to understand your body completely.
Our doctor will help you create a plan that’s right for him. Most use a simple system that’s set up like a traffic light: green for “go,” yellow for “caution,” and red for “stop — danger!” See how you fit into each color zone, and you’ll know how to respond.
The Green Zone
This is where you want to be. You’ll know you’re in the green zone when you:
- are breathing easy
- aren’t coughing or wheezing
- can do your regular activities
- sleep through the night without coughing
If you can say “yes” to those four items, you’re doing well. No need to hold back from your usual routine. Enjoy your activities.
Even when you’re doing well, keep up your regular medication. Your doctor may call it “controller” medicine because it keeps your asthma in check over the long haul. Make sure you follow the instructions for the dose and when to take it.
The Yellow Zone
Think of this category as a big yellow “caution” sign. You’ll know you belongs here when you:
- Feel short of breath
- Have some trouble doing your usual activities
- Have a tight feeling in your chest, or congestion
- Wake up at night with breathing problems
If you have some or all of those, make sure you are taking your regular treatment plus any additional medications that doctor recommends. The doctor might prescribe some that give quick relief when you have symptoms, called “rescue” medicines.
The Red Zone
This zone means DANGER. Call your doctor right away if you are in this zone. You may take your rescue medications immediately to mitigate the symptoms. If you think the symptoms are severe and persistent, then don’t hesitate to call 911.
Here’s what to watch for:
- You’re breathing hard and fast.
- Your nostrils are open wide.
- You have trouble walking.
- You’re not talking well.
- Your ribs retract with each breath.
Autistic Treatment Center
Our Unparalleled Approach
The Autistic Treatment Center at Prime Med of Ozark provides comprehensive assessment, diagnostic and treatment services for people with autism spectrum disorders. Our mission is to improve the quality of life for individuals with Autism Spectrum Disorders and their families. We continually strive to be the premier resource for specialized autism services in Alabama and its surrounding counties by providing programs that meet the specific needs of each individual affected by autism. Our Autistic Treatment Center provides comprehensive services in one centralized location to make it as convenient as possible for children to receive the evaluation and treatment needed to help them reach their potential.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder that affects many children. It continues to be an important public health concern. There is strong evidence that genetic factors play a critical role. It affects a child’s social skills such as difficulty making friends or knowing when to use gestures or make eye contact when talking to someone.
In 2013, Autistic Disorder, Asperger’s Disorder and Pervasive Developmental Disorder, NOS (not otherwise specified) were rolled into one umbrella category: Autism Spectrum Disorder (ASD).
ASD is characterized by developmental delays, communication problems, abnormal social skills, learning disabilities and behavioral problems—all ranging from mild to severe. While some symptoms are apparent during infancy, most children exhibit ASD symptoms between the ages of 1 and 2.
The frequency of being diagnosed with an ASD has increased over the past few decades. Recent statistics from the Centers for Disease Control estimate that ASD affects 1 in 68 children. Currently, 1 in 42 boys and 1 in 189 girls are diagnosed with it, making boys almost 5 times more likely than girls to have this disorder.
It is now known that ASD is not caused by just one thing. Rather, this broad condition can have many different causes. Similarly, there is not just one brain problem found in ASD, but actually 8-10 factors that can influence abnormal brain function.
Originally thought to be genetic in nature but despite much research in this area which has identified many chromosomal differences associated with the condition, an autism genetic test has remained elusive, as these genetic variations are also seen in normal people.
Recent research is pointing towards the environment as being more involved with the development of autism than genetics. Autism could be described as developing following an environmental insult(s) in genetically susceptible individuals.
The studies of people suffering from ASD reveal that their brain patterns tend to have high activity or low activity (and both in some cases).
Activity Patterns in ASD
High Activity Patterns
Increased activity in the anterior cingulate gyrus (the “gear shifter”) and lateral (side) prefrontal cortex, relating to symptoms such as:
- Repetitious speech and behavior
- Getting stuck on thoughts
- Problems with transitions and change
A “Ring of Fire” pattern—an overall increase of activity throughout the brain—which may be associated with inflammation and be related to:
- Mood instability
- Emotional “meltdowns”
Low Activity Patterns
A smaller, less active cerebellum, contributing to:
- Impeded or poor motor skills
- Problems with learning and thought coordination
Decreased activity in the back portion of the brain, especially in the parietal and temporal lobes, contributing to:
- Communication difficulties
- Learning problems
- Sensory processing issues
- Problems with abstract thinking
Overall decreased activity and “scalloping” (a bumpy looking surface), which is associated with environmental toxicity. Sometimes, a head injury pattern is revealed.
What Makes Autistic Treatment Center at Prime Med of Ozark Unique?
The program at Autistic Treatment Center at Prime Med Clinic located in Ozark, Alabama is different than – even opposite to – almost everything you’ve been told to do to help your child. Most schools and therapists, too, are operating on a deep misconception about what autism is and what works to treat it.
Traditional methods see autism as a disorder that is primarily behavioral (some even have the word “behavior” in their name). They seek to eliminate or extinguish unwanted behaviors and promote wanted behaviors through repetition, training, and rewards.
In the shadow of our extensive practices, research and treatment, we understand that autism is, at its core, a social relational disorder. Fundamentally, our children, regardless of whether they are not yet verbal or have Asperger’s Syndrome, have difficulty connecting to, relating to, and communicating with others. Sure, our children may have behaviors that look different, but these are symptoms, not causes, and trying to stamp them out is not the answer.
This means that, rather than trying for force our children to conform to a world that they don’t yet understand, we join them in their world first.
We have seen that children on the autism spectrum can:
- Learn to speak, even if they’ve never spoken.
- Experience real happiness, satisfaction, and love, even if they seem frustrated or combative right now.
- Have deep, meaningful, caring relationships with others, even though they may have appeared disconnected for years.
- Have fun, reciprocal conversations, even if they have a history of rigid communication.
- Make close friends, even if they don’t start with the interest or the tools to do so.
- Live a life that may include college, dates, sports, jobs, hobbies, travel, girlfriends/boyfriends – regardless of how many of these life experiences their parents have been told were simply not possible.
Chronic obstructive pulmonary disease, or COPD, is a group progressive disease where inflammation in the lungs damages lung tissue and traps air in the lungs. As the disease worsens, it takes longer and longer to exhale. The lungs become overinflated and shortness of breath develops. Inflammation is most often due to cigarette smoking. Once started, the inflammation is difficult to stop. The most common are emphysema and chronic bronchitis. Many people with COPD have both of these conditions.
Chronic bronchitis is inflammation of the lining of the bronchial tubes, which carry air to and from the air sacs (alveoli) of the lungs. It’s characterized by daily cough and mucus (sputum) production. Bronchitis causes inflammation and narrowing of the bronchial tubes, which allows mucus to build up.
Emphysema is a condition in which the alveoli at the end of the smallest air passages (bronchioles) of the lungs are destroyed as a result of damaging exposure to cigarette smoke and other irritating gases and particulate matter. Emphysema slowly destroys air sacs in your lungs, which interferes with outward air flow.
COPD versus Asthma
COPD (chronic obstructive pulmonary disease) is a lung disease caused by chronic interference with lung airflow that impairs breathing, and is not fully reversible.
Asthma is a respiratory condition marked by spasms of the bronchi, due to inflamed and narrowed airways in the lungs. Asthma causes difficulty in breathing that often results from an allergic reaction.
Symptoms and Signs — 6 similarities between COPD and Asthma
Similarities in signs and symptoms are between the two conditions are:
- Shortness of breath
- Chest tightness
- Exercise intolerance
- Wheezing (a whistling or squeaking sound in the chest)
- Anxiety with increased heart rate may occur in both diseases.
Symptoms and Signs — 6 Differences between COPD and Asthma
- In asthma, breathing can return to normal between attacks, while breathing with COPD usually does not return to normal.
- The symptoms of COPD gradually become more severe. (This also may occur if you have asthma.)
- COPD produces more mucus and phlegm compared to asthma.
- Chronic cough is common with COPD.
- People with COPD often have chronic blueness to fingernail beds and/or lips (cyanosis).
- Asthma can occur in a person of almost any age, while COPD usually occurs in those over age 40. (Although it is possible in some individuals to develop COPD a younger age.)
Causes of COPD
- Long-term exposure to lung irritants that damage the lungs and the airways usually is the cause of COPD.
- In the United States, the most common irritant that causes COPD is cigarette smoke. Pipe, cigar, and other types of tobacco smoke also can cause COPD, especially if the smoke is inhaled.
- Breathing in secondhand smoke, which is in the air from other people smoking; air pollution; or chemical fumes or dusts from the environment or workplace also can contribute to COPD.
- Rarely, a genetic condition called alpha-1 antitrypsin deficiency may play a role in causing COPD. People who have this condition have low blood levels of alpha-1 antitrypsin (AAT)—a protein made in the liver. Having a low level of the AAT protein can lead to lung damage and COPD if you are exposed to smoke or other lung irritants. If you have alpha-1 antitrypsin deficiency and also smoke, COPD can worsen very quickly.
- Some people who have asthma can develop COPD. Asthma is a chronic lung disease that inflames and narrows the airways. Treatment usually can reverse the inflammation and narrowing that occurs in asthma.
Symptoms of COPD
Symptoms of chronic obstructive pulmonary disease include:
- chest discomfort
- shortness of breath (dyspnea)
Progressive or more serious symptoms may include:
- respiratory distress
- tachypnea (excessively rapid breathing)
- cyanosis (chronic blueness to fingernail beds and/or lips)
- use of accessory respiratory muscles
- peripheral edema (accumulation of fluid causing swelling in tissues perfused by the peripheral vascular system, usually in the lower limbs)
- chronic wheezing
- abnormal lung sounds
- prolonged expiration
- elevated jugular venous pulse
Comorbidities are diseases and conditions that you have in addition to the main disease. Comorbidities for asthma and COPD are also often similar. They include:
- high blood pressure
- impaired mobility
- stomach ulcers
Stages of COPD
One measure of COPD disease is by stage. The stages are:
Stage 0 – At Risk
Symptoms include coughing and noticeable mucus. You don’t actually have COPD, so treatment isn’t necessarily needed. But do heed the warning. If you smoke, stop now. It would be wise to reassess your diet and exercise routines to improve overall health. Once you have COPD, it’s not reversible or curable.
Stage 1 – Mild
At this stage, some people still don’t notice symptoms, which may include chronic cough and increased mucus production. If you visit a doctor at this point, chances are you’ll start using a bronchodilator as needed.
Stage 2 – Moderate
Symptoms are becoming more noticeable. In addition to the cough and mucus, you may start to experience shortness of breath. You may need a long-acting bronchodilator.
Stage 3 – Severe
Symptoms become more frequent and you may have occasional flare-ups of severe symptoms. You might find that it’s difficult to function normally. Your doctor may recommend corticosteroids, other medications, or oxygen therapy.
Stage 4 – Very Severe
Symptoms are progressing and it’s harder to complete everyday tasks. Flare-ups can be life-threatening. You may be a candidate for surgical treatment.
Diagnosis of COPD
The staging as mentioned above is based on the results of a pulmonary function test. Pulmonary function tests measure how much air you can breathe in and out, how fast you can breathe air out, and how well your lungs deliver oxygen to your blood. The main test for COPD is spirometry. Other lung function tests, such as a lung diffusion capacity test, also might be used.
Specifically, the forced expiratory volume (how much air one can exhale forcibly) in one second (FEV1) of a standard predicted value is measured, based on the individual patient’s physical parameters. The staging of chronic obstructive pulmonary disease by this method is as follows:
- Stage I is FEV1 of equal or more than 80% of the predicted value
- Stage II is FEV1 of 50% to 79% of the predicted value
- Stage III is FEV1 of 30% to 49% of the predicted value
- Stage IV is FEV1 of less than 30% of predicted value or an FEV1 less than 50% of predicted value plus respiratory failure
The clinician will take a history of the patient emphasising on:
- Symptoms suggesting COPD and how these affect your life
- Hospitalizations, particularly ones for breathing problems
- Smoking and home/work exposure history
- Family history of lung disease
- Other medical conditions, particularly asthma, sinus disease, sleep apnea, lung infections, cancer, heart disease, anxiety/depression, osteoporosis (thin bones) and muscle disease
You should have a physical examination focused on the heart and lungs. The examination is often normal unless COPD is severe.
You should have spirometry (breathing tests) performed to measure lung function. COPD can’t be diagnosed without them.
Other tests that may help in diagnose or treat COPD include:
- A chest X-ray
- Oxygen level, measured by pulse oximetry (finger or ear probe) or by a blood sample
- A blood test for Alpha-1, an inherited form of COPD
- Additional breathing tests
- Exercise testing. The most common test measures how far you can walk in 6 minutes.
Treatment for COPD
Certain lifestyle changes may also help alleviate your symptoms or provide relief. These include:
- If you smoke, quit. Your doctor can recommend appropriate products or support services.
- Whenever possible, avoid secondhand smoke and chemical fumes.
- Get the nutrition your body needs. Work with your doctor or dietician to create a healthy eating plan.
- Talk to your doctor about how much exercise is safe for you.
If your blood oxygen levels are low, you can receive oxygen through a mask or nasal prongs to help you breathe better. A portable unit can make it easier to get around.
Oral Medications to Quit Smoking (Smoking Cessation)
Varenicline (Chantix) is an oral medication that is prescribed to promote cessation of smoking. This is also an alternative to try to quit smoking.
Bupropion (Zyban) is an antidepressant that helps reduce symptoms of nicotine withdrawal.
Some medications are used “off label” (that is, they are normally prescribed for another condition) to help people quit smoking. These drugs are recommended by the Agency for Healthcare Research and Quality to help smokers kick the habit, but have not been approved by the FDA for this use. These medications include nortriptyline (Pamelor), an older type of antidepressant. It’s been found to help smokers double their chances of quitting compared to taking no medicine. Another drug used off label is clonidine (Catapres). Normally used to treat high blood pressure it can help smokers quit.
Medications for COPD
Bronchodilators are used for COPD treatment because they open up the airway tubes and allow air to more freely pass in and out of the lung tissue. There are both short-term (several hours) and long-term (12 or more hours) types of bronchodilators.
Examples of short-term bronchodilators
- albuterol (Ventolin, Proventil)
- metaproterenol (Alupent)
- levalbuterol (Xopenex)
- pirbuterol (Maxair)
Examples of long-term bronchodilators
- salmeterol (Serevent)
- formoterol (Foradil)
- arformoterol (Brovana)
- indacaterol (Arcapta)
- ipratropium (Atrovent)
- tiotropium (Spiriva)
- aclidinium (Tudorza)
Other bronchodilators such as theophylline (Elixophyllin, Theo-24) are occasionally used, but are not favored because of unwanted side effects including anxiety, tremors, seizures, and arrhythmias.
Also on the market are combined to drugs using steroids and long-acting bronchodilators. Roflumilast (Daxas, Daliresp) is a new drug that inhibits the enzyme phosphodiesterase type 4, has been utilized in patients with symptoms of chronic bronchitis.
Sometimes bronchodilators are combined with inhaled glucocorticosteroids. Using the two together can reduce inflammation in the airways and lower mucus production. Corticosteroids are also available in pill form.
This newer medication in pill form reduces inflammation and changes mucus production. It’s generally prescribed for severe COPD.
This medicine eases chest tightness and shortness of breath. It may help prevent flare-ups. It’s available in pill form.
Antibiotics and antivirals
Antibiotics or antivirals may be prescribed when you develop respiratory infections.
Surgery may not be available or desirable for many people with COPD.
- Bullectomy surgery is the removal of giant bullae. Air-filled spaces usually located in the lung periphery that occupy lung space most often in people with emphysema are termed bullae. Giant bullae may occupy over 33% of the lung tissue, compress adjacent lung tissue, and reduce blood flow and ventilation to healthy tissue. Surgical removal can allow compressed lung tissue that is still functional to expand.
- Lung volume reduction surgery is removal of lung tissue that has been most damaged by tobacco smoking, usually the 20% to 30% of lung tissue located in the upper part of each lung. This procedure is not done often; it is usually done on people who have severe emphysema and marked hyperinflation of the airways and air spaces.
- Lung transplantation is surgical therapy for people with advanced lung disease. People with COPD are the largest single category of people who undergo lung transplantation. In general, these people with COPD usually are at COPD stage three or four with severe symptoms and generally, without transplantation, have a life expectancy of about two years or less.
Home Remedies for COPD include:
- Vitamin E to improve lung function
- Omega-3 fatty acids to decrease inflammation (found in supplements or foods such as salmon, herring, mackerel, sardines, soybeans, canola oil)
- Antioxidants to reduce inflammation (found in kale, tomatoes, broccoli, green tea, red grapes)
- Breathing techniques relaxation therapy, meditation
- Acupuncture COPD symptom reduction by needle placement
Other supplementary therapies such as treatment with antibiotics to reduce pathogen (viral, fungal, bacterial) damage to lung tissue, mucolytic agents to help unblock mucus-clogged airways, or oxygenation therapies to increase the available oxygen to lung tissues may also reduce the symptoms of COPD.
In some people, oxygen therapy will increase his/her life expectancy, and improve the quality of life. This is especially true with people with COPD who have chronically low oxygen levels in the blood. It may also help exercise endurance. Oxygen delivery systems are now easily portable and have reduced in cost in comparison to earlier designs.
Yoga may be another form of beneficial exercise that helps with breathing efficiency and breathing muscle control.
Diabetes Mellitus commonly known as Diabetes is a disease that occurs when your blood glucose, also called blood sugar, is too high. Blood glucose is your main source of energy and comes from the food you eat. Insulin, a hormone made by the pancreas, helps glucose from food get into your cells to be used for energy. Sometimes your body doesn’t make enough—or any—insulin or doesn’t use insulin well. Glucose then stays in your blood and doesn’t reach your cells.
Over time, having too much glucose in your blood can cause health problems. Although diabetes has no cure, you can take steps to manage your diabetes and stay healthy.
Sometimes people call diabetes “a touch of sugar” or “borderline diabetes.” These terms suggest that someone doesn’t really have diabetes or has a less serious case, but every case of diabetes is serious.
What are the different types of diabetes?
The most common types of diabetes are type 1 (previously known as insulin-dependent, juvenile or childhood-onset) , type 2 (formerly called non-insulin-dependent, or adult-onset), and gestational diabetes.
Type 1 Diabetes
If you have type 1 diabetes, your body does not make insulin. Your immune system attacks and destroys the cells in your pancreas that make insulin. Type 1 diabetes is usually diagnosed in children and young adults, although it can appear at any age. People with type 1 diabetes need to take insulin every day to stay alive. Type 1 diabetes is an autoimmune condition. It’s caused by the body attacking its own pancreas with antibodies. In people with type 1 diabetes, the damaged pancreas doesn’t make insulin. This type of diabetes may be caused by a genetic predisposition. It could also be the result of faulty beta cells in the pancreas that normally produce insulin.
Exposure to certain viral infections (mumps and Coxsackie viruses) or other environmental toxins may serve to trigger abnormal antibody responses that cause damage to the pancreas cells where insulin is made. Some of the antibodies seen in type 1 diabetes include anti-islet cell antibodies, anti-insulin antibodies and anti-glutamic decarboxylase antibodies. These antibodies can be detected in the majority of patients, and may help determine which individuals are at risk for developing type 1 diabetes.
Type 2 Diabetes
If you have type 2 diabetes, your body does not make or use insulin well. You can develop type 2 diabetes at any age, even during childhood. However, this type of diabetes occurs most often in middle-aged and older people. Type 2 is the most common type of diabetes. Type 2 diabetes comprises the majority of people with diabetes around the world, and is largely the result of excess body weight and physical inactivity.
In addition to the problems with an increase in insulin resistance, the release of insulin by the pancreas may also be defective and suboptimal. In fact, there is a known steady decline in beta cell production of insulin in type 2 diabetes that contributes to worsening glucose control. (This is a major factor for many patients with type 2 diabetes who ultimately require insulin therapy.) Finally, the liver in these patients continues to produce glucose through a process called gluconeogenesis despite elevated glucose levels. The control of gluconeogenesis becomes compromised.
Gestational diabetes is hyperglycaemia with blood glucose values above normal but below those diagnostic of diabetes, occurring during pregnancy. However, if you’ve had gestational diabetes, you have a greater chance of developing type 2 diabetes later in life. Sometimes diabetes diagnosed during pregnancy is actually type 2 diabetes. Women with gestational diabetes are at an increased risk of complications during pregnancy and at delivery. They and their children are also at increased risk of type 2 diabetes in the future. Gestational diabetes is diagnosed through prenatal screening, rather than through reported symptoms.
Other Types of Diabetes
Less common types include monogenic diabetes (Neonatal Diabetes Mellitus & MODY), which is an inherited form of diabetes that result from mutations or changes in a single gene. Neonatal diabetes mellitus (NDM) and maturity-onset diabetes of the young (MODY) are the two main forms of monogenic diabetes. NDM occurs in newborns and young infants. MODY is much more common than NDM and usually first occurs in adolescence or early adulthood. Another rare and less common form is cystic fibrosis-related diabetes; which is a unique type of diabetes that is common in people with cystic fibrosis CF.
Impaired Glucose Tolerance and Impaired Fasting Glycaemia
Impaired glucose tolerance (IGT) and impaired fasting glycaemia (IFG) are intermediate conditions in the transition between normality and diabetes. People with IGT or IFG are at high risk of progressing to type 2 diabetes, although this is not inevitable.
Prevalence of Diabetes
Globally, an estimated 422 million adults were living with diabetes in 2014, compared to 108 million in 1980. The global prevalence (age-standardized) of diabetes has nearly doubled since 1980, rising from 4.7% to 8.5% in the adult population. There are 30.3 million people with diabetes (9.4% of the US population) including 23.1 million people who are diagnosed and 7.2 million people (23.8%) undiagnosed. The numbers for prediabetes indicate that 84.1 million adults (33.9% of the adult U.S. population) have prediabetes, including 23.1 million adults aged 65 years or older (the age group with highest rate). The estimated percentage of individuals with type 1 diabetes remains at 5% among those with diabetes. Diabetes caused 1.5 million deaths in 2012. Higher-than-optimal blood glucose caused an additional 2.2 million deaths, by increasing the risks of cardiovascular and other diseases. Forty-three percent of these 3.7 million deaths occur before the age of 70 years.
Early Signs and Symptoms of Diabetes
The early symptoms of untreated diabetes are related to elevated blood sugar levels, and loss of glucose in the urine. High amounts of glucose in the urine can cause increased urine output (frequent urination) and lead to dehydration.
The dehydration also causes increased thirst and water consumption.
A relative or absolute insulin deficiency eventually leads to weight loss.
The weight loss of diabetes occurs despite an increase in appetite.
Some untreated diabetes patients also complain of fatigue.
Nausea and vomiting can also occur in patients with untreated diabetes.
Frequent infections (such as infections of the bladder, skin, and vaginal areas) are more likely to occur in people with untreated or poorly-controlled diabetes.
Fluctuations in blood glucose levels can lead to blurred vision.
Extremely elevated glucose levels can lead to lethargy and coma.
Symptoms of Type 1 Diabetes
- excessive excretion of urine (polyuria)
- thirst (polydipsia)
- constant hunger
- weight loss
- vision changes
Symptoms of Type 2 Diabetes
Symptoms may be similar to those of type 1 diabetes, but are often less marked. As a result, the disease may be diagnosed several years after onset, once complications have already arisen.
Treatment for Diabetes
Simple lifestyle measures have been shown to be effective in preventing or delaying the onset of type 2 diabetes. To help prevent type 2 diabetes and its complications, people should:
- achieve and maintain healthy body weight;
- be physically active – at least 30 minutes of regular, moderate-intensity activity on most days. More activity is required for weight control;
- eat a healthy diet, avoiding sugar and saturated fats intake; and
- avoid tobacco use – smoking increases the risk of diabetes and cardiovascular diseases.
Diagnosis and Treatment
Early diagnosis can be accomplished through relatively inexpensive testing of blood sugar.
Treatment of diabetes involves diet and physical activity along with lowering blood glucose and the levels of other known risk factors that damage blood vessels. Tobacco use cessation is also important to avoid complications.
Interventions that are both cost-saving and feasible in developing countries include:
- blood glucose control, particularly in type 1 diabetes. People with type 1 diabetes require insulin, people with type 2 diabetes can be treated with oral medication, but may also require insulin
- blood pressure control
- foot care
- in overweight patients with type 2 diabetes mellitus, early use of metformin reduced the risk for diabetes-related end points and all-cause mortality
Other cost saving interventions include:
- screening and treatment for retinopathy (which causes blindness)
- blood lipid control (to regulate cholesterol levels)
- screening for early signs of diabetes-related kidney disease and treatment.
- a periodic test called the A1C blood test estimates glucose levels in your blood over the previous three months. It’s used to help identify overall glucose level control and the risk of complications from diabetes, including organ damage.
Medications for Nerve Pain due to Diabetes:
The pain of diabetic nerve damage may respond to traditional treatments with certain medications such as gabapentin (Neurontin), phenytoin (Dilantin), and carbamazepine (Tegretol) that are traditionally used in the treatment of seizure disorders. Amitriptyline (Elavil, Endep) and desipramine (Norpraminine) are medications that are traditionally used for depression. The pain of diabetic nerve damage may also improve with better blood sugar control, though unfortunately blood glucose control and the course of neuropathy do not always go hand in hand. Newer medications for nerve pain include Pregabalin (Lyrica) and duloxetine (Cymbalta).
Risk factors for type 1 diabetes are not as well understood as those for type 2 diabetes. Family history is a known risk factor for type 1 diabetes. Other risk factors can include having certain infections or diseases of the pancreas.
Risk factors for type 2 diabetes and prediabetes are many. The following can raise your risk of developing type 2 diabetes:
- Being obese or overweight
- High blood pressure
- Elevated levels of triglycerides and low levels of “good” cholesterol (HDL)
- Sedentary lifestyle
- Family history
- Increasing age
- Polycystic ovary syndrome
- Impaired glucose tolerance
- Insulin resistance
- Gestational diabetes during a pregnancy
- Ethnic background: Hispanic/Latino Americans, African-Americans, Native Americans, Asian-Americans, Pacific Islanders, and Alaska natives are at greater risk.
When diabetes is not well managed, complications develop that threaten health and endanger life. Acute complications are a significant contributor to mortality, costs and poor quality of life. Abnormally high blood glucose can have a life-threatening impact if it triggers conditions such as diabetic ketoacidosis (DKA) in types 1 and 2, and hyperosmolar coma in type 2. Abnormally low blood glucose can occur in all types of diabetes and may result in seizures or loss of consciousness. It may happen after skipping a meal or exercising more than usual, or if the dosage of anti-diabetic medication is too high.
Over time, high blood glucose leads to complications such as:
- heart disease
- kidney disease (diabetic nephropathy)
- eye problems (Cataracts and Glaucoma )
- vision loss
- dental disease
- nerve damage (diabetic neuropathy, erectile dysfunction)
- foot problems
- leg amputation
- in pregnancy, poorly controlled diabetes increases the risk of fetal death and other complications.
Diabetes and its complications bring about substantial economic loss to people with diabetes and their families, and to health systems and national economies through direct medical costs and loss of work and wages. While the major cost drivers are hospital and outpatient care, a contributing factor is the rise in cost for analogue insulins which are increasingly prescribed despite little evidence that they provide significant advantages over cheaper human insulins.
The starting point for living well with diabetes is an early diagnosis – the longer a person lives with undiagnosed and untreated diabetes, the worse their health outcomes are likely to be. Easy access to basic diagnostics, such as blood glucose testing, should therefore be available in primary health-care settings. Established systems for referral and back-referral are needed, as patients will need periodic specialist assessment or treatment for complications. For those who are diagnosed with diabetes, a series of cost-effective interventions can improve their outcomes, regardless of what type of diabetes they may have. These interventions include blood glucose control, through a combination of diet, physical activity and, if necessary, medication; control of blood pressure and lipids to reduce cardiovascular risk and other complications; and regular screening for damage to the eyes, kidneys and feet, to facilitate early treatment. Diabetes management can be strengthened through the use of standards and protocols.
Efforts to improve capacity for diagnosis and treatment of diabetes should occur in the context of integrated noncommunicable disease (NCD) management to yield better outcomes. At a minimum, diabetes and cardiovascular disease management can be combined. Integrated management of diabetes and tuberculosis and/or HIV/AIDS can be considered where there is high prevalence of these diseases.
Get free Metformin from Tristate Community Pharmacy in Dothan, AL.
Prime Med of Ozark specializes in treating patients suffering from eating disorders.
When you become so preoccupied with food and weight issues that you find it harder and harder to focus on other aspects of your life, it may be an early sign of an eating disorder. There is a commonly held view that eating disorders are a lifestyle choice. Studies suggest that 1 in 20 people will be affected at some point in their lives. Ultimately without treatment, eating disorders can take over a person’s life and lead to serious, potentially fatal medical complications. Eating Disorders describe illnesses that are characterized by irregular eating habits and severe distress or concern about body weight or shape. Eating disturbances may include inadequate or excessive food intake which can ultimately damage an individual’s well-being. Males suffering from eating disorders and body image issues have an immense stigma to overcome and, as a result, have been significantly neglected in both diagnosis and treatment. Lifetime prevalence estimates of DSM-IV anorexia nervosa, bulimia nervosa, and binge eating disorder are .9%, 1.5%, and 3.5% among women, and .3% .5%, and 2.0% among men.
Types of Eating Disorders and Their Symptoms
People with anorexia nervosa may see themselves as overweight, even when they are dangerously underweight. People with anorexia nervosa typically weigh themselves repeatedly, severely restrict the amount of food they eat, and eat very small quantities of only certain foods. Anorexia nervosa has the highest mortality rate of any mental disorder. While many young women and men with this disorder die from complications associated with starvation, others die of suicide. In women, suicide is much more common in those with anorexia than with most other mental disorders.
- Extremely restricted eating
- Extreme thinness (emaciation)
- A relentless pursuit of thinness and unwillingness to maintain a normal or healthy weight
- Intense fear of gaining weight
- Distorted body image, a self-esteem that is heavily influenced by perceptions of body weight and shape, or a denial of the seriousness of low body weight
Other symptoms may develop over time, including:
- Thinning of the bones (osteopenia or osteoporosis)
- Mild anemia and muscle wasting and weakness
- Brittle hair and nails
- Dry and yellowish skin
- Growth of fine hair all over the body (lanugo)
- Severe constipation
- Low blood pressure, slowed breathing and pulse
- Damage to the structure and function of the heart
- Brain damage
- Multiorgan failure
- Drop in internal body temperature, causing a person to feel cold all the time
- Lethargy, sluggishness, or feeling tired all the time
People with bulimia nervosa have recurrent and frequent episodes of eating unusually large amounts of food and feeling a lack of control over these episodes. This binge-eating is followed by behavior that compensates for the overeating such as forced vomiting, excessive use of laxatives or diuretics, fasting, excessive exercise, or a combination of these behaviors. Unlike anorexia nervosa, people with bulimia nervosa usually maintain what is considered a healthy or relatively normal weight.
- Chronically inflamed and sore throat
- Swollen salivary glands in the neck and jaw area
- Worn tooth enamel and increasingly sensitive and decaying teeth as a result of exposure to stomach acid
- Acid reflux disorder and other gastrointestinal problems
- Intestinal distress and irritation from laxative abuse
- Severe dehydration from purging of fluids
- Electrolyte imbalance (too low or too high levels of sodium, calcium, potassium and other minerals) which can lead to stroke or heart attack
People with binge-eating disorder lose control over his or her eating. Unlike bulimia nervosa, periods of binge-eating are not followed by purging, excessive exercise, or fasting. As a result, people with binge-eating disorder often are overweight or obese. Binge-eating disorder is the most common eating disorder in the U.S.
- Eating unusually large amounts of food in a specific amount of time
- Eating even when you’re full or not hungry
- Eating fast during binge episodes
- Eating until you’re uncomfortably full
- Eating alone or in secret to avoid embarrassment
- Feeling distressed, ashamed, or guilty about your eating
- Frequently dieting, possibly without weight loss
Eating disorders are very complex conditions, and scientists are still learning about the causes. Although eating disorders all have food and weight issues in common, most experts now believe that eating disorders are caused by people attempting to cope with overwhelming feelings and painful emotions by controlling food. Unfortunately, this will eventually damage a person’s physical and emotional health, self-esteem and sense of control.
Factors that may be involved in developing an eating disorder include:
- Genetics: People with first degree relatives, siblings or parents, with an eating disorder appear to be more at risk of developing an eating disorder, too. This suggests a genetic link. Evidence that the brain chemical, serotonin, is involved also points a contributing genetic and biological factors.
- Environment: Cultural pressures that stress “thinness” as beautiful for women and muscular development and body size for men places undue pressure on people of achieve unrealistic standards. Popular culture and media images often tie being thin to popularity, success, beauty and happiness. This creates a strong desire to very thin.
- Peer Pressure: With young people, this can be a very powerful force. Pressure can appear in the form of teasing, bullying or ridicule because of size or weight.
- Physical or Sexual Abuse: A history of physical or sexual abuse can also contribute to some people developing an eating disorder.
- Emotional Health: Perfectionism, impulsive behavior and difficult relationships can all contribute to lowering a person’s self-esteem and make them vulnerable to developing eating disorders.
Examples of environmental factors that would contribute to the occurrence of eating disorders are:
Dysfunctional family dynamic
Professions and careers that promote being thin and weight loss, such as ballet and modeling
Aesthetically oriented sports, where an emphasis is placed on maintaining a lean body for enhanced performance. Examples include:
- Long distance running
Eating disorders affect all types of people. However there are certain risk factors that put some people at greater risk for developing an eating disorder.
- Age: Eating disorders are much more common during teens and early 20s.
- Gender: Statistically, teenage girls and young women are more likely to have eating disorders, but they are more likely to be noticed/treated for one. Teenage boys and men are less likely seek help, but studies show that 1 out of 10 people diagnosed with eating disorders are male.
- Family history: Having a parent or sibling with an eating disorder increases the risk.
- Dieting: Dieting taken too far can become an eating disorder.
- Changes: Times of change like going to college, starting a new job, or getting divorced may be a stressor towards developing an eating disorder.
- Vocations and activities: Eating disorders are especially common among gymnasts, runners, wrestlers and dancers.
Men may develop this type of disorder marked by an extreme concern with becoming more muscular.
Comorbidity of Eaiting Disorder with Trauma and PTSD
Researchers have found trauma is more common in bulimic eating disorders compared to nonbulimic eating disorders, these findings linking eating disorders with trauma have been extended to children and adolescents with eating disorders; which results in multiple episodes, especially in boys. Trauma is associated with greater comorbidity (including and often mediated by PTSD) in eating disorder subjects; partial or sub-threshold PTSD may also be a risk factor for bulimia nervosa and bulimic symptoms; and the trauma and PTSD or its symptoms must be expressly and satisfactorily addressed in order to facilitate full recovery from the ED and all associated comorbidity.
Eating Disorders and Major Depressive Disorders
Central serotonin pathways modulate eating patterns, and may also participate in the regulation of behavioral impulsivity and mood. The impaired postingestive satiety in bulimia nervosa is associated with reduced hypothalamic serotonergic responsiveness. Serotonin dysregulation has been implicated in major depression, and may play a role in the increased prevalence of depressive episodes in patients with eating disorders. Early menarche (prior to 11.6 years) was associated with elevated depression and substance abuse.
Eating disorders can cause serious health problems related to inadequate nutrition, overeating, bingeing and other factors. The type of health problems caused by eating disorders depends on the type and severity of the eating disorder. In many cases, problems caused by an eating disorder require ongoing treatment and monitoring.
Health problems linked to eating disorders may include:
- Electrolyte imbalances, which can interfere with the functioning of your muscles, heart and nerves
- Heart problems and high blood pressure
- Digestive problems
- Nutrient deficiencies
- Dental cavities and erosion of the surface of your teeth from frequent vomiting (bulimia)
- Low bone density (osteoporosis) as a result of irregular or absent menstruation or long-term malnutrition (anorexia)
- Stunted growth caused by poor nutrition (anorexia)
- Mental health conditions such as depression, anxiety, obsessive-compulsive disorder or substance abuse
- Lack of menstruation and problems with infertility and pregnancy
Psychotherapies such as a family-based therapy called the Maudsley approach, where parents of adolescents with anorexia nervosa assume responsibility for feeding their child, appear to be very effective in helping people gain weight and improve eating habits and moods. To reduce or eliminate binge-eating and purging behaviors, people may undergo cognitive behavioral therapy (CBT), which is another type of psychotherapy that helps a person learn how to identify distorted or unhelpful thinking patterns and recognize and change inaccurate beliefs.
Medication can be a valuable tool in the treatment of eating disorders.
Medication is used less frequently to treat anorexia compared to other eating disorders. However, when medication is called for, antidepressants are typically prescribed to treat underlying mental health problems. Fluoxetine (Prozac) may help people with anorexia overcome their depression and maintain a healthy weight once they have gotten their weight and eating under control. Fluoxetine is in a class of drugs called selective serotonin uptake inhibitors (SSRIs). These drugs increase serotonin levels, a brain chemical connected to mood. If the patient does not do well on an SSRI, doctors may prescribe olanzapine (Zyprexa), an antipsychotic drug typically used to treat schizophrenia. This medication has been found to help some people with anorexia gain weight and change their obsessive thinking.
People with bulimia respond well to SSRI antidepressants, even if they aren’t depressed. Fluoxetine (Prozac) can help people stop binging and purging when used alone or with CBT. In fact, Fluoxetine is the only antidepressant approved by the U.S. Food and Drug Administration to treat bulimia. Other SSRI antidepressants may be helpful in treating bulimia and are often used, although scientific studies to support their use are limited. Another possible bulimia medication is topiramate (Topamax), an anti-seizure drug. Topiramate may help people with bulimia suppress their urge to binge and reduce their preoccupation with eating and weight. However, topiramate can have troublesome side effects compared to the SSRIs. Accumulating evidence suggests that antidepressants in combination with psychotherapy can be effective in the treatment of bulimia nervosa. Clinical experience supports the use of most selective serotonin reuptake inhibitors (i.e., fluoxetine, sertraline and citalopram) as well as some of the newer antidepressants (i.e., venlafaxine).
About 2 percent of U.S. adults, or about 5 million people, have binge eating disorder, according to the Department of Health and Human Services. Standard treatment for binge eating and other eating disorders usually involves counseling and psychotherapy. Some doctors also prescribe antidepressants to try and curb eating disorders, though they are not approved for that use. Antidepressants can help treat binge eating disorder. SSRIs, such as Fluoxetine (Prozac) and Sertraline (Zoloft), may help reduce binge eating and can improve mood in patients who are also struggling with depression or anxiety. However, antidepressants in general will not help much with weight loss. Some have also tried anticonvulsants (Topiramate) for treating binge-eating disorder.
Vyvanse, known chemically as lisdexamfetamine dimesylate, is part of a family of drugs that stimulate the central nervous system. Federal health regulators have approved an attention deficit disorder drug for a new use: A first-of-its kind treatment for binge-eating disorder. The Food and Drug Administration originally approved Vyvanse in 2007 as a once-a-day pill for attention deficit hyperactivity disorder. In February of 2015, the agency cleared the drug for adults who compulsively overeat. The drug is not approved for weight loss. Bupropion (Aplenzin, Forfivo, Wellbutrin), although it can cause seizures if taken by someone who binges then tries to rid the body of the food (purges).
Below is a listing of some of the most common medications prescribed in treating some victims of Eating Disorders (it is important to discuss medications, indications, side’s effects, etc. with your medical doctor and/or psychiatrist):
Zoloft (sertraline hydrochloride)
- Antidepressant (SSRI – selective serotonin reuptake inhibitor); SSRIs selectively affect neurotransmitter (the chemicals that send messages to and from the brain) mechanisms in the central nervous system
- Oral administration
- Used to treat mental depression, obsessive-compulsive disorder and panic disorders
Paxil (paroxetine hydrochloride)
- Antidepressant (SSRI – selective serotonin reuptake inhibitor); SSRIs selectively affect neurotransmitter (the chemicals that send messages to and from the brain) mechanisms in the central nervous system
- Oral administration
- Used to treat mental depression, obsessive-compulsive disorder and panic disorders
Prozac (fluoxetine hydrochloride)
- Antidepressant (SSRI – selective serotonin reuptake inhibitor); SSRIs selectively affect neurotransmitter (the chemicals that send messages to and from the brain) mechanisms in the central nervous system
- Oral administration
- Used to treat mental depression, obsessive-compulsive disorder and panic disorders
Effexor (venlafaxine hydrochloride)
- Antidepressant (unique class of antidepressants called serotonin and norepinephrine reuptake inhibitors; believed to work by increasing neurotransmitter effects in the brain)
- Oral administration
- Used to treat depression.
Wellbutrin (bupropion hydrochloride)
- Antidepressant (structurally unrelated to tricyclic antidepressants (TCA), selective serotonin reuptake inhibitors (SSRI) and monoamine oxidase inhibitors (MAOI)
- Oral administration
- Used to treat major depressive disorders, by increasing the levels of certain nerve transmitters, such as norepinephrine, serotonin and dopamine; it is believed that it also acts as a brain stimulant
* The extended release formulation of this drug is also indicated to help in smoking cessation.
- Oral administration
- Used in the treatment of depression and for the symptomatic relief of depressive illness, significantly reduces the symptoms of obsessive-compulsive disorder
Despiramine/Norpramin (desipramine hydrochloride)
- Tricyclic antidepressant
- Oral administration
- Used in treatment of endogenous depressive illness, including the depressed phase of manic depressive illness, involutional melancholia and psychotic depression. It may also be indicated in the management of depression of a nonpsychotic degree such as in selected cases of depressive neurosis. Patients with transient mood disturbances or normal grief reaction are not expected to benefit from tricyclic antidepressants. It has also been used to treat cocaine withdrawal, panic disorder and Bulimia Nervosa
Imipramine/Tofranil (imipramine hydrochloride)
- Tricyclic antidepressant
- Oral administration
- Used for relief of depressive illness, panic disorder, chronic pain (from migraines, tension headaches, diabetes, cancer, arthritis), and Bulimia Nervosa
- Tricyclic antidepressant
- Oral administration
- Used for the symptomatic relief of depressive illness
- Anxiety medication (a type of central nervous system (CNS) depressant or medicine that slows down the nervous system
- Oral administration
- Used to treat anxiety, anxiety associated with depression and panic disorders
Lithium (lithium carbonate)
- Oral administration
- Used in the treatment of acute manic episodes in patients with manic-depressive disorders. Maintenance therapy has been found useful in preventing or diminishing the frequency of subsequent relapses in patients with bipolar disorder. It has also been used to treat migraine headaches, bulimia, and alcoholism
Naltrexone / Revia (naltrexone hydrochloride)
- Oral administration
- Used for the treatment of Alcoholism, binge-related Eating Disorders. Naltrexone may also be useful in treating those who are “cutters” or who practice in self-multilation
Bronchitis is an inflammation of the lining of your bronchial tubes, which carry air to and from your lungs. People who have bronchitis often cough up thickened mucus, which can be discolored. Bronchitis may be either acute or chronic.
Often developing from a cold or other respiratory infection, acute bronchitis is very common. Chronic bronchitis, a more serious condition, is a constant irritation or inflammation of the lining of the bronchial tubes, often due to smoking.
Acute bronchitis, also called a chest cold, usually improves within a week to 10 days without lasting effects, although the cough may linger for weeks.
However, if you have repeated bouts of bronchitis, you may have chronic bronchitis, which requires medical attention. Chronic bronchitis is one of the conditions included in chronic obstructive pulmonary disease (COPD).
For either acute bronchitis or chronic bronchitis, signs and symptoms may include:
- Production of mucus (sputum), which can be clear, white, yellowish-gray or green in color — rarely, it may be streaked with blood
- Shortness of breath
- Slight fever and chills
- Chest discomfort
If you have acute bronchitis, you might have cold symptoms, such as a mild headache or body aches. While these symptoms usually improve in about a week, you may have a nagging cough that lingers for several weeks.
Chronic bronchitis is defined as a productive cough that lasts at least three months, with recurring bouts occurring for at least two consecutive years.
If you have chronic bronchitis, you're likely to have periods when your cough or other symptoms worsen. At those times, you may have an acute infection on top of chronic bronchitis.
When to see a doctor
See your doctor if your cough:
- Lasts more than three weeks
- Prevents you from sleeping
- Is accompanied by fever higher than 100.4 F (38 C)
- Produces discolored mucus
- Produces blood
- Is associated with wheezing or shortness of breath
Acute bronchitis is usually caused by viruses, typically the same viruses that cause colds and flu (influenza). Antibiotics don't kill viruses, so this type of medication isn't useful in most cases of bronchitis.
The most common cause of chronic bronchitis is cigarette smoking. Air pollution and dust or toxic gases in the environment or workplace also can contribute to the condition.
Factors that increase your risk of bronchitis include:
- Cigarette smoke. People who smoke or who live with a smoker are at higher risk of both acute bronchitis and chronic bronchitis.
- Low resistance. This may result from another acute illness, such as a cold, or from a chronic condition that compromises your immune system. Older adults, infants and young children have greater vulnerability to infection.
- Exposure to irritants on the job. Your risk of developing bronchitis is greater if you work around certain lung irritants, such as grains or textiles, or are exposed to chemical fumes.
- Gastric reflux. Repeated bouts of severe heartburn can irritate your throat and make you more prone to developing bronchitis.
Although a single episode of bronchitis usually isn't cause for concern, it can lead to pneumonia in some people. Repeated bouts of bronchitis, however, may mean that you have chronic obstructive pulmonary disease (COPD).
To reduce your risk of bronchitis, follow these tips:
- Avoid cigarette smoke. Cigarette smoke increases your risk of chronic bronchitis.
- Get vaccinated. Many cases of acute bronchitis result from influenza, a virus. Getting a yearly flu vaccine can help protect you from getting the flu. You may also want to consider vaccination that protects against some types of pneumonia.
- Wash your hands. To reduce your risk of catching a viral infection, wash your hands frequently and get in the habit of using alcohol-based hand sanitizers.
- Wear a surgical mask. If you have COPD, you might consider wearing a face mask at work if you're exposed to dust or fumes, and when you're going to be among crowds, such as while traveling.
During the first few days of illness, it can be difficult to distinguish the signs and symptoms of bronchitis from those of a common cold. During the physical exam, your doctor will use a stethoscope to listen closely to your lungs as you breathe.
In some cases, your doctor may suggest the following tests:
- Chest X-ray. A chest X-ray can help determine if you have pneumonia or another condition that may explain your cough. This is especially important if you ever were or currently are a smoker.
- Sputum tests. Sputum is the mucus that you cough up from your lungs. It can be tested to see if you have illnesses that could be helped by antibiotics. Sputum can also be tested for signs of allergies.
- Pulmonary function test. During a pulmonary function test, you blow into a device called a spirometer, which measures how much air your lungs can hold and how quickly you can get air out of your lungs. This test checks for signs of asthma or emphysema.
Most cases of acute bronchitis get better without treatment, usually within a couple of weeks.
Because most cases of bronchitis are caused by viral infections, antibiotics aren't effective. However, if your doctor suspects that you have a bacterial infection, he or she may prescribe an antibiotic.
In some circumstances, your doctor may recommend other medications, including:
- Cough medicine. If your cough keeps you from sleeping, you might try cough suppressants at bedtime.
- Other medications. If you have allergies, asthma or chronic obstructive pulmonary disease (COPD), your doctor may recommend an inhaler and other medications to reduce inflammation and open narrowed passages in your lungs.
If you have chronic bronchitis, you may benefit from pulmonary rehabilitation — a breathing exercise program in which a respiratory therapist teaches you how to breathe more easily and increase your ability to exercise.
Lifestyle and home remedies
To help you feel better, you may want to try the following self-care measures:
- Avoid lung irritants. Don't smoke. Wear a mask when the air is polluted or if you're exposed to irritants, such as paint or household cleaners with strong fumes.
- Use a humidifier. Warm, moist air helps relieve coughs and loosens mucus in your airways. But be sure to clean the humidifier according to the manufacturer's recommendations to avoid the growth of bacteria and fungi in the water container.
- Consider a face mask outside. If cold air aggravates your cough and causes shortness of breath, put on a cold-air face mask before you go outside.
High Blood Pressure (Hypertension)
Hypertension; Hypertension (HTN), defined as systolic blood pressure (SBP) > 140 mmHg or diastolic blood pressure (DBP) > 90 mmHg, affects around 40 % of the worldwide population aged over 25 years, and is estimated to be implicated in approximately half of the deaths from stroke or cardiovascular disease, an estimated 970 million people worldwide suffer from the disease resulting in significant morbidity, mortality and financial burden globally. Diagnosing and treating hypertension plays an important role in minimising the risk of cardiovascular disease and stroke. Early and accurate diagnosis of hypertension, as well as regular monitoring, is essential to meet treatment targets. It is estimated that uncontrolled HTN is responsible for 7.5 million deaths per year worldwide and in USA alone 75 million people affect from hypertension, and accounts for over 47 billion dollars spent in health care services, medications and absent workforce.
Based on recommendations of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), the classification of BP for adults aged 18 years or older has been as follows:
- Normal: Systolic lower than 120 mm Hg, diastolic lower than 80 mm Hg
- Prehypertension: Systolic 120-139 mm Hg, diastolic 80-89 mm Hg
- Stage 1: Systolic 140-159 mm Hg, diastolic 90-99 mm Hg
- Stage 2: Systolic 160 mm Hg or greater, diastolic 100 mm Hg or greater
Hypertension may be primary, which may develop as a result of environmental or genetic causes, or secondary, which has multiple etiologies, including renal, vascular, and endocrine causes. Primary or essential hypertension accounts for 90-95% of adult cases, and secondary hypertension accounts for 2-10% of cases.
It happens when the force of the blood pumping through your arteries is too strong. When your heart beats, it pushes blood through your arteries to the rest of your body. When the blood pushes harder against the walls of your arteries, your blood pressure goes up. Your blood pressure may be different at different times of the day. It is usually higher when you first wake up, after you exercise, or when you are under stress.
Measuring Blood Pressure
How is Blood Pressure Measured?
Usually, a cuff is filled with air to squeeze the artery in your upper arm while a “gauge” (measuring tool) records your blood pressure as the air is released from the cuff. Most home devices use digital (electronic) gauges.
What Do the Numbers Mean?
A blood pressure measurement has two parts—a top (first) number and a bottom (second) number. The top number is the “systolic” (pronounced sis-TOL-ik) pressure and the bottom number is the “diastolic” (pronounced di-a-STOL-ik) pressure.
- Systolic pressure is your blood pressure when your heart beats and pumps blood through your arteries. Your blood pressure is higher while your heart is pumping, so the systolic number is higher.
- Diastolic pressure is your blood pressure in between heartbeats when your heart is not pumping. Your blood pressure is lower while your heart is not pumping, so the diastolic number is lower.
Your blood pressure numbers are given one on top of the other, with your systolic pressure “over” your diastolic pressure.
- A normal blood pressure is less than “120 over 80,” or 120/80. This means the systolic pressure is 120 and the diastolic pressure is 80.
- A blood pressure between 120/80 and 139/89 is called “prehypertension.” This means that your blood pressure is higher than normal and that you are at risk for having high blood pressure.
- If your blood pressure is 140/90 or higher most of the time it is measured, you have high blood pressure.
Symptoms of High Blood Pressure
Most people with high blood pressure have no signs or symptoms, even if blood pressure readings reach dangerously high levels. It may take years or even decades for the condition to reach levels severe enough that symptoms become obvious. Even then, these symptoms may be attributed to other issues.
Symptoms of hypertension include:
- shortness of breath
- chest pain
- visual changes
- blood in the urine
These symptoms don’t occur in everyone with hypertension, but waiting for a symptom of this condition to appear could be fatal. The best way to know if you have hypertension is to get regular blood pressure readings. Most doctors’ offices will take a blood pressure reading at every appointment.
Causes of Hypertension
There are two types of hypertension. Each type has a different cause.
Primary hypertension is also called essential hypertension. This kind of hypertension develops over time with no identifiable cause. Researchers are still unclear what mechanisms cause blood pressure to slowly increase. A combination of factors may play a role. These factors include:
- Genes: Some people are genetically predisposed to hypertension. This may be from gene mutations or genetic abnormalities inherited from your parents.
- Physical changes: If something in your body malfunctions, you may begin experiencing issues throughout your body. High blood pressure may be one of those issues.
- Environment: Over time, unhealthy lifestyle choices like lack of physical activity and poor diet can take their toll on your body. Lifestyle choices can lead to weight problems. Being overweight or obese can increase your risk for hypertension.
For example, it’s thought that changes in your kidney function may upset the body’s natural balance of salts and fluid. This change may cause your body’s blood pressure to increase.
Although the aetiology of essential HTN is unknown, it is often associated with increased salt intake and obesity and has a strong relationship with family history, underscoring the possibility of genetic predisposition for the disease
Secondary hypertension often occurs quickly and can become more severe than primary hypertension. Several conditions that may cause secondary hypertension include:
- chronic kidney disease
- congenital heart defects
- problems with your thyroid
- side effects of medications
- use of illegal drugs
- alcohol abuse or chronic use
- adrenal gland problems
- certain endocrine tumors
- sleep apnea
- renal artery stenosis
The common phenomenon in both scenarios is the derangement of multiple mechanisms involved in the maintenance of normal blood pressures and as such, the sympathetic nervous system, renin-angiotensin-aldosterone system, endothelial function plus sodium and water retention have been extensively studied to ascertain mechanisms involved in the development of the disease.
Cardiac output and peripheral vascular resistance (PVR)
Cardiac output and PVR are two important factors that maintain normal blood pressures and it has been suggested that increased cardiac output resulting from sympathetic dysfunction is the trigger for the development of HTN and increases in PVR is essentially the physiologic response to accommodate change in pressure and maintain homeostasis.
Sympathetic nervous system
Over the last decade the role of SNS in the development and maintenance of blood pressure has been studied exhaustively and it has been identified that sympathetic stimulation of the heart, peripheral vasculature, and kidneys, resulting in increased cardiac output, increased vascular resistance, plus fluid retention is important in the development and maintenance of this disease. As evidenced in the Coronary Artery Risk Development in Young Adults (CARDIA) study, sympathetic overdrive is often accompanied by low parasympathetic tone, which further exacerbates the condition. The renal sympathetic nervous system is a major player in the development and maintenance of HTN affecting blood pressure via two pathways, namely, the efferent and afferent pathways. The efferent pathway carries signals from the SNS to the kidney and increases renin release thereby activating the RAAS system and increasing sodium and water retention, all resulting in increased circulating volumes and therefore increased blood pressures. In addition to the aforementioned processes the efferent pathway also decreases renal blood flow and to increase perfusion the kidney triggers the afferent pathway that carries impulses to the SNS exacerbating sympathetic over activity and thereby maintaining the high blood pressures.
Renin-angiotensin-aldosterone system (RAAS)
The RAAS system plays a major role in orchestrating the maintenance of normal blood pressures and is activated by dual mechanisms, stimulation of the SNS and glomerular under perfusion. These stimuli trigger the release of renin from the juxtaglomerular apparatus which converts angiotensinogen to inactive angiotensin I, the latter is further cleaved by endothelium bound angiotensin converting enzyme (ACE) into angiotensin II, the active component of this cascade and a potent vasoconstrictor. Although this conversion of angiotensin I to angiotensin II was initially believed to occur primarily in the lungs, it has since been established that the process occurs practically in all tissues. In response to decreased salt intake RAAS also triggers the release of aldosterone from the adrenal glands that increases salt reabsorption coupled with water retention resulting in further increase of blood pressure. Under these circumstances one would expect that patients with HTN would invariably have high circulating levels of renin and angiotensin II, however, studies have demonstrated that plasma renin activity is increased in 15 percent patients, normal in 60 percent patients, and reduced in approximately 25 percent patients. This can be reconciled by growing evidence for the presence of local renin systems regulating regional blood flow that might play an essential part in the pathophysiology of HTN.
Whether endothelial dysfunction is a cause or an effect of hypertension is debatable, nonetheless there is substantial evidence linking endothelial dysfunction with hypertension. In fact, there is evidence of a positive association between the degree of endothelial dysfunction and the severity of hypertension. The major underlying mechanism for endothelial dysfunction seen in HTN is the decrease in the availability of nitric oxide (NO), a consequence of increased oxidative stress in these patients. To this, extent although effective antihypertensive therapy restores impaired nitric oxide production, endothelium dependent vasorelaxation continues to be altered suggesting an irreversible course once HTN is established. This evidence as well as studies demonstrating that inhibition of endothelium-derived nitric oxide synthase (eNOS) results in hypertension in humans, insinuates endothelial dysfunction as a potential aetiological factor in the initiation of HTN. On the other hand the Multiethnic Study of Atherosclerosis (MESA) showed that impaired flow-mediated dilation (FMD) was not a significant independent predictor of the future development of hypertension and an association of higher blood pressures in adolescence with endothelial dysfunction in adulthood. In addition to NO other vasorelaxing factors such as arachidonic acid metabolites, reactive oxygen species (ROS), vasoactive peptides and microparticles of endothelial origin play important roles in maintenance of vascular tone. Emerging data suggests that these factors contribute to excessive vascular oxidative stress and vascular inflammation resulting in endothelial dysfunction. In the recent years endothelial progenitor cells (EPC’s) that develop to form mature endothelial cells has been implicated in the maintenance of arterial stiffness and as such are now considered as determinants of endothelial function. Thus endothelial dysfunction is multifactorial and a myriad of alterations in the vascular milieu lead to structural and functional changes within the arteries and therapies targeting key pathways involved in the process have shown to decrease vascular remodeling, improve vascular function and therefore attenuate overall cardiovascular risk.
Whilst due to its relevance endothelial function was initially measured in the coronary arteries invasively using acetylcholine or other pharmacologic flow manipulation, current methodologies include venous plethysmography, digital pulse tonometery, laser Doppler flowmetry and the most common high-resolution ultrasound. These methods have not only made early identification of endothelial dysfunction possible and but has also broadened the horizon of FMD in determining efficacy of treatment and assessing prognosis in patients with HTN and other cardiovascular diseases.
Endothelin, a potent vasoconstrictor is one of the major substances involved in maintaining vascular tone. It is secreted by endothelial cells and exerts its affects in a paracrine or autocrine manner on vascular smooth muscle cells and counteracts the relaxing activity of NO Studies have demonstrated that both in animals and humans infusion of endothelin-1 (ET-1) results in increased blood pressures and blocking the system using antagonists reverts the phenomenon . However, plasma levels of ET-1 are normal in patients with essential hypertension suggesting that activity of this system might not play a role in all types of HTN but rather in specific disease states such as salt-sensitive HTN and renal HTN. Large clinical trials aimed at determining both the importance of endothelin in the development and maintenance of HTN and, ascertaining necessity of treatments targeted towards maintenance of this system are warranted.
Bradykinin a vasodilatory peptide with autocrine and paracrine function has long had an indirect association with HTN since apart from its direct vasodilatory affects, bradykinin stimulates release of other vasoactive substances like prostaglandins. This peptide from the kinin-kallikrein system is shown to reduce blood pressures by vasodilation as well as enhanced natriuresis and diuresis both achieved via increased renal blood flow mediated by NO and prostaglandin release. Although vastly overlooked due to side effects of coughing and angioedema the hypotensive effects of ACE inhibitors is due to increased bradykinin levels owing to its reduced degradation therefore therapies targeted directly at bradykinin system are likely in the not so distant future.
Atrial natriuretic peptide (ANP) belongs to a family of structurally and functionally related peptide hormones with cardio-renal functions. ANP mediates its functions via membrane-bound guanylatecyclase linked receptor (NPR-A), which further activates intracellular cGMP mediated processes. Released from the atria in response to atrial distention stemming from hemodynamic overload, ANP causes natriuresis and diuresis resulting in modest reductions in blood pressures with concomitant decreases in plasma renin and aldosterone. Thus, the natriuretic peptide system by decreasing peripheral vascular resistance balances the activity of the SNS and the RAAS system in maintaining blood pressures.
High blood pressure has many risk factors, including:
- Age: The risk of high blood pressure increases as you age. Through early middle age, or about age 45, high blood pressure is more common in men. Women are more likely to develop high blood pressure after age 65.
- Race: High blood pressure is particularly common among blacks, often developing at an earlier age than it does in whites. Serious complications, such as stroke, heart attack and kidney failure, also are more common in blacks.
- Family history: High blood pressure tends to run in families.
- Being overweight or obese: The more you weigh the more blood you need to supply oxygen and nutrients to your tissues. As the volume of blood circulated through your blood vessels increases, so does the pressure on your artery walls.
- Not being physically active: People who are inactive tend to have higher heart rates. The higher your heart rate, the harder your heart must work with each contraction and the stronger the force on your arteries. Lack of physical activity also increases the risk of being overweight.
- Using tobacco: Not only does smoking or chewing tobacco immediately raise your blood pressure temporarily, but the chemicals in tobacco can damage the lining of your artery walls. This can cause your arteries to narrow, increasing your blood pressure. Secondhand smoke also can increase your blood pressure.
- Too much salt (sodium) in your diet: Too much sodium in your diet can cause your body to retain fluid, which increases blood pressure.
- Too little potassium in your diet: Potassium helps balance the amount of sodium in your cells. If you don’t get enough potassium in your diet or retain enough potassium, you may accumulate too much sodium in your blood.
- Too little vitamin D in your diet: It’s uncertain if having too little vitamin D in your diet can lead to high blood pressure. Vitamin D may affect an enzyme produced by your kidneys that affects your blood pressure.
- Drinking too much alcohol: Over time, heavy drinking can damage your heart. Having more than two drinks a day for men and more than one drink a day for women may affect your blood pressure.If you drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women of all ages and men older than age 65, and up to two drinks a day for men age 65 and younger. One drink equals 12 ounces of beer, 5 ounces of wine or 1.5 ounces of 80-proof liquor.
- Stress: High levels of stress can lead to a temporary increase in blood pressure. If you try to relax by eating more, using tobacco or drinking alcohol, you may only increase problems with high blood pressure.
- Certain chronic conditions: Certain chronic conditions also may increase your risk of high blood pressure, such as kidney disease, diabetes and sleep apnea.
Sometimes pregnancy contributes to high blood pressure, as well.
Although high blood pressure is most common in adults, children may be at risk, too. For some children, high blood pressure is caused by problems with the kidneys or heart. But for a growing number of kids, poor lifestyle habits, such as an unhealthy diet, obesity and lack of exercise, contribute to high blood pressure.
Diagnosis of Hypertension
Measurement of blood pressures can be done either manually using a sphygmomanometer or an automated electronic device (both office and home) or when feasible ambulatory blood pressure monitoring is utilized. The latter two are preferred since they are reproducible and rule out observer bias. Readings are measured in both arms using arm cuffs for accuracy. The use of finger cuffs is strongly discouraged due to lack of reproducibility. Blood pressure measurements are taken on an empty bladder with the patient well positioned, legs resting on the ground and arms resting comfortably on a table. An average of two readings taken approximately 5 minutes apart is taken at two visits to determine blood pressure. In older patients postural hypertension is also assessed. In addition to blood work and electrocardiography, it is important to consider all previous cardiovascular events, risk factors plus other medical and medication history (stroke, transient ischemic attacks, coronary artery disease, heart failure, chronic kidney disease, peripheral artery disease, diabetes and sleep apnea) to determine an appropriate treatment plan.
If your blood pressure remains high, your doctor will likely conduct more tests to rule out underlying conditions. These tests include:
- urine test
- cholesterol screening
- test of your heart’s electrical activity
These tests can help your doctor identify any secondary issues causing your elevated blood pressure.
Treatment of High Blood Pressure
The recommendations to lower BP and decrease cardiovascular disease risk include the following, with greater results achieved when 2 or more lifestyle modifications are combined:
- Weight loss (range of approximate systolic BP reduction [SBP], 5-20 mm Hg per 10 kg)
- Limit alcohol intake to no more than 1 oz (30 mL) of ethanol per day for men or 0.5 oz (15 mL) of ethanol per day for women and people of lighter weight (range of approximate SBP reduction, 2-4 mm Hg)
- Reduce sodium intake to no more than 100 mmol/day (2.4 g sodium or 6 g sodium chloride; range of approximate SBP reduction, 2-8 mm Hg)
- Maintain adequate intake of dietary potassium (approximately 90 mmol/day)
- Maintain adequate intake of dietary calcium and magnesium for general health
- Stop smoking and reduce intake of dietary saturated fat and cholesterol for overall cardiovascular health
- Engage in aerobic exercise at least 30 minutes daily for most days (range of approximate SBP reduction, 4-9 mm Hg)
Although diet and exercise are the most appropriate tactics to lower your blood pressure, some supplements also may help lower it. However, more research is needed to determine the potential benefits. These include:
- Fiber, such as blond psyllium and wheat bran
- Minerals, such as magnesium, calcium and potassium
- Folic acid
- Supplements or products that increase nitric oxide or widen blood vessels (vasodilators), such as cocoa, coenzyme Q10, L-arginine or garlic
- Omega-3 fatty acids, found in fatty fish, fish oil supplements or flaxseed
- Thiazide diuretics. Diuretics, sometimes called water pills, are medications that act on your kidneys to help your body eliminate sodium and water, reducing blood volume. Thiazide diuretics are often the first, but not the only, choice in high blood pressure medications. Thiazide diuretics include hydrochlorothiazide (Microzide), chlorthalidone and others.If you’re not taking a diuretic and your blood pressure remains high, talk to your doctor about adding one or replacing a drug you currently take with a diuretic. Diuretics or calcium channel blockers may work better for black and older people than do angiotensin-converting enzyme (ACE) inhibitors alone. A common side effect of diuretics is increased urination.
- Beta blockers. These medications reduce the workload on your heart and open your blood vessels, causing your heart to beat slower and with less force. Beta blockers include acebutolol (Sectral), atenolol (Tenormin) and others.When prescribed alone, beta blockers don’t work as well, especially in black and older people, but may be effective when combined with other blood pressure medications.
- Angiotensin-converting enzyme (ACE) inhibitors. These medications — such as lisinopril (Zestril), benazepril (Lotensin), captopril (Capoten) and others — help relax blood vessels by blocking the formation of a natural chemical that narrows blood vessels. People with chronic kidney disease may benefit from having an ACE inhibitor as one of their medications.
- Angiotensin II receptor blockers (ARBs). These medications help relax blood vessels by blocking the action, not the formation, of a natural chemical that narrows blood vessels. ARBs include candesartan (Atacand), losartan (Cozaar) and others. People with chronic kidney disease may benefit from having an ARB as one of their medications.
- Calcium channel blockers. These medications — including amlodipine (Norvasc), diltiazem (Cardizem, Tiazac, others) and others — help relax the muscles of your blood vessels. Some slow your heart rate. Calcium channel blockers may work better for black and older people than do ACE inhibitors alone.Grapefruit juice interacts with some calcium channel blockers, increasing blood levels of the medication and putting you at higher risk of side effects. Talk to your doctor or pharmacist if you’re concerned about interactions.
- Renin inhibitors. Aliskiren (Tekturna) slows down the production of renin, an enzyme produced by your kidneys that starts a chain of chemical steps that increases blood pressure.Tekturna works by reducing the ability of renin to begin this process. Due to a risk of serious complications, including stroke, you shouldn’t take aliskiren with ACE inhibitors or ARBs.
Additional Medications Sometimes Used to Treat High Blood Pressure
If you’re having trouble reaching your blood pressure goal with combinations of the above medications, your doctor may prescribe:
- Alpha blockers. These medications reduce nerve impulses to blood vessels, reducing the effects of natural chemicals that narrow blood vessels. Alpha blockers include doxazosin (Cardura), prazosin (Minipress) and others.
- Alpha-beta blockers. In addition to reducing nerve impulses to blood vessels, alpha-beta blockers slow the heartbeat to reduce the amount of blood that must be pumped through the vessels. Alpha-beta blockers include carvedilol (Coreg) and labetalol (Trandate).
- Central-acting agents. These medications prevent your brain from signaling your nervous system to increase your heart rate and narrow your blood vessels. Examples include clonidine (Catapres, Kapvay), guanfacine (Intuniv, Tenex) and methyldopa.
- Vasodilators. These medications, including hydralazine and minoxidil, work directly on the muscles in the walls of your arteries, preventing the muscles from tightening and your arteries from narrowing.
- Aldosterone antagonists. Examples are spironolactone (Aldactone) and eplerenone (Inspra). These drugs block the effect of a natural chemical that can lead to salt and fluid retention, which can contribute to high blood pressure.
To reduce the number of daily medication doses you need, your doctor may prescribe a combination of low-dose medications rather than larger doses of one single drug. In fact, two or more blood pressure drugs often are more effective than one. Sometimes finding the most effective medication or combination of drugs is a matter of trial and error.
The excessive pressure on your artery walls caused by high blood pressure can damage your blood vessels, as well as organs in your body. The higher your blood pressure and the longer it goes uncontrolled, the greater the damage.
Uncontrolled high blood pressure can lead to:
- Heart attack or stroke. High blood pressure can cause hardening and thickening of the arteries (atherosclerosis), which can lead to a heart attack, stroke or other complications.
- Aneurysm. Increased blood pressure can cause your blood vessels to weaken and bulge, forming an aneurysm. If an aneurysm ruptures, it can be life-threatening.
- Heart failure. To pump blood against the higher pressure in your vessels, your heart muscle thickens. Eventually, the thickened muscle may have a hard time pumping enough blood to meet your body’s needs, which can lead to heart failure.
- Weakened and narrowed blood vessels in your kidneys. This can prevent these organs from functioning normally.
- Thickened, narrowed or torn blood vessels in the eyes. This can result in vision loss.
- Metabolic syndrome. This syndrome is a cluster of disorders of your body’s metabolism, including increased waist circumference; high triglycerides; low high-density lipoprotein (HDL) cholesterol, the “good” cholesterol; high blood pressure; and high insulin levels. These conditions make you more likely to develop diabetes, heart disease and stroke.
- Trouble with memory or understanding. Uncontrolled high blood pressure may also affect your ability to think, remember and learn. Trouble with memory or understanding concepts is more common in people with high blood pressure.
Interventional Pain Management
A Comprehensive Approach to Chronic Pain
Our vision is to help patients from the chronic pain condition. Our goals are to relieve, reduce, or manage pain and improve a patient’s overall quality of life through minimally invasive techniques specifically designed to diagnose and treat painful conditions.
For chronic pain sufferers, finding relief from their pain can be difficult and time consuming. Sometimes patients are shuffled back and forth between primary care physicians, specialists, and therapists of all kinds in search of a solution to their pain problems. Interventional Pain Management can be a useful alternative for patients who have exhausted other treatment methods without success and may be the solution chronic pain sufferers are looking for.
When we’ve been injured or have been living with pain, it affects our life. It prevents us from working or from just getting around and performing the most basic daily tasks. Unresolved pain, in particular, can affect our personal relationships and keep you from social activities or any form of fulfilling life. It can cause despair and even depression, as it does for nearly a third of chronic pain sufferers.
IPMAC is the pioneer in providing non-surgical pain treatment services in Dothan, Alabama. Treatment for all major chronic pain conditions like back pain, slipped disc, sciatic pain, knee pain, joint pains, arthritis, neuralgic pain, headaches and migraines is provided using the latest and most advanced treatment modalities like ozone discectomy, radiofrequency lesioning, Platelet Rich Plasma (PRP) therapy, spinal cord stimulator implant, and vertebroplasty.
IPMAC focuses in treating a wide variety of painful conditions from acute pain (post-injury and post-surgical pain) to chronic pain (chronic spine pain, nerve pain, chronic musculoskeletal pain, headaches). IPMAC aim to provide comprehensive care, treating the whole person and working to resolve all types of pain with a multidisciplinary approach and with the most complete array of modern treatment options. It’s also why you won’t have to wait weeks to be cared for and will always be treated with honesty, respect and total commitment to your needs.
Back Pain and Interventional Pain Management Treatments
For back pain sufferers, interventional pain management techniques can be particularly useful. In addition to a thorough medical history and physical examination, interventional pain management physicians have a wide array of treatments that can be used including the following:
- Epidural injections (in all areas of the spine): the use of anesthetic and steroid medications injected into the epidural space to relieve pain or diagnose a specific condition.
- Nerve, root, and medial branch blocks: injections done to determine if a specific spinal nerve root is the source of pain. Blocks also can be used to reduce inflammation and pain.
- Facet joint injections: an injection used to determine if the facet joints are the source of pain. These injections can also provide pain relief.
- Discography: an “inside” look into the discs to determine if they are the source of a patient’s pain. This procedure involves the use of a dye that is injected into a disc and then examined using x-ray or CT Scan.
- Pulsed Radiofrequency Neurotomy (PRFN): a minimally invasive procedure that disables spinal nerves and prevents them from transmitting pain signals to the brain.
- Rhizotomy: a procedure in which pain signals are “turned off” through the use of heated electrodes that are applied to specific nerves that carry pain signals to the brain.
- Spinal cord stimulation: the use of electrical impulses that are used to block pain from being perceived in the brain.
- Intrathecal pumps: a surgically implanted pump that delivers pain medications to the precise location in the spine where the pain is located.
- Percutaneous Discectomy/Nucleoplasty: a procedure in which tissue is removed from the disc in order to decompress and relieve pressure.
Interventional pain management physicians often include other treatments such as physical therapy, occupational therapy, and lifestyle modification (such as exercise, diet, and smoking cessation) to further enhance these procedures.
Interventional Pain Management of Prime Med
We offer the following:
- Epidural injections (cervical, thoracic, lumbar and caudal)
- Selective epidural and root blocks (cervical, thoracic, lumbar and sacral)
- Facet injections and medical branch blocks (cervical, thoracic and lumbar)
- Sympathetic blocks (stellate ganglion, thoracic, lumbar and hypogastric)
- Peripheral nerve blocks
- Radiofrequency denervation
- Spinal cord stimulation
- Neurolytic of celiac plexus and cancer pain
- Intrathecal and epidural infusion systems
- Kyphoplasty & Vertebroplasty
- Sacroiliac joint procedures
- Botulinum toxin injections (chronic migraines)
- Joint Procedures and injections
- Multiple Sclerosis
- Cerebral Palsy
- Carpal Tunnel
Our team of specialists can treat, guide or assist in the pain management and mitigation of the broad spectrum of various chronic and temporary pain, including:
- Acute Pain
- Advanced Prostate Cancer
- AIDS-Related Pain
- Ankylosing Spondylitis
- Ataxic Cerebral Palsy
- Autoimmune Atrophic Gastritis
- Autoimmune Diseases
- Avascular Necrosis
- Back Pain
- Breakthrough Pain
- Burning Mouth Syndrome
- Cancer Pain
- Carpal Tunnel
- Cauda Equina Syndrome
- Central Pain Syndrome
- Cerebral Palsy
- Cerebrospinal Fluid (CSF) Leaks
- Cervical Stenosis
- Charcot-Marie-Tooth (CMT) Disease
- Chronic Fatigue Syndrome (CFS)
- Chronic Functional Abdominal Pain (CFAP)
- Chronic Pain
- Chronic Pancreatitis
- Collapsed Lung (Pneumothorax)
- Complementary and Alternative Medicine
- Complex Regional Pain Syndrome (RSD)
- Corneal Neuropathic Pain
- Crohn’s Disease
- Degenerative Disc Disease
- Dependence (Physical)
- Dercum’s Disease
- Diabetic Peripheral Neuropathy (DPN)
- Ehlers-Danlos Syndrome (EDS)
- Failed Back Surgery Syndrome (FBSS)
- Growing Pains
- Herniated disc
- Intercostal Neuraligia
- Interstitial Cystitis
- Irritable Bowel syndrome (IBS)
- Juvenile Dermatositis
- Knee Injury
- Leg Pain
- Loin Pain-Haematuria Syndrome
- Lyme Disease
- Medullary Sponge Kidney (MSK)
- Meralgia Paresthetica
- Mitochondrial Disorders
- Multiple Sclerosis
- Musculoskeletal Pain
- Myofascial Pain
- Neck Pain
- Neuropathic Pain
- Occipital Neuralgia
- Paget’s Disease
- Patient Rights
- Pelvic Pain
- Peripheral Neuropathy
- Phantom Limb Pain
- Pinched Nerve
- Polycystic Kidney Disease
- Polymyalgia Rhuematica
- Post Herniorraphy Pain Syndrome
- Post Mastectomy Pain Syndrome
- Post Stroke Pain
- Post Thorocotomy Pain Syndrome
- Postherpetic Neuralgia (Shingles)
- Post-Polio Health International
- Post-Polio Syndrome
- Post-Traumatic Stress Disorder (PTSD)
- Primary Lateral Sclerosis
- Psoriatic Arthritis
- Pudendal Neuralgia
- Raynaud’s Disease
- Restless Leg Syndrome
- Rheumatoid Arthritis (RA)
- Sacroiliac Joint Dysfunction
- Scheuemann’s Kyphosis Disease
- Shingles (Herpes Zoster)
- Sickle Cell
- Sjogren’s Syndrome
- Sleep apnea
- Spasmodic Torticollis
- Sphincter of Oddi Dysfunction
- Spinal Cerebellum Ataxia (SCA Ataxia)
- Spinal Cord Injury
- Spinal Stenosis
- Tarlov Cysts
- Thoracic Outlet Syndrome (TOS)
- Transverse Myelitis
- Trigeminal Neuralgia
- Trigger Points
- Ulcerative Colitis
- Vascular Pain
Mood and Personality Disorder Program Treatment (MAPeD-PACT)
Seeking help isn’t easy. But left untreated, issues affecting your psychological well-being can leave you feeling alone and lost. They can also affect relationships with family and friends and disrupt life at home and at work.
The Mood and Personality Disorder Program at Prime Med of Ozark Treatment helps patients address trauma and early childhood attachment styles that contribute to mood disorders, personality disorders and co-occurring issues like substance abuse.
Personality disorders are rigid, inflexible and maladaptive, causing impairment in functioning or internal distress. A personality disorder is an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual’s culture, is pervasive and inflexible, has an onset in adolescence or early adulthood, is stable over time and leads to distress or impairment.
Personality disorders exist on a continuum ranging from mild to severe and include diagnoses like Schizotypal Personality Disorder, Schizoaffective Personality Disorder, Schizophrenia, Narcissistic Personality Disorder, Borderline Personality Disorder, Paranoid Personality Disorder, Dependent Personality Disorder, Avoidant Personality Disorder, Anorexia, Bulimia, Overeating disorders, Substance-abuse and addiction, and other co-occurring conditions. While most people can live pretty normal lives with mild personality disorders (or more simply, personality traits), during times of increased stress or external pressures (work, family, a new relationship, etc.), the symptoms of the personality disorder may begin to seriously interfere with their emotional and psychological functioning. Our personality disorders treatment program helps clients identify unhealthy ways of relating to others, learn ways to break these patterns, and better manage stress and triggers.
Mood disorders are a category of illnesses that describe a serious change in mood. Illness under mood disorders include: major depressive disorder, bipolar disorder (mania – euphoric, hyperactive, over inflated ego, unrealistic optimism), persistent depressive disorder (long lasting low grade depression), cyclothymia (a mild form of bipolar disorder), and SAD (seasonal affective disorder). Mood Disorders includes Major Depression, Bipolar Syndrome, Dysthymia, Dysphoria, Panic Disorder, Anxiety, Obsessive-Compulsive Disorder OCD, Post-Traumatic Stress Disorder PTSD, Social Anxiety Disorder, General Anxiety, Disorder, Premenstrual Syndrome (PMS), Postpartum Depression (PPD), Attention-Deficit/Hyperactivity Disorder (ADHD), Pervasive Developmental Disorders (PDD), and mood changes due to Smoking Cessation.
Major depressive disorder is a serious medical illness affecting an estimated 15 million American adults. For many, their antidepressant may not be working well enough. A large study showed that 2 out of 3 people taking an antidepressant still experienced symptoms of depression. It’s important to know that antidepressants may increase suicidal thoughts or actions in some children, teenagers, or young adults within the first few months of treatment. Pay close attention to any changes, especially sudden changes in mood, behaviors, thoughts, or feelings and report such changes to the healthcare provider.
As an internationally known and respected treatment provider of medical, therapeutic, and experiential services, our treatment center is pleased to offer state-of-the-art treatment for a wide range of behavioral health concerns. Through the integration of evidence-based practices and integrative therapies, MAPeD-PACT prides itself on being a leading provider of services that are effective in treating addictions and other behavioral health problems. Holistic and individualized treatment is the cornerstone of the best care offered at MAPeD-PACT, and is provided by a staff of qualified and experienced professionals. Our primary goal is to deliver services in such a manner that all who come to us for treatment will benefit from them and resume the pursuit of a healthy and productive lifestyle.
Offered within our behavioral health residential treatment center, services supplied in this treatment plan are designed to produce the most favorable outcomes for all residents. The neuropsychiatric treatment provided in this plan is designed to care for the whole person – mind, body, and spirit – in a naturally scenic, tranquil setting that offers the best comprehensive care. Using an interdisciplinary team approach through a customized blend of conventional, complementary, and evidence-based treatments, our caring and compassionate staff strives to support each person’s unique capacity to flourish and achieve overall wellness. The all-encompassing goal of the MAPeD-PACT is to help residents decrease the symptoms that plague them, while also helping them to gain the tools needed to resume healthy daily functioning, free from the turmoil elicited by depression.
What We Offer at MAPeD-PACT
- Full Psychiatric Checkup and Medications
- Cognitive Behavioral Therapy (CBT)
- Counselling for Ropes Course
- Mindfulness Based Cognitive Therapy (MBCT)
- Somatic Experiencing
- Eye Movement Desensitization and Reprocessing, commonly referred to as EMDR
- Dialectical Behavior Therapy (DBT)
- Cognitive Behavioral Analysis System of Psychotherapy (CBASP)
- Acceptance and Commitment Therapy (ACT)
Overview of Mood Disorders
Anxiety is a feeling of uneasiness and apprehension over normal life stressors like beginning a new job or taking a test. When anxiety becomes overwhelming, it can interfere with a person’s physical and mental health and is then referred to as an anxiety disorder.
Bipolar disorder is a mood disorder in which a person experiences powerful swings between periods of mania (feeling “up”) and depression (feeling “down”). Bipolar disorder, also known as manic-depressive illness, can occur in both children and adults.
Depression, a serious brain disorder, is more than just “feeling down” or “blue.” It’s a persistent problem that affects everyday life. Symptoms of depression include sadness, feelings of uselessness, loss of interest in activities, weight changes, loss of energy and suicidal thoughts.
Obsessive-Compulsive Disorder (OCD)
Obsessive-compulsive disorder (OCD) is a type of anxiety disorder. People with OCD have uncontrollable, unwanted thoughts (obsessions) and try to control them by repeating certain behaviors (compulsions).
Panic disorder, also referred to as a panic attack, is a type of anxiety disorder that is characterized by sudden attacks of terror when there is no real threat of danger. A person may feel as if he or she is losing control.
Post-Traumatic Stress Disorder (PTSD)
Post-traumatic stress disorder, or PTSD, is an anxiety disorder that some people develop after seeing or living through a dangerous or distressing event. The “fight or flight” reaction that’s normal at the time can linger long after the danger has passed.
Social Anxiety Disorder
Social anxiety disorder (SAD) is a mental disorder. People with social anxiety have an extreme fear of others’ criticism or judgment in social situations. Some people with social anxiety disorder experience this fear in all social situations. Others experience it in only certain situations (for example, when speaking in public).
Overview of Personality Disorder
The study of human personality or ‘character’ (from the Greek charaktêr, the mark impressed upon a coin) dates back at least to antiquity. In his Characters, Tyrtamus (371-287 bc)—nicknamed Theophrastus or ‘divinely speaking’ by his contemporary Aristotle— divided the people of the Athens of the 4th century BC into thirty different personality types, including ‘arrogance’, ‘irony’, and ‘boastfulness’. The Characters exerted a strong influence on subsequent studies of human personality such as those of Thomas Overbury (1581-1613) in England and Jean de la Bruyère (1645-1696) in France.
The concept of personality disorder itself is much more recent and tentatively dates back to psychiatrist Philippe Pinel’s 1801 description of manie sans délire, a condition which he characterized as outbursts of rage and violence (manie) in the absence of any symptoms of psychosis such as delusions and hallucinations (délires).
Across the English Channel, physician JC Prichard (1786-1848) coined the term ‘moral insanity’ in 1835 to refer to a larger group of people characterized by ‘morbid perversion of the natural feelings, affections, inclinations, temper, habits, moral dispositions and natural impulses’, but the term, probably considered too broad and non-specific, soon fell into disuse.
Personality is the way of thinking, feeling and behaving that makes a person different from other people. An individual’s personality is influenced by experiences, environment (surroundings, life situations) and inherited characteristics. A personality disorder is a way of thinking, feeling and behaving that deviates from the expectations of the culture, causes distress or problems functioning, and lasts over time.
Some 60 years later, in 1896, psychiatrist Emil Kraepelin (1856-1926) described seven forms of antisocial behaviour under the umbrella of ‘psychopathic personality’, a term later broadened by Kraepelin’s younger colleague Kurt Schneider (1887-1967) to include those who ‘suffer from their abnormality’.
Schneider’s seminal volume of 1923, Die psychopathischen Persönlichkeiten (Psychopathic Personalities), still forms the basis of current classifications of personality disorders such as that contained in the influential American classification of mental disorders, the Diagnostic and Statistical Manual of Mental Disorders 5th Revision (DSM-5).
According to DSM-5, a personality disorder can be diagnosed if there are significant impairments in self and interpersonal functioning together with one or more pathological personality traits. In addition, these features must be (1) relatively stable across time and consistent across situations, (2) not better understood as normative for the individual’s developmental stage or socio-cultural environment, and (3) not solely due to the direct effects of a substance or general medical condition.
DSM-5 lists ten personality disorders, and allocates each to one of three groups or ‘clusters’: A, B, or C
Cluster A (Odd, bizarre, eccentric)
- Paranoid Personality Disorder
- Schizoid Personality Disorder
- Schizotypal Personality Disorder
Cluster B (Dramatic, erratic)
- Antisocial Personality Disorder
- Borderline Personality Disorder
- Histrionic Personality Disorder
- Narcissistic Personality Disorder
Cluster C (Anxious, fearful)
- Avoidant Personality Disorder
- Dependent Personality Disorder
- Obsessive-compulsive Personality Disorder
Before going on to characterize these ten personality disorders, it should be emphasized that they are more the product of historical observation than of scientific study, and thus that they are rather vague and imprecise constructs. As a result, they rarely present in their classic ‘textbook’ form, but instead tend to blur into one another. Their division into three clusters in DSM-5 is intended to reflect this tendency, with any given personality disorder most likely to blur with other personality disorders within its cluster. For instance, in cluster A, paranoid personality is most likely to blur with schizoid personality disorder and schizotypal personality disorder.
The majority of people with a personality disorder never come into contact with mental health services, and those who do usually do so in the context of another mental disorder or at a time of crisis, commonly after self-harming or breaking the law. Nevertheless, personality disorders are important to health professionals because they predispose to mental disorder, and affect the presentation and management of existing mental disorder. They also result in considerable distress and impairment, and so may need to be treated ‘in their own right’. Whether this ought to be the remit of the health professions is a matter of debate and controversy, especially with regard to those personality disorders which predispose to criminal activity, and which are often treated with the primary purpose of preventing crime.
1. Paranoid Personality Disorder
Cluster A comprises paranoid, schizoid, and schizotypal personality disorders. Paranoid personality disorder is characterized by a pervasive distrust of others, including even friends, family, and partner. As a result, the person is guarded and suspicious, and constantly on the lookout for clues or suggestions to validate his fears. He also has a strong sense of personal rights: he is overly sensitive to setbacks and rebuffs, easily feels shame and humiliation, and persistently bears grudges. Unsurprisingly, he tends to withdraw from others and to struggle with building close relationships. The principal ego defence in paranoid PD is projection, which involves attributing one’s unacceptable thoughts and feelings to other people. A large long-term twin study found that paranoid PD is modestly heritable, and that it shares a portion of its genetic and environmental risk factors with schizoid PD and schizotypal PD.
2. Schizoid Personality Disorder
The term ‘schizoid’ designates a natural tendency to direct attention toward one’s inner life and away from the external world. A person with schizoid PD is detached and aloof and prone to introspection and fantasy. He has no desire for social or sexual relationships, is indifferent to others and to social norms and conventions, and lacks emotional response. A competing theory about people with schizoid PD is that they are in fact highly sensitive with a rich inner life: they experience a deep longing for intimacy but find initiating and maintaining close relationships too difficult or distressing, and so retreat into their inner world. People with schizoid PD rarely present to medical attention because, despite their reluctance to form close relationships, they are generally well functioning, and quite untroubled by their apparent oddness.
3. Schizotypal Disorder
Schizotypal PD is characterized by oddities of appearance, behaviour, and speech, unusual perceptual experiences, and anomalies of thinking similar to those seen in schizophrenia. These latter can include odd beliefs, magical thinking (for instance, thinking that speaking of the devil can make him appear), suspiciousness, and obsessive ruminations. People with schizotypal PD often fear social interaction and think of others as harmful. This may lead them to develop so-called ideas of reference, that is, beliefs or intuitions that events and happenings are somehow related to them. So whereas people with schizotypal PD and people with schizoid PD both avoid social interaction, with the former it is because they fear others, whereas with the latter it is because they have no desire to interact with others or find interacting with others too difficult. People with schizotypal PD have a higher than average probability of developing schizophrenia, and the condition used to be called ‘latent schizophrenia’.
4. Antisocial Personality Disorder
Cluster B comprises antisocial, borderline, histrionic, and narcissistic personality disorders. Until psychiatrist Kurt Schneider (1887-1967) broadened the concept of personality disorder to include those who ‘suffer from their abnormality’, personality disorder was more or less synonymous with antisocial personality disorder. Antisocial PD is much more common in men than in women, and is characterized by a callous unconcern for the feelings of others. The person disregards social rules and obligations, is irritable and aggressive, acts impulsively, lacks guilt, and fails to learn from experience. In many cases, he has no difficulty finding relationships—and can even appear superficially charming (the so-called ‘charming psychopath’)—but these relationships are usually fiery, turbulent, and short-lived. As antisocial PD is the mental disorder most closely correlated with crime, he is likely to have a criminal record or a history of being in and out of prison.
5. Borderline Personality Disorder
In borderline PD (or emotionally unstable PD), the person essentially lacks a sense of self, and, as a result, experiences feelings of emptiness and fears of abandonment. There is a pattern of intense but unstable relationships, emotional instability, outbursts of anger and violence (especially in response to criticism), and impulsive behaviour. Suicidal threats and acts of self-harm are common, for which reason many people with borderline PD frequently come to medical attention. Borderline PD was so called because it was thought to lie on the ‘borderline’ between neurotic (anxiety) disorders and psychotic disorders such as schizophrenia and bipolar disorder. It has been suggested that borderline personality disorder often results from childhood sexual abuse, and that it is more common in women in part because women are more likely to suffer sexual abuse. However, feminists have argued that borderline PD is more common in women because women presenting with angry and promiscuous behaviour tend to be labelled with it, whereas men presenting with similar behaviour tend instead to be labelled with antisocial PD.
6. Histrionic Personality Disorder
People with histrionic PD lack a sense of self-worth, and depend for their wellbeing on attracting the attention and approval of others. They often seem to be dramatizing or ‘playing a part’ in a bid to be heard and seen. Indeed, ‘histrionic’ derives from the Latin histrionicus, ‘pertaining to the actor’. People with histrionic PD may take great care of their appearance and behave in a manner that is overly charming or inappropriately seductive. As they crave excitement and act on impulse or suggestion, they can place themselves at risk of accident or exploitation. Their dealings with others often seem insincere or superficial, which, in the longer term, can adversely impact on their social and romantic relationships. This is especially distressing to them, as they are sensitive to criticism and rejection, and react badly to loss or failure. A vicious circle may take hold in which the more rejected they feel, the more histrionic they become; and the more histrionic they become, the more rejected they feel. It can be argued that a vicious circle of some kind is at the heart of every personality disorder, and, indeed, every mental disorder.
7. Narcissistic Personality Disorder
In narcissistic PD, the person has an extreme feeling of self-importance, a sense of entitlement, and a need to be admired. He is envious of others and expects them to be the same of him. He lacks empathy and readily lies and exploits others to achieve his aims. To others, he may seem self-absorbed, controlling, intolerant, selfish, or insensitive. If he feels obstructed or ridiculed, he can fly into a fit of destructive anger and revenge. Such a reaction is sometimes called ‘narcissistic rage’, and can have disastrous consequences for all those involved.
8. Avoidant Personality Disorder
Cluster C comprises avoidant, dependent, and anankastic personality disorders. People with avoidant PD believe that they are socially inept, unappealing, or inferior, and constantly fear being embarrassed, criticized, or rejected. They avoid meeting others unless they are certain of being liked, and are restrained even in their intimate relationships. Avoidant PD is strongly associated with anxiety disorders, and may also be associated with actual or felt rejection by parents or peers in childhood. Research suggests that people with avoidant PD excessively monitor internal reactions, both their own and those of others, which prevents them from engaging naturally or fluently in social situations. A vicious circle takes hold in which the more they monitor their internal reactions, the more inept they feel; and the more inept they feel, the more they monitor their internal reactions.
9. Dependent Personality Disorder
Dependent PD is characterized by a lack of self-confidence and an excessive need to be looked after. The person needs a lot of help in making everyday decisions and surrenders important life decisions to the care of others. He greatly fears abandonment and may go through considerable lengths to secure and maintain relationships. A person with dependent PD sees himself as inadequate and helpless, and so surrenders personal responsibility and submits himself to one or more protective others. He imagines that he is at one with these protective other(s), whom he idealizes as competent and powerful, and towards whom he behaves in a manner that is ingratiating and self-effacing. People with dependent PD often end up with people with a cluster B personality disorder, who feed on the unconditional high regard in which they are held. Overall, people with dependent PD maintain a naïve and child-like perspective, and have limited insight into themselves and others. This entrenches their dependency, and leaves them vulnerable to abuse and exploitation.
10. Anankastic (Obsessive-Compulsive) Personality Disorder
Anankastic PD is characterized by excessive preoccupation with details, rules, lists, order, organization, or schedules; perfectionism so extreme that it prevents a task from being completed; and devotion to work and productivity at the expense of leisure and relationships. A person with anankastic PD is typically doubting and cautious, rigid and controlling, humorless, and miserly. His underlying anxiety arises from a perceived lack of control over a world that eludes his understanding; and the more he tries to exert control, the more out of control he feels. In consequence, he has little tolerance for complexity or nuance, and tends to simplify the world by seeing things as either all good or all bad. His relationships with colleagues, friends, and family are often strained by the unreasonable and inflexible demands that he makes upon them.
We treat following movement disorders at the Alabama Clinics. We have neurologists and psychologists that closely examine the patients and in the light of detail diagnostic procedural we diagnose, and treat the movement disorders.
- Parkinson’s Disease
- Tremor (Essential)
- Huntington’s Disease
- Focal dystonia
- Writer’s cramp
- Restless Leg Syndrome
- Tics or Tourette’s Syndrome
- Ataxias (Gait disorders)
- Tardive Dyskinesia
- Multiple System Atrophy (Shy-Drager syndrome)
- Wilson’s Disease
- Progressive Supranuclear Palsy
- Corticobasal degeneration
- Olivopontocerebellar atrophy
- Hemifacial spasm
Multiple sclerosis affects around 2.5 million people worldwide; it is one of the most common neurological disorders and cause of disability of young adults, especially in Europe and North America.
Multiple Sclerosis is an unpredictable disease of the central nervous system; marked by weakness, numbness, a loss of muscle coordination, and problems with vision, speech, and bladder control. Multiple sclerosis (MS) can range from relatively benign to somewhat disabling to devastating, as communication between the brain and other parts of the body is disrupted.
Multiple sclerosis (MS) involves an immune-mediated process in which an abnormal response of the body’s immune system is directed against the central nervous system (CNS), which is made up of the brain, spinal cord and optic nerves. The exact antigen — or target that the immune cells are sensitized to attack — remains unknown, which is why MS is considered by many experts to be “immune-mediated” rather than “autoimmune.”
- Within the CNS, the immune system attacks myelin — the fatty substance that surrounds and insulates the nerve fibers — as well as the nerve fibers themselves.
- The damaged myelin forms scar tissue (sclerosis), which gives the disease its name.
- When any part of the myelin sheath or nerve fiber is damaged or destroyed, nerve impulses traveling to and from the brain and spinal cord are distorted or interrupted, producing a wide variety of symptoms.
- The disease is thought to be triggered in a genetically susceptible individual by a combination of one or more environmental factors.
- People with MS typically experience one of four disease courses, which can be mild, moderate or severe.
Types of Multiple Sclerosis
Clinically Isolated Syndrome (CIS)
Clinically isolated syndrome (CIS) is one of the MS disease courses. CIS refers to a first episode of neurologic symptoms that lasts at least 24 hours and is caused by inflammation or demyelination (loss of the myelin that covers the nerve cells) in the central nervous system (CNS). CIS can be either monofocal or multifocal:
- Monofocal episode: The person experiences a single neurologic sign or symptom — for example, an attack of optic neuritis — that’s caused by a single lesion.
- Multifocal episode: The person experiences more than one sign or symptom — for example, an attack of optic neuritis accompanied by numbness or tingling in the legs — caused by lesions in more than one place.
The episode usually has no associated fever or infection and is followed by a complete or partial recovery.
- High risk of developing MS: When CIS is accompanied by magnetic resonance imaging (MRI)-detected brain lesions that are similar to those seen in MS, the person has a 60 to 80 percent chance of a second neurologic event and diagnosis of MS within several years.
- Low risk of developing MS: When CIS is not accompanied by MRI-detected brain lesions, the person has about a 20 percent chance of developing MS over the same period of time.
Like MS, CIS is two to three times more common in women than men. Seventy percent of people diagnosed with CIS are between the ages of 20 and 40 years (average 30 years) but people can develop CIS at older or younger ages.
Relapsing-remitting MS (RRMS)
RRMS – the most common disease course – is characterized by clearly defined attacks of new or increasing neurologic symptoms. These attacks – also called relapses or exacerbations – are followed by periods of partial or complete recovery (remissions). During remissions, all symptoms may disappear, or some symptoms may continue and become permanent. However, there is no apparent progression of the disease during the periods of remission.
At different points in time, RRMS can be further characterized as either active (with relapses and/or evidence of new MRI activity) or not active, as well as worsening (a confirmed increase in disability over a specified period of time following a relapse) or not worsening. An increase in disability is confirmed when the person exhibits the same level of disability at the next scheduled neurological evaluation, typically 6 to 12 months later.Approximately 85 percent of people with MS are initially diagnosed with RRMS.
Relapsing-remitting MS is defined by inflammatory attacks on myelin (the layers of insulating membranes surrounding nerve fibers in the central nervous system (CNS)), as well as the nerve fibers themselves. During these inflammatory attacks, activated immune cells cause small, localized areas of damage which produce the symptoms of MS. Because the location of the damage is so variable, no two people have exactly the same symptoms.
Primary-Progressive Multiple Sclerosis (PPMS)
PPMS is characterized by worsening neurologic function (accumulation of disability) from the onset of symptoms, without early relapses or remissions. PPMS can be further characterized at different points in time as either active (with an occasional relapse and/or evidence of new MRI activity) or not active, as well as with progression (evidence of disease worsening on an objective measure of change over time, with or without relapse or new MRI activity) or without progression. Approximately 15 percent of people with MS are diagnosed with PPMS.
Although there is a lot of variability among people with PPMS, we know that as a group, they differ in several ways from people with relapsing forms of MS:
- Relapsing forms of MS (including relapsing-remitting MS, and secondary progressive in those individuals who continue to experience relapses) are defined by inflammatory attacks on myelin. PPMS involves much less inflammation of the type seen in relapsing MS. As a result, people with PPMS tend to have fewer brain lesions (also called plaques) than people with relapsing MS and the lesions tend to contain fewer inflammatory cells. People with PPMS also tend to have more lesions in the spinal cord than in the brain. Together, these differences make PPMS more difficult to diagnose and treat than relapsing forms of MS.
- In the relapsing forms, women are affected two to three times as often as men; in PPMS, the numbers of women and men are approximately equal.
- The average age of onset is approximately 10 years later in PPMS than in relapsing MS.
- People with PPMS tend to experience more problems with walking and more difficulty remaining in the workforce.
- In general, people with PPMS may also require more assistance with their everyday activities.
Secondary-progressive MS (SPMS)
SPMS follows an initial relapsing-remitting course. Most people who are diagnosed with RRMS will eventually transition to a secondary progressive course in which there is a progressive worsening of neurologic function (accumulation of disability) over time. SPMS can be further characterized at different points in time as either active (with relapses and/or evidence of new MRI activity) or not active, as well as with progression (evidence of disease worsening on an objective measure of change over time, with or without relapses) or without progression.
SPMS occurs in people who initially had a relapsing-remitting disease course. In other words, SPMS occurs as a second phase of the disease for many individuals. Primary progressive MS (PPMS) is the first — and only — phase of the illness for approximately 15 percent of people with MS.
In SPMS, people may or may not continue to experience relapses caused by inflammation; the disease gradually changes from the inflammatory process seen in RRMS to a more steadily progressive phase characterized by nerve damage or loss.
Symptoms of Multiple Sclerosis
- Fatigue; occurs in about 80% of people, can significantly interfere with the ability to function at home and work, and may be the most prominent symptom in a person who otherwise has minimal activity limitations.
- Vision Problems; the first symptom of MS for many people. Onset of blurred vision, poor contrast or color vision, and pain on eye movement can be frightening — and should be evaluated promptly.
- Bladder Problems; occurs in at least 80% of people with MS, can usually be managed quite successfully with medications, fluid management, and intermittent self-catheterization.
- Depression; studies have suggested that clinical depression — the severest form of depression — is among the most common symptoms of MS. It is more common among people with MS than it is in the general population or in persons with many other chronic, disabling conditions.
- Numbness or Tingling; numbness of the face, body, or extremities (arms and legs) is often the first symptom experienced by those eventually diagnosed as having MS.
- Weakness; that results from deconditioning of unused muscles or damage to nerves that stimulate muscles, can be managed with rehabilitation strategies and the use of mobility aids and other assistive devices.
- Bowel Problems; constipation is a particular concern among people with MS, as is loss of control of the bowels. Bowel issues can typically be managed through diet, adequate fluid intake, physical activity and medication.
- Pain; is very common in MS. In one study, 55% of people with MS had “clinically significant pain” at some time, and almost half had chronic pain.
- Cognitive Changes; refers to a range of high-level brain functions affected in more than 50% of people with MS, including the ability to process incoming information, learn and remember new information, organize and problem-solve, focus attention and accurately perceive the environment.
- Spasticity; refers to feelings of stiffness and a wide range of involuntary muscle spasms; can occur in any limb, but it is much more common in the legs.
- Dizziness and Vertigo; people with MS may feel off balance or lightheaded, or — much less often — have the sensation that they or their surroundings are spinning (vertigo).
- Emotional Changes; can be a reaction to the stresses of living with MS as well as the result of neurologic and immune changes. Significant depression, mood swings, irritability, and episodes of uncontrollable laughing and crying pose significant challenges for people with MS and their families.
- Sexual Problems; very common in the general population including people with MS. Sexual responses can be affected by damage in the central nervous system.
Less Common Symptoms
- Speech Problems; including slurring (dysarthria) and loss of volume (dysphonia) occur in approximately 25-40% of people with MS, particularly later in the disease course and during periods of extreme fatigue. Stuttering is occasionally reported as well.
- Swallowing Problems; referred to as dysphagia — result from damage to the nerves controlling the many small muscles in the mouth and throat.
- Tremor; or uncontrollable shaking, can occur in various parts of the body because of damaged areas along the complex nerve pathways that are responsible for coordination of movements.
- Seizures; which are the result of abnormal electrical discharges in an injured or scarred area of the brain — have been estimated to occur in 2-5% people with MS, compared to the estimated 3% of the general population.
- Breathing Problems; respiration problems occur in people whose chest muscles have been severely weakened by damage to the nerves that control those muscles.
- Itching; Pruritis (itching) is one of the family of abnormal sensations — such as “pins and needles” and burning, stabbing or tearing pains — which may be experienced by people with MS.
- Hearing Loss; about 6% of people who have MS complain of impaired hearing. In very rare cases, hearing loss has been reported as the first symptom of the disease.
- Headache; although headache is not a common symptom of MS, some reports suggest that people with MS have an increased incidence of certain types of headache.
Secondary Symptoms that results from the primary symptoms
- Bladder dysfunction can cause repeated urinary tract infections.
- Inactivity can result in loss of muscle tone and disuse weakness (not related to demyelination), poor postural alignment and trunk control, decreased bone density (and resulting increased risk of fracture), and shallow, inefficient breathing.
- Immobility can lead to pressure sores.
Tertiary symptoms are the “trickle down” effects of the disease on your life. These symptoms include social, vocational and psychological complications. For example, if you are no longer able to drive or walk, you may not be able to hold down your usual job. The stress and strain of dealing with MS often alters social networks and sometimes fractures relationships. Problems with bladder control, tremor or swallowing may cause people to withdraw from social interactions and become isolated.
Causes for Multiple Sclerosis
The worldwide distribution of MS can be only an indirect refl ection of its cause, implicating some environmental factor that varies with latitude, and can be interpreted in at least three different ways in the search for clues to a specific etiology. a), an environmental risk factor may be more common in temperate than tropical climates, b), such a factor may be more common in tropical climates, where it is acquired at an earlier age and consequently has less impact c), this factor may be equally common in all regions, but the chance of its acquisition or of the manifestation of symptoms is either increased by some enhancing factor present in temperate climates or reduced by a protective factor present in tropical areas.
Among those factors that have been most closely scrutinized are:
- infections, including a number of viral infections such as measles and Epstein–Barr virus;
- climate and solar conditions;
- living conditions;
- diet and trace elements.
It is now generally accepted that the etiology of MS involves some interplay of genetic and environmental factors. Evidence of racial or ethnic resistance, the increased risk among MS family members, and elevated monozygotic twin concordance rate all favor a genetic contribution to acquisition of the disease. The studies from which this evidence is derived, however, also indicate that heredity cannot entirely explain the occurrence of MS. This is underlined by the fact that no population-based study of monozygotic twins has found a concordance rate in excess of 30%. Some environmental factor, such as a virus or toxin, must still play a role.
Regardless of any factor, the demyelination occurs in all subjects suffering from Multiple Sclerosis.
The latest research identifies that the chloride-channel protein anoctamin 2 (ANO2) as a new target for autoantibody production in multiple sclerosis (MS) patients.
Your doctor will need to perform a neurological exam, a clinical history, and a series of other tests to determine if you have MS.
Diagnostic testing may include the following:
- MRI is the best imaging test for MS. Using a contrast dye allows the MRI to detect active and inactive lesions throughout the brain and spinal cord.
- Evoked potentials require stimulation of nerve pathways to analyze electrical activity in the brain. The three types of evoked potentials doctors use to help diagnose MS are visual, brainstem, and sensory.
- A spinal tap, or lumbar puncture, can help your doctor find abnormalities in your spinal fluid. It can help rule out infectious diseases.
- Doctors use blood tests to eliminate other conditions with similar symptoms.
The diagnosis of MS requires evidence of demyelination in more than one area of the brain, spinal cord, or optic nerves. That damage must have occurred at different times.
It also requires ruling out other conditions that have similar symptoms. This includes Lyme disease, lupus, and Sjogren’s syndrome.
Treatment for Multiple Sclerosis
No cure is available for MS, but multiple treatment options exist.
If you have relapsing-remitting MS (RRMS), you can choose one of the disease-modifying drugs. These medications are designed to slow disease progression and lower your relapse rate.
Self-injectable disease-modifying drugs include glatiramer (Copaxone, Glatopa) and beta interferons, such as:
Oral medications for RRMS include:
- dimethyl-fumarate (Tecfidera)
- fingolimod (Gilenya)
- teriflunomide (Aubagio)
Intravenous infusion treatments for RRMS include:
- alemtuzumab (Lemtrada)
- natalizumab (Tysabri)
- mitoxantrone (Novantrone), which is for severe MS only
Disease-modifying drugs aren’t effective in treating progressive MS.
Your doctor can prescribe corticosteroids, such as methylprednisolone (Medrol) and prednisone (Deltasone) to treat relapses.
Other treatments may ease your symptoms and improve your quality of life. Because the disease is different for everybody, treatment depends on your specific symptoms. For most people, a flexible approach is necessary.
These factors may increase your risk of developing multiple sclerosis:
- Age. MS can occur at any age, but most commonly affects people between the ages of 15 and 60.
- Sex. Women are about twice as likely as men are to develop MS.
- Family history. If one of your parents or siblings has had MS, you are at higher risk of developing the disease.
- Certain infections. A variety of viruses have been linked to MS, including Epstein-Barr, the virus that causes infectious mononucleosis.
- Race. White people, particularly those of Northern European descent, are at highest risk of developing MS. People of Asian, African or Native American descent have the lowest risk.
- Climate. MS is far more common in countries with temperate climates, including Canada, the northern United States, New Zealand, southeastern Australia and Europe.
- Certain autoimmune diseases. You have a slightly higher risk of developing MS if you have thyroid disease, type 1 diabetes or inflammatory bowel disease.
- Smoking. Smokers who experience an initial event of symptoms that may signal MS are more likely than nonsmokers to develop a second event that confirms relapsing-remitting MS.
People with multiple sclerosis also may develop:
- Muscle stiffness or spasms
- Paralysis, typically in the legs
- Problems with bladder, bowel or sexual function
- Mental changes, such as forgetfulness or mood swings
Statistics about MS
- MS is the most widespread neurological condition disabling young adults worldwide.
- About 400,000 people in the United States have MS, though that’s only an estimate. Doctors in the United States aren’t required to report MS to any agency. According to the National MS Society, there hasn’t been a scientifically sound, national study on the prevalence of MS in the United States since 1975.
- Most people are between the ages of 20 and 40 when their doctor diagnoses them with MS. Women develop MS 2 to 3 times more often than men, a difference that has grown steadily for five decades. MS is more common among Caucasians of northern European ancestry than other ethnic groups.
- Rates of MS tend to be lower in places that are closer to the equator. The rates of MS are higher in places farther away from the equator. This may have to do with sunlight and vitamin D. People who relocate to a new location before age 15 generally acquire the risk factors associated with the new location.
- Data from 1999-2008 showed that direct and indirect costs of MS were between $8,528 and $54,244 per year. Current disease-modifying drugs can cost up to $60,000 per year.
Neurological disorders are intertwined and complex, some may even exhibit the symptoms as late as 60 years and has fatality less than a year, therefore a regular checkup with neurologist is always a good idea, because a great proportion of the diseases or disorders are preventable or treatable on the early diagnosis.
- Absence of the Septum Pellucidum
- Acid Lipase Disease
- Acid Maltase Deficiency [Pompe’s Disease]
- Acquired Epileptiform Aphasia [Landau-Kleffner syndrome (LKS)]
- Acute Disseminated Encephalomyelitis
- Adie’s Pupil
- Adie’s Syndrome [Adie’s syndrome, Adie’s Tonic Pupil or Holmes-Adie’s syndrome]
- Agenesis of the Corpus Callosum (ACC)
- Aicardi Syndrome
- Alexander Disease
- Alpers’ Disease
- Alternating Hemiplegia
- Alzheimer’s Disease
- Amyotrophic Lateral Sclerosis
- Angelman Syndrome
- Antiphospholipid Syndrome (APS)
- Arachnoid Cysts
- Arnold-Chiari Malformation
- Arteriovenous Malformation (AVMs)
- Asperger Syndrome
- Ataxia – Friedreich’s ataxia
- Ataxia Telangiectasia
- Ataxias and Cerebellar or Spinocerebellar Degeneration (SCA)
- Atrial Fibrillation and Stroke
- Autonomic Dysfunction
- Back Pain (Dorsalgia)
- Barth Syndrome
- Batten Disease
- Becker’s Myotonia
- Behcet’s Disease
- Bell’s Palsy
- Benign Essential Blepharospasm (BEB)
- Benign Focal Amyotrophy
- Benign Intracranial Hypertension
- Bernhardt-Roth Syndrome
- Binswanger’s Disease
- Bloch-Sulzberger Syndrome
- Brachial Plexus Injuries
- Bradbury-Eggleston Syndrome
- Brain and Spinal Tumors
- Brain Aneurysm
- Brain Injury
- Brown-Sequard Syndrome
- Bulbospinal Muscular Atrophy
- Cadasil [Cerebral Autosomal Dominant Arteriopathy with Sub-cortical Infarcts and Leukoencephalopathy]
- Canavan Disease
- Carpal Tunnel Syndrome
- Cavernomas [cerebral cavernous malformation (CCM)]
- Cavernous Angioma
- Central Cord Syndrome
- Central Pain Syndrome
- Central Pontine Myelinolysis (CPM)
- Cephalic Disorders
- Ceramidase Deficiency
- Cerebellar Degeneration
- Cerebellar Hypoplasia
- Cerebral Aneurysm – (intracranial or intracerebral aneurysm)
- Cerebral Arteriosclerosis
- Cerebral Atrophy
- Cerebral Beriberi
- Cerebral Gigantism [Sotos syndrome]
- Cerebral Hypoxia
- Cerebral Palsy
- Cerebro-Oculo-Facio-Skeletal Syndrome (COFS)
- Charcot-Marie-Tooth Disease (CMT)
- Chiari Malformation (CMs)
- Chronic Inflammatory Demyelinating Polyneuropathy (CIDP
- Chronic Pain
- Coffin Lowry Syndrome
- Coma and Persistent Vegetative State
- Congenital Facial Diplegia [Mobius syndrome]
- Congenital Myasthenia
- Congenital Myopathy
- Corticobasal Degeneration
- Cranial Arteritis
- Creutzfeldt-Jakob Disease (CJD)
- Cumulative Trauma Disorders
- Cushing’s Syndrome [Hypercortisolism]
- Cytomegalic Inclusion Body Disease
- Dancing Eyes-Dancing Feet Syndrome [Opsoclonus myoclonus]
- Dandy-Walker Syndrome (DWS)
- Dawson Disease
- Dementia – Multi-Infarct (MID)
- Dementia – Semantic [Frontotemporal dementia (FTD)]
- Dementia [Subcortical – Binswanger’s disease (BD)]
- Dementia With Lewy Bodies (DLB)
- Dentate Cerebellar Ataxia
- Dentatorubral Atrophy [Dentatorubral pallidoluysian atrophy]
- Developmental Dyspraxia
- Devic’s Syndrome [Neuromyelitis optica (NMO)]
- Diabetic Neuropathy
- Diffuse Sclerosis [Schilder’s disease]
- Dravet Syndrome [severe myoclonic epilepsy of infancy (SMEI)]
- Dyssynergia Cerebellaris Myoclonica
- Early Infantile Epileptic Encephalopathy [Ohtahara syndrome]
- Empty Sella Syndrome (ESS)
- Encephalitis Lethargica (EL) [von Economo disease]
- Encephalotrigeminal Angiomatosis
- Erb-Duchenne and Dejerine-Klumpke Palsies
- Erb’s Palsy
- Essential Tremor
- Extrapontine Myelinolysis (CPM)
- Fabry Disease
- Fahr’s Syndrome [Idiopathic Basal Ganglia Calcification]
- Fainting [Syncope]
- Familial Dysautonomia (FD) [Riley-Day syndrome]
- Familial Hemangioma [Cavernous malformation]
- Familial Periodic Paralyzes
- Familial Spastic Paralysis [Hereditary spastic paraplegia (HSP)]
- Farber’s Disease [Farber’s lipogranulomatosis or ceramidase deficiency]
- Febrile Seizures
- Fibromuscular Dysplasia (FMD)
- Fisher Syndrome
- Floppy Infant Syndrome [hypotonia or infantile hypotonia]
- Foot Drop
- Friedreich’s Ataxia
- Frontotemporal Dementia [frontotemporal lobar degeneration]
- Gaucher’s Disease
- Gerstmann’s Syndrome
- Gerstmann-Straussler-Scheinker Disease
- Giant Cell Arteritis (GCA)
- Giant Cell Inclusion Disease
- Globoid Cell Leukodystrophy [Krabbe disease]
- Glossopharyngeal Neuralgia
- Glycogen Storage Disease [glycogenosis, dextrinosis]
- Guillain-Barre Syndrome (GBS)
- Hallervorden-Spatz Disease [Neurodegeneration with brain iron accumulation (NBIA)]
- Head Injury
- Hemicrania Continua
- Hemifacial Spasm
- Hemiplegia Alterans
- Hereditary Neuropathies
- Hereditary Spastic Paraplegia (HSP)
- Heredopathia Atactica Polyneuritiformis [Adult Refsum disease (ARD)]
- Herpes Zoster [Shingles]
- Herpes Zoster Oticus [Ramsay Hunt Syndrome or Ramsay Hunt Syndrome type II]
- Hirayama Syndrome [Monomelic amyotrophy (MMA)]
- Holmes-Adie syndrome (HAS)
- HTLV-1 Associated Myelopathy
- Hughes Syndrome [Antiphospholipid syndrome (APS or APLS)]
- Huntington’s Disease
- Hypernychthemeral Syndrome
- Immune-Mediated Encephalomyelitis [Acute disseminated encephalomyelitis (ADE)]
- Inclusion Body Myositis [Sporadic inclusion body myositis (sIBM)]
- Incontinentia Pigmenti (IP)
- Infantile Hypotonia
- Infantile Neuroaxonal Dystrophy (INAD)
- Infantile Phytanic Acid Storage Disease (IRD)
- Infantile Refsum Disease
- Infantile Spasms (IS)
- Inflammatory Myopathies
- Intestinal Lipodystrophy [Whipple’s disease]
- Intracranial Cysts
- Intracranial Hypertension [Idiopathic intracranial hypertension (IIH) / benign intracranial hypertension (BIH) / pseudotumor cerebri (PTC)]
- Isaac’s Syndrome [Neuromyotonia / Isaac-Mertens syndrome / continuous muscle fiber activity syndrome/ quantal squander syndrome]
- Joubert syndrome [Joubert-Boltshauser syndrome / cerebelloparenchymal disorder IV / familial cerebellar vermis agenesis / cerebello-oculo-renal syndrome]
- Kearns-Sayre Syndrome (KSS)
- Kennedy’s Disease (KD) [X-linked spinal and bulbar muscular atrophy (SBMA)]
- Kinsbourne syndrome [Opsoclonus myoclonus syndrome (OMS)]
- Kleine-Levin Syndrome (KLS)
- Klippel-Feil Syndrome
- Klippel-Trenaunay Syndrome (KTS)
- Kluver-Bucy Syndrome
- Korsakoff’s Amnesic Syndrome [ Korsakoff’s psychosis, amnesic-confabulatory syndrome]
- Krabbe Disease [globoid cell leukodystrophy / galactosylceramide lipidosis]
- Kugelberg-Welander Disease [Spinal Muscular Atrophy (SMA) Types I, II, and III]
- Lambert-Eaton Myasthenic Syndrome (LEMS)
- Landau-Kleffner Syndrome (LKS)
- Lateral Medullary Syndrome [Wallenberg’s syndrome / posterior inferior cerebellar artery syndrome]
- Learning Disabilities
- Leigh’s Disease [Leigh syndrome / Subacute Necrotizing Encephalomyelopathy (SNEM)]
- Lennox-Gastaut Syndrome
- Lesch-Nyhan Syndrome [Nyhan’s syndrome]
- Levine-Critchley Syndrome
- Lewy Body Dementia
- Lipid Storage Diseases
- Lipoid Proteinosis
- Locked-In Syndrome
- Lou Gehrig’s Disease [Amyotrophic lateral sclerosis (ALS)]
- Lupus – Neurological Sequelae [systemic lupus erythematosus]
- Lyme Disease
- Machado-Joseph Disease [(MJD) / spinocerebellar ataxia type 3]
- Melkersson-Rosenthal Syndrome
- Menkes Disease
- Meralgia Paresthetica
- Metachromatic Leukodystrophy [MLD / Arylsulfatase A deficiency]
- MigraineMiller Fisher Syndrome
- Mini-Strokes [transient ischemic attack (TIA)]
- Mitochondrial Myopathies
- Motor Neuron Diseases (MNDs)
- Moyamoya Disease
- Multiple System Atrophy
- Muscular Dystrophy
- Myasthenia Gravis
- Neurodegeneration with Brain Iron Accumulation (NBIA)
- Neurological Complications of AIDS
- Neurological Complications Of Lyme Disease
- Neurological Consequences of Cytomegalovirus Infection
- Neurological Manifestations of Pompe Disease
- Neurological Sequelae Of Lupus
- Neuromyelitis Optica or Devic’s disease
- Neuronal Ceroid Lipofuscinosis (NCL) [Batten Disease]
- Neuronal Migration Disorders
- Neuropathy – Hereditary
- Nevus Cavernosus – or cavernous angioma
- Niemann-Pick Disease
- Non 24 Sleep Wake Disorder
- Normal Pressure Hydrocephalus
- Occipital Neuralgia
- Occult Spinal Dysraphism Sequence
- Ohtahara Syndrome
- Olivopontocerebellar Atrophy (OPCA)
- Opsoclonus Myoclonus (OMS)
- Orthostatic Hypotension [postural hypotension / orthostatic reflect / orthostatic intolerance / head rush / dizzy spell]
- O’Sullivan-McLeod Syndrome [Monomelic amyotrophy (MMA)]
- Overuse Syndrome
- Pantothenate Kinase-Associated Neurodegeneration (PKAN) [Hallervorden-Spatz syndrome]
- Paraneoplastic Syndromes
- Parkinson’s Disease
- Paroxysmal Choreoathetosis
- Paroxysmal Hemicrania
- Pelizaeus-Merzbacher Disease (PMD)
- Perineural Cysts
- Periodic Paralyzes
- Peripheral Neuropathy
- Periventricular Leukomalacia (PVL)
- Pervasive Developmental Disorders
- Pinched Nerve
- Piriformis Syndrome
- Pompe Disease
- Postherpetic Neuralgia (PHN)
- Postinfectious Encephalomyelitis [Acute disseminated encephalomyelitis (ADEM)]
- Post-Polio Syndrome (PPS)
- Postural Hypotension
- Postural Orthostatic Tachyardia Syndrome (POTS)
- Primary Lateral Sclerosis (PLS)
- Prion Diseases [Transmissible spongiform encephalopathies (TSEs)]
- Progressive Multifocal Leukoencephalopathy (PML)
- Progressive Sclerosing Poliodystrophy (Alper’s Disease)
- Progressive Supranuclear Palsy (PSP)
- Pseudotumor Cerebri
- Ramsay Hunt Syndrome I
- Ramsay Hunt Syndrome I
- Rasmussen’s Encephalitis
- Reflex Sympathetic Dystrophy Syndrome (RSDS) [Causalgia / CRPS / Reflex sympathetic dystrophy]
- Refsum Disease – Adult Refsum disease (ARD)
- Refsum Disease – Infantile (IRD)
- Repetitive Motion Disorders
- Repetitive Stress Injuries (RSI) [cumulative trauma disorder (CTD) / occupational overuse syndrome / work related upper limb disorder (WRULD)]
- Restless Legs Syndrome – (RLS) [Wittmaack-Ekbom’s syndrome / Nocturnal myoclonus]
- Retrovirus-Associated Myelopathy [Tropical Spastic Paraparesis]
- Rett Syndrome
- Reye’s Syndrome
- Rheumatic Encephalitis [Sydenham chorea (SD)]
- Riley-Day Syndrome
- Saint Vitus Dance [Sydenham chorea (SD)]
- Sandhoff Disease
- Septo-Optic Dysplasia (SOD) [de Morsier syndrome]
- Shaken Baby Syndrome
- Shingles [herpes zoster]
- Shy-Drager Syndrome
- Sjogren’s Syndrome
- Sleep Apnea
- Sleeping Sickness
- Sotos Syndrome
- Spinal Cord Infarction
- Spinal Cord Injury
- Spinal Cord Tumors
- Spinocerebellar Atrophy (SCA)
- Spinocerebellar Degeneration
- Stiff-Person Syndrome (SPS)
- Striatonigral Degeneration
- Stroke (CVA)
- Sturge-Weber Syndrome
- SUNCT Headache
- Syphilitic Spinal Sclerosis
- Tabes Dorsalis
- Tardive Dyskinesia
- Tarlov Cysts
- Tay-Sachs Disease (TSD) [GM2 gangliosidosis / Hexosaminidase A deficiency / Sphingolipidosis]
- Temporal Arteritis [giant cell arteritis (GCA)]
- Tethered Spinal Cord Syndrome
- Thomsen’s Myotonia
- Thoracic Outlet Syndrome (TOS)
- Thyrotoxic Myopathy
- Tic Douloureux [Trigeminal neuralgia (TN)]
- Todd’s Paralysis
- Tourette Syndrome
- Transient Ischemic Attack
- Transmissible Spongiform Encephalopathies
- Transverse Myelitis
- Traumatic Brain Injury
- Trigeminal Neuralgia ( prosopalgia )
- Tropical Spastic Paraparesis (TSP)
- Troyer Syndrome
- Tuberous Sclerosis [tuberous sclerosis complex (TSC)]
- Vasculitis including Temporal Arteritis
- Von Economo’s Disease [Encephalitis lethargica (EL)]
- Von Hippel-Lindau Disease (VHL)
- Von Recklinghausen’s Disease [Neurofibromatosis 1 (NF1)]
- Wallenberg’s Syndrome [Lateral medullary syndrome]
- Werdnig-Hoffman Disease [Infantile spinal muscular atrophy / spinal muscular atrophy type 1 / spinal muscular atrophy type I]
- Wernicke-Korsakoff Syndrome
- West Syndrome
- Whipple’s Disease
- Williams Syndrome [Williams-Beuren syndrome]
- Wilson’s Disease
- Wolman’s Disease [Wolman’s syndrome / acid lipase deficiency]
- X-Linked Spinal and Bulbar Muscular Atrophy [Kennedy disease]
- Zellweger Syndrome
Descriptions of Parkinson’s disease date back as far as 5000 BC. Around that time, an ancient Indian civilization called the disorder Kampavata and treated it with the seeds of a plant containing therapeutic levels of what is today known as levodopa. Parkinson’s disease was named after the British doctor James Parkinson, who in 1817 first described the disorder in detail as “shaking palsy.”
Parkinson’s disease (PD) is a chronic, progressive neurodegenerative motor system disorders characterized by both motor and nonmotor features, which are the result of the loss of dopamine-producing brain cells. Parkinson’s is a progressive disease, which means that in most cases it will continue to gradually get worse. Many people who develop Parkinson’s will require nursing care. There is no cure for the disease and its exact cause is not known, but there are effective treatments that can relieve the symptoms.
Parkinson’s is the second most common age-related neurodegenerative disorder after Alzheimer’s disease, an estimated 10 million people worldwide have PD, with over 1 million people in US. The incidence of PD in the U.S. is approximately 20 cases per 100,000 people per year (60,000 per year), with the mean age of onset close to 60 years. The prevalence of PD ranges from 41 people per 100,000 in the fourth decade of life to more than 1,900 people per 100,000 among those 80 and older. Men are 1 1/2 times more likely to have Parkinson’s than women.
Idiopathic Parkinson’s (IDP)
Idiopathic Parkinson’s disease – or Parkinson’s – is the most common type of parkinsonism. Idiopathic means that the cause is unknown. Necropsy studies of patients with Parkinson’s syndrome show that idiopathic Parkinson’s disease (IPD) comprises between 60 and 75% of cases.
The main symptoms of idiopathic Parkinson’s are tremor, rigidity (stiffness) and slowness of movement.
A definitive diagnosis of IDP requires the postmortem findings of degeneration of the substantia nigra pars compacta and the presence of Lewy bodies (insoluble cytoplasmic inclusions composed of aggregated alpha-synuclein).
Vascular parkinsonism (also known as arteriosclerotic parkinsonism) affects people with restricted blood supply to the brain – usually older people who have health issues such as diabetes.
Sometimes people who have had a mild stroke may experience this form of parkinsonism.
The common symptoms of Vascular Parkonism are walking difficulties, urinary incontinence and memory problems.
The common symptoms of Vascular Parkonism are walking difficulties, urinary incontinence and memory problems.
Some people with vascular parkinsonism may swing their arms less than those with Parkinson’s.
A small number (around 7%) of people diagnosed with parkinsonism develop symptoms following treatment with particular medication.
Neuroleptic drugs (used to treat schizophrenia and other psychotic disorders) which block the action of dopamine are thought to be the biggest cause of drug-induced parkinsonism.
The symptoms of drug-induced parkinsonism tend to be static. Only in rare cases do they change in the manner that the symptoms of Parkinson’s do.
Most people will recover within months, and often within hours or days, of stopping the drug that is the cause.
Drugs to avoid in Parkonism
- chlorpromazine (Largactil)
- fluphenazine (Modecate)
- perphenazine (Fentazin/Triptafen)
- trifluoperazine (Stelazine)
- flupenthixol (Fluanxol/Depixol)
- haloperidol (Serenace/Haldol)
- metoclopramide (Maxalon)
- prochlorperazine (Stemetil)
Multiple System Atrophy (MSA)
- Both multiple system atrophy and Parkinson’s cause stiffness and slowness of movement in the early stages.
- People with multiple system atrophy can also develop symptoms such as incontinence, difficulty with swallowing and dizziness. These symptoms are unusual in early Parkinson’s.
- The condition used to be known as striatonigral degeneration, Shy-Drager syndrome, or olivopontocerebellar atrophy.
Progressive Supranuclear Palsy (PSP)
Progressive supranuclear palsy affects eye movement, balance, mobility, speech and swallowing. It is sometimes called Steele-Richardson-Olszewski syndrome.
Normal Pressure Hydrocephalus
- The symptoms of normal pressure hydrocephalus mainly affect the lower half of the body.
- The common symptoms are walking difficulties, urinary incontinence and memory problems.
- Removing some cerebrospinal fluid can help with these symptoms in the short term. If there is improvement after this procedure, an operation to divert the spinal fluid permanently (known as lumbar puncture) can help in the long term.
Stages of Parkinson’s Disease
Stage 1 is the mildest form of Parkinson’s. At this stage, there may be symptoms, but they’re not severe enough to interfere with daily tasks and overall lifestyle. In fact, the symptoms are so minimal at this stage that they’re often missed. But family and friends may notice changes in your posture, walk, or facial expressions.
A distinct symptom of stage 1 Parkinson’s is that tremors and other difficulties in movement are generally exclusive to one side of the body. Prescribed medications can work effectively to minimize and reduce symptoms at this stage.
Stage 2 is considered a moderate form of Parkinson’s, and the symptoms are much more noticeable than those experienced in stage 1. Stiffness, tremors, and trembling may be more noticeable, and changes in facial expressions can occur.
While muscle stiffness prolongs task completion, stage 2 does not impair balance. Difficulties walking may develop or increase, and the person’s posture may start to change.
People at this stage feel symptoms on both sides of the body (though one side may only be minimally affected) and sometimes experience speech difficulties.
The majority of people with stage 2 Parkinson’s can still live alone, though they may find that some tasks take longer to complete. The progression from stage 1 to stage 2 can take months or even years. And there is no way to predict individual progression.
Stage 3 is the middle stage in Parkinson’s, and it marks a major turning point in the progression of the disease. Many of the symptoms are the same as those in stage 2. However, you’re now more likely to experience loss of balance and decreased reflexes. Your movements become slower overall. This is why falls become more common in stage 3.
Parkinson’s significantly affects daily tasks at this stage, but people are still able to complete them. Medication combined with occupational therapy may help decrease symptoms.
Independence separates people with stage 3 Parkinson’s from those with stage 4. During stage 4, it’s possible to stand without assistance. However, movement may require a walker or other type of assistive device.
Many people are unable to live alone at this stage of Parkinson’s because of significant decreases in movement and reaction times. Living alone at stage 4 or later may make many daily tasks impossible, and it can be extremely dangerous.
Stage 5 is the most advanced stage of Parkinson’s disease. Advanced stiffness in the legs can also cause freezing upon standing, making it impossible to stand or walk. People in this stage require wheelchairs, and they’re often unable to stand on their own without falling. Around-the-clock assistance is required to prevent falls.
Up to 30 percent of people at stage 4 and 5 experience confusion, hallucinations, and delusions. Hallucinations occur when you see things that aren’t there. Delusions happen when you believe things that aren’t true, even when you have been presented with evidence that your belief is wrong. Dementia is also common, affecting up to 75 percent of people with Parkinson’s. Side effects from medications at these later stages can often outweigh the benefits.
Signs and Symptoms
- Motor symptomatology (bradykinesia, rest tremor, rigidity, and postural disturbances)
- Other non-motor symptoms may be present and may even manifest before the motor symptoms
- Rapid Eye Movement
- Sleep Disorders and Sleep Apnea
- Mood & Personality Change
- Urinary disturbances
- Orthostatic Hypotension
- Neuropsychiatric disturbances (dementia, hallucinations and delirium) usually become evident and troublesome after several years in the course of the disease
- Overt dementia is a late complication that most frequently affects older patients with prolonged disease duration
- Skin problems
- Male erectile dysfunction
- Constipation and bowel disorders
- Late-onset motor symptoms include
- Postural Instability & Falls
- Freezing of Gait
- Speech & Swallowing difficulties
Risk Factors Associated With Parkinson’s Disease
- Elevated cholesterol
- Environmental toxins
- Carbon disulfide
- Methanol and organic solvents
- Head traum
- High caloric intake
- Increased body mass index
- Inflammation associated with activation of microglia
- Methcathinone (manganese content)
- Methamphetamine/amphetamine abuse
- Mitochondrial dysfunction
- Nitric oxide toxicity
- Oxidative stress
- Formation of free radicals (e.g., hydrogen peroxide)
- Potent neurotoxins (e.g., 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)
- Post-infection states
- Signal-mediated apoptosis
A substance called dopamine acts as a messenger between two brain areas – the substantia nigra and the corpus striatum – to produce smooth, controlled movements. Most of the movement-related symptoms of Parkinson’s disease are caused by a lack of dopamine due to the loss of dopamine-producing cells in the substantia nigra. When the amount of dopamine is too low, communication between the substantia nigra and corpus striatum becomes ineffective, and movement becomes impaired; the greater the loss of dopamine, the worse the movement-related symptoms. Other cells in the brain also degenerate to some degree and may contribute to non-movement related symptoms of Parkinson’s disease.
Mutations in the -synuclein gene (SNCA) in the Contursi kindred implicated this gene in Parkinson’s disease (PD). Subsequently, -synuclein was identified as the major component of Lewy bodies (cytoplasmic proteinaceous inclusions) in surviving dopaminergic neurons is the pathological hallmark of PD, and of glial cell cytoplasmic inclusions.
Genetic predisposing factors in combination with environmental factors are thought to be responsible for the cellular changes leading to progressive neuronal degeneration in which mitochondrial dysfunction, oxidative mechanisms and failure of the protein degradation machinery at the cellular level are probably involved. So far, five genes have been identified that are definitively associated with Parkinson’s disease.
SNCA (synuclein, alpha non A4 component of amyloid precursor): SNCA makes the protein alpha-synuclein. In brain cells of individuals with Parkinson’s disease, this protein aggregates in clumps called Lewy bodies. Mutations in the SNCA gene are found in early-onset Parkinson’s disease.
PARK2 (Parkinson’s disease autosomal recessive, juvenile 2): The PARK2 gene makes the protein parkin. Mutations of the PARK2 gene are mostly found in individuals with juvenile Parkinson’s disease. Parkin normally helps cells break down and recycle proteins.
PARK7 (Parkinson’s disease autosomal recessive, early onset 7): PARK7 mutations are found in early-onset Parkinson’s disease. The PARK7 gene makes the DJ-1 protein, which may protect cells from oxidative stress.
PINK1 (PTEN-induced putative kinase 1): Mutations of this gene are found in early-onset Parkinson’s disease. The exact function of the protein made by PINK1 is not known, but it may protect structures within the cell called mitochondria from stress.
LRRK2 (leucine-rich repeat kinase 2): LRRK2 makes the protein dardarin. Mutations in the LRRK2 gene have been linked to late-onset Parkinson’s disease.
Several other chromosome regions and the genes GBA (glucosidase beta acid), SNCAIP (synuclein alpha interacting protein), and UCHL1 (ubiquitin carboxyl-terminal esterase L1) may also be linked to Parkinson’s disease.
Diagnosis of Parkinson’s Disease
Bradykinesia and at least one of the following:
- Muscular rigidity
- 4–6 Hz resting tremor
- Postural instability; not caused by primary visual, vestibular, cerebellar, or proprioceptive dysfunction
Exclusion Criteria for PD
History of the following:
- Repeated strokes with stepwise progression
- Repeated head injury
- Antipsychotic or dopamine-depleting drugs
- Definite encephalitis and/or oculogyric crises on no drug treatment
- More than 1 affected relative
- Sustained remission
- Negative response to large doses of levodopa (up to 1,000-1,500 mg/day if tolerated), if malabsorption is excluded
- Strictly unilateral features after 3 years
- Other neurological features: supranuclear gaze palsy, cerebellar signs, early severe autonomic involvement, Babinski sign, early severe dementia with disturbances of language, memory, or praxis
- Exposure to known neurotoxin
- Presence of cerebral tumor or communicating hydrocephalus on neuroimaging
Features that Support a Diagnosis of PD
Three or more required for diagnosis of definite PD:
- Unilateral onset
- Rest tremor present
- Progressive disorder
- Persistent asymmetry affecting the side of onset most
- Excellent (70%–100%) response to levodopa
- Severe levodopa-induced chorea
- Levodopa response for ≥5 years
- Clinical course of ≥10 years
Treatment for Parkinson’s Disease
At present, there is no cure for PD, but a variety of medications provide dramatic relief from the symptoms. Usually, affected individuals are given levodopa combined with carbidopa. Carbidopa delays the conversion of levodopa into dopamine until it reaches the brain. Nerve cells can use levodopa to make dopamine and replenish the brain’s dwindling supply. Although levodopa helps at least three-quarters of parkinsonian cases, not all symptoms respond equally to the drug. Bradykinesia and rigidity respond best, while tremor may be only marginally reduced. Problems with balance and other symptoms may not be alleviated at all. Anticholinergics may help control tremor and rigidity. Other drugs, such as bromocriptine, pramipexole, and ropinirole, mimic the role of dopamine in the brain, causing the neurons to react as they would to dopamine. An antiviral drug, amantadine, also appears to reduce symptoms. In May 2006, the FDA approved rasagiline to be used along with levodopa for patients with advanced PD or as a single-drug treatment for early PD. In March 2017, the FDA approved safinamide tablets as an add-on treatment for individuals with PD how are currently taking levodopa/carbisopa and experiencing “off” episodes (when the person’s medicatins are not working well, causing an increase in PD symptoms).
In some cases, surgery may be appropriate if the disease doesn’t respond to drugs. A therapy called deep brain stimulation (DBS) has now been approved by the U.S. Food and Drug Administration. In DBS, electrodes are implanted into the brain and connected to a small electrical device called a pulse generator that can be externally programmed. DBS can reduce the need for levodopa and related drugs, which in turn decreases the involuntary movements called dyskinesias that are a common side effect of levodopa. It also helps to alleviate fluctuations of symptoms and to reduce tremors, slowness of movements, and gait problems. DBS requires careful programming of the stimulator device in order to work correctly.
Even if you experience symptoms common among people with PD, they may in fact be brought on by a different condition. Consult a doctor if you notice a change in your body with no obvious cause. While visiting the doctor, try to be as specific as possible when describing your symptoms. You may be referred to a movement disorders specialist; a neurologist with particular expertise in PD and other movement disorders.
Psychiatry Disorders Department
Psychiatry Department at Prime Med of Ozark, headed by Dr. Meghani, is one of the best in Alabama, and has unparalleled accomplishments to account under the department. Dr. Meghani, one of the most renowned Psychiatrists in the United States, has a unique way of treating the patients. Dr. Meghani believes in the philosophy that what is not started today is never finished tomorrow and you can’t get too much winter in the winter.
Treatment is our job, Faith is yours.
The following conditions are treated by the Psychiatry Department at Prime Med Clinic of Ozark:
- Absence seizure
- Acute Stress Disorder
- Adjustment Disorders
- Adverse effects of medication NOS
- Age-related Cognitive Decline
- Alcohol Addiction
- Alzheimer’s Disease
- Amphetamine Addiction
- Anorexia Nervosa:
- Anterograde Amnesia
- Antisocial personality disorder
- Anxiety Disorder
- Anxiolytic related disorders
- Asperger’s Syndrome
- Attention Deficit Disorder
- Attention Deficit Hyperactivity Disorder
- Autism Spectrum Disorder
- Avoidant Personality Disorder
- Barbiturate related disorders
- Benzodiazepine-related disorders
- Binge Eating Disorder
- Bipolar disorder
- Body Dysmorphic Disorder
- Borderline intellectual functioning
- Borderline Personality Disorder
- Breathing-Related Sleep Disorder
- Brief Psychotic Disorder
- Bulimia Nervosa
- Caffeine Addiction
- Cannabis Addiction
- Catatonic disorder
- Catatonic schizophrenia
- Childhood amnesia
- Childhood Disintegrative Disorder
- Childhood Onset Fluency Disorder
- Circadian Rhythm Disorders
- Cocaine related disorders
- Communication disorder
- Conduct Disorder
- Conversion Disorder
- Cotard delusion
- Delusional Disorder
- Dependent Personality Disorder (also known as Asthenic Personality Disorder)
- Depersonalization disorder (now known as Depersonalization / Derealization Disorder)
- Depression (also known as Major Depressive Disorder)
- Depressive personality disorder
- Derealization disorder (now known as Depersonalization / Derealization Disorder)
- Developmental coordination disorder
- Diogenes Syndrome
- Disorder of written expression
- Dissocial Personality Disorder
- Dissociative Amnesia
- Dissociative Fugue
- Dissociative Identity Disorder (formerly known as Multiple Personality Disorder)
- Down syndrome
- Dysthymia (now known as Persistent Depressive Disorder)
- Eating disorder NOS
- Ekbom’s Syndrome (Delusional Parasitosis)
- Emotionally unstable personality disorder
- Enuresis (bedwetting)
- Exhibitionistic Disorder
- Expressive language disorder
- Factitious Disorder
- Female Sexual Disorders
- Fetishistic Disorder
- Folie à deux
- Fregoli delusion
- Frotteuristic Disorder
- Fugue State
- Ganser syndrome
- Gambling Addiction
- Gender Dysphoria (formerly known as Gender Identity Disorder)
- Generalized Anxiety Disorder
- General adaptation syndrome
- Grandiose delusions
- Hallucinogen Addiction
- Haltlose personality disorder
- Histrionic Personality Disorder
- Primary hypersomnia
- Huntington’s Disease
- Hypoactive sexual desire disorder
- Hyperkinetic syndrome
- Impulse control disorder
- Impulse control disorder NOS
- Inhalant Addiction
- Intellectual Development Disorder
- Intermittent Explosive Disorder
- Joubert syndrome
- Korsakoff’s syndrome
- Lacunar amnesia
- Language Disorder
- Learning Disorders
- Major Depression (also known as Major Depressive Disorder)
- major depressive disorder
- Male Sexual Disorders
- Mathematics disorder
- Medication-related disorder
- Mental Retardation (now known as Intellectual Development Disorder)
- Morbid jealousy
- Multiple Personality Disorder (now known as Dissociative Identity Disorder)
- Munchausen Syndrome
- Munchausen by Proxy
- Narcissistic Personality Disorder
- Neglect of child
- Neurocognitive Disorder (formerly known as Dementia)
- Neuroleptic-related disorder
- Nightmare Disorder
- Non Rapid Eye Movement
- Obsessive-Compulsive Disorder
- Obsessive-Compulsive Personality Disorder (also known as Anankastic Personality Disorder)
- Opioid Addiction
- Oppositional Defiant Disorder
- Orthorexia (ON)
- Pain disorder
- Panic attacks
- Panic Disorder
- Paranoid Personality Disorder
- Parkinson’s Disease
- Partner relational problem
- Passive-aggressive personality disorder
- Pathological gambling
- Pedophilic Disorder
- Persecutory delusion
- Persistent Depressive Disorder (also known as Dysthymia)
- Personality change due to a general medical condition
- Personality disorder
- Pervasive developmental disorder (PDD)
- Phencyclidine related disorder
- Phobic disorder
- Phonological disorder
- Physical abuse
- Polysubstance related disorder
- Postpartum Depression
- Post-traumatic embitterment disorder (PTED)
- Post Traumatic Stress Disorder
- Premature ejaculation
- Premenstrual Dysphoric Disorder
- Psychogenic amnesia
- Psychological factor affecting medical condition
- Psychoneurotic personality disorder
- Psychotic disorder, not otherwise specified
- Reactive Attachment Disorder
- Reading disorder
- Recurrent brief depression
- Relational disorder
- REM Sleep Behavior Disorder
- Restless Leg Syndrome
- Retrograde amnesia
- Retts Disorder (now part of Autism Spectrum Disorder)
- Rumination syndrome
- Sadistic personality disorder
- Schizoaffective Disorder
- Schizoid Personality Disorder
- Schizophreniform disorder
- Schizotypal Personality Disorder
- Seasonal Affective Disorder
- Sedative, Hypnotic, or Anxiolytic Addiction
- Selective Mutism
- Self-defeating personality disorder
- Separation Anxiety Disorder
- Sexual Disorders Female
- Sexual Disorders Male
- Sexual Addiction
- Sexual Masochism Disorder
- Sexual Sadism Disorder
- Shared Psychotic Disorder
- Sleep Arousal Disorders
- Sleep Paralysis
- Sleep Terror Disorder (now part of Nightmare Disorder
- Social Anxiety Disorder
- Somatization Disorder
- Specific Phobias
- Stendhal syndrome
- Stereotypic movement disorder
- Stimulant Addiction
- Stuttering (now known as Childhood Onset Fluency Disorder)
- Substance related disorder
- Tardive dyskinesia
- Tobacco Addiction
- Tourettes Syndrome
- Transient tic disorder
- Transient global amnesia
- Transvestic Disorder
- Voyeuristic Disorder
Seizures happen when your brain cells, which communicate through electrical signals, send out the wrong signals. Having just one seizure does not mean you have epilepsy. Generally, several seizures are needed before there is a diagnosis of epilepsy.
Epilepsy can happen at any age, but it is most common in the elderly. Many children with epilepsy outgrow the condition. However, even mild seizures that happen more than once should be treated. Seizures can be very dangerous if they happen while you are driving, walking, or swimming, for example.
A seizure is an abnormal electrical discharge that occurs in your brain. Usually brain cells, or neurons, flow in an organized fashion along the surface of your brain. A seizure occurs when there is an excess of electrical activity.
Typically, you are diagnosed with a seizure disorder once you’ve had two or more “unprovoked” seizures. Unprovoked seizures have what are considered natural causes, such as genetic factors or metabolic imbalances in your body.
“Provoked” seizures are triggered by a specific event like a brain injury or stroke. To be diagnosed with epilepsy or a seizure disorder, you need to have at least two unprovoked seizures.
Seizures are classified into two primary types: partial seizures, also called focal seizures, and generalized seizures. Both can be associated with seizure disorders.
Partial, or focal, seizures begin in a specific part of your brain. If they originate on one side of your brain and spread to other areas, they are called simple partial seizures. If they begin in an area of your brain that affects consciousness, they are called complex partial seizures.
Simple partial seizures have symptoms including:
- involuntary muscle twitching
- vision changes
- sensory changes
Complex partial seizures can cause similar symptoms, and may also lead to loss of consciousness.
Generalized seizures begin on both sides of your brain at the same time. Because these seizures spread quickly, it can be difficult to tell where they originated. This makes certain kinds of treatments more difficult.
There are several different types of generalized seizures, each with their own symptoms:
- Absence seizures are brief episodes that may make you stare off while remaining motionless, as though you are daydreaming. They typically occur in children.
- Myoclonic seizures can cause your arms and legs to twitch on both sides of your body
- Tonic-clonic seizures can go on for a long time, sometimes up to 20 minutes. This type of seizure can cause more serious symptoms, such as loss of bladder control and loss of consciousness, in addition to uncontrolled movements.
Another type of seizure is a febrile seizure that occurs in infants as the result of a fever. About one in every 25 children, between the ages of 6 months to 5 years, has a febrile seizure. Generally, children who have febrile seizures don’t need to be hospitalized, but if the seizure is prolonged, your doctor may order hospitalization to observe your child.
Signs and Symptoms
Many different symptoms happen during a seizure. This new classification separates them simply into groups that involve movement.
For generalized onset seizures:
- Motor (Grand Mal) symptoms may include sustained rhythmical jerking movements (clonic), muscles becoming weak or limp (atonic), muscles becoming tense or rigid (tonic), brief muscle twitching (myoclonus), or epileptic spasms (body flexes and extends repeatedly).
- Non-motor symptoms are usually called absence seizures or petit mal. These can be typical or atypical absence seizures (staring spells). Absence seizures can also have brief twitches (myoclonus) that can affect a specific part of the body or just the eyelids.
For focal onset seizures:
- Motor symptoms may also include jerking (clonic), muscles becoming limp or weak (atonic), tense or rigid muscles (tonic), brief muscle twitching (myoclonus), or epileptic spasms. There may also be automatisms or repeated automatic movements, like clapping or rubbing of hands, lipsmacking or chewing, or running.
- Non-motor symptoms: Examples of symptoms that don’t affect movement could be changes in sensation, emotions, thinking or cognition, autonomic functions (such as gastrointestinal sensations, waves of heat or cold, goosebumps, heart racing, etc.), or lack of movement (called behavior arrest).
For unknown onset seizures:
- Motor seizures are described as either tonic-clonic or epileptic spasms.
- Non-motor seizures usually include a behavior arrest. This means that movement stops – the person may just stare and not make any other movements.
- Viral encephalitis
- High blood levels of sugar or sodium
- Low blood levels of sugar, calcium, magnesium, or sodium
- Kidney failure or liver failure, which can lead to dysfunction of the brain (encephalopathy)
- An underactive parathyroid gland
- Vitamin B6 deficiency (in newborns)
Inadequate oxygen supply to the brain
- Abnormal heart rhythms
- Cardiac arrest
- Carbon monoxide poisoning
- Near drowning
- Near suffocation
Structural damage to the brain
- Brain tumor (noncancerous or cancerous)
- Head injury
- Intracranial hemorrhage (bleeding within the skull)
- Alzheimer’s Disease
Abnormalities present or occurring at birth
- Birth defect
- Hereditary metabolic disorders, such as Tay-Sachs disease or phenylketonuria
- Injury during birth
Fluid accumulation in the brain (cerebral edema)
- Hypertensive encephalopathy
- Buspirone (used to treat anxiety disorders)
- *Chlorpromazine (used to treat schizophrenia)
- Ciprofloxacin (an antibiotic)
- Chloroquine (used to treat malaria)
- Clozapine (usually used to treat schizophrenia)
- Cyclosporine (used to prevent and treat rejection of organ transplants)
- Imipenem (an antibiotic)
- *Indomethacin (used to relieve pain and reduce inflammation)
- *Meperidine (used to relieve pain)
- Theophylline (used to treat asthma and other airway disorders)
- Tricyclic antidepressants
- Cocaine (overdose)
Withdrawal of a drug after heavy use
- General anesthetics (used during surgery)
- Sedatives, including sleep aids
Exposure to toxins
*Various drugs can cause seizures if too much is taken. Some drugs can also lower the seizure threshold
†Phenytoin, used to treat seizure disorders, can cause seizures if too much is taken.
Your doctor will do blood tests and an electroencephalogram (EEG), which records the electrical activity in your brain. You may also have a computerized tomography (CT) scan, a magnetic resonance imaging (MRI) scan, and a positron emission tomography (PET) scan.
Your doctor may prescribe medicines called antiepileptics, which aim to alter or reduce excess electrical activity in your brain. Some of the many kinds of these medicines include phenytoin and carbamazepine.
Surgery may be another treatment option if you have partial seizures that aren’t helped by medicine. The goal of surgery is to remove the part of your brain where your seizures begin.
Nutrition and Supplements
A ketogenic diet. A diet that is high in fat and low in protein and carbohydrates — may help control the frequency of seizures. This type of diet is most commonly used in children, and seems to work better for children than adults. If you are on a ketogenic diet, your doctor should monitor you both for side effects and effectiveness. You may need to take vitamin and mineral supplements, because this diet is very restricted. DO NOT attempt a ketogenic diet on your own. Work with your physician to make sure you are doing it safely.
Some studies have shown a connection between food allergies and seizures in some children. But the evidence is not clear. Avoid alcohol, caffeine, and any supplements that have stimulating effects. A holistically-oriented health care provider may help you identify possible food allergies.
Some supplements may make certain antiseizure medications less effective. Ask your doctor before taking any herbs or supplements.
- Taurine is an amino acid that may be involved in the brain’s electrical activity and is often low in people with seizures. It acts like GABA (gamma aminobutyric acid), another amino acid that is often low in people with seizures. But there is no scientific evidence that taking either supplement will reduce seizures. Taurine may interact with many medications. DO NOT take taurine or GABA supplements without your doctor’s supervision. DO NOT take taurine or GABA if you have a history of bipolar disorder, or if you take psychoactive medications.
- Folic acid levels may drop during seizures and may be low in some people with seizures, however, taking extra folic acid may make anticonvulsant drugs less effective. That could raise your risk for more seizures. DO NOT take folic acid without your doctor’s supervision.
- Vitamin B12. Some anticonvulsant drugs may cause low levels of B12 in the body.
- Vitamin E may help reduce the frequency of seizures when used with prescription drugs. But some studies show that it does not help. DO NOT take vitamin E if you take blood thinners. Vitamin E can interact with a number of medications. So ask your doctor before taking it.
- Anticonvulsant drugs may cause low levels of calcium, vitamin D, and vitamin K. If you take anticonvulsant drugs, ask your doctor about taking a supplement. Calcium can interfere with anticonvulsant drugs. So DO NOT take calcium without your doctor’s supervision.
Herbs are a way to strengthen and tone the body’s systems. As with any therapy, you should work with your health care provider to diagnose your problem before starting treatment. You may use herbs as dried extracts (capsules, powders, or teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, make teas with 1 tsp. (5 g) herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups per day. You may use tinctures alone or in combination as noted.
Many of the herbs used to treat seizures have sedative effects, and they interact with other herbs, supplements, and prescription medications. Take these herbs only under a doctor’s supervision. It is important for a health care professional to monitor side effects and interactions. Most of these herbs have been used traditionally for seizures, but lack scientific evidence showing they work.
- Bacopa (Bacopa monnieri). An herb used in Ayurvedic medicine to treat epilepsy. Some studies found that bacopa may reduce the frequency of seizures. More research is needed. Take special care if you have a history of lung or urinary problems or a history of ulcers.
- Chamomile (Matricaria recutita). A sedative herb. Ask your doctor to help you find the right dose. Chamomile can make the effects of other sedatives stronger. It also interacts with many other medications.
- Kava (Piper methysticum). Has been used traditionally as a sedative herb for seizures. However, there is some concern that kava can damage the liver, even if taken for a short time. Take kava only under your doctor’s supervision, so they can monitor liver function. Kava may interact with a number of other drugs. DO NOT take kava if you have Parkinson’s disease.
- Valerian (Valeriana officinalis). A sedative and anticonvulsive. It interacts with several medications, herbs, and alcohol, so take it only under your doctor’s supervision. Valerian is sometimes combined with lemon balm (Melissa officinalis), another herb that has sedative effects.
- Passionflower (Passiflora incarnata). May help treat and prevent seizures.
DO NOT take the following herbs:
- Ginkgo (Ginkgo biloba) and ginseng (Panax ginseng and Panax quinquefolius) have caused seizures in some people.
- There is some evidence that GLA, a kind of fatty acid found in evening primrose oil(Oenothera biennis) and borage oil (Borago officinalis), may worsen epilepsy. More research is needed.
- St. John’s wort (Hypericum perforatum) interacts with a number of medications and herbs used to treat epilepsy.
- White willow (Salix alba) may interact with epilepsy medications.
Avoid these essential oils:
- Eucalyptus (Eucalyptus globulus)
- Fennel (Foeniculum vulgare)
- Hyssop (Hyssopus officinalis)
- Pennyroyal (Mentha pulegium)
- Rosemary (Rosmarinus officinalis)
- Sage (Salvia officinalis)
- Tansy (Tanacetum vulgare)
- Thuja (Thuya occidentalis)
- Wormwood (Artemesia absinthium)
Few studies have examined the effectiveness of specific homeopathic remedies. Professional homeopaths, however, may recommend one or more of the following treatments for seizure disorders based on their knowledge and clinical experience. Before prescribing a remedy, homeopaths take into account a person’s constitutional type, includes your physical, emotional, and intellectual makeup. An experienced homeopath assesses all of these factors when determining the most appropriate remedy for a particular individual.
- Belladonna. For seizures that occur in individuals with a high fever.
- Causticum. For individuals whose seizures may be triggered by receiving bad news or by feelings of sadness such as from grief; this remedy is most appropriate for individuals who tend to feel hopeless and fearful.
- Cicuta. For individuals who develop seizures after a head injury.
- Cuprum metallicum. For individuals whose seizures are accompanied by mental dullness; may be triggered by menstruation or vomiting.
Rhinosinusitis (Sinusitis or Sinus Infection)
If you have nasal congestion, facial pressure, cough and thick nasal discharge, you may have rhinosinusitis, commonly referred to as sinusitis.
Sinuses are hollow spaces in the bones around the nose that connect to the nose through small, narrow channels. The sinuses stay healthy when the channels are open, which allows air from the nose to enter the sinuses and mucus made in the sinuses to drain into the nose.
Sinusitis, also called rhinosinusitis, affects about 1 in 8 adults annually and generally occurs when viruses or bacteria infect the sinuses (often during a cold) and begin to multiply. Part of the body’s reaction to the infection causes the sinus lining to swell, blocking the channels that drain the sinuses. This causes mucus and pus to fill up the nose and sinus cavities.
Humans have four pair of these cavities each referred to as the:
- frontal sinus (in forehead),
- maxillary sinus (behind cheeks),
- ethmoid sinuses (between the eyes), and
- sphenoid sinus (deep behind the ethmoids).
The four pair of sinuses are often described as a unit and termed the “paranasal sinuses.” The cells of the inner lining of each sinus are mucus-secreting cells, epithelial cells and some cells that are part of the immune system (macrophages, lymphocytes, and eosinophils).
What Causes It?
Lots of people. About 35 million Americans have sinusitis at least once each year. Conditions that can cause sinus blockage include:
- Nasal polyps: These tissue growths can block the nasal passages or sinuses.
- Deviated nasal septum: A crooked septum — the wall between the nostrils — may restrict or block sinus passages.
- Other medical conditions: The complications of cystic fibrosis, gastroesophageal reflux, or HIV and other immune system-related diseases can result in nasal blockage.
- Respiratory tract infections: Infections in your respiratory tract — most commonly colds — can inflame and thicken your sinus membranes and block mucus drainage. These infections can be viral, bacterial or fungal.
- Allergies such as hay fever: Inflammation that occurs with allergies can block your sinuses.
- Allergic rhinitis: which is swelling of the lining of the nose.
- Immune system deficiencies or medications that suppress the immune system, such as; Budesonide (Entocort EC), Cortisone (Cortone), Dexamethasone (Decadron), Hydrocortisone (Cortef), Methylprednisolone (Medrol), Prednisolone (Prelone), Prednisone (Deltasone), Triamcinolone and others.
For children, things that can cause sinusitis include:
- Illnesses from other kids at day care or school
- Bottle drinking while lying on the back
- Smoke in the environment
- Acute sinusitis usually starts with cold-like symptoms such as a runny, stuffy nose and facial pain. It may start suddenly and last 2-4 weeks. Acute viral sinusitis is likely if you have been sick less than 10 days and are not getting worse. Acute bacterial sinusitis is likely when you do not improve at all within 10 days of getting sick or when you get worse within 10 days after beginning to get better.
- Subacute sinusitis inflammation usually lasts 4 to 12 weeks.
- Chronic sinusitis inflammation symptoms last 12 weeks or longer. People with allergic rhinitis or asthma are more likely to suffer from chronic sinusitis. This is because the airways are more likely to become inflamed when allergic rhinitis or asthma are present.
- Recurrent sinusitis happens several times a year.
At least two of the four primary signs and symptoms of chronic sinusitis must be present with confirmation of nasal inflammation for a diagnosis of the condition. They are:
- Thick, discolored discharge from the nose or drainage down the back of the throat (postnasal drainage) or
- Yellowish-greenish nasal discharge that may have an odor
- Nasal obstruction or congestion, causing difficulty breathing through your nose
- Pain, tenderness and swelling around your eyes, cheeks, nose or forehead
- Reduced sense of smell and taste in adults or cough in children
- Post nasal drip is mucus overproduction from sinusitis that flows to the throat and irritates throat tissue
Other signs and symptoms can include:
- Ear pain
- Aching in your upper jaw and teeth
- Cough that might worsen at night
- Sore throat
- Bad breath (halitosis)
- Fatigue or irritability
- Tooth pain
- Itching eyes or sneezing
Chronic sinusitis and acute sinusitis have similar signs and symptoms, but acute sinusitis is a temporary infection of the sinuses often associated with a cold. The signs and symptoms of chronic sinusitis last longer and often cause more fatigue. Fever isn’t a common sign of chronic sinusitis, but you might have one with acute sinusitis.
Is Chronic Sinusitis Treated Differently Than Acute Sinusitis?
Because chronic sinusitis is caused more by inflammation than infection, the treatments for chronic sinusitis are meant to control the inflammation. Salt water nasal irrigation and/or nasal steroid sprays are the main treatments for the symptoms of chronic sinusitis. It may help to look for other factors that can go along with chronic sinusitis and possibly make the problem worse, and have them treated too. Some of these factors are allergies, nasal polyps, asthma, and problems with the body’s ability to fight infections.
Do I Need Surgery For My Sinusitis?
Surgery for the sinuses is done when the symptoms can’t be controlled with medications and other treatments. The most common type of surgery for the sinuses is called endoscopic sinus surgery, because a pencil-sized scope (“endoscope”) is used to see inside the nose and sinuses and guide the surgery. The purpose of the surgery is to widen the natural drainage pathways between the sinuses and the nose, allowing mucus to get out of the sinuses and air to get in. Medications that are delivered to the surface of the nose and sinuses, like sprays and irrigations, can get into the sinuses better after surgery as well.
You’re at increased risk of getting chronic or recurrent sinusitis if you have:
- A nasal passage abnormality, such as a deviated nasal septum or nasal polyps
- Asthma, which is highly connected to chronic sinusitis
- Aspirin sensitivity that causes respiratory symptoms
- An immune system disorder, such as HIV/AIDS or cystic fibrosis
- Hay fever or another allergic condition that affects your sinuses
- Regular exposure to pollutants such as cigarette smoke
Chronic sinusitis complications include:
- Meningitis: This infection causes inflammation of the membranes and fluid surrounding your brain and spinal cord.
- Other infections: Uncommonly, infection can spread to the bones (osteomyelitis) or skin (cellulitis).
- Partial or complete loss of sense of smell: Nasal obstruction and inflammation of the nerve for smell (olfactory nerve) can cause temporary or permanent loss of smell.
- Vision problems: If infection spreads to your eye socket, it can cause reduced vision or even blindness that can be permanent.
Take these steps to reduce your risk of getting chronic sinusitis:
- Avoid upper respiratory infections. Minimize contact with people who have colds. Wash your hands frequently with soap and water, especially before meals.
- Manage your allergies. Work with your doctor to keep symptoms under control.
- Avoid cigarette smoke and polluted air. Tobacco smoke and air contaminants can irritate and inflame your lungs and nasal passages.
- Use a humidifier. If the air in your home is dry, such as it is if you have forced hot air heat, adding moisture to the air may help prevent sinusitis. Be sure to keep the humidifier clean and free of mold with regular, thorough cleaning.
Substance Abuse Recovery Program
SUBOXONE/SUBUTEX Treatment Program at Prime Med of Ozark for Heroin/Opioid/Pain Medicine Dependence and Substance-Abuse
Have You Gone Too Far?
There’s still a way back.
Substance abuse is a broad term that can describe a wide range of dangerous and harmful behaviors involving both legal and illegal substances. Alcohol, tobacco, marijuana, and prescription medications are among the most commonly abused substances in the United States, while the abuse of heroin, cocaine, methamphetamine, and other drugs remains problematic in communities throughout the nation. Depending upon the specific substance being abused, the amount and frequency of that abuse, and certain other factors, individuals who engage in substance abuse are at risk for myriad negative outcomes, including significant physical and psychological damage and the development of a substance use disorder.
Commonly referred to as addiction or chemical dependency, substance use disorders are characterized by a variety of unpleasant symptoms that include prioritizing substance abuse over important issues such as relationships, career, and academic progress, continuing to abuse substances even after experiencing negative repercussions, and experiencing painful withdrawal symptoms when attempting to stop or limit one’s substance abuse.
Drug overdose deaths and opioid-involved deaths continue to increase in the United States. The majority of drug overdose deaths (more than six out of ten) involve an opioid. Since 1999, the number of overdose deaths involving opioids (including prescription opioids and heroin) quadrupled.2 From 2000 to 2015 more than half a million-people died from drug overdoses. 91 Americans die every day from an opioid overdose.
We now know that overdoses from prescription opioids are a driving factor in the 15-year increase in opioid overdose deaths. The amount of prescription opioids sold to pharmacies, hospitals, and doctors’ offices nearly quadrupled from 1999 to 2010, yet there had not been an overall change in the amount of pain that Americans reported. Deaths from prescription opioids—drugs like oxycodone, hydrocodone, and methadone—have more than quadrupled since 1999.
In their search for a less addictive opiate, in the mid-1990s drug companies first designed extended release opiates like Vicodin (containing hydrocodone and Tylenol) and Percocet, which contains oxycodone and Tylenol. Subsequently, they created a purer opiate, containing only oxycodone, most commonly known under the brand Oxycontin.
At Prime Med Substance-Abuse Treatment Program, we are familiar with the many ways that substance abuse can devastate individuals and families. Perhaps more importantly, we are also dedicated to developing innovative and effective programming that can help adolescents and adults overcome their dependence upon alcohol and/or other drugs and learn to live healthier and more satisfying lives, free from the limitations of addiction. At programs throughout Prime Med of Ozark network, experienced and dedicated professionals provide the life-changing therapeutic interventions and other clinical services that help individuals emerge from the darkness of substance abuse and addiction and take their first steps along the path toward a brighter, drug-free future.
Why Consider Treatment for Substance Abuse?
It is difficult to overstate the degree of devastation that can occur in the lives of individuals who do not receive effective care for substance abuse and chemical dependency. The potential impact of a single experience with substance abuse can range from temporary incapacitation to irreversible damage, including death. As an individual continues to engage in a pattern of substance abuse, both the likelihood and the possible severity of these negative outcomes continues to increase. The physical damage of substance abuse can include, but is not limited to, heart problems, breathing impairments, vision trouble, liver and kidney damage, tics and tremors, and increased risk for certain cancers. Psychological effects may include diminished cognition, anxiety, depression, paranoia, hallucinations, and delusions. An individual whose mind and body has been weakened by substance abuse is at increased risk for academic failures, diminished occupational performance, and deteriorating interpersonal relationships. Other negative outcomes that have been associated with chronic substance abuse and addiction include unemployment, financial setbacks, arrest and incarceration, homelessness, social ostracization, hopelessness, and suicide.
Our Experience with the Suboxone or Subutex Treatment for Substance and Opioid Dependence
Office-based buprenorphine-naloxone (Suboxone) treatment in the United States has significantly improved access to safe and effective opioid-dependence therapy. Patients averaged 32 years old, 4.3 years of opioid dependence, and were primarily white (93%) and employed (70%). Fifty-two percent used heroin primarily (most by injection), and 70% had no agonist substitution therapy history. Almost half (47%) paid for their own treatment. Suboxone maintenance was associated with good treatment retention and significantly reduced opioid use, and it is helping to reach patients, including injection drug users, without histories of agonist substitution therapy.
The recent advancements in the understanding of the neurobiology underlying addiction related behavior have contributed to the recognition that opioid addiction is a serious complication of chronic opioid intake in some individuals (note that patients receiving opioids for chronic pain do not necessarily develop addiction). Nowadays, addiction is considered a chronic disease of the brain rather than a mental illness carrying a social stigma.
Opiate addiction is a chronic relapsing disorder associated with significant morbidity and mortality as well as with severe psychosocial complications and which requires long-term care and management strategies.
Our treatment program devises careful dosages of medicines that competitively inhibits the pharmacologic effects of exogenously administered opioids and, in line with the classical receptor theory, produces a parallel right shift in the dose-response curves of opioids. Suboxone is readily transported across the blood-brain barrier and, therefore, has a fast onset of action in reversing opioid effects. Its duration of action is limited due to its short elimination half-life of 30 minutes. The ability of suboxone to reverse opioid effects in vivo is mainly determined by the pharmacologic characteristics of the interacting opioid agonist (i.e., the opioid that requires antagonism).
Anesthesiologists use buprenorphine/naloxone for reversal of postoperative respiratory depression induced by potent opioid analgesics, such as fentanyl, sufentail and morphine. Similarly, buprenorphine/naloxone may be used to treat opioid overdose in opioid-dependent patients.
SUBOXONE/SUBUTEX Treatment Program for Substance-Abuse Disorder including Opioid, Heroin, Pain Medicines, Methamphetamine, Marijuana and Alcoholic Annoymous is the foremost proven treatment provided in special patient-based strategies that Prime Med of Ozark is champion.
Tinnitus (Ringing in the Ear)
Tinnitus—the false perception of sound in the absence of an acoustic stimulus, a phantom noise—is one of the most common clinical syndromes in the United States, affecting 12 % men and 14% women who are sixty-five and older; which accounts for 1 in 5 people. It only rarely afflicts the young, with one significant exception: those serving in the armed forces. Tinnitus affects nearly half the soldiers exposed to blasts in Iraq and Afghanistan. Tinnitus is often described as ringing in the ears, but that’s not the only sound that qualifies. It can also present as buzzing, roaring, clicking, hissing, or a noise like crickets, among other things. A type known as pulsatile tinnitus is rhythmic, often keeping time with the person’s heartbeat.
Normally, the outer ear, known as the pinna, collects sound waves and directs them into the ear canal, which carries the sound waves to the eardrum. In turn, the eardrum vibrates, and these tremors are picked up by the three tiny bones in the middle ear: the malleus (resembling a club), the incus (shaped like an anvil), and the stapes (similar to a stirrup). These bones amplify the sound vibrations and transmit them to the inner ear, where the cochlea converts the vibrations into electrical impulses, which travel from the acoustic nerve to the part of the brain that processes sound, the auditory cortex. Tinnitus can be temporary, caused by excess wax, an infection of the inner ear, or the toxic effects of drugs like aspirin (which appears to weaken the neural signals from the ear to the brain) or those used to treat cancer. Some people with normal hearing develop spontaneous tinnitus when placed in total silence; this is believed to be a response of the auditory cortex to the abnormal absence of all ambient sounds. But the majority of people with chronic symptoms develop them in conjunction with hearing loss. With the recent proliferation of MP3 players, rates of hearing loss and tinnitus may rise sharply in the coming years.
The health related causes for tinnitus includes:
- Noise-induced hearing loss
- Ear and sinus infections
- Diseases of the heart or blood vessels
- Ménière’s disease
- Brain tumors
- Hormonal changes in women
- Thyroid abnormalities
Tinnitus is sometimes the first sign of hearing loss in older people. It also can be a side effect of medications. More than 200 drugs are known to cause tinnitus when you start or stop taking them.
People who work in noisy environments—such as factory or construction workers, road crews, or even musicians—can develop tinnitus over time when ongoing exposure to noise damages tiny sensory hair cells in the inner ear that help transmit sound to the brain. This is called noise-induced hearing loss.
Tinnitus involves the annoying sensation of hearing sound when no external sound is present. Tinnitus symptoms include these types of phantom noises in your ears:
The phantom noise may vary in pitch from a low roar to a high squeal, and you may hear it in one or both ears. In some cases, the sound can be so loud it can interfere with your ability to concentrate or hear actual sound. Tinnitus may be present all the time, or it may come and go.
There are two kinds of tinnitus.
- Subjective tinnitus is tinnitus only you can hear. This is the most common type of tinnitus. It can be caused by ear problems in your outer, middle or inner ear. It also can be caused by problems with the hearing (auditory) nerves or the part of your brain that interprets nerve signals as sound (auditory pathways).
- Objective tinnitus is tinnitus your doctor can hear when he or she does an examination. This rare type of tinnitus may be caused by a blood vessel problem, a middle ear bone condition or muscle contractions.
What should I do if I have tinnitus?
The first thing is to see your primary care doctor, who will check if anything, such as ear wax, is blocking the ear canal. Your doctor will ask you about your current health, medical conditions, and medications to find out if an underlying condition is causing your tinnitus.
If your doctor cannot find any medical condition responsible for your tinnitus, you may be referred to an otolaryngologist (commonly called an ear, nose, and throat doctor, or an ENT). The ENT will physically examine your head, neck, and ears and test your hearing to determine whether you have any hearing loss along with the tinnitus. You might also be referred to an audiologist who can also measure your hearing and evaluate your tinnitus.
Questions that a doctor might ask include:
- How or when did it start?
- Are the noises constant, intermittent, or pulsating?
- Is there any hearing loss or dizziness?
- Is there any pain or jaw clicking?
- Have you had a recent illness or injury?
- Has there been any exposure to loud noise, such as a rock concert or explosives?
Tests may include:
- a complete examination of the ear, head, neck, and torso
- hearing tests
- laboratory blood tests
- imaging studies
The first step is to treat any underlying cause of tinnitus. This may involve:
- prompt care for an ear infection
- discontinuing any ototoxic medications
- treating any temporomandibular joint (TMJ) problems, which affect the joint betwen the jaw bone and the cheek bone
There is no cure for most cases of tinnitus. Most people become accustomed to it and learn to tune it out. Ignoring it rather than focusing on it can provide relief.
When this does not work, the individual may benefit from treatment for the effects of tinnitus, insomnia, anxiety, hearing difficulties, social isolation, and depression. Dealing with these issues can significantly improve a person’s quality of life.
Here are some other things a person can do to manage tinnitus and its effects.
Sound therapy uses external noise to mask the individual’s perception of tinnitus. Low-level background music, white noise, or specialized ear maskers can help. The choice of sound should be pleasant to the individual. Masking devices offer temporary relief, and the awareness of tinnitus returns when the sound therapy is turned off. Hearing aids are a common type of sound therapy. They amplify environmental sounds and redirect attention to those noises instead of the tinnitus.
Tinnitus retraining therapy (TRT) involves retraining the auditory system to accept the abnormal sounds of tinnitus as natural rather than disruptive. It involves help from a trained professional and wearing a device that emits low-level white noise. Ongoing counseling sessions can help people cope with the tinnitus. This therapy’s success is proportionate to the severity of the tinnitus and the individual’s overall mental health. Follow-up studies suggest that TRT provides relief for around 80 percent of people with tinnitus.
Other techniques to mitigate the impact of tinnitus includes:
- Get your blood pressure checked. If it is high, get your doctor’s help to control it
- Exercise daily to improve your circulation
- Get adequate rest and avoid fatigue
- Use physical (sound machine) and mental techniques to push the perception of tinnitus to the background; the more you think about the tinnitus, the louder it will seem. If you cannot do this on your own, seek help as outlined above.
In 2009, the National Institute on Deafness and Other Communication Disorders (NIDCD) sponsored a workshop that brought together tinnitus researchers to talk about the condition and develop fresh ideas for potential cures. During the course of the workshop, participants discussed a number of promising research directions, including:
- Electrical or magnetic stimulation of brain areas involved in hearing. Implantable devices already exist to reduce the trembling of Parkinson’s disease and the anxieties of obsessive-compulsive disorder. Similar devices could be developed to normalize the neural circuits involved in tinnitus.
- Repetitive transcranial magnetic stimulation (rTMS). This technique, which uses a small device placed on the scalp to generate short magnetic pulses, is already being used to normalize electrical activity in the brains of people with epilepsy. Preliminary trials of rTMS in humans, funded by the NIDCD, are helping researchers pinpoint the best places in the brain to stimulate in order to suppress tinnitus. Researchers are also looking for ways to identify which people are most likely to respond well to stimulation devices.
- Hyperactivity and deep brain stimulation. Researchers have observed hyperactivity in neural networks after exposing the ear to intense noise. Understanding specifically where in the brain this hyperactivity begins and how it spreads to other areas could lead to treatments that use deep brain stimulation to calm the neural networks and reduce tinnitus.
- Resetting the tonotopic map. Researchers are exploring how to take advantage of the tonotopic map, which organizes neurons in the auditory cortex according to the frequency of the sound to which they respond. Previous research has shown a change in the organization of the tonotopic map after exposing the ear to intense noise. By understanding how these changes happen, researchers could develop techniques to bring the map back to normal and relieve tinnitus.
Tremor is an unintentional, rhythmic muscle movement involving to-and-fro movements (oscillations) of one or more parts of the body. It is the most common of all involuntary movements and can affect the hands, arms, head, face, voice, trunk, and legs. Most tremors occur in the hands. In some people, tremor is a symptom of a neurological disorder or appears as a side effect of certain drugs. The most common form of tremor, however, occurs in otherwise largely healthy people. Although tremor is not life-threatening, it can be embarrassing to some people and make it harder to perform daily tasks.
Causes of Tremor
Tremor is generally caused by problems in parts of the brain that control muscles throughout the body or in particular areas, such as the hands. Neurological disorders or conditions that can produce tremor include multiple sclerosis, stroke, traumatic brain injury, and neurodegenerative diseases that damage or destroy parts of the brainstem or the cerebellum. Other causes include the use of some drugs (such as amphetamines, corticosteroids, and drugs used for certain psychiatric disorders), alcohol abuse or withdrawal, mercury poisoning, overactive thyroid, or liver failure. Some forms of tremor are inherited and run in families, while others have no known cause.
Characteristics of Tremor
Characteristics may include a rhythmic shaking in the hands, arms, head, legs, or trunk; shaky voice; difficulty writing or drawing; or problems holding and controlling utensils, such as a fork. Some tremors may be triggered by or become exaggerated during times of stress or strong emotion, when the individual is physically exhausted, or during certain postures or movements.
Tremor may occur at any age but is most common in middle-aged and older persons. It may be occasional, temporary, or occur intermittently. Tremor affects men and women equally.
A useful way to understand and describe tremors is to define them according to the following types. Resting tremor occurs when the muscle is relaxed, such as when the hands are lying on the lap or hanging next to the trunk while standing or walking. It may be seen as a shaking of the limb, even when the person is at rest. Often, the tremor affects only the hand or fingers. This type of tremor is often seen in patients with Parkinson’s disease. An action tremor occurs during any type of movement of an affected body part. There are several subclassifications of action tremor. Postural tremor occurs when the person maintains a position against gravity, such as holding the arms outstretched. Kinetic tremor appears during movement of a body part, such as moving the wrists up and down, while intention tremor is present during a purposeful movement toward a target, such as touching a finger to one’s nose during a medical exam. Task-specific tremor appears when performing highly skilled, goal-oriented tasks such as handwriting or speaking. Isometric tremor occurs during a voluntary muscle contraction that is not accompanied by any movement.
Types of Tremor
Tremor is most commonly classified by its appearance and cause or origin. Some of the better-known forms of tremor, with their symptoms, include the following:
Essential tremor (sometimes called benign essential tremor) is the most common of the forms of abnormal tremor. Although the tremor may be mild and nonprogressive in some people over a long period of time, in others, the tremor is slowly progressive, starting on one side of the body but affecting both sides within a few years. The hands are most often affected but the head, voice, tongue, legs, and trunk may also be involved, typically to a lesser extend than the hands. Tremor of the hands is typically present as an action tremor. Head tremor may be seen as a “yes-yes” or “no-no” motion. Essential tremor may be accompanied by mild gait disturbance. Tremor frequency may decrease as the person ages, but the severity may increase, affecting the person’s ability to perform certain tasks or activities of daily living. Heightened emotion, stress, fever, physical exhaustion, or low blood sugar may trigger tremors and/or increase their severity. Onset is most common after age 40, although symptoms can appear at any age. It may occur in more than one family member. Children of a parent who has essential tremor have a 50 percent chance of inheriting the condition. A variant in the gene LINGO1 has been identified as a risk gene, although not all individuals with essential tremor carry this variant–which also can be present in people without essential tremor. While essential tremor was thought not to be associated with any known pathology over many years, recent studies suggest that there is a mild degeneration of certain parts of the cerebellum in individuals with essential tremor.
Parkinsonian tremor is caused by damage to structures within the brain that control movement. This tremor, which appears characteristically as a resting tremor, can occur as an isolated symptom or be seen in other disorders and is often the first symptom of Parkinson’s disease (more than 25 percent of patients with Parkinson’s disease have an associated action tremor). The tremor, which is classically seen as a “pill-rolling” action of the hands that may also affect the chin, lips, legs, and trunk, can be markedly increased by stress or emotions. Onset of parkinsonian tremor is generally after age 60. Movement starts in one limb or on one side of the body and usually progresses to include the other side.
Dystonic tremor occurs in individuals of all ages who are affected by dystonia, a movement disorder in which sustained involuntary muscle contractions cause twisting and repetitive motions and/or painful and abnormal postures or positions, such as twisting of the neck (torticollis) or writer’s cramp. Dystonic tremor may affect any muscle in the body and is seen most often when the patient is in a certain position or moves a certain way. The pattern of dystonic tremor may differ from essential tremor. Dystonic tremors occur irregularly and often can be relieved by complete rest. Touching the affected body part or muscle may reduce tremor severity. The tremor may be the initial sign of dystonia localized to a particular part of the body.
Cerebellar tremor is a slow tremor of the extremities that occurs at the end of a purposeful movement (intention tremor), such as trying to press a button or touching a finger to the tip of one’s nose. Cerebellar tremor is caused by lesions in or damage to the cerebellum resulting from stroke, tumor, or disease such as multiple sclerosis or some inherited degenerative disorder. It can also result from chronic alcoholism or overuse of some medicines. In classic cerebellar tremor, a lesion on one side of the brain produces a tremor in that same side of the body that worsens with directed movement. Cerebellar damage can also produce a “wing-beating” type of tremor called rubral or Holmes’ tremor — a combination of rest, action, and postural tremors. The tremor is often most prominent when the affected person is active or is maintaining a particular posture. Cerebellar tremor may be accompanied by dysarthria (speech problems), nystagmus (rapid involuntary movements of the eyes), gait problems, and postural tremor of the trunk and neck.
Psychogenic tremor (also called functional tremor) can appear as any form of tremor movement. The characteristics of this kind of tremor may vary but generally include sudden onset and remission, increased incidence with stress, change in tremor direction and/or body part affected, and greatly decreased or disappearing tremor activity when the individual is being distracted. Many indviduals with psychogenic tremor have a conversion disorder (defined as a psychological disorder that produces physical symptoms) or another psychiatric disease.
Orthostatic tremor is characterized by rhythmic muscle contractions that occur in the legs and trunk immediately after standing. The person typically perceives orthostatic tremor as unsteadiness rather than actual tremor. Because of its high tremor frequency, often the tremor cannot be seen, but sometimes be heard when putting a stethoscope to the thigh muscles. No other clinical signs or symptoms are present and the unsteadiness ceases when the individual sits, is lifted off the ground, or starts walking.
Physiologic tremor occurs in every normal individual. It is rarely visible to the eye and may be heightened by strong emotion (such as anxiety or fear), physical exhaustion, hypoglycemia, hyperthyroidism, heavy metal poisoning, stimulants, alcohol withdrawal, caffeine, or fever. It can occur in all voluntary muscle groups and can be detected by extending the arms and placing a piece of paper on top of the hands. Enhanced physiologic tremor is a strengthening of physiologic tremor to more visible levels. It is generally not caused by a neurological disease but by reaction to certain drugs, alcohol withdrawal, or medical conditions including an overactive thyroid and hypoglycemia. It is usually reversible once the cause is corrected.
Tremor can result from other conditions as well. Alcoholism, excessive alcohol consumption, or alcohol withdrawal can kill certain nerve cells, resulting in tremor, especially in the hand. (Conversely, small amounts of alcohol may even help to decrease essential tremor, but the mechanism behind this is unknown. Doctors may use small amounts of alcohol to aid in the diagnosis of certain forms of tremor but not as a regular treatment for the condition.) Tremor in peripheral neuropathymay occur when the nerves that supply the body’s muscles are traumatized by injury, disease, abnormality in the central nervous system, or as the result of systemic illnesses. Peripheral neuropathy can affect the whole body or certain areas, such as the hands, and may be progressive. Resulting sensory loss may be seen as a tremor or ataxia (inability to coordinate voluntary muscle movement) of the affected limbs and problems with gait and balance. Clinical characteristics may be similar to those seen in individuals with essential tremor.
Diagnosing essential tremor involves reviewing your medical history, family history and symptoms and conducting a physical examination.
There are no medical tests to diagnose essential tremor. Diagnosing it is often a matter of ruling out other conditions that could be causing your symptoms. To do this, your doctor may suggest the following tests:
In a neurological examination, your doctor surveys your nervous system functioning, including checking your:
- Tendon reflexes
- Muscle strength and tone
- Ability to feel certain sensations
- Posture and coordination
Your blood and urine may be tested for several factors, including:
- Thyroid disease
- Metabolic problems
- Drug side effects
- Alcohol levels
- Levels of chemicals that may cause tremor
To evaluate the tremor itself, your doctor may ask you to:
- Drink from a glass
- Hold your arms outstretched
- Draw a spiral
If your doctor is still unsure if your tremor is essential tremor or Parkinson’s disease, he or she might order a dopamine transporter scan. This can tell the difference between the two types of tremor. The doctor may order an electromyogram to diagnose muscle or nerve problems. This test measures involuntary muscle activity and muscle response to nerve stimulation.
Treatments for Tremor
There is no cure for most tremors. The appropriate treatment depends on accurate diagnosis of the cause.
Some tremors respond to treatment of the underlying condition. For example, in some cases of psychogenic tremor, treating the patient’s underlying psychological problem may cause the tremor to disappear.
Symptomatic drug therapy is available for several forms of tremor.
Drug treatment for parkinsonian tremor involves levodopa and/or dopamine-like drugs such as pramipexole and ropinirole. Other drugs used to lessen parkinsonian tremor include amantadine hydrochloride and anticholinergic drugs.
Essential tremor may be treated with propranolol or other beta blockers (such as nadolol) and primidone, an anticonvulsant drug.
Cerebellar tremor typically does not respond well to medical treatment.
Dystonic tremor may respond to clonazepam, anticholinergic drugs, and intramuscular injections of botulinum toxin.
OnabotulinumtoxinA (Botox) injections might be useful in treating some types of tremors, especially head and voice tremors. Botox injections can improve tremors for up to three months at a time. However, if Botox is used to treat hand tremors, it can cause weakness in your fingers. If it’s used to treat voice tremors, it can cause a hoarse voice and difficulty swallowing.
Clonazepam and primidone may be prescribed for primary orthostatic tremor.
Enhanced physiologic tremor is usually reversible once the cause is corrected. If symptomatic treatment is needed, beta blockers can be used.
Physical therapy may help to reduce tremor and improve coordination and muscle control for some individuals. A physical therapist will evaluate the individual for tremor positioning, muscle control, muscle strength, and functional skills. Teaching the person to brace the affected limb during the tremor or to hold an affected arm close to the body is sometimes useful in gaining motion control. Coordination and balancing exercises may help some people. Some therapists recommend the use of weights, splints, other adaptive equipment, and special plates and utensils for eating.
Surgical intervention such as thalamotomy and deep brain stimulation may ease certain tremors. These surgeries are usually performed only when the tremor is severe and cannot be controlled satisfactorily with drugs.
Deep brain stimulation (DBS), the most common form of surgical treatment of tremor, uses implantable electrodes to send high-frequency electrical signals to the thalamus. A battery-operated device called a neurostimulator is used to deliver electrical stimulation to targeted areas in the brain that control movement. The person uses a hand-held magnet to turn on and turn off a pulse generator that is surgically implanted under the skin. The electrical stimulation temporarily disables the tremor and can be “reversed,” if necessary, by turning off the implanted electrode. Batteries in the generator last about 5 years and can be replaced surgically. DBS is currently used to treat parkinsonian tremor, essential tremor, and dystonia.
Thalamotomy, involving the creation of lesions in the brain region called the thalamus, is quite effective in treating individuals with essential, cerebellar, or parkinsonian tremor. This in-hospital procedure is performed under local anesthesia, with the individual being awake. After the person’s head is secured in a metal frame, the surgeon maps the brain to locate the thalamus. A small hole is drilled through the skull and a temperature-controlled electrode is inserted into the thalamus. A low-frequency current is passed through the electrode to activate the tremor and to confirm proper placement. Once the site has been confirmed, the electrode is heated to create a temporary lesion. Testing is done to examine speech, language, coordination, and tremor activation, if any. If no problems occur, the probe is again heated to create a 3-mm permanent lesion. The probe, when cooled to body temperature, is withdrawn and the skull hole is covered. The lesion causes the tremor to permanently disappear without disrupting sensory or motor control.
The most common side effects of tremor surgery include dysarthria (problems with motor control of speech), temporary or permanent cognitive impairment (including visual and learning difficulties), and problems with balance.
Lifestyle and home remedies
To reduce or relieve tremors:
- Avoid caffeine. Caffeine and other stimulants can increase tremors.
- Use alcohol sparingly, if at all. Some people notice that their tremors improve slightly after they drink alcohol, but drinking isn’t a good solution. Tremors tend to worsen once the effects of alcohol wear off. Also, increasing amounts of alcohol eventually are needed to relieve tremors, which can lead to alcoholism.
- Learn to relax. Stress and anxiety tend to make tremors worse, and being relaxed may improve tremors. Although you can’t eliminate all stress from your life, you can change how you react to stressful situations using a range of relaxation techniques, such as massage or meditation.
- Make lifestyle changes. Use the hand less affected by tremor more often. Find ways to avoid writing with the hand affected by tremor, such as using online banking and debit cards instead of writing checks.Try voice-activated dialing on your cellphone and speech-recognition software on your computer.
Therapies for Tremors
- Use heavier objects. You may need to replace lightweight or delicate objects, such as glasses, silverware, or plates, with heavier versions. The extra weight may make the item easier to handle.
- Use specially designed utensils and tools. Gripping and controlling pens, pencils, garden tools, and kitchen utensils may be difficult if you have shaky hands. You may need to seek out versions of these items that are designed for individuals with grip and control issues.
- Wear wrist weights. The extra weight on your arm may make control easier.
Urinary Tract Infections (UTI)
A urinary tract infection (UTI) is an infection involving the kidneys, ureters, bladder, or urethra. These are the structures that urine passes through before being eliminated from the body.
- The kidneys are a pair of small organs that lie on either side of the spine at about waist level. They have several important functions in the body, including removing waste and excess water from the blood and eliminating them as urine. These functions make them important in the regulation of blood pressure. Kidneys are also very sensitive to changes in blood sugar levels and blood pressure and electrolyte balance. Both diabetes and hypertension can cause damage to these organs.
- Two ureters, narrow tubes about 10 inches long, drain urine from each kidney into the bladder.
- The bladder is a small saclike organ that collects and stores urine. When the urine reaches a certain level in the bladder, we experience the sensation that we have to void, then the muscle lining the bladder can be voluntarily contracted to expel the urine.
- The urethra is a small tube connecting the bladder with the outside of the body. A muscle called the urinary sphincter, located at the junction of the bladder and the urethra, must relax at the same time the bladder contracts to expel urine.
Any part of this system can become infected. As a rule, the farther up in the urinary tract the infection is located, the more serious it is.
- The upper urinary tract is composed of the kidneys and ureters. Infection in the upper urinary tract generally affects the kidneys (pyelonephritis), which can cause fever, chills, nausea, vomiting, and other severe symptoms.
- The lower urinary tract consists of the bladder and the urethra. Infection in the lower urinary tract can affect the urethra (urethritis) or the bladder (cystitis).
In the United States, urinary tract infections account for more than 10 million visits to medical offices and hospitals each year.
- Urinary tract infections are much more common in adults than in children, but about 1%-2% of children do get urinary tract infections. Urinary tract infections in children are more likely to be serious than those in adults (especially in younger children).
- Urinary tract infection is the most common urinary tract problem in children besides bedwetting.
- Urinary tract infection is second only to respiratory infection as the most common type of infection.
- These infections are much more common in girls and women than in boys and men younger than 50 years of age. The reason for this is not well understood, but anatomic differences between the genders (a shorter urethra in women) might be partially responsible.
- About 40% of women and 12% of men have a urinary tract infection at some time in their life.
Causes and Risk Factors
The urine is normally sterile. An infection occurs when bacteria get into the urine and begin to grow. The bacterial infection usually starts at the opening of the urethra where the urine leaves the body and moves upward into the urinary tract.
- The culprit in at least 90% of uncomplicated infections is a type of bacteria called Escherichia coli, better known as E. coli. These bacteria normally live in the bowel (colon) and around the anus.
- These bacteria can move from the area around the anus to the opening of the urethra. The two most common causes of this are improper wiping and sexual intercourse.
- Usually, the act of emptying the bladder (urinating) flushes the bacteria out of the urethra. If there are too many bacteria, urinating may not stop their spread.
- The bacteria can travel up the urethra to the bladder, where they can grow and cause an infection.
- The infection can spread further as the bacteria move up from the bladder via the ureters.
- If they reach the kidney, they can cause a kidney infection (pyelonephritis), which can become a very serious condition if not treated promptly.
The following people are at increased risk of urinary tract infection:
- People with conditions that block (obstruct) the urinary tract, such as kidney stones
- People with medical conditions that cause incomplete bladder emptying (for example, spinal cord injury)
- Postmenopausal women: Decreased circulating estrogen makes the urinary tract more vulnerable to a UTI.
- People with suppressed immune systems: Examples of situations in which the immune system is suppressed are HIV/AIDS and diabetes. People who take immunosuppressant medications such as chemotherapy for cancer also are at increased risk.
- Women who are sexually active: Sexual intercourse can introduce larger numbers of bacteria into the bladder. Urinating after intercourse seems to decrease the likelihood of developing a urinary tract infection.
- Women who use a diaphragm for birth control
- Men with an enlarged prostate: Prostatitis or obstruction of the urethra by an enlarged prostate can lead to incomplete bladder emptying, thus increasing the risk of infection. This is most common in older men.
- Breastfeeding has been found to decrease the risk for urinary tract infections in children.
The following special groups may be at increased risk of urinary tract infection:
- Very young infants: Bacteria gain entry to the urinary tract via the bloodstream from other sites in the body.
- Young children: Young children have trouble wiping themselves and washing their hands well after a bowel movement. Poor hygiene has been linked to an increased frequency of urinary tract infections.
- Children of all ages: Urinary tract infection in children can be (but is not always) a sign of an abnormality in the urinary tract, usually a partial blockage. An example is a condition in which urine moves backward from the bladder up the ureters (vesicoureteral reflux).
- Hospitalized patients or nursing-home residents: Many of these individuals are catheterized for long periods and are thus vulnerable to infection of the urinary tract. Catheterization means that a thin tube (catheter) is placed in the urethra to drain urine from the bladder. This is done for people who have problems urinating or cannot reach a toilet to urinate on their own.
- Patients using catheters: If a patient is required to empty their bladder using a catheter, they are at increased risk for infection.
Symptoms of UTIs
Lower urinary tract infection (infections of the bladder or urethra)
- Bladder (cystitis, or bladder infection): The lining of the urethra and bladder becomes inflamed and irritated.
- Dysuria: pain or burning during urination
- Frequency: more frequent urination (or waking up at night to urinate, sometimes referred to as nocturia); often with only a small amount of urine
- Urinary urgency: the sensation of having to urinate urgently
- Cloudy, bad-smelling, or bloody urine
- Lower abdominal pain or pelvic pressure or pain
- Mild fever (less than 101 F), chills, and “just not feeling well” (malaise)
- Urethra (urethritis): Burning with urination
Upper urinary tract infection (pyelonephritis, or kidney infection)
Symptoms develop rapidly and may or may not include the symptoms for a lower urinary tract infection.
- Fairly high fever (higher than 101 F)
- Shaking chills
- Shaking chills
- Flank pain: pain in the back or side, usually on only one side at about waist level
In newborns, infants, children, and elderly people, the classic symptoms of a urinary tract infection may not be present. Other symptoms may indicate a urinary tract infection.
- Newborns: fever or hypothermia (low temperature), poor feeding, jaundice
- Infants: vomiting, diarrhea, fever, poor feeding, not thriving
- Children: irritability, eating poorly, unexplained fever that doesn’t go away, loss of bowel control, loose bowels, change in urination pattern
- Elderly people: fever or hypothermia, poor appetite, lethargy, change in mental status
Pregnant women are at increased risk for an UTI. Typically, pregnant women do not have unusual or unique symptoms. If a woman is pregnant, her urine should be checked during prenatal visits because an unrecognized infection can cause pregnancy health complications.
Although most people have symptoms with a urinary tract infection, some do not.
The symptoms of urinary tract infection can resemble those of sexually transmitted diseases.
Diagnosis of a urinary tract infection is based on information someone gives about his or her symptoms, medical and surgical history, medications, habits, and lifestyle. A physical examination and lab tests complete the evaluation.
A health care professional may simply perform a urine dipstick test in the office. Only a few minutes are needed to obtain results. Your health-care provider may also send a urine sample to the lab for culture testing (see below). These results take a few days to come back. This tells the doctor the exact bacteria causing the infection and to which antibiotics these bacteria have resistance or sensitivity. The culture is usually sent for special populations, including men, because they are less likely to get UTIs. It is not necessary to send a culture for everyone because the majority of UTIs are caused by the same bacteria.
- The single most important lab test is urinalysis. A urine culture will be tested for signs of infection, such as the presence of white blood cells and bacteria.
- In certain circumstances, urine also may be “cultured.” This means that a small amount of the urine is brushed on a sterile nutrient substance in a plastic plate. The plate is allowed to sit for a few days and then examined to see what kind of bacteria are growing on it. These bacteria are treated with different antibiotics to see which works best against them. This helps determine the best treatment for the specific infection.
- Blood tests usually are not required unless a complicated condition, such as pyelonephritis or kidney failure, is suspected.For a culture specimen, the patient will be asked to give a clean-catch, midstream urine specimen. This avoids contamination of the urine with bacteria from the skin. Patients will be instructed in how to do this.
For a culture specimen, the patient will be asked to give a clean-catch, midstream urine specimen. This avoids contamination of the urine with bacteria from the skin. Patients will be instructed in how to do this.
- Midstream means urinating a little into the toilet before collecting a specimen. The idea is to avoid collecting the urine that comes out first, as this urine is often contaminated.
- Clean-catch refers to a midstream sample that was collected after cleaning the area of the urethral opening.
- Adult women and older girls: Cleanse the area around the urethral opening gently (but completely) using a sterile wipe or soap and water. Catch the urine midstream. For some women, catheterization (inserting a tube into the bladder) may be the only way to obtain a sterile, uncontaminated specimen.
- Men and boys: A sterile specimen can usually be obtained with a midstream catch. Uncircumcised males should retract the foreskin and cleanse the area before urinating.
- Newborns: Urine may be obtained with a catheter or a procedure in which a needle is introduced through the lower abdominal wall to draw (aspirate) urine from the bladder.
- Infants and children: Either catheterization or the needle aspiration method is used.
If someone cannot produce a urine specimen or is unable to follow instructions for a clean-catch specimen, a health-care professional may obtain a urine specimen by catheterization.
- This means placing a thin tube (catheter) in the urethra to drain urine from the bladder.
- The catheter usually is removed after the bladder is emptied.
- The catheter may remain in place if someone is very ill or if it is necessary to collect all urine or measure urine output.
Depending on their symptoms, sexually active women could require a pelvic examination because pelvic infections can have similar symptoms as a urinary tract infection. Males will require a genital examination, and depending on the symptoms, most likely a prostate examination. A prostate infection (prostatitis) requires a longer course of antibiotics than a urinary tract infection.
Men will most likely require a rectal examination so that the prostate can be checked. A prostate infection (prostatitis) requires a longer course of antibiotics than a urinary tract infection.
Rarely, an imaging test may be indicated to detect any underlying problem in the urinary tract that could cause an infection. This is usually only necessary in repeat infections or special circumstances (unusual bacteria, suspected anatomic abnormalities).
- An ultrasound examination can evaluate kidney and bladder problems.
- A fluoroscopic study can show any physical problems that predispose children to urinary tract infections.
- Intravenous pyelogram (IVP) is a special series of X-rays that uses a contrast dye to highlight abnormalities in the urinary tract.
- Cystoscopy involves insertion of a thin, flexible tube with a tiny camera on the end through the urethra into the bladder. This allows detection of abnormalities inside the bladder that might contribute to infections.
- A CT scan gives a very detailed three-dimensional picture of the urinary tract.
Imaging tests are most often needed for the following groups:
- Children with repeat urinary tract infections, especially boys
- Up to 50% of infants and 30% of older children with a urinary tract infection have an anatomic abnormality. The child’s pediatrician should investigate this possibility.
- Adults with frequent or recurrent urinary tract infections
- People who have blood in the urine
You can prevent getting another UTI with the following tips:
- Empty your bladder frequently as soon as you feel the need to go; don’t rush, and be sure you’ve emptied your bladder completely.
- Wipe from front to back.
- Drink lots of water.
- Choose showers over baths.
- Stay away from feminine hygiene sprays, scented douches, and scented bath products — they’ll only increase irritation.
- Cleanse your genital area before sex.
- Urinate after sex to flush away any bacteria that may have entered your urethra.
- If you use a diaphragm, unlubricated condoms, or spermicidal jelly for birth control, consider switching to another method. Diaphragms can increase bacteria growth, while unlubricated condoms and spermicides can cause irritation. All can make UTI symptoms more likely.
- Keep your genital area dry by wearing cotton underwear and loose-fitting clothes. Avoid tight jeans and nylon underwear — they can trap moisture, creating the perfect environment for bacteria growth.
The usual treatment for both simple and complicated urinary tract infections is antibiotics. The type of antibiotic and duration of treatment depend on the circumstances. Examples of common antibiotics used in treatment include, but are not limited to, amoxicillin, sulfamethoxazole/trimethoprim (Bactrim), ciprofloxacin, nitrofurantoin (Macrobid), and many others. Your health-care provider will chose the appropriate medication for your condition and the specific causative organisms.
Lower urinary tract infection (cystitis, or bladder infection)
- In an otherwise healthy person, a three-day course of antibiotics is usually enough. Some providers prefer a seven-day course of antibiotics. Occasionally, a single dose of an antibiotic is used. A health-care professional will determine which of these options is best.
- In adult males, if the prostate is also infected (prostatitis), four weeks or more of antibiotic treatment may be required.
- Adult females with potential for or early involvement of the kidneys, urinary tract abnormalities, or diabetes are usually given a five- to seven-day course of antibiotics.
- Children with uncomplicated cystitis are usually given a 10-day course of antibiotics.
- To alleviate burning pain during urination, phenazopyridine (Pyridium) or a similar drug, can be used in addition to antibiotics for one to two days.
Upper urinary tract infection (pyelonephritis)
- Young, otherwise healthy patients with symptoms of pyelonephritis can be treated as outpatients. They may receive IV fluids and antibiotics or an injection of antibiotics in the emergency department, followed by 10-14 days of oral antibiotics. They should follow up with their health-care professional in one to two days to monitor improvement.
- If someone is very ill, dehydrated, or unable to keep anything in his or her stomach because of vomiting, an IV will be inserted into the arm. He or she will be admitted to the hospital and given fluids and antibiotics through the IV until he/she is well enough to switch to an oral antibiotic.
- A complicated, acute infection may require treatment for several weeks.
A person may be hospitalized if he or she has symptoms of pyelonephritis and any of the following:
- Appear very ill
- Are pregnant
- Have not gotten better with outpatient antibiotic treatment
- Have underlying diseases that compromise the immune system (diabetes is one example) or are taking immunosuppressive medication
- Are unable to keep anything in the stomach because of nausea or vomiting
- Had previous kidney disease, especially pyelonephritis, within the last 30 days
- Have a device such as a urinary catheter in place
- Have kidney stones
Urethritis in men and women can be caused by the same bacteria as sexually transmitted diseases (STDs). Therefore, people with symptoms of STDs (vaginal or penile discharge, for example) should be treated with appropriate antibiotics. Your doctor will have to evaluate you for STDs as well as UTIs if you experience any pain in the genital area.
Prognosis of UTIs
For people with uncomplicated cystitis or pyelonephritis, antibiotic treatment usually brings complete resolution of the infection.
If not treated promptly, urinary tract infections can cause permanent scarring of the urinary tract.
Recurrent urinary tract infections can become a problem and will require close monitoring by your health care provider.
Pyelonephritis, if not treated promptly, can spread to the bloodstream and cause a very severe infection.
- Short-term and long-term kidney damage can be a result of pyelonephritis.
- Death from pyelonephritis is rare in otherwise healthy people.
- Factors associated with poor outcome are old age or general debility, kidney stones, recent hospitalization, diabetes, sickle cell disease, cancer, or chronic kidney disease.