Sciatica

Sciatica facts

• Sciatica is nerve pain from irritation of the sciatic nerve.
• The sciatic nerve is the largest nerve in the body.
• Sciatica pain is typically felt from the low back to behind the thigh and radiating down below the knee.
• Treatments for sciatica depend on the underlying cause and the severity of the pain.

What is sciatica?

Sciatica is pain in the lower extremity resulting from irritation of the sciatic nerve. The pain of sciatica is typically felt from the low back (lumbar area) to behind the thigh and radiating down below the knee. The sciatic nerve is the largest nerve in the body and begins from nerve roots in the lumbar spinal cord in the low back and extends through the buttock area to send nerve endings down the lower limb. The pain of sciatica is sometimes referred to as sciatic nerve pain.

What are causes of sciatica?

While sciatica is most commonly a result of a lumbar disc herniation directly pressing on the nerve, any cause of irritation or inflammation of the sciatic nerve can reproduce the symptoms of sciatica. This irritation of nerves as a result of an abnormal intervertebral disc is referred to as radiculopathy. Aside from a pinched nerve from a disc, other causes of sciatica include irritation of the nerve from adjacent bone, tumors, muscle, internal bleeding, infections, injury, and other causes. Sometimes sciatica can occur because of irritation of the sciatic nerve during pregnancy.

Picture of a herniated disc, a common cause of sciatica 

What are risk factors for sciatica?

Risk factors for sciatica include degenerative arthritis of the lumbar spine, lumbar disc disease, and trauma or injury to the lumbar spine.

What are sciatica symptoms?

Sciatica causes pain, a burning sensation, numbness, or tingling radiating from the lower back and upper buttock down the back of the thigh to the back of the leg. The result is lumbar pain, buttock pain, hip pain, and leg pain. Sometimes the pain radiates around the hip or buttock to feel like hip pain. While sciatica is often associated with lower back pain (lumbago), it can be present without low back pain. Severe sciatica can make walking difficult if not impossible. Sometimes the symptoms of sciatica are aggravated by walking or bending at the waist and relieved by lying down. The pain relief by changing positions can be partial or complete.

How is sciatica diagnosed?

Sciatica is diagnosed with a physical exam and medical history. The typical symptoms and certain examination maneuvers help the health care professional to diagnose sciatica. Sometimes, X-rays and other tests, such as CT scan, MRI scan, and electromyogram, are used to further define the exact causes of sciatica.

What are treatment options for sciatica?

Bed rest has been traditionally advocated for the treatment of acute sciatica. But how useful is it?
To study the effectiveness of bed rest in patients with sciatica of sufficient severity to justify treatment with bed rest for two weeks, a research team in the Netherlands led by Dr. Patrick Vroomen randomly assigned 183 such patients to bed rest or, alternatively, to watchful waiting for this period.
To gauge the outcome, both primary and secondary measures were examined. The primary outcome measures were the global assessments of improvement after two and 12 weeks by the doctor and the patient. The secondary outcome measures were changes in functional status and in pain scores, absenteeism from work, and the need for surgical intervention. Neither the doctors who assessed the outcomes nor those involved in data entry and analysis were aware of the patients' treatment assignments.
The results, reported in the New England Journal of Medicine, showed that after two weeks, 64 of the 92 (70%) patients in the bed-rest group reported improvement, as compared with 59 of the 91 (65%) of the patients in the control (watchful-waiting) group. After 12 weeks, 87% of the patients in both groups reported improvement. The results of assessments of the intensity of pain, the aggravation of symptoms, and functional status revealed no significant differences between the two groups. The extent of absenteeism from work and rates of surgical intervention were similar in the two groups.
The researchers concluded that "among patients with symptoms and signs of a lumbosacral radicular syndrome, bed rest is not a more effective therapy than watchful waiting." Sometimes, conventional wisdom is not as wise as research!
Other treatment options for sciatica include addressing the underlying cause, medications to relieve pain and inflammation (including oral and injectable cortisone) and relax muscles, and physical therapy. A variety of low back conditioning and stretching exercises are employed to help people recover from sciatica. Surgical procedures can sometimes be required for persisting sciatica that is caused by nerve compression at the lower spine. Sometimes pain management specialists help with chronic sciatica conditions.

What is the outlook (prognosis) for patients with sciatica?

Depending on the precise cause of the sciatica and the duration of symptoms, the outlook for recovery from sciatica ranges from excellent to having long-term chronic symptoms.

Can sciatica be prevented?

Sciatica can be prevented only to the extent that low back trauma injuries can be avoided can sciatica.

Reflex Sympathetic Dystrophy (RSD, Complex Regional Pain Syndrome, CRPS)

Reflex sympathetic dystrophy (RSD) facts

• Reflex sympathetic dystrophy (RSD) is characterized by a group of symptoms including pain (often "burning" type), tenderness, and swelling of an extremity associated with varying degrees of sweating, warmth and/or coolness, flushing, discoloration, and shiny skin.
• How RSD occurs is not known, but there are often triggering events.
• Symptoms of RSD often occur in three stages: 1) acute, 2) dystrophic, and 3) atrophic.
• Diagnosis of RSD is based on clinical findings, supported by radiological tests.
• Treatment of RSD is most effective in the earlier stages.

What is reflex sympathetic dystrophy (RSD)?

Reflex sympathetic dystrophy (RSD) is a condition that features a group of typical symptoms, including pain (often "burning" type), tenderness, and swelling of an extremity associated with varying degrees of sweating, warmth and/or coolness, flushing, discoloration, and shiny skin. RSD is also referred to as "complex regional pain syndrome," "the shoulder-hand syndrome," "causalgia," and "Sudeck's atrophy."

What causes reflex sympathetic dystrophy (RSD)?

The exact mechanism of how RSD develops is poorly understood. The theories include irritation and abnormal excitation of nervous tissue, leading to abnormal impulses along nerves that affect blood vessels and skin. The involuntary nervous system, peripheral nerves, and brain seem to be involved.
A variety of events can trigger the RSD, including:

• injury,
• surgery,
• heart disease,
• degenerative arthritis of the neck,
• stroke or other brain diseases,
• nerve irritation by entrapment (such as carpal tunnel syndrome),
• shingles,
• shoulder problems,
• breast cancer, and
• drugs for tuberculosis and barbiturates.

There is no associated or identified inciting event in one-third of individuals with RSD. Fibromyalgia has been reported to coexist with RSD in some people.

What are the symptoms of reflex sympathetic dystrophy (RSD)?

The onset of RSD symptoms may be rapid or gradual. The condition may not display all features. It is bilateral (involving both sides of the body) in up to half of people with RSD. There are several stages of RSD with symptoms that include:

1. Acute (three to six months): burning, flushing, blanching, sweating, swelling, pain, and tenderness. This stage can show early X-ray changes of patchy bone thinning.
2. Dystrophic (three to six months): early skin changes of shiny, thickened skin and contracture with persistent pain, but diminished swelling and flushing.
3. Atrophic (may be long-standing): loss of motion and function of the involved hand or foot with contracture (flexed scarring process), and thinning of the fatty layers under the skin. X-ray can show significant osteoporosis.
   

   How is reflex sympathetic dystrophy (RSD) diagnosed?

   RSD is diagnosed based on the clinical features described previously. Blood tests are not abnormal because of RSD, though the associated triggering events mentioned previously may lead to abnormalities in laboratory testing. Plain film X-ray testing and MRI scanning can show patchy thinning or significant osteoporosis. Nuclear bone scanning can show characteristic uptake patterns.
   
   

   What is the treatment for reflex sympathetic dystrophy (RSD)?

   Response to treatment of RSD is greater in the earlier stages of the condition than in the later stages.
   
4. Cool, moist applications to the affected areas can provide some relief of burning symptoms.
5. Gradual exercise can help prevent contractures.
6. Medications for pain and inflammation can also reduce symptoms.
7. For persisting symptoms, high doses of prednisone (cortisone) may be used for periods of weeks, depending on the response, and then gradually reduced.
8. Other medications that may be of benefit include amitriptyline (Elavil, Endep), pregabalin (Lyrica), and clonidine (Catapres, Catapres=TTS, Jenloga).
9. Occasionally, a nerve block with anesthetic injected into a specialized area of the involuntary nervous system (for example, a stellate ganglion blockade) can help both in treatment and in establishing the diagnosis. Sometimes a series of these blocks is tried.
10. Other treatments include surgically interrupting the nerves (the sympathetic nerves) of the involuntary nervous system (surgical sympathectomy), implanting pumps with pain medication into the spinal canal (intrathecal drug pumps), and spinal cord stimulation devices.

1. What is the prognosis for reflex sympathetic dystrophy (RSD)

   The prognosis (outlook) and response to treatment in patients with RSD is unpredictable. As previously mentioned, instituting treatment early in the course of the condition leads to better outcomes.
   
   

   Can reflex sympathetic dystrophy (RSD) be prevented?

   There is some evidence that early immobilization of patients with stroke or heart attack can help decrease the chances of developing RSD. Also, there have been studies demonstrating a decrease in the risk of developing RSD in patients with bony fractures using daily Vitamin C supplementation.

Infectious Mononucleosis (Mono)

Infectious mononucleosis (mono) facts

• Infectious mononucleosis (mono) is a contagious illness caused by the Epstein-Barr virus (EBV).
• The infection can be spread by saliva, and the incubation period for mono is four to eight weeks.
• Most adults have laboratory evidence (antibodies against the EBV) indicative of a previous infection with EBV and are immune to further infection.
• The symptoms of mono include fever, fatigue, sore throat, and swollen lymph nodes.
• The diagnosis of mono is confirmed by blood tests.
• Mono can cause liver inflammation (hepatitis) and enlargement of the spleen.
• People who have had mono can continue to shed virus particles in their saliva during reactivations of the viral infection throughout their lifetime.
• Vigorous contact sports should be avoided in the illness and recovery phase to prevent rupture of the spleen.

What is infectious mononucleosis?

Infectious mononucleosis, "mono," "kissing disease," and glandular fever are all terms popularly used for the very common infection caused by the Epstein-Barr virus (EBV). EBV is a member of the herpesvirus family. The characteristic symptoms of infection with EBV include fever, fatigue, malaise, and sore throat. The designation "mononucleosis" refers to an increase in a particular type of white blood cells (lymphocytes) in the bloodstream relative to the other white blood cells as a result of the EBV infection.
The disease was first described in 1889 and was referred to as "Drüsenfieber," or glandular fever. The term infectious mononucleosis was first used in 1920 when an increased number of lymphocytes were found in the blood of a group of college students who had fever and symptoms of the condition.

What is the cause of mono?

The EBV that causes mono is found throughout the world. By the time most people reach adulthood, an antibody against EBV can be detected in their blood. In the U.S., up to 95% of adults 35-40 years of age have antibodies directed against EBV. This means that most people, sometime in their lives, have been infected with EBV. The body's immune system produces antibodies to attack and help destroy invading viruses and bacteria. These specific antibodies can be detected in the blood of people who have been infected.
When infection occurs in childhood, the virus most often produces no symptoms. It is estimated that only about 10% of children who become infected with EBV develop the illness. Likewise, probably because of immunity from prior infection, adults typically do not develop the illness. Most cases of infectious mononucleosis occur in the 15-24 age group.
While there are other illnesses falling under the broad classification of mononucleosis that can cause similar symptoms (cytomegalovirus [CMV] infection is one example) and an increase in blood lymphocytes, the form caused by the EBV is by far the most common.

What are the risk factors for mono?

The EBV can infect any person. As previously discussed, the majority of people have become infected with the virus by the time that they reach adulthood, and the majority of these infections produce no symptoms or are not recognized as mono. Mono is most often diagnosed in adolescents and young adults, with a peak incidence at 15-17 years of age. However, it can also be seen in children. Generally, the illness is less severe in young children and may mimic the symptoms of other common childhood illnesses, which may explain why it is less commonly diagnosed or recognized in this younger age group.

Infectious mononucleosis symptoms and signs

How is mono transmitted or spread?

Mono is spread by person-to-person contact. Saliva is the primary method of transmitting mono, which leads to the infection of B lymphocytes in the mouth and throat. Infectious mononucleosis developed its common name of "kissing disease" from this prevalent form of transmission among teenagers. It typically takes between four to eight weeks for symptoms of mono to appear after the initial infection with EBV. A person with mono can also pass the disease by coughing or sneezing, causing small droplets of infected saliva and/or mucus to be suspended in the air which can be inhaled by others. Sharing food or beverages from the same container or utensil can also transfer the virus from one person to another since contact with infected saliva may result.
Most people have been exposed to the virus as children, and as a result of the exposure, they have developed immunity to the virus. It is of note that most people who are exposed to the EBV don't ever develop mononucleosis. The incubation period for mono, meaning the time from the initial viral infection until the appearance of symptoms, is between four and eight weeks. During an infection, a person is likely able to transmit the virus to others for at least a few weeks and possibly longer, even after symptoms have disappeared (see below).
Research has shown that, depending on the method used to detect the virus, anywhere from 20%-80% of people who have had mononucleosis and have recovered will continue to secrete the EBV in their saliva for years due to periodic "reactivations" of the viral infection. Since healthy people without symptoms also secrete the virus during reactivation episodes throughout their lifetime, isolation of people infected with EBV is not necessary. It is currently believed that these healthy people, who nevertheless secrete EBV particles, are the primary reservoir for transmission of EBV among humans.

What are the symptoms of mono?

The initial symptoms of mono are

• a general lack of energy or malaise,
• fatigue,
• a loss of appetite,
• chills.

These initial symptoms can last from one to three days before the more intense symptoms of the illness begin. The more common intense symptoms include

• a severe sore throat,
• fever, which may be persistent,
• swollen lymph nodes (glands) in the neck area.

It is typically the severe sore throat that prompts people to contact their doctor.

What are the signs of mono?

In addition to a fever from 102 F-104 F, the most common signs of mono are

• a very reddened throat and tonsils,
• swollen lymph glands in the neck that typically occur on both sides.

The tonsils have a whitish coating in at least one-third of the cases. The spleen (sometimes referred to as the body's biggest lymph node) is an organ found in the left upper abdomen underneath the rib cage, which becomes enlarged or swollen in about 50% of patients with mono. An enlarged liver and abnormalities in liver function tests (blood tests) may be detected (see Complications, below). About 5% of patients have a splotchy red rash over the body, which has a similar appearance to the rash of measles. Early in the course of disease (over the first few days of illness), a temporary swelling (edema) of both upper eyelids may appear.

What is the usual course and treatment of mono?

In most cases of mono, no specific treatment is necessary. The illness is usually self-limited and passes much the way other common viral illnesses resolve. Treatment is directed toward the relief of symptoms. Available antiviral drugs have no significant effect on the overall outcome of mono and may actually prolong the course of the illness. Occasionally, Strep throat occurs in conjunction with mono and is best treated with penicillin or erythromycin (E-Mycin, Eryc, Ery-Tab, PCE, Pediazole, Ilosone). Ampicillin (Omnipen, Polycillin, Principen) and amoxicillin (Amoxil, DisperMox, Trimox) should be avoided if there is a possibility of mono since up to 90% of patients with mono develop a rash when taking these medications. They may then be inappropriately thought to have an allergy to penicillin.
For the most part, supportive or comfort measures are all that is necessary. Acetaminophen (Tylenol) can be given for fever and any headache or body aches. A sufficient amount of sleep and rest is important. The throat soreness is worst during the first five to seven days of illness and then subsides over the next seven to 10 days. The swollen, tender lymph nodes generally subside by the third week.
A feeling of fatigue or tiredness may persist for months following the acute phase of the illness. It is recommended that patients with mono avoid participation in any contact sports for three to four weeks after the onset of symptoms to prevent trauma to the enlarged spleen. The enlarged spleen is susceptible to rupture, which can be life threatening. Cortisone medication is occasionally given for the treatment of severely swollen tonsils or throat tissues which threaten to obstruct breathing.
Patients can continue to have virus particles present in their saliva for as long as 18 months after the initial infection. When symptoms persist for more than six months, the condition is frequently called "chronic" EBV infection. However, laboratory tests generally cannot confirm continued active EBV infection in people with "chronic" EBV infection.

Bird Flu (Avian Influenza, Avian Flu)

Bird flu facts

• Bird flu refers to strains of influenza that primarily affect wild and domesticated birds.
• Bird flu is also known as avian flu or avian influenza.
• Although bird flu is contagious and spreads easily among birds, it is uncommon for it to be transmitted to humans.
• In the late 1990s, a new strain of bird flu arose which was unusually severe ("highly pathogenic"), resulting in the deaths of hundreds of millions of birds, including poultry.
• Control efforts, including culling infected flocks and vaccinating healthy birds, have limited the spread of highly pathogenic bird flu.
• In 2011, a mutated strain of highly pathogenic bird flu appeared, which is concerning because the existing poultry vaccines are not very effective against the new strain.
• Human infection with the highly pathogenic strain of bird flu is uncommon, with fewer than 600 cases reported since 1997.
• Human infection occurs primarily in people who have close contact with sick poultry in countries where the virus is found. There have been isolated cases of human-to-human transmission.
• Human infection with bird flu is fatal in approximately 60% of cases.
• Bird flu from the highly pathogenic strain is not found in the United States at this time.

What is bird flu?

Bird flu (avian influenza) is a disease caused by an influenza virus that primarily affects birds. In the late 1990s, a new strain of bird flu arose that was remarkable for its ability to cause severe disease and death, especially in domesticated birds such as ducks, chickens, or turkeys. As a result, this strain was called highly pathogenic (meaning very severe) avian influenza.
Since the identification of highly pathogenic influenza, infected birds have been found in Asia, Europe, the Middle East, and Africa. Careful control measures, including destroying infected flocks and vaccinating healthy birds, have reduced the number of cases, but the virus continues to exist in poultry flocks in areas of Asia and Africa. Bird flu from the highly pathogenic strain is not found in the United States at this time.
The virus spreads from bird to bird through infected birds shedding the virus in their saliva, nasal secretions, and droppings. Healthy birds get infected when they come into contact with contaminated secretions or feces from infected birds. Contact with contaminated surfaces such as cages might also allow the virus to transfer from bird to bird. Symptoms in birds range from mild drops in egg production to failure of multiple major organs and death.
The first human case of illness from highly pathogenic avian influenza was identified in 1997, and more than 560 cases have been identified since then, with deaths worldwide exceeding 300. Human cases of highly pathogenic bird flu have been largely confined to Southeast Asia and Africa. However, mutations often occur in the virus, and it is possible that some mutations could create a more contagious virus that could cause a regional epidemic or a worldwide pandemic of bird flu among humans. Fortunately, the mutations that have occurred to date have not made the virus more contagious, although the concern remains.

What causes bird flu?

Bird flu is caused by strains of the influenza virus that have evolved to be specially adapted to enter avian cells. There are three main types of influenza: A, B, and C. The virus that causes bird flu is an influenza A type with eight RNA strands that make up its genome. Influenza viruses are further classified by analyzing two proteins on the surface of the virus. The proteins are called hemagglutinin (H) and neuraminidase (N). There are many different types of hemagglutinin and neuraminidase proteins. The current highly pathogenic bird flu virus has type 5 hemagglutinin and type 1 neuraminidase. Thus, it is a "H5N1" influenza A virus.
There are many types of influenza viruses, and most prefer to live in a limited number of animals. Thus, swine flu primarily infects swine and bird flu primarily infects birds. Human influenza is best adapted to humans. A few cases may occur in an accidental host, such as when people who have extensive contact with sick birds get the bird flu. In addition to humans and birds, we know that pigs, tigers, leopards, ferrets, and domestic cats can sometimes be infected with avian influenza viruses.
Influenza viruses mutate easily and often. These mutations can arise spontaneously in a single virus or can occur when two different influenza strains get close enough together to exchange genetic material. There are two major types of mutations in influenza viruses: antigenic shifts, where large RNA segments are interchanged between different influenza virus type, and antigenic shifts, where small RNA sequences are changed. The antigenic shifts are usually responsible for developing new strains. For example, the 2009 swine flu pandemic was caused by a virus that included genetic material from pig influenza, avian influenza, and human influenza strains. New mutations can allow the virus to evade the body's immune system and makes older vaccines ineffective. In 2011, one strain of the highly pathogenic avian influenza virus mutated in this way, making the existing vaccine used against avian flu ineffective against the new strain. Sometimes a flu virus will mutate in a way that makes it able to infect a new species.
Serious pandemic influenza occurs when a relatively new strain of the influenza virus arises that is highly contagious to humans. The most deadly pandemic in modern history was the 1918 influenza, also known as the Spanish flu (although it did not originate in Spain). The 1918 virus spread rapidly and killed tens of millions of people worldwide. Mortality was especially high in healthy young adults. Although the 1918 virus was a human influenza virus it, had many genes that likely came from a strain of bird flu. One reason that health officials carefully watch for and try to limit human contact with birds that develop avian flu is to avoid chances for a new strain to arise that may prefer to develop in human tissue.

What are risk factors for bird flu?

Humans may get bird flu from contact with infected birds (chickens, for example) or their droppings or surfaces with infected droppings. Risk factors include caring for sick birds, killing sick birds, and preparing sick birds for consumption. Despite the large number of people who have contact with poultry every day in the world, human cases of bird flu remain rare. This highlights how difficult it is for the bird flu virus to infect human cells, but mutations like antigenic shifts may reduce such difficulties.
Although direct contact with sick poultry poses the highest risk, indirect exposure to bird feces is also a risk. Thus, contact with unwashed eggs from sick birds or water contaminated by poultry feces poses a potential risk of disease.
Human to human spread has occurred in isolated cases. Thus, caring for a person infected with bird flu is also a risk factor for the disease. There is a theoretical risk in laboratory workers who handle the avian flu virus. One alleged incident in 2009 occurred when a company inadvertently sent live avian flu virus samples to research laboratories, which subsequently were used to vaccinate ferrets. The contaminated vaccine did not result in any human cases of infection.

What are bird flu symptoms and signs?

Symptoms occur approximately two to eight days after exposure, on average. Infected people experience typical flu-like symptoms, including fever, cough, sore throat, and muscle aches. Some people also have nausea, vomiting, diarrhea, or eye infections. This can progress to pneumonia and even respiratory failure. Bird flu causes a very aggressive form of pneumonia (acute respiratory distress syndrome or ARDS) that is often fatal.

How is bird flu diagnosed?

Routine tests for human influenza A will be positive in patients with bird flu but are not specific for the avian virus. To make a specific diagnosis of bird flu, specialized tests are needed. In the United States, local health departments and the Centers for Disease Control and Prevention can provide access to the specialized testing. The virus can be detected in sputum by several methods, including culture or polymerase chain reaction (PCR). Culture should be done in laboratories that have an appropriate biosafety certification. PCR detects nucleic acid from the influenza A virus. Specialized PCR testing is available in reference laboratories to identify avian strains.
During and after infection with bird flu, the body makes antibodies against the virus. Blood tests can detect these antibodies, but this requires one sample at the onset of disease and another sample several weeks later. Thus, results are not available until the patient has recovered or died.

What is the treatment for bird flu?

Because of the small number of human cases, it has not been possible to conduct rigorous treatment trials for bird flu. The current recommendation from the World Health Organization is to use an antiviral medication called oseltamivir (Tamiflu). In Sept. 2011, the CDC stated the following: "Two other antiviral medications, oseltamivir and zanamivir, would probably work to treat influenza caused by H5N1 virus, but additional studies still need to be done to demonstrate their effectiveness."

Cholesterol Test

High cholesterol facts

• Cholesterol is a naturally occurring substance in the body that is an important part of normal body function.
• Cholesterol has two main types: HDL, or good cholesterol, that protects against heart disease, stroke and peripheral vascular disease; and LD, or bad ,cholesterol, that increases the risk of these conditions.
• Cholesterol tests measure total cholesterol as well as HDL and LDL levels in the blood. Triglycerides, another type of fat present in the bloodstream, may also be measured.
• Cholesterol tests are usually ordered and blood drawn in the health care provider's office. There are also home test kits available. It is important to be fasting for the tests to be accurate. Typically, a fasting test is performed first thing in the morning before the individual has eaten anything for the day.
• Cholesterol test results should be discussed with the health care provider to determine if treatment of high cholesterol is necessary to decrease the risk of heart disease and stroke.

What is cholesterol?

Cholesterol is a naturally occurring fat that the body needs to produce important structures and chemicals. It is one of the main components of cell membranes, the outer lining that protects the internal structures that make body cells work and function properly. Cholesterol is also a building block for many of the hormones in the body including mineralocorticoids that control electrolyte levels in the body, glucocorticoids involved in carbohydrate metabolism, and sex hormones including testosterone, estrogen, and progesterone. Cholesterol is one of the building blocks that assists in forming Vitamin D in the body. Vitamin D is responsible for calcium metabolism in the body.
There are two important types of cholesterol, high density lipoprotein (HDL) and low density lipoprotein (LDL). LDL is the bad cholesterol that deposits in arteries when too much is present. HDL is considered the good cholesterol because it can bind to LDL cholesterol and return it to the liver where it can be removed from the body.
While most of the cholesterol in the body is obtained through the foods we eat, it is also produced in the liver to meet the body's demands. The body attempts to regulate the amount of total cholesterol, but when too much cholesterol is present, the excess can be deposited in arteries throughout the body. This leads to artery narrowing and increases the risk of heart attack, stroke, and peripheral vascular disease. Elevated LDL levels increase the risk of these diseases, and elevated HDL levels decrease the risk.

What does a cholesterol test measure?

Cholesterol tests are blood tests that measure the amount of cholesterol in the body. The health care provider may order only a cholesterol test with results showing total cholesterol, HDL, and LDL levels; or the health care provider also may order a lipid profile. In addition to cholesterol levels, the lipid profile test will also measure triglyceride levels, another fatty substance found in the blood.

How do I prepare for a cholesterol test?

For the best and most accurate results, it is important to fast for many hours before the cholesterol blood test is taken. Each laboratory has its own guidelines for not eating, and the fast may range from 9-16 hours. It is acceptable to drink water.

Do I need to call my doctor for my test results?

It usually takes a day or two from the time the blood is drawn until your health care provider receives the results of the cholesterol test. Ideally, the health care provider will contact you with those results and explain their significance. However, if you have not been contacted in a short period of time, it is reasonable to contact your health care provider and ask for the test results.
There are home cholesterol test kits available that have been U.S. FDA approved, but their accuracy is not necessarily as good as that of a certified laboratory. These tests usually measure total cholesterol only, but some also can measure HDL, LDL and cholesterol. If you use one of the home kits, it is wise to discuss the results with your health care provider.
The purpose of the cholesterol blood test is to determine whether treatment is needed for high cholesterol. That treatment may include dietary and lifestyle modifications, medications, or both to control cholesterol levels and decrease the risk of heart disease, stroke, and peripheral vascular disease.

How do I interpret my cholesterol test results?

Cholesterol levels are but one of the risk factors for heart disease, stroke, and peripheral vascular disease. It is important to control cholesterol levels to minimize risk just as it is important to control diabetes, high blood pressure, and avoid smoking.
Guidelines for cholesterol levels have been developed by many health organizations including the American Heart Association. It is important to remember that tests may need to be repeated over time to help monitor treatment and disease risk prevention.

Total cholesterol

Less than 200 mg/dL: desirable

200-239 mg/dL: borderline high risk

240 and over: high risk

HDL (high density lipoprotein)

Less than 40 mg/dL (men), less than 50 mg/dL (women): increased risk of heart disease

Greater than 60mg/dL: some protection against heart disease

LDL (low density lipoprotein)

Less than 100 mg/dL: optimal

100-129 mg/dL: near optimal/above optimal

130-159 mg/dL: borderline high

160- 189 mg/dL: high

190 mg/dL and above: very high

Triglycerides

Less than n150 mg/dL: normal

150-199 mg/dL: borderline to high

200-499mg/dL: high

Above 500 mg/dL: very high

Brain Aneurysm (Cerebral Aneurysm)

Brain aneurysm facts

• Blood to the brain is supplied by four major blood vessels that join together at the Circle of Willis at the base of the brain. Smaller branch arteries leave the circle to supply brain cells with oxygen and nutrients.
• Artery junction points may become weak, causing ballooning of the blood vessel wall that can form a small sac or aneurysm.
• Cerebral aneurysms are common, but most are asymptomatic and are found incidentally at autopsy.
• Aneurysms can leak or rupture causing symptoms from severe headache to stroke-like symptoms, or death.
• The health care practitioner needs to maintain a high incidence of suspicion to make the diagnosis, since many patients may have an initial small leak of blood causing symptoms before a catastrophic bleed occurs.
• Diagnosis of a brain aneurysm may require CT scans, lumbar puncture, or angiography.
• Treatment to repair the aneurysm may involve neurosurgery to put a clip across the weak blood vessel wall or clipping by interventional radiology.

What is a brain aneurysm and what causes a brain aneurysm?

The Circle of Willis is the junction of the four many arteries that supply the brain with nutrition (oxygen and glucose), two carotid arteries and two vertebral arteries. This loop of arteries is located at the base of the brain and sends out smaller branch arteries to all parts of the brain. The junctions where these arteries come together may develop weak spots. These weak spots can balloon out and fill with blood, creating the outpouchings of blood vessels known as aneurysms. These sac-like areas may leak or rupture, spilling blood into surrounding tissues.
Aneurysms have a variety of causes including high blood pressure and atherosclerosis, trauma, heredity, and abnormal blood flow at the junction where arteries come together.
There are other rare causes of aneurysms. Mycotic aneurysms are caused by infections of the artery wall. Tumors and trauma can also cause aneurysms to form. Drug abuse, especially cocaine, can cause the artery walls to inflame and weaken.
Brain aneurysms (aneurysms within arteries in the brain) are a common occurrence. At autopsy, incidental asymptomatic aneurysms are found in more than 1% of people. Most aneurysms remain small and never become an issue or are diagnosed. Some, however, may gradually become larger and exert pressure on surrounding brain tissue and nerves and may be diagnosed because of symptoms such as:

• headache,
• numbness, or weakness of one side of the face,
• a dilated pupil, or
• change in vision.

The greater concern is a brain aneurysm that leaks or ruptures, and potentially causes stroke or death. Bleeding leaks into one of the membranes that covers the brain and spinal canal and is known as a subarachnoid hemorrhage (sub= beneath + arachnoid=one of the brain coverings + hemorrhage=bleeding).

What are the signs and symptoms of brain aneurysm?

The headache associated with a leaking aneurysm is severe. Blood is very irritating to the brain and causes significant pain. Patients may describe the "worst headache of their life," and the health care practitioner needs to have an appreciation of brain aneurysm as a potential cause of this type of pain. The headache may be associated with nausea, vomiting, and change in vision. A subarachnoid hemorrhage also causes pain and stiffness of the neck.

How is brain aneurysm diagnosed?

The diagnosis of brain aneurysm begins with a high index of suspicion by the health care practitioner. The history of the headache, an acute onset of the worst headache of the patient's life, associated with a stiff neck and an ill-appearing patient on physical examination, typically lead the health care practitioner to order a CT (computerized tomography) scan of the head. This will show a subarachnoid hemorrhage in more than 90% of cases of ruptured aneurysm. In the few cases that are not recognized by CT, the health care practitioner may consider performing a lumbar puncture (LP, or spinal tap) to identify blood in the cerebrospinal fluid that runs in the subarachnoid space.
If the CT or the LP reveals the presence of blood, angiography is performed to identify where the aneurysm is located and to plan treatment. Angiography (angio=artery +graphy= picture) is a procedure in which a small flexible tube is threaded into one of the brain's arteries, and dye is injected while pictures are taken. Newer technology allows angiography to be done in association with CT or magnetic resonance imaging (MRI).
Though the symptoms may suggest a brain aneurysm, other diagnoses may need to be considered. Migraine headache, meningitis, tumor, and stroke all may cause neurologic symptoms. Based on the patient's presentation, the health care practitioner will need to decide which tests and studies to use to establish the correct diagnosis.

What is the treatment for brain aneurysm?

Treatment for a symptomatic aneurysm is to repair the blood vessels. Clipping and coiling are two treatment options.

• Clipping: A neurosurgeon can operate on the brain by cutting open the skull, identifying the damaged blood vessel and putting a clip across the aneurysm. This prevents blood from entering the aneurysm and causing further growth or blood leakage.
  
• Coiling: A neurosurgeon or interventional radiologist can thread a tube through the arteries, as with an angiogram, identify the aneurysm, and fill it with coils of platinum wire or with latex. This prevents further blood from entering the aneurysm and resolves the problem.

Both these options have the risk of damaging the blood vessel and causing more bleeding, damaging nearby brain tissue, and causing the surrounding blood vessels to go into spasm; depriving brain tissue of blood supply and causing a stroke.
Prior, during, and after surgery, attention is paid to protect the brain and its blood vessels from potential further damage. Vitals signs are monitored frequently, and heart monitors are used to watch for abnormal heart rhythms. Medications may be used to prevent blood vessel spasm, seizure, agitation, and pain.

What is the outcome of brain aneurysm?

Brain aneurysms are deadly. About 10% of patients with a ruptured aneurysm die before receiving medical care. If untreated, another 50% will die within a month, with 25% of patients sustaining another bleeding episode within a week. Aside from the bleeding issues, there is significant risk of artery spasm leading to stroke.
Survival rates are increased by early presentation to the hospital, early aneurysm repair, and control of potential blood vessel spasm with medications.

What are future directions for the treatment of brain aneurysm?

For those who survive an initial aneurysm rupture, blood vessel spasm (vasospasm) may be the villain in causing continued brain damage. Experiments to develop new drugs to control vasospasm are ongoing. Molecules that can cause spasm are being identified, and antibodies may be able to be produced to blunt their effect.
Studies are also looking at the possibility that brain aneurysms may be hereditary, and perhaps screening of high-risk populations may be possible in the future.

Transient Ischemic Attack

What is the treatment for a transient ischemic attack (TIA)?

TIA Therapy
Treatment for a transient ischemic attack is aimed at preventing a second stroke. Since there is no way of determining the severity of future episodes, and no guarantee that the symptoms will resolve, prevention of a future TIA or CVA is crucial.
Treatment guidelines address a variety of targeted goals.
Antiplatelet therapy

• If the patient was not taking aspirin when the TIA occurred, it usually is started at a dose of 325mg per day.
• If the patient was taking aspirin, another antiplatelet drug called dipyridamole may be added. Aggrenox is a combination of aspirin and dipyridamole. Headache is often a side effect.
• If the patient cannot tolerate aspirin because of allergy or stomach upset clopidogrel (Plavix) may be used.

High blood pressure therapy

• Even if the patient does not have hypertension or high blood pressure, there may be benefit in taking anti-hypertensive medications.  
• Two classes of drugs are recommended to be started at the same time, a diuretic and an ACE inhibitor.
• The goal for normal blood pressure is 120/80.

Cholesterol lowering therapy

• Guidelines recommend that a statin drug be started, even if cholesterol levels are normal. Simvastatin (Zocor) is the most commonly recommended medication, but new guidelines limit the amount prescribed per day because of the risk of liver side effects.

Risk modification
Smoking, excessive alcohol, obesity and lack of physical activity are considered risks for future stroke. The following recommendations are now suggested:

• Smoking: Counseling, smoking cessation aids like nicotine gum or medications like varenicline (Chantix) should be considered. Environmental smoke should be avoided.
• Alcohol: Intake should be limited to two or fewer drinks a day for men and one or less for women.
• Obesity: Overweight people should try to lose weight using a combination of diet, exercise and counseling. The goal is a BMI of 18.5-24.9 and a waist line of 35 inches or less for women and 40 inches or less for men.
• Exercise: 30 minutes of moderate exercise daily is recommended for those who are able. For patients with disabilities, a tailored exercise program to their capabilities should be arranged. 

What is the prognosis for transient ischemic attack (TIA)?

A transient ischemic attack should be considered a major warning sign of an impending future stroke. Up to 10% of people will experience a stroke within three months of TIA. Since there is no way of predicting that stroke-like symptoms will resolve, the patient and family need to be educated should symptoms occur, they need to access medical care emergently activating the emergency medical services system and calling 911.
If a stroke occurs, there is a very short period of time where thrombolytic (clot dissolving) drugs, (for example, alteplase [TPA]), can be used to reverse a stroke. In most hospitals, the drug can only be given within 4 1/2 hours of onset of stroke symptoms. In that time frame, the patient needs to get to the hospital, the diagnosis needs to be made, laboratory tests and head CT scans need to be performed, neurologic consultation needs to occur, and the drug administered. The longer the delay, there is a higher the risk that the drug won't work and that complications such as bleeding into the brain will occur.
Specialized interventional radiologists can inject TPA directly into the clot that has blocked the blood vessel in the brain. This can extend the time frame to six hours, but currently this treatment is not widely available.
TIAs should be considered the equivalent of angina of the brain. In heart disease, angina is the heart pain that warns of potential heart attack. When heart muscle is damaged, it cannot be replaced or repaired. Similarly, brain tissue is at risk when there is decreased blood supply and it, too, cannot be replaced.

Transient Ischemic Attack (TIA, Mini-Stroke)

Transient ischemic attack (TIA) facts

• A transient ischemic attack (TIA) is a brief interruption of blood flow to part of the brain that causes temporary stroke like symptoms.
• The risks for TIA are the same as for heart attack, stroke, and peripheral artery disease, and include smoking, high blood pressure, high cholesterol, diabetes, and family history.
• The artery blockage may occur because of a ruptured plaque due to atherosclerosis or hardening of the arteries, debris that floats downstream from narrowed carotid arteries or blood clots (emboli) that form (often in the heart) and travel to block an artery in the brain.
• Since TIAs resolve on their own, the goal for treatment is to minimize the risk of future TIAs and stroke. Treatment involves looking for the reason why the TIA occurred.
• Treatment may include aspirin or other anti-platelet medications like Aggrenox or clopidogrel (Plavix).
• It is important to educate the patient and family that should another stroke-like event occur, 911 must be called and emergency medical services activated, since there is no guarantee that symptoms will resolve.

What is a transient ischemic attack (TIA)?

The primary role of the brain is to send signals to the body for motor function and to receive signals through the five senses (sight, hearing, touch, smell, and taste), and to respond to them. The brain processes information through conscious thought, and unconsciously through nerve systems that control basic bodily functions, like heart rate, breathing, and temperature control.
In simple terms:

• The brain is arranged so that the right side of the brain controls the left side of the body, and the left side of the brain controls the right of the body.
• Vision is located in the back of the brain (occiput), and balance and coordination are located at the bottom of the brain (cerebellum).
• Blood supply to the brain comes from the carotid arteries that are located in the front of the neck, and the vertebral arteries that run in the back of the neck through small canals in the bony spine (vertebrae) of the neck.
• All of these connect at a junction of blood vessels located in the base of the brain (called the Circle of Willis), and from there smaller arteries supply the brain with oxygen and nutrients.

When a portion of the brain loses its blood supply, it can become damaged and stop functioning. When a portion of the brain does not function, the part of the body that it controls also stops working. This is called a stroke or a cerebrovascular accident (CVA). If the brain is able to regain its blood supply quickly, then the CVA symptoms may resolve; this is known as a transient ischemic attack (TIA). A TIA is similar to a stroke that resolves by itself because of a temporary lack of oxygen to a portion of the brain.

What are the causes of transient ischemic attack (TIA)?

Loss of blood supply to portions of the brain can occur for a variety of reasons. A blood vessel can become blocked, and blood supply to a part of the brain is lost, or a blood vessel can leak blood into the brain (brain hemorrhage). Most commonly however, the blood vessel is blocked. The blockage can be caused by a blood clot that forms in the blood vessel (thrombosis) or it can be caused by a clot or debris that floats downstream (embolus).
Blocked blood vesselsFatty plaque formation in the blood vessel wall is called atherosclerosis or "hardening of the arteries." Plaque can rupture and cause a small blood clot to form and occlude the blood vessel. Blockage can also occur when debris from narrowing of a carotid artery breaks off, and floats downstream to cause the occlusion. Sometimes, in people with an irregular heart beat called atrial fibrillation, small blood clots can be formed within the heart and travel to the brain to cause the obstruction.

  Picture of Carotid Artery Disease and Plaque Buildup
Brain hemorrhage or bleeding in the brain can be due to an aneurysm, a weak spot in a blood vessel that ruptures and spills blood into the brain tissue, or it may be due to spontaneous bleeding caused by poorly controlled hypertension (high blood pressure). Such bleeding more commonly results in the irreversible damage of a stroke, as opposed to a TIA.

What are the risk factors for transient ischemic attack (TIA)?

The risk factors for TIA or stroke are the same as those for other vascular disease, similar to heart attack (coronary artery disease) or peripheral vascular disease, which causes decreased blood flow to the legs. These risk factors include:

• family history
• smoking,
• high blood pressure,
• high cholesterol, and
• diabetes.

Moreover, any condition that results in stagnant blood flow and or clotting may result in a TIA due to embolization of a blood clot. Such conditions may include atrial fibrillation, large heart attacks, and severe weakness of the heart muscle.

What are the symptoms of transient ischemic attack (TIA)?

The intensity and location of the blood limitation to the brain will determine what symptoms will occur as a result of a stroke or TIA. Many people experience confusion, weakness, and lethargy. If the loss of blood supply is in an area supplied by the middle cerebral artery, a classic sign may include weakness or paralysis and numbness of one side of the body. The whole side may be affected, or just one limb. Often there is a facial droop. If the stroke is on the left side of the body where the speech centers are usually  located, there may be difficulty understanding words or speaking. Partial vision loss may also be part of the constellation of symptoms.
Strokes involving the vertebral arteries decrease blood supply to the base of the brain and may cause a drop attack (a sudden fall while walking or standing, and then a quick recovery), an unexpected collapse, incoordination, or difficulty walking.
The important distinction between stroke and TIA is resolution of the symptoms. By definition, the symptoms of a TIA must completely resolve. And, while this most often occurs within the first few minutes after symptom onset, it may take up to 24 hours to have complete return to normal function.
A special type of TIA is amaurosis fugax. Transient blindness in one eye occurs because debris from a narrowed carotid artery clogs the artery (ophthalmic artery) that supplies blood to the back of the eye.

How is transient ischemic attack (TIA) diagnosed?

TIA is diagnosed by history and physical examination. Since most often the symptoms have resolved, the physician will need to complete a thorough history from the patient and family or friends who witnessed the event. The physical exam will include careful attention to the neurologic examination. This may include:

• Assess mental status to make certain the patient is alert and oriented.
• Check eye range of motion and facial movement to evaluate the cranial nerves (the short nerves that run from the brain to the face and neck).
• Listen to the neck with a stethoscope to detect abnormal sounds that may signal narrowing of the blood vessel (carotid bruits).
• Check for a regular heart rhythm to rule out the presence of atrial fibrillation.
• Examine the arms and legs for tone, power, and sensation.
• Check coordination and balance.

If the diagnosis of TIA is made, further urgent testing is usually recommended, including:

• Electrocardiogram (EKG) to confirm a regular heart rate
• Computerized tomography (CT scan) of the brain to assess bleeding
• Carotid ultrasound to assess for narrowing of the large blood vessels in the neck
• Some hospitals have CT angiogram available to evaluate the cerebral, carotid, and vertebral arteries. This test is the same as a CT of the head with the addition of intravenous dye into the blood vessels to the arteries.
• Routine blood tests may include a complete blood count (CBC) to assess for anemia or low red blood cell count or too few platelets (thrombocytopenia). If the patient takes warfarin (Coumadin), a blood thinner, then an international normalized ratio (INR - a blood test that measures the degree of blood thinning) or prothrombin time (PT), may be performed to assess blood clotting measurements.
• If there is concern that the heart is the source of blood clot or debris, then an echocardiogram or sound wave tracing of the heart may be considered.

Sleep Disorders: Hypersomnia

Introduction to Hypersomnia

Hypersomnia, or excessive sleepiness, is a condition in which a person has trouble staying awake during the day. People who have hypersomnia can fall asleep at any time; for instance, at work or while they are driving. They may also have other sleep-related problems, including a lack of energy and trouble thinking clearly.
According to the National Sleep Foundation, up to 40% of people have some symptoms of hypersomnia from time to time.

What Causes Hypersomnia?

There are several potential causes of hypersomnia, including:

• The sleep disorders narcolepsy (daytime sleepiness) and sleep apnea (interruptions of breathing during sleep)
  
• Not getting enough sleep at night (sleep deprivation)
  
• Being overweight
  
• Drug or alcohol abuse
  
• A head injury or a neurological disease, such as multiple sclerosis
  
• Prescription drugs, such as tranquilizers
  
• Genetics (having a relative with hypersomnia)

How Is Hypersomnia Diagnosed?

If you consistently feel drowsy during the day, talk to your doctor. In making a diagnosis of hypersomnia, your doctor will ask you about your sleeping habits, how much sleep you get at night, if you wake up at night, and whether you fall asleep during the day. Your doctor will also want to know if you are having any emotional problems or are taking any medications that may be interfering with your sleep.
Your doctor may also order some tests, including blood tests, computed tomography (CT) scans, and a sleep test called polysomnography. In some cases, an additional electroencephalogram (EEG), which measures the electrical activity of the brain, is needed.

How Is Hypersomnia Treated?

If you are diagnosed with hypersomnia, your doctor can prescribe various drugs to treat it, including stimulants, antidepressants, as well as several newer medications (for example, Provigil and Xyrem).
If you are diagnosed with sleep apnea, your doctor may prescribe a treatment known as continuous positive airway pressure, or CPAP. With CPAP, you wear a mask over your nose while you are sleeping. A machine that delivers a continuous flow of air into the nostrils is hooked up to the mask. The pressure from air flowing into the nostrils helps keep the airways open.
If you are taking a medication that causes drowsiness, ask your doctor about changing the medication to one that is less likely to make you sleepy. You may also want to go to bed earlier to try to get more sleep at night, and eliminate alcohol and caffeine
.

Bedwetting (Nocturnal Enuresis)

What is bedwetting?

Bedwetting, also called nocturnal enuresis, is the involuntary passage of urine (urinary incontinence) while asleep. Inherent in the definition of bedwetting is satisfactory bladder control while the person is awake. Therefore, urination while awake is a different condition and has a variety of difference causes than bedwetting.

What are the types of bedwetting?

There are two types of bedwetting:

1. Primary enuresis: bedwetting since infancy
2. Secondary enuresis: wetting developed after being continually dry for a minimum of six months

What is primary bedwetting?

Primary bedwetting is viewed as a delay in maturation of the nervous system. At 5 years of age, approximately 20% of children wet the bed at least once a month, with about 5% of males and 1% of females wetting nightly. By 6 years of age, only about 10% of children are bedwetters -- the large majority being boys. The percentage of all children who are bedwetters continues to diminish by 50% each year after 5 years of age. Family history plays a big role in predicting primary bedwetting. If one parent was a bedwetter, the offspring have a 45% chance of a developing primary enuresis as well.

What is the basic problem in primary bedwetting?

The fundamental problem for children with primary bedwetting is the inability to recognize messages of the nervous system sent by the full bladder to the sleep arousal centers of the brain while asleep. In addition, bladder capacity is often smaller in bedwetting children than in their peers.

Is primary bedwetting due to emotional problems?

Parents sometimes believe that their child's primary bedwetting is emotional. No medical or scientific literature exists to support this impression.

How is primary bedwetting treated?

The "cure" for primary bedwetting is "tincture (or passage) of time." However, since many parents and children are frustrated with bedwetting as it starts to interfere with self-esteem or social events (for example, sleepovers), a patient step-by-step approach is best. Fortunately, it can be anticipated to have a successful outcome in over 75% of such patients. You should always discuss treatment options with your child's physician, since it is important to differentiate between primary and secondary enuresis prior to starting specific treatments.
It is also important to remember that different children develop differently and that primary enuresis can be a normal developmental stage. Toilet training a child requires special patience. While most children are fully toilet trained by 3-4 years of age, many will not stay dry overnight, even though they can during the day. Reassurance and encouragement often will work in time, but for some children, there are steps that can be taken to address the issues.
Some common recommended management and treatment options include the following:

1. Encourage voiding prior to bedtime, and restrict fluid intake before bed. 2. Cover the mattress with plastic. 3. Bedwetting alarms: There are generally reserved for older school-age children. There are commercial alarms that are available at most pharmacies. When the device senses urine, it alarms and wakes up the child so he/she can use the toilet. The cure rate is variable. 4. Bladder-stretching exercises are aimed at increasing the bladder volume and increasing the periods between daytime urinations. 5. Medications, such as DDAVP (desmopressin acetate or antidiuretic hormone) and Tofrinil (imipramine), have been shown to be very effective and are used to temporarily treat the nighttime urination, but they do not "cure" the enuresis. Many pediatricians will prescribe one of these medications, especially if the child is engaged in behavioral conditioning as well. Medications are very helpful when a child is not sleeping at home (camp or sleepovers), since the trauma of bedwetting in those settings is predictable. In addition, a recent study presented at the 2009 Pediatric Academic Society's annual meeting suggested that ibuprofen (Motrin, Advil, etc.) may also decrease the incidence of bedwetting by possibly stabilizing the bladder muscle that contracts during urination (detrusor muscle). 

How common is secondary bedwetting?

Only approximately 2%-3% of all children with bedwetting have a medical cause for the condition.

What causes secondary bedwetting?

Urinary tract infections, metabolic disorders (such as diabetes), external pressure on the bladder (such as from a rectal stool mass), and spinal cord disorders are among the causes of secondary bedwetting.

How is the cause of secondary bedwetting diagnosed?

A complete history and thorough physical examination are central to the initial evaluation of a child with primary bedwetting. A urinalysis and urine culture generally complete the workup. Further laboratory and radiological studies are for the child with secondary bedwetting.

What is the treatment for secondary bedwetting?

Therapy of secondary bedwetting is directed at the primary problem causing the symptom of wetting the bed. As expected, cure rates vary depending on the cause of the loss of control.

What is the outlook (prognosis) for children with bedwetting?

In the medical world of today, both primary and secondary bedwetting can be a manageable condition. Treatment programs can successfully eliminate both parental and patient anxiety, frustration, and embarrassment.
Resources for parents
http://www.aap.org
http://www.aafp.org

Bedwetting At A Glance

• Bedwetting is also called nocturnal enuresis.
• There are two types of bedwetting: primary and secondary.
• Primary bedwetting is bedwetting since infancy.
• Primary bedwetting is due to a delay in the maturing of the nervous system.
• Primary bedwetting is an inability to recognize messages sent by the bladder to the sleeping brain.
• The "cure" for primary bedwetting is "tincture (or passage) of time."
• There are a number of interventions including medical and behavioral options.
• Secondary bedwetting is wetting after being dry for at least six months.
• Secondary bedwetting is due to urine infections, diabetes, and other medical conditions.
• All bedwetting is manageable.
• Always speak to your child's physician for guidance.

 

Liver Blood Test

What are the basic functions of the liver?

The liver, located in the right upper portion of the abdominal cavity just beneath the right side of the rib cage, has many vital functions. Briefly, some of these functions are:

• Detoxification of blood
  
• Production of important clotting factor and other important proteins
  
• Metabolizing (processing) medications and nutrients
  
• Processing of waste products of hemoglobin
  
• Storing of vitamins, fat, cholesterol, and bile
  
• Production of glucose

What are common liver blood tests?

Liver blood tests are some of the most commonly performed blood tests. These tests can assess liver functions or liver injury. An initial step in detecting liver damage is a simple blood test to determine the presence of certain liver enzymes (proteins) in the blood. Under normal circumstances, these enzymes reside within the cells of the liver. But when the liver is injured for any reason, these enzymes are spilled into the blood stream. Enzymes are proteins that are present throughout the body, each with a unique function. Enzymes help to speed up (catalyze) routine and necessary chemical reactions in the body.
Among the most sensitive and widely used liver enzymes are the aminotransferases. They include aspartate aminotransferase (AST or SGOT) and alanine aminotransferase (ALT or SGPT). These enzymes are normally contained within liver cells. If the liver is injured or damaged, the liver cells spill these enzymes into the blood, raising the enzyme levels in the blood and signaling liver disease.
Other blood tests pertaining to the liver are measurements of some of the other enzymes found the liver. In addition to AST and ALT, alkaline phosphatase, 5' nucleotidase, and gamma-glutamyl transpeptidase (GGT) are other enzymes located in the liver. The focus of this article is mainly on the most common liver enzymes, AST and ALT.

What are the aminotransferases?

The aminotransferases catalyze chemical reactions in which an amino group from one amino acid (amino acids are building blocks of proteins) is transferred from a donor molecule to a recipient molecule. Hence, the names "aminotransferases."
Medical terms can sometimes be confusing, as is the case with these enzymes.

• Another name for aminotransferase is transaminase.
  
• The enzyme aspartate aminotransferase (AST) is also known as serum glutamic oxaloacetic transaminase (SGOT).
  
• Alanine aminotransferase (ALT) is also known as serum glutamic pyruvic transaminase (SGPT).

To put matters briefly, AST = SGOT and ALT = SGPT.

Normally, where are the aminotransferases?

AST (SGOT) is normally found in a variety of tissues including liver, heart, muscle, kidney, and brain. It is released into the serum when any one of these tissues is damaged. For example, its level in serum rises in heart attacks or with muscle disorders. It is therefore, not a highly specific indicator of liver injury as it can occur from other injured tissues.
ALT (SGPT) is, by contrast, normally found largely in the liver. This is not to say that it is exclusively located in liver, but that is where it is most concentrated. It is released into the bloodstream as the result of liver injury. Thus, it serves as a fairly specific indicator of liver status.

What are normal levels of AST and ALT?

• The normal range of values for AST (SGOT) is from 5 to 40 units per liter of serum (the liquid part of the blood).
  
• The normal range of values for ALT (SGPT) is from 7 to 56 units per liter of serum.

The ranges of AST and ALT numbers may differ slightly depending on the technique and protocols used by different laboratories. However, normal reference ranges are routinely provided by each laboratory and printed in the report.

What do elevated liver tests (AST and ALT) mean?

AST (SGOT) and ALT (SGPT) are sensitive indicators of liver damage or injury from different types of diseases. But it must be emphasized that higher-than-normal levels of these liver enzymes should not be automatically equated with liver disease. They may mean liver problems or they may not. For example, elevations of these enzymes can occur with muscle damage. The interpretation of elevated AST and ALT levels depends upon the entire clinical evaluation of an individual, and so it is best done by physicians experienced in evaluating liver disease and muscle disease.
Moreover, the precise levels of these enzymes do not correlate well with the extent of liver damage or the prognosis (outlook). Thus, the exact levels of AST (SGOT) and ALT (SGPT) cannot be used to determine the degree of liver disease or predict the future. For example, individuals with acute viral hepatitis A may develop very high AST and ALT levels (sometimes in the thousands of units/liter range). But most people with acute viral hepatitis A recover fully without residual liver disease. Conversely, people with chronic hepatitis C infection typically have only a little elevation in their AST and ALT levels while having substantial liver injury and even  advanced scarring of the liver (cirrhosis).

Heart Disease and Stress

Heart disease and stress introduction

Are stress and heart disease related? Does stress increase the risk of heart disease? Stress is a normal part of life. But if left unmanaged, stress can lead to emotional, psychological, and even physical problems, including heart disease, high blood pressure, chest pains, or irregular heart beats.

How Does Stress Increase the Risk for Heart Disease?

Medical researchers aren't sure exactly how stress increases the risk of heart disease. Stress itself might be a risk factor, or it could be that high levels of stress make other risk factors (such as high cholesterol or high blood pressure) worse. For example, if you are under stress, your blood pressure goes up, you may overeat, you may exercise less, and you may be more likely to smoke.
If stress itself is a risk factor for heart disease, it could be because chronic stress exposes your body to unhealthy, persistently elevated levels of stress hormones like adrenaline and cortisol. Studies also link stress to changes in the way blood clots, which increases the risk of heart attack.

Does Stress Affect Everyone the Same?

No. People respond in different ways to events and situations. One person may find an event joyful and gratifying, but another person may find the same event miserable and frustrating. Sometimes, people may handle stress in ways that make bad situations worse by reacting with feelings of anger, guilt, fear, hostility, anxiety, and moodiness. Others may face life's challenges with ease.

What Causes Stress?

Stress can be caused by a physical or emotional change, or a change in your environment that requires you to adjust or respond. Things that make you feel stressed are called "stressors."
Stressors can be minor hassles, major lifestyle changes, or a combination of both. Being able to identify stressors in your life and releasing the tension they cause are the keys to managing stress.
Below are some common stressors that can affect people at all stages of life.

• Illness, either personal or of a family member or friend.
• Death of a friend or loved one.
• Problems in a personal relationship.
• Work overload.
• Starting a new job.
• Unemployment.
• Retirement.
• Pregnancy.
• Crowds.
• Relocation.
• Daily hassles.
• Legal problems.
• Financial concerns.
• Perfectionism.

• What Are the Warning Signs of Stress?

  When you are exposed to long periods of stress, your body gives warning signals that something is wrong. These physical, cognitive, emotional and behavioral warning signs should not be ignored. They tell you that you need to slow down. If you continue to be stressed and you don't give your body a break, you are likely to develop health problems like heart disease. You could also worsen an existing illness.
  Below are some common warning signs and symptoms of stress.
  

  Physical signs	Dizziness, general aches and pains, grinding teeth, clenched jaws, headaches, indigestion, muscle tension, difficulty sleeping, racing heart, ringing in the ears, stooped posture, sweaty palms, tiredness, exhaustion, trembling, weight gain or loss, upset stomach
  Mental signs	Constant worry, difficulty making decisions, forgetfulness, inability to concentrate, lack of creativity, loss of sense of humor, poor memory
  Emotional signs	Anger, anxiety, crying, depression, feeling powerless, frequent mood swings, irritability, loneliness, negative thinking, nervousness, sadness
  Behavioral signs	Bossiness, compulsive eating, critical attitude of others, explosive actions, frequent job changes, impulsive actions, increased use of alcohol or drugs, withdrawal from relationships or social situations

   

Polio

What is the history of polio?

Polio is caused by a virus and has been around for thousands of years. There are even Egyptian artifacts portraying individuals with typical features of post-polio paralysis. Polio has been called many different names, including infantile paralysis, debility of the lower extremities, and spinal paralytic paralysis. We now refer to the virus and disease as polio, which is short for poliomyelitis and has Greek derivation: polios (gray), myelos (marrow), and itis (inflammation).
Polio is caused by a very infectious enterovirus, poliovirus (PV), which primarily affects young children and is spread through direct person-to-person contact, with infected mucus, phlegm, feces, or by contact with food and water contaminated by feces of another infected individual. The virus multiplies in the gastrointestinal tract where it can also invade the nervous system, causing permanent neurological damage in some individuals.
Most individuals infected with polio remain asymptomatic or develop only mild flu-like symptoms, including fatigue, malaise, fever, headache, sore throat, and vomiting. In fact, the symptoms, if present, may only last 48-72 hours; however, those individuals will continue to shed virus in their stools for a prolonged period, serving as a reservoir for subsequent infections. About 2%-5% of infected individuals go on to develop more serious symptoms that may include respiratory problems and paralysis. Currently, there is no cure for polio; only vaccination can prevent the spread of the disease, and although in the developed world it is almost unheard of, globally, polio remains a fairly common disease. Originally, international organizations believed it possible to eradicate polio by 2000, though this has been more difficult than initially hoped for.

What causes polio?

The symptoms of polio are caused by the poliovirus, which is a small RNA virus that is spread through contact with the oral mucosa (mouth, nose, etc). Most commonly, the virus attaches to and infects intestinal cells, multiplies, and is excreted in the stool of the infected individual. Rarely, in 2% of the cases, the virus spreads from the gastrointestinal tract to the nervous system and causes paralytic disease.

How is polio spread?

Polio is spread in an "oral-fecal" manner. Person-to-person infection occurs by contact with infected mucus, phlegm, feces, or by contact with food and water contaminated by feces of another infected individual.

What are signs and symptoms of polio?

The signs and symptoms of polio differ depending on the extent of the infection. Signs and symptoms can be divided into paralytic and non-paralytic polio.
In non-paralytic polio which accounts for most individuals infected with polio, patients remain asymptomatic or develop only mild flu-like symptoms, including fatigue, malaise, fever, headache, sore throat, and vomiting. The symptoms, if present, may only last 48-72 hours, though usually they last for one to two weeks.
Paralytic polio occurs in about 2% of people infected with the polio virus and is a much more serious disease. Symptoms occur as a result of nervous system and spinal cord infection and inflammation. Symptoms can include

• abnormal sensation,
• breathing difficulty,
• difficulty swallowing,
• urinary retention,
• constipation,
• drooling,
• headache,
• mood swings,
• muscle pain and spasms, and
• paralysis.

Approximately 5%-10% of patients who develop paralytic polio often die from respiratory failure, since they are unable to breathe on their own. That is why it is imperative that patients receive appropriate medical evaluation and treatment. Prior to the vaccine era and the use of modern ventilators, patients would be placed in an "iron lung" (a negative pressure ventilator, which was used to support breathing in patients suffering from paralytic polio).

How is polio diagnosed?

The diagnosis of polio is a clinical one. History of exposure with no history of previous vaccination is the initial hint. Often, a spinal tap for CSF fluid is done to help distinguish polio from other diseases that initially have similar symptoms (for example, meningitis). After that, viral cultures (taken from throat washings, stools, or CSF fluid) and measurement of polio antibodies support the diagnosis.

How is polio treated?

There is no cure for polio, so prevention is very important. Patients with non-paralytic polio need to be monitored for progression to paralytic polio. Patients with paralytic polio need to be monitored for signs and symptoms of respiratory failure, which may require lifesaving therapies such as respiratory support. In addition, a number of treatments are available to decrease some of the less severe symptoms. There are medications to treat urinary infections and urinary retention and pain management plans for muscle spasms. Unfortunately, there are only supportive measures available to treat the symptoms of paralytic polio. Patients who recover from polio may require physical therapy, leg braces, or even orthopedic surgery to improve physical function.

Is there a vaccine that prevents polio?

The story of polio vaccine is a true medical success story. It is not over yet since polio still causes significant illness in less developed areas of the world such as in India and Africa.
During the last half of the 19th century and into the first half of the 20th century, polio was a global epidemic. Even the future U.S. president, Franklin D. Roosevelt, contracted paralytic polio in 1921. President Franklin D. Roosevelt was quite influential in increasing both public awareness and scientific research dedicated to eradicating the disease. In 1938, after the founding of the National Foundation for Infantile Paralysis (March of Dimes), there was a significant effort to develop a vaccine to prevent polio. This came to fruition in 1955 when Dr. Jonas Salk developed an injectable inactivated polio vaccine (IVP) which was soon distributed and administered to children all over the United States and Canada. The current inactivated polio vaccine has evolved over time, but since 1999, it has been the recommended form of the polio vaccine in developed nations.
In 1961, an oral live virus vaccine against polio (OVP) was developed by Albert Sabin which became available and widely used from 1963 to 1999 in developed countries and to present day in underdeveloped countries. This oral virus vaccine is still recommended to control polio pandemics all over the world due to its ease of administration (no needles needed).
Both vaccines were developed for children since they are the group that generally seemed to be at highest risk. However, the oral vaccine (OVP) should not be given to children who are immunodepressed as they can develop vaccine-associated paralytic poliomyelitis (VAPP).
The newest injected vaccine is an enhanced inactivated polio vaccine that is more immunogenic (produces a strong immune system response) than the previous IVP and is used in the U.S.; it does not cause VAPP. The original OVP (also termed tOVP) was a trivalent oral vaccine (polio viruses types 1-3) but caused a measurable immune response in only about 40%-50% of people who obtained it. Unfortunately, this trivalent oral vaccine was often not immunogenic fast enough to withstand dilution or removal from the gastrointestinal tract by chronic diarrhea that existed in many patients. OVP was modified in 2005 to a monovalent (type 1 polio virus only) termed mOVP1. This change caused the vaccine to be three times more immunogenic than the original trivalent OVP and generated an immune response in over 80% of people who obtained this oral vaccine. This newer oral vaccine is used in many developing countries where no needles or trained personnel are available and where chronic diarrhea further reduces the effectiveness of the original trivalent OVP. Other monovalent OVP (for example, mOVP3, used for the infrequent polio type 3 outbreaks) are occasionally used.
Currently, four doses of inactivated polio vaccine (IPV) are recommended for children when they are 2 months old, 4 months old, 6-18 months old, and finally at 4-6 years of age.
Due to vaccination programs, there have been very few cases of polio in the western hemisphere since the 1970s, and although current worldwide eradication programs continue to be successful, there is still work to be done to eliminate polio in developing countries.

Anorexia Nervosa

What is anorexia nervosa?

Anorexia nervosa, commonly referred to simply as anorexia, is one type of eating disorder. More importantly, it is also a psychological disorder. Anorexia is a condition that goes beyond concern about obesity or out-of-control dieting. A person with anorexia often initially begins dieting to lose weight. Over time, the weight loss becomes a sign of mastery and control. The drive to become thinner is actually secondary to concerns about control and/or fears relating to one's body. The individual continues the ongoing cycle of restrictive eating, often accompanied by other behaviors such as excessive exercising or the overuse of diet pills to induce loss of appetite, and/or diuretics, laxatives, or enemas in order to reduce body weight, often to a point close to starvation in order to feel a sense of control over his or her body. This cycle becomes an obsession and, in this way, is similar to an addiction.

Who is at risk for anorexia nervosa?

Approximately 95% of those affected by anorexia are female, most often teenage girls, but males can develop the disorder as well. While anorexia typically begins to manifest itself during early adolescence, it is also seen in young children and adults. In the U.S. and other countries with high economic status, it is estimated that about one out of every 100 adolescent girls has the disorder. Caucasians are more often affected than people of other racial backgrounds, and anorexia is more common in middle and upper socioeconomic groups. According to the U.S. National Institute of Mental Health (NIMH), other statistics about this disorder include the fact that an estimated 0.5%-3.7% of women will suffer from this disorder at some point in their lives. About 0.3% of men are thought to develop anorexia in their lifetimes
Many experts consider people for whom thinness is especially desirable, or a professional requirement (such as athletes, models, dancers, and actors), to be at risk for eating disorders such as anorexia nervosa. Health-care professionals are usually encouraged to present the facts about the dangers of anorexia through education of their patients and of the general public as a means of preventing this and other eating disorders.

What causes anorexia nervosa?

At this time, no definite cause of anorexia nervosa has been determined. However, research within the medical and psychological fields continues to explore possible causes.
Studies suggest that a genetic (inherited) component may play a more significant role in determining a person's susceptibility to anorexia than was previously thought. Researchers are currently attempting to identify the particular gene or genes that might affect a person's tendency to develop this disorder, and preliminary studies suggest that a gene located at chromosome 1p seems to be involved in determining a person's susceptibility to anorexia nervosa.
Other evidence had pinpointed a dysfunction in the part of the brain, the hypothalamus (which regulates certain metabolic processes), as contributing to the development of anorexia. Other studies have suggested that imbalances in neurotransmitter (brain chemicals involved in signaling and regulatory processes) levels in the brain may occur in people suffering from anorexia.
Feeding problems as an infant, a general history of undereating, and maternal depressive symptoms tend to be risk factors for developing anorexia. Other personal characteristics that can predispose an individual to the development of anorexia include a high level of negative feelings and perfectionism. For many individuals with anorexia, the destructive cycle begins with the pressure to be thin and attractive. A poor self-image compounds the problem. People who suffer from any eating disorder are more likely to have been the victim of childhood abuse.
While some professionals remain of the opinion that family discord and high demands from parents can put a person at risk for developing this disorder, the increasing evidence against the idea that families cause anorexia has mounted to such an extent that professional mental-health organizations no longer ascribe to that theory. Possible factors that protect against the development of anorexia include high maternal body mass index (BMI) as well as personal high self-esteem.

How is anorexia nervosa diagnosed?

Anorexia nervosa can be a difficult disorder to diagnose, since individuals with anorexia often attempt to hide the disorder. Denial and secrecy frequently accompany other symptoms. It is unusual for an individual with anorexia to seek professional help because the individual typically does not accept that she or he has a problem (denial). In many cases, the actual diagnosis is not made until medical complications have developed. The individual is often brought to the attention of a professional by family members only after marked weight loss has occurred. When anorexics finally come to the attention of the health-care professional, they often lack insight into their problem despite being severely malnourished and may be unreliable in terms of providing accurate information. Therefore, it is often necessary to obtain information from parents, a spouse, or other family members in order to evaluate the degree of weight loss and extent of the disorder. Health professionals will sometimes administer questionnaires for anorexia as part of screening for the disorder.
Warning signs of developing anorexia or one of the other eating disorders include excessive interest in dieting or thinness. One example of such interest includes a movement called "thinspiration," which promotes extreme thinness as a lifestyle choice rather than as a symptom of illness. There are a variety of web sites that attempt to inspire others toward extreme thinness by featuring information on achieving that goal, photos of famous, extremely thin celebrities, and testimonials, as well as before and after pictures of individuals who ascribe to extreme thinness.
The actual criteria for anorexia nervosa are found in the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR).
There are four basic criteria for the diagnosis of anorexia nervosa that are characteristic:

1. The refusal to maintain body weight at or above a minimally normal weight for age and height (maintaining a body weight less than 85% of the expected weight)
2. An intense fear of gaining weight or becoming fat, even though the person is underweight
3. Self-perception that is grossly distorted, excessive emphasis on body weight in self-assessment, and weight loss that is either minimized or not acknowledged completely
4. In women who have already begun their menstrual cycle, at least three consecutive periods are missed (amenorrhea), or menstrual periods occur only after a hormone is administered.

The DSM-IV-TR further identifies two subtypes of anorexia nervosa. In the binge-eating/purging type, the individual regularly engages in binge eating or purging behavior which involves self-induced vomiting or the misuse of laxatives, diuretics, or enemas during the current episode of anorexia. In the restricting type, the individual severely restricts food intake but does not regularly engage in the behaviors seen in the binge-eating type.

What are anorexia symptoms and signs (psychological and behavioral)?

Anorexia can have dangerous psychological and behavioral effects on all aspects of an individual's life and can affect other family members as well.

• The individual can become seriously underweight, which can lead to depression and social withdrawal.
• The individual can become irritable and easily upset and have difficulty interacting with others.
• Sleep can become disrupted and lead to fatigue during the day.
• Attention and concentration can decrease.
• Most individuals with anorexia become obsessed with food and thoughts of food. They think about it constantly and become compulsive about eating rituals. They may collect recipes, cut their food into tiny pieces, prepare elaborate calorie-laden meals for other people, or hoard food. Additionally, they may exhibit other obsessions and/or compulsions related to food, weight, or body shape that meet the diagnostic criteria for an obsessive compulsive disorder.
• Other psychiatric problems are also common in people with anorexia nervosa, including affective (mood) disorders, anxiety disorders, and personality disorders.
• Generally, individuals with anorexia are compliant in every other aspect of their life except for their relationship with food. Sometimes, they are overly compliant, to the extent that they lack adequate self-perception. They are eager to please and strive for perfection. They usually do well in school and may often overextend themselves in a variety of activities. The families of anorexics often appear to be "perfect." Physical appearances are important to the anorexia sufferer. Performance in other areas is stressed as well, and they are often high achievers in many areas.
• While control and perfection are critical issues for individuals with anorexia, aspects of their life other than their eating habits are often found to be out of control as well. Many have, or have had at some point in their lives, addictions to alcohol, drugs, or gambling. Compulsions involving sex, exercising, housework, and shopping are not uncommon. In particular, people with anorexia often exercise compulsively to speed the weight-loss process.
• Symptoms of anorexia in men tend to co-occur with other psychological problems and more commonly follow a period of being overweight than in women. Men with anorexia also tend to be more likely to have a distorted body image.
• Compared to symptoms in men, symptoms of anorexia in women tend to more frequently include a general displeasure with their body and a possibly stronger desire to be thin. Women with anorexia also tend to experience more perfectionism and cooperativeness.

Due to the growth and development inherent during childhood and adolescence, symptoms and signs of anorexia in children and teenagers can include a slowing of the natural increase in height or a slowed increase in development of other body functions.
All of these features can negatively affect one's daily activities. Diminished interest in previously preferred activities can result. Some individuals also have symptoms that meet the diagnostic criteria for a major depressive disorder.

What are anorexia symptoms and signs (physical)?

Most of the medical complications of anorexia nervosa result from starvation. Few organs are spared the progressive deterioration brought about by anorexia.

• Heart and circulatory system: Although not life-threatening, an abnormally slow heart rate (bradycardia) and unusually low blood pressure (hypotension) are frequent manifestations of starvation and are commonly associated with anorexia. Of greater significance are disturbances in the heart rhythm (arrhythmia). A reduction in the work capacity of the heart is associated with severe weight loss and starvation.
• Gastrointestinal complications are also associated with anorexia. Constipation and abdominal pain are the most common symptoms. The rate at which food is absorbed into the body is slowed down. Starvation and overuse of laxatives can seriously disrupt the body's normal functions involved in the elimination process. While liver function is generally found to be normal, there is evidence that some individuals with anorexia develop changes in enzyme levels and overall damage to the liver.
• The glandular (endocrine) system in the body is profoundly affected by anorexia. The complex physical and chemical processes involved in the maintenance of life can be disrupted, with serious consequences. Disturbances in the menstrual cycle are frequent, and secondary amenorrhea (absence of menstrual periods) affects about 90% of adolescent girls with anorexia. Menstrual periods typically return with weight gain and successful treatment. Hormonal imbalances are found in men with anorexia as well. Continual restrictive eating can trick the thyroid into thinking that the body is starving, causing it to slow down in an attempt to preserve calories. When anorexia occurs in a person who also has diabetes mellitus (a tendency toward very high blood sugar levels), the risk of death is higher than in people who have either anorexia or diabetes mellitus alone.
• Kidney (renal) function may appear normal. However, there are significant changes in kidney function in many people with anorexia, resulting in increased or decreased urination or potentially fatal potassium deficiency. Diabetes insipidus, characterized by excessive urination and extreme thirst, has also been seen in anorexia.
• Bone density loss (osteopenia or thinning of the bones) is a significant complication of anorexia, since women acquire 40%-60% of their bone mass during adolescence. Studies have shown that bone loss can occur fairly rapidly in girls with anorexia. While some studies have shown that bone density may be restored if overall health improves and anorexia is successfully treated, other studies suggest that an increased risk for fracture may persist later in life.
• Anorexics who use a large quantity of laxatives or who frequently vomit are in danger of electrolyte imbalance, which can have life-threatening consequences.
• Anemia is frequently found in anorexic patients. In addition to having fewer red blood cells, people with anorexia tend to have lower numbers of white blood cells, which play a major role in protecting the body from developing infections. Suppressed immunity and a high risk for infection are suspected but not clinically proven.
• Contrary to what might be expected, anorexia nervosa is associated with a high total cholesterol levels.
• Physical symptoms, other than the obvious loss of weight, can be seen. Anorexia can cause dry, flaky skin that takes on a yellow tinge. Fine, downy hair grows on the face, back, arms, and legs. Despite this new hair growth, loss of hair on the head is not uncommon. Nails can become brittle. Frequent vomiting can erode dental enamel and eventually lead to tooth loss. People with anorexia might also develop trouble maintaining a consistent body temperature.

What is the treatment for anorexia nervosa?

Anorexia may be treated in an outpatient setting or hospitalization may be necessary. For an individual with severe weight loss that has impaired organ function, hospital treatment must initially focus on correction of malnutrition, and intravenous feeding or tube feeding that goes past the mouth may be required. A gain of between 1 to 3 pounds per week is a safe and attainable goal when malnutrition must be corrected. Sometimes weight gain is achieved using schedules for eating, decreased physical activity, and increased social activity, either on an inpatient or outpatient basis. For individuals who have suffered from anorexia for several years, the goals of treatment may need to be achieved more slowly in order to prevent the anorexia sufferer from relapsing as a result of being overwhelmed by treatment.
The overall treatment of anorexia, however, must focus on more than weight gain. There are a variety of treatment approaches dependent upon the resources available to the individual. Because of increasing insurance restrictions, many patients find that a short hospitalization followed by a day treatment program is an effective alternative to longer inpatient programs. Most individuals, however, initially seek outpatient treatment involving psychological as well as medical intervention. It is common to engage a multidisciplinary treatment team consisting of a medical-care provider, a dietician or nutritionist, and a mental-health-care provider.
Different kinds of psychological therapy have been employed to treat people with anorexia. Individual therapy, cognitive behavior therapy, group therapy, and family therapy have all been successful in the treatment of anorexia. In adolescents, research shows that the Maudsley model of family therapy can be particularly effective in treating this disorder in this population. In contrast to many past approaches to treatment, the Maudsley model approaches the family of the individual with anorexia as part of the solution rather than part of the reason their loved one has the disorder. With ongoing specific guidance from the professional mental-health team, this approach has the family actively help their loved one eat in a more healthy manner.
Any appropriate treatment approach addresses underlying issues of control, perfectionism, and self-perception. Family dynamics are explored. Nutritional education provides a healthy alternative to weight management for the patient. Group counseling or support groups may assist the individual in the recovery process. The ultimate goal of treatment should be for the individual to accept herself/himself and lead a physically and emotionally healthy life.
While no medications have been identified that can definitively reduce the compulsion to starve themselves, olanzapine (Zyprexa, Zydis), risperidone (Risperdal), and quetiapine (Seroquel) are medications that are also used as mood stabilizers and to treat schizophrenia that may be useful in treating anorexia. These medications may also help increase weight and to manage some of the emotional symptoms like anxiety and depression that can accompany anorexia. Some of the selective serotonin reuptake inhibitor (SSRI) antidepressant drugs have been shown to be helpful in weight maintenance after weight has been gained, as well as having beneficial effects on the mood and anxiety symptoms that may be associated with the condition.