Definition

Amitriptyline is a medication used to treat various forms of depression, pain associated with the nerves (neuropathic pain), and to prevent migraine headaches. It is sold in the United States under the brand names Elavil and Endep.

Purpose

Amitriptyline helps relieve depression and pain. This medication, usually given at bedtime, also helps patients sleep better.

Description

This medication is one of several tricyclic antidepressants, so-called because of the three-ring chemical structure common to these drugs. Amitriptyline acts to block reabsorption of neurotransmitters (chemicals that transmit nerve messages in the brain). Amitriptyline and the other tricyclic antidepressants are primarily used to treat mental depression but are increasingly being replaced by a newer and more effective group of antidepressant drugs called selective serotonin reuptake inhibitors (SSRIs). Amitriptyline is sometimes prescribed to help treat pain associated with cancer. In addition, it is sometimes prescribed for various types of chronic pain. Tablets are available in 10, 25, 50, 70, and 150 mg.

Recommended dosage

The usual adult dose for pain management ranges from 10 mg to 150 mg at bedtime. Patients are generally started on a low dose and the amount may be increased as needed. Side effects, such as a dry mouth and drowsiness, may make it difficult to increase the dose in older adults. Bedtime dosing helps the patient sleep. Doctors generally prescribe 75–150 mg for depression. It is given at bedtime or in divided doses during the day. It may take 30 days for the patient to feel less depressed. Pain relief is usually noticed sooner than the mood change. Teens and older adults usually receive a lower dose. If the nightly dose is missed, it should not be taken the next morning. Taking amitriptyline during waking hours could result in noticeable side effects. Patients should check with their doctor if the daily dose is missed. Those on more than one dose per day should take a missed dose as soon as it is remembered but should not take two doses at the same time. While amitriptyline is usually administered orally, injectable amitriptyline is available. It should not be used in this form long-term; patients should switch to tablets as soon as possible.

Precautions

Patients should not stop taking this medication suddenly. The dose should gradually be decreased, then discontinued. If the drug is stopped abruptly, the patient may experience headache, nausea, or discomfort throughout the body, and a worsening of original symptoms. The effects of the medication last for three to seven days after it has been stopped, and older patients usually are more prone to some side effects such as drowsiness, dizziness, mental confusion, blurry vision, dry mouth, difficulty urinating, and constipation. Taking a lower dose may help resolve these problems. Patients may need to stop this medication before surgery.

Amitriptyline should not be given to anyone with allergies to the drug or to patients recovering from a heart attack. Patients taking the monoamine oxidase inhibitors (MAOIs) Parnate (tranylcypromine) and Nardil (phenelzine) —different types of antidepressants—should not use amitriptyline in combination. It should be administered with caution to patients with glaucoma, seizures, urinary retention, overactive thyroid, poor liver or kidney function, alcoholism, asthma, digestive disorders, enlarged prostate, seizures, or heart disease. This medication should not be given to children under 12 years of age. Pregnant women should discuss the risks and benefits of this medication with their doctor as fetal deformities have been associated with taking this drug during pregnancy. Women should not breast feed while using amitriptyline.

Side effects

Common side effects include dry mouth, drowsiness, constipation, and dizziness or lightheadedness when standing. Patients can suck on ice cubes or sugarless hard candy to combat the dry mouth. Increased fiber in the diet and additional fluids may help relieve constipation. Dizziness is usually caused by a drop in blood pressure when suddenly changing position. Patients should slowly rise from a sitting or lying position if dizziness is noticed. Amitriptyline may increase the risk of falls in older adults. Patients should not drive or operate machinery or appliances while under the influence of this drug. Alcohol and other central nervous system depressants can increase drowsiness. Amitriptyline may also produce blurry vision, irregular or fast heartbeat, high or low blood pressure, palpitations, and an increase or decrease in a diabetic patient’s blood sugar levels. Patients’ skin may become more sensitive to the sun and thus direct sunlight should be avoided by wearing protective clothing and the application of sunscreen with a protective factor of 15 or higher.

Amitriptyline may increase appetite, cause weight gain, or produce an unpleasant taste in the mouth. It may also cause diarrhea, vomiting, or heartburn. Taking this medication with food may decrease digestive side effects. Other less likely side effects include muscle tremors, nervousness, impaired sexual function, sweating, rash, itching, hair loss, ringing in the ears, or changes in the makeup of the patient’s blood. Patients with schizophrenia may develop an increase in psychiatric symptoms.

Interactions

Patients should always tell all doctors and dentists that they are taking this medication. It may decrease the effectiveness of some drugs used to treat high blood pressure and should not be taken with other antidepressants, epinephrine and other adrenaline-type drugs, or methylphenidate. Patients should not take over-thecounter medications without checking with their doctor. For instance, amitriptyline should not be taken with Tagamet (cimetidine) or Neosynephrine. Patients taking this drug should avoid the dietary supplements St. John’s wort, belladonna, henbane, and scopolia. Black tea may decrease the absorption of this drug. Patients should ingest the drug and tea at least two hours apart.

Definition

Alzheimer’s disease, or AD, is a progressive, incurable disease of the brain caused by the degeneration and eventual death of neurons (nerve cells) in several areas of the brain.

Description

Patients with AD first lose such mental functions as short-term memory and the ability to learn new things. In the later stages of AD they gradually lose control over their sense of orientation, their emotions, and other aspects of behavior. End-stage AD is characterized by loss of control of body functions, an increased likelihood of seizures, loss of the ability to eat or swallow, and eventual death from infection or malnutrition. Alzheimer’s disease is the most common cause of dementia (loss of cognitive abilities) in the elderly; it is thought to be responsible for 50%–70% of cases of dementia in the United States.

Alzheimer’s disease was first identified in 1906 by a German psychiatrist and neuroanatomist named Alois Alzheimer. He was studying slides prepared from the brain of a fifty-one-year-old woman, known as Frau D., who had died after several years of dementia with symptoms that did not fit the definition of any brain disorder known at the time. Alzheimer was the first to describe the plaques and neurofibrillary tangles that are now used to identify AD at autopsy. Plaques are clumps or clusters of dead or dying nerve cells and other cellular debris found in the brains of patients with Alzheimer’s disease. Neurofibrillary tangles are the accumulations of twisted protein fragments found inside the nerve cells in the brains of Alzheimer’s patients. Because dementia had been associated with elderly people and Frau D. had been middle-aged, AD was first known as presenile dementia and was thought to be a very rare disorder. It was not until the early 1950s that researchers at St. Elizabeth’s Hospital in Washington, DC, came to recognize that AD is the single most common cause of dementia in adults.

Alzheimer’s disease is now considered a very serious public health problem because of the growing numbers of people who are affected by it, the increasing length of their lives, and the direct and indirect costs of their care. It is estimated that four million people in the United States had AD as of 2000, with 360,000–400,000 new cases identified every year. One person in ten over the age of 65 has AD, and nearly 50% of those over 85 have the disease. Unless a cure or preventive treatment is discovered, 14 million Americans will have Alzheimer’s by 2050. Very few people are wealthy enough to cover the cost of caring for an Alzheimer’s patient in the seven–10 years that typically extend between the beginning of the person’s dependency and death. The average lifetime cost of caring for one patient with AD is estimated at $174,000. The costs of laboratory tests, physicians’ visits, medications, nursing services, home care, and adult day care come to $114.4 billion per year in the United States alone. This sum is greater than the combined annual budgets of six Federal departments (Commerce, Education, Justice, Labor, Energy, and Interior).

The problem is expected to be complicated in future years by the fact that the so-called “baby boomer” generation is better nourished and better educated than the generation now at risk for AD. When the baby boomers are old enough to be at risk for late-onset Alzheimer’s, they are expected to live longer than the average Alzheimer’s patient does in 2002. Public health researchers who are making future projections about the impact of AD in the mid-twenty-first century point out that a treatment that would delay the onset of the disease would reduce the overall prevalence of AD. One study estimates that a therapy that would delay the onset of Alzheimer’s by only one year would save the United States $9 billion by 2007. The second approach, that of discovering a treatment for people who already have Alzheimer’s, would alter the proportion of mild cases to those considered moderate or severe. The researchers conclude by stating: “None of our models predicts less than a threefold rise in the total number of persons with Alzheimer’s disease between 2000 and 2050.”

Types of Alzheimer’s disease

As of 2002, some researchers think that Alzheimer’s may be more accurately described as a group or family of diseases rather than a single disease. Moreover, more recent research is helping to differentiate Alzheimer’s disease from other less common causes of dementia. In particular, some cases of dementia that were formerly thought to have been related to AD are now known to have been caused by Pick’s disease or Lewy body dementia. Pick’s disease is a rare type of dementia that affects certain areas of the brain and is characterized by a progressive loss of social skills, language, and memory. Lewy body dementia is a type of dementia in which the brain has characteristic Lewy bodies—areas of injury found on damaged nerve cells in certain parts of the brain.

Physicians now recognize three different forms of Alzheimer’s disease.

EARLY-ONSET AD. Early-onset AD is a rare form of Alzheimer’s found in fewer than 10% of AD patients. This group of patients, however, develops more of the brain abnormalities associated with AD than patients with the late-onset form. In addition, patients with early-onset Alzheimer’s are more likely to develop myoclonus (a condition in which a muscle or group of muscles has sudden spasms or twitching).

LATE-ONSET AD. Late-onset AD is the most common form of the disease; its symptoms usually begin to appear after age 65. Late-onset Alzheimer’s, which may or may not be affected by genetic variables, is also called sporadic Alzheimer’s disease because it does not necessarily run in families.

FAMILIAL ALZHEIMER’S DISEASE (FAD). Familial Alzheimer’s disease, or FAD, is a rare form that is entirely inherited. FAD accounts for fewer than 5% of all cases of AD. It has a very early onset, often in the patient’s 40s, and there is a clear family history of the disease.

Stages

Health care professionals use the term “insidious” to describe Alzheimer’s, which means that it is very gradual in onset. Many times people recognize the first symptoms of the disorder in a friend or family member only in hindsight. In addition, the present generation of people old enough to be at risk for Alzheimer’s is the first generation in history to know what the diagnosis means; there are therefore very powerful emotional reasons for attributing the early signs of AD to normal aging, job stress, adjusting to retirement, and other less troubling factors. The insidious onset of Alzheimer’s is a characteristic, however, that allows doctors to distinguish it from other causes of dementia, including vascular dementia.

EARLY-STAGE ALZHEIMER’S. Early-stage Alzheimer’s may begin almost imperceptibly. The first symptoms usually include short-term memory loss, temporary episodes of spatial disorientation, groping for words while one is speaking, minor problems with arithmetic, and small errors of judgment. For example, the person may light a stove burner under a saucepan before noticing that he has forgotten to put the food or water in the pan first, or he may have difficulty balancing a checkbook as quickly as he used to. At this stage in the disease, however, the patient can usually keep up with most activities of daily life. Although some persons at this point can still operate a motor vehicle safely, it is advisable to consult a physician about possible impairment behind the wheel. Many patients with early-stage AD voluntarily give up their driver’s licenses for their own safety and that of other drivers on the roads.

MIDDLE-STAGE ALZHEIMER’S. In the middle stage, which typically begins two to three years after onset, the person begins to lose awareness of his or her cognitive deficits. Memory lapses are more frequent and the person begins to have more severe problems with language. Unlike early-stage AD, the problems caused by loss of cognitive functioning are impossible to ignore. The middle stage of AD is the point at which the behavioral and psychiatric symptoms that are so stressful to caregivers often begin— the agitation, wandering, temper outbursts, depression, and disorientation. The patient is at high risk for falls and similar accidents. In addition, the patient becomes increasingly unable to understand simple instructions or to follow a conversation, and begins to lose his or her basic sense of personal identity.

END-STAGE ALZHEIMER’S. End-stage Alzheimer’s is marked by the loss of the ability to walk and eventually even to sit up. Patients may be able to use a wheelchair for awhile but eventually become completely bedridden. They lose bladder and bowel control. When the disease begins to affect the patient’s brain stem, the basic processes of digestion, respiration, and excretion shut down. Patients usually stop eating at this point and sleep most of the time. The hands and feet begin to feel cold, the breathing becomes shallow, and the patient is generally unresponsive to caregivers. Eventually the patient’s breathing simply stops.

Causes and symptoms

Causes

Evidence has accumulated that Alzheimer’s disease is multifactorial— that is, it is caused by a combination of several genetic and environmental factors.

GENETIC. Early-onset AD is caused by a defect in one of three genes known as APP, presenilin-1, and presenilin-2, found on human chromosomes 21, 14, and 1, respectively. Early-onset AD is also associated with Down syndrome, in that people with trisomy 21 (three forms of human chromosome 21 instead of a pair) often develop this form of Alzheimer’s. The brains of people with Down syndrome age prematurely, so that those who develop early-onset AD are often only in their late 40s or early 50s when the symptoms of the disease first appear.

Genetic research indicates that late-onset Alzheimer’s disease is a polygenic disorder; that is, its development is influenced by more than one gene. It has been known since 1993 that a specific form of a gene for apolipoprotein E (apoE4) on human chromosome 19 is a genetic risk factor for late-onset AD. People who have the apoE4 gene from one parent have a 50% chance of developing AD; a 90% chance if they inherited the gene from both parents. They are also likely to develop AD earlier in life. One of the remaining puzzles about this particular gene, however, is that it is not a consistent marker for AD. In other words, some people who have the apoE4 gene do not develop Alzheimer’s, and some who do not have the gene do develop the disorder. In 1998 another gene on chromosome 12 that controls the production of bleomycin hydrolase (BH, an enzyme involved in the body’s processing of amyloid precursor protein) was identified as a second genetic risk factor that acts independently of the APOE gene. In December 2000, three separate research studies reported that a gene on chromosome 10 that may affect the processing of a particular protein is also involved in the development of late-onset AD.

Familial Alzheimer’s disease appears to be related to abnormal genes on human chromosomes 21 and 14.

NEUROBIOLOGICAL. Investigators since Alois Alzheimer’s time have studied the abnormalities found at autopsy in the brains of patients with AD. One abnormality is plaques, or clumps, of a starchy protein called beta amyloid. Beta amyloid is formed when a substance called amyloid precursor protein, or APP, fails to be metabolized properly in the body. APP is a substance found in many parts of the body, but its precise function is not yet known. Following the formation of beta amyloid, pieces of it then stick to one another and gradually build up into plaques. The other abnormal finding is neurofibrillary tangles, which are twisted threads formed from parts of the dying nerve cell called the tau protein, which was discovered in 1986. If the tau protein is damaged by the addition of molecules of phosphorus, a process called hyperphosphorylation, it forms filaments that twist around each other to form the neurofibrillary tangles. As the plaques and tangles accumulate in the brain, they cause the nerve cells to wither and eventually die. As the nerve cells die, the affected parts of the brain start to shrink in size. It is not known as of 2002, however, whether the plaques and tangles are causes of AD or results of it. The relationship between the plaques and the tangles is another question that has not yet been answered. Although the plaques usually appear in brain tissue before the tangles, it is not clear that they cause the tangles. There are other brain disorders, such as Pick’s disease, in which tangles appear in the brain cells without plaques.

Another nervous system abnormality in AD is the lowered level of neurotransmitters produced by the cells in the brain. Neurotransmitters are chemicals that carry nerve impulses across the small gaps (synapses) between nerve cells. The neurotransmitters whose production is affected by Alzheimer’s include serotonin, norepinephrine, and acetylcholine. Many of the behavioral and psychiatric problems associated with AD are thought to result from the inadequate supply of these neurotransmitters.

ENVIRONMENTAL. Researchers have been studying the possibility that certain chemicals or other toxins in the environment may have a role in causing or triggering AD. The environmental factors that have been considered include aluminum, zinc, toxins in contaminated food, and viruses. Although there is little evidence as of 2002 that AD is caused by a virus or other infectious agent, the possibility cannot be completely excluded.

Other hypotheses about the causes of Alzheimer’s include damage caused by oxidation, estrogen deficiency, and inflammation. All of these possibilities are presently under investigation.

RISK FACTORS. A number of factors have been identified that increase a person’s risk of developing Alzheimer’s:

• Age. The risk of developing AD rises after age 65, and rises sharply after age 75. While 1% of the population has AD at age 65, almost 50% of those over 85 have it.
• Sex. Women are more likely to develop AD than men. As of 2002, however, it is not known whether women are more susceptible to the disorder, or more likely to develop it because they live longer than men, on average.
• Family history of AD.
• Having Down syndrome.
• History of head injury.
• Substances in the environment. Higher-than-average amounts of aluminum have been found in the brains of patients with Alzheimer’s. Some researchers in the late 1990s thought that exposure to aluminum might be a risk factor for the disorder. It now appears that the levels of aluminum in the brains of patients are a result rather than a cause of AD.
• Low occupational attainment and education level. Studies have found a clear correlation between employment in jobs that are not mentally challenging and an increased risk of AD. In addition, taking less rather than more challenging jobs as one grows older is associated with a higher risk of AD.
• High systolic blood pressure.
• High blood cholesterol levels. When both high systolic blood pressure and high cholesterol are present, the risk of developing AD increases by a factor of 3.5.
• Mild cognitive impairment (MCI). Mild cognitive impairment is a transitional decline in cognitive functioning that precedes the onset of AD. MCI is characterized primarily by memory loss while other cognitive functions remain intact. People with MCI are at higher risk for AD than people who do not develop the condition; 12% of people with mild cognitive impairment develop Alzheimer’s disease each year, compared with 1–2% per year of people without MCI. After four years, 40% of people diagnosed with mild cognitive impairment have clear symptoms of Alzheimer’s disease.

Treatments

At present the mainstay of Alzheimer’s treatment is medication, both to slow symptom progression and to manage the behavioral and psychiatric symptoms of AD.

Medications to slow symptom progression

The medications most commonly given to delay the progression of symptoms in Alzheimer’s are a group of drugs called cholinesterase inhibitors. These drugs were approved by the FDA over a decade ago. They work by slowing down the body’s destruction of the neurotransmitter acetylcholine.

The cholinesterase inhibitors include:

• Tacrine (Cognex). This drug is the oldest cholinesterase inhibitor in use. It is used less often than newer agents because it must be taken four times a day and may cause liver damage.
• Donepezil (Aricept). This drug is the one used most commonly as of 2002 to treat AD. It has fewer side effects than tacrine and can be given in one daily dose.
• Rivastigmine (Exelon). This drug is taken twice daily.
• Galantamine (Reminyl). This is the newest cholinesterase inhibitor, approved in late 2001. It acts on an additional acetylcholine receptor.

None of these medications provide more than modest benefits to patients with AD: they slow the progression of symptoms for about six months to a year in one-third to one-half of patients with AD. In addition, the cholinesterase inhibitors have side effects, most commonly nausea, vomiting, diarrhea, muscle cramps, and sleep disturbances.

Medications for BPSD

Medications are also prescribed to manage the behavioral and psychiatric symptoms of AD, which are often quite stressful for caregivers if the patient is being cared for at home. These medications are usually prescribed for specific symptoms:

• Delusions: Antipsychotic drugs, usually haloperidol(Haldol) or risperidone (Risperdal).
• Agitation: Short-term anti-anxiety drugs, usually lorazepam (Ativan) or buspirone (BuSpar).
• Depression: One of the selective serotonin reuptake inhibitors (SSRIs), at half the dosage for a young adult.
• Pain: Acetaminophen or a very low dose of codeine.

In general, older patients require lower dosages than those given to younger adults. Patients with AD are also more susceptible to the side effects of medications. For these reasons, physicians often recommend making changes in the patient’s environment to reduce the behavioral symptoms before trying medications.

Alternative and complementary treatments

Some complementary therapies have been shown to benefit patients with Alzheimer’s.

NATUROPATHY. A naturopathic approach to Alzheimer’s includes supplementing antioxidant vitamins (vitamins A, E, and C) in the patient’s diet, along with adding carotenoids, small amounts of selenium and zinc, and thiamin. Botanical supplements that have been said to improve cognitive function include Huperzine A, a Chinese tea, and an extract made from Gingko biloba, a tree that is native to China and is said to be the world’s oldest living deciduous tree. GBE, or gingko biloba extract, is the most frequently used herbal medicine in Europe. It is available in Germany by prescription and in an over-the-counter form; and has been approved by the German Commission E for dementia-related memory loss. Gingko extract is thought to work in a manner similar to the cholinesterase inhibitors. At present the National Center for Complementary and Alternative Medicine (NCCAM) is conducting studies of gingko extract as a treatment for Alzheimer’s.

MUSIC THERAPY. Music therapy has been found to calm agitated patients with Alzheimer’s, to improve mood, and to enhance their long-term memory. Old familiar songs are particularly effective in improving recall. In other studies, music therapy has been shown to reduce sensations of chronic pain in patients with AD.

Prognosis

There is no cure for Alzheimer’s disease as of 2002. The prognosis is progressive loss of mental and bodily functions leading to death within seven to ten years. Some patients, however, die within three years of diagnosis and others may survive for as long as fifteen.

Prevention

Researchers are considering several different strategies to prevent Alzheimer’s, ranging from development of a vaccine to prevent the formation of beta amyloid plaques to finding a drug that would stop the conversion of APP to beta amyloid. As of 2002, the vaccine, which was originally developed and tested on mice, does not appear to have any serious side effects in humans. It is presently being tested in Phase II trials on human subjects.

Definition

Amantadine is a synthetic antiviral agent that also has strong antiparkinsonian properties. It is sold in the United States under the brand name Symmetrel, and is also available under its generic name.

Purpose

Amantadine is used to treat a group of side effects (called parkinsonian side effects) that include tremors, difficulty walking, and slack muscle tone. These side effects may occur in patients who are taking antipsychotic medications used to treat mental disorders such as schizophrenia. An unrelated use of amantadine is in the treatment of viral infections of some strains of influenza A.

Description

Some medicines, called antipsychotic drugs, that are used to treat schizophrenia and other mental disorders can cause side effects similar to the symptoms of Parkinson’s disease. The patient does not have Parkinson’s disease, but he or she may experience shaking in muscles while at rest, difficulty with voluntary movements, and poor muscle tone. These symptoms are similar to the symptoms of Parkinson’s disease.

One way to eliminate these undesirable side effects is to stop taking the antipsychotic medicine. Unfortunately, the symptoms of the original mental disorder usually come back, so in most cases simply stopping the antipsychotic medication is not a reasonable option. Some drugs such as amantadine that control the symptoms of Parkinson’s disease also control the parkinsonian side effects of antipsychotic medicines.

Amantadine works by restoring the chemical balance between dopamine and acetylcholine, two neuro-transmitter chemicals in the brain. Taking amantadine along with the antipsychotic medicine helps to control symptoms of the mental disorder, while reducing parkinsonian side effects. Amantadine is in the same family of drugs (commonly known as anticholinergic drugs) as biperiden and trihexyphenidyl.

Recommended dosage

Amantadine is available in 100-mg tablets and capsules, as well as a syrup containing 50 mg of amantadine in each teaspoonful. For the treatment of drug-induced parkinsonian side effects, amantadine is usually given in a dose of 100 mg orally twice a day. Some patients may need a total daily dose as high as 300 mg. Patients who are taking other antiparkinsonian drugs at the same time may require lower daily doses of amantadine (100 mg daily, for example).

People with kidney disease or who are on hemodialysis must have their doses lowered. In these patients, doses may range from 100 mg daily to as little as 200 mg every seven days.

Precautions

Amantadine increases the amount of the neurotransmitter dopamine (a central nervous system stimulant) in the brain. Because of this, patients with a history of epilepsy or other seizure disorders should be carefully monitored while taking this drug. This is especially true in the elderly and in patients with kidney disease. Amantadine may cause visual disturbances and affect mental alertness and coordination. People should not operate dangerous machinery or motor vehicles while taking this drug.

Side effects

Five to ten percent of patients taking amantadine may experience the following nervous system side effects:

• dizziness or lightheadedness
• insomnia
• nervousness or anxiety
• impaired concentration

One to five percent of patients taking amantadine may experience the following nervous system side effects:

• irritability or agitation
• depression
• confusion
• lack of coordination
• sleepiness or nightmares
• fatigue
• headache

In addition, up to 1% of patients may experience hallucinations, euphoria (excitement), extreme forgetfulness, aggressive behavior, personality changes, or seizures. Seizures are the most serious of all the side effects associated with amantadine.

Gastrointestinal side effects may also occur in patients taking amantadine. Five to ten percent of people taking this drug experience nausea and up to 5% have dry mouth, loss of appetite, constipation, and vomiting. In most situations, amantadine may be continued and these side effects treated symptomatically.

One to five percent of patients taking amantadine have also reported a bluish coloring of their skin (usually on the legs) that is associated with enlargement of the blood vessels (called livedo reticularis). This side effect usually appears within one month to one year of starting the drug and subsides within weeks to months after the drug is discontinued. People who think they may be experiencing this or other side effects from any medication should tell their physician.

Interactions

Taking amantadine along with other drugs used to treat parkinsonian side effects may cause increased confusion or even hallucinations. The combination of amantadine and central nervous system stimulants (such as amphetamines or decongestants) may cause increased central nervous stimulation or increase the likelihood of seizures.

Definition

Alcoholism is defined as alcohol seeking and consumption behavior that is harmful. Long-term and uncontrollable harmful consumption can cause alcohol-related disorders that include: antisocial personality disorder, mood disorders (bipolar and major depression) and anxiety disorders.

Description

Alcoholism is the popular term for the disorder recognized by the American Psychiatric Association (APA) as alcohol dependence. The hallmarks of this disorder are addiction to alcohol, inability to stop drinking, and repeated interpersonal, school- or work-related problems that can be directly attributed to the use of alcohol. Alcoholism can have serious consequences, affecting an individual’s health and personal life, as well as impacting society at large.

Alcohol dependence is a complex disorder that includes the social and interpersonal issues mentioned above, and also includes biological elements, as well. These elements are related to tolerance and withdrawal, cognitive (thinking) problems that include craving, and behavioral abnormalities including the impaired ability to stop drinking. Withdrawal is a term that refers to the symptoms that occur when a person dependent on a substance stops taking that substance for a period of time; withdrawal symptoms vary in type and severity depending on the substance, but alcohol withdrawal symptoms can include shaking, irritability, and nausea. Tolerance is a reduced response to the alcohol consumed and can be acute or chronic. Acute tolerance occurs during a single episode of drinking and is greater when blood alcohol concentration rises. Chronic tolerance occurs over the long term when there is greater resistance to the intoxicating effects of alcohol, and, as a result, the affected person has to drink more to achieve desired effect.

The APA also recognizes another alcohol use disorder called alcohol abuse. Alcohol abuse is similar to dependence in that the use of alcohol is impairing the affected person’s ability to achieve goals and fulfill responsibilities, and his or her interpersonal relationships are affected by the alcohol abuse. However, unlike a person with dependence, a person diagnosed with alcohol abuse does not experience tolerance or, when not drinking, withdrawal symptoms. People who abuse alcohol can become dependent on the substance over time.

Alcohol-related disorders are groups of disorders that can result in persons who are long-term users of alcohol. These disorders can affect the person’s metabolism, gastrointestinal tract, nervous system, bone marrow (the matter in bones that forms essential blood cells) and can cause endocrine (hormone) problems. Additionally, alcoholism can result in nutritional deficiencies. Some common alcohol-related medical disorders include vitamin deficiencies, alterations in sugar and fat levels in blood, hepatitis, fatty liver, cirrhosis, esophagitis (inflammation of the esophagus), gastritis (inflammation of the lining of the stomach), dementia, abnormal heart rates and rhythms, lowered platelets (cells important for forming a clot), leukopenia (decrease in the number of white blood cells that are important for body defenses and immunity), and testicular atrophy (shrinking of the testicles). People with anxiety, depression, or bipolar disorder may consume alcohol for temporary relief from their symptoms. Others, such as people with antisocial personality disorder, may use alcohol as part of a dual diagnosis of criminality and substance dependence.

Causes and symptoms

Causes

The cause of alcoholism is related to behavioral, biological, and genetic factors.

Behaviorally, alcohol consumption is related to internal or external feedback. Internal feedback is the internal state a person experiences during and after alcohol consumption. External feedback is made up of the cues that other people send the person when he or she drinks. Internal states pertaining to alcohol can include shame or hangover. Alcohol-related external cues can include reprimands, criticism, or encouragement. People may drink to the point of dependence because of peer pressure, acceptance in a peer group, or because drinking is related to specific moods (easygoing, relaxed, calm, sociable) that are related to the formation of intimate relationships.

Biologically, repeated use of alcohol can impair the brain levels of a “pleasure” neurotransmitter called dopamine. Neurotransmitters are chemicals in the brain that pass impulses from one nerve cell to the next. When a person is dependent on alcohol, his or her brain areas that produce dopamine become depleted and the individual can no longer enjoy the pleasures of everyday life— his or her brain chemistry is rearranged to depend on alcohol for transient euphoria (state of happiness).

Genetic studies have isolated a gene that causes alcohol dependence and that is usually transmitted from affected fathers to sons. Other genetic studies have demonstrated that close relatives of an alcoholic are four times more likely to become alcoholics themselves. Furthermore, this risk holds true even for children who were adopted away from their biological families at birth and raised in a nonalcoholic adoptive family, with no knowledge of their biological family’s difficulties with alcohol.

Symptoms

ALCOHOL DEPENDENCE. Individuals who are alcohol-dependent compulsively drink ethanol (the chemical name for alcohol) to the level of intoxication. Intoxication occurs at blood alcohol levels of 50 to 150 mg/dl and is characterized by euphoria at first, and then if blood concentrations of alcohol continue to rise, a person can become explosively combative. Neurologically, acute intoxication causes impaired thinking, incoordination, slow or irregular eye movements, and impaired vision. As the person repeatedly drinks, the body develops a reduced response to ethanol called tolerance.

People with chronic tolerance may apparently be sober (not intoxicated) even after consumption of alcohol that could cause death in non-drinkers. People with alcohol dependence may also develop alcoholic blackouts after large amounts of ethanol consumption. These blackouts are typically characterized by amnesia (loss of memory) lasting several hours without impaired consciousness. In other words, people experiencing blackouts appear to be conscious, but will not remember their actions during the blackouts after the intoxication has worn off.

People with alcohol dependence also develop alcohol withdrawal (a state of non-drinking) syndrome. The nervous system adapts to chronic ethanol exposure by increasing the activity of nerve cell mechanisms that counteract alcohol’s depressant effects. Therefore, when drinking is abruptly reduced, the affected person develops disordered perceptions, seizures, tremor (often accompanied by irritability, nausea, and vomiting). Tremor of the hands called “morning shakes,” usually occurs in the morning due to overnight abstinence. The most serious manifestation of alcohol withdrawal syndrome is delirium tremens, which occurs in approximately 5% of people dependent on alcohol. Delirium tremens consists of agitation, disorientation, insomnia, hallucinations, delusions, intense sweating, fever, and increased heart rate (tachycardia). This state is a medical emergency because it can be fatal, and affected persons must be immediately hospitalized and treated with medications that control vital physiological functions.

The APA publishes a manual for mental health professionals called the Diagnostic and Statistical Manual of Mental Disorders, also known as the DSM. This manual lists criteria that each disorder must meet for diagnosis. The criteria are symptoms that must be present so that the diagnosis can be made. Alcohol dependence can be diagnosed if three or more of the following symptoms are present:

• tolerance
• withdrawal
• denial of problem
• preoccupation with seeking alcohol
• drinking is the focal point of person’s life (using takes up most of the person’s time)
• continued use despite problems

ALCOHOL ABUSE. In order for a person to be diagnosed with alcohol abuse, one of the following four criteria must be met. Because of drinking, a person repeatedly:

• fails to live up to his or her most important responsibilities
• physically endangers him- or herself, or others (for example, by drinking when driving)
• gets into trouble with the law
• experiences difficulties in relationships or jobs

Demographics

The lifetime prevalence in the general population for alcoholism is between 9.4% and 14.1%. The disorder occurs twice as often in males than in females. Alcoholism and alcohol abuse affect 20% or more of hospitalized and ambulatory patients (those receiving care on an outpatient basis). Alcoholism can develop in all people of all races and socioeconomic classes. Approximately two-thirds of Americans older than 14 years drink alcohol. People who drink excessive amounts of alcohol account for about half of the total alcohol consumed, and account for almost all the socioeconomic and medical complications of alcoholism at an annual cost of $100 billion. Alcoholism ranks third in the United States as a preventable disease and accounts for 5% of the total deaths in the U.S. amounting to about 100,000 people dying annually.

Diagnosis

The diagnosis of alcoholism can either be based on medical and/or psychological conditions. With a long-term history of abusive drinking, medical conditions can result, and these could lead the physician to suspect a patient’s alcoholism. These medical conditions may include organ complications such as: cirrhosis (liver), hepatitis (liver), pancreatitis (pancreas), peripheral neuropathy (nervous system) or cardiomyopathy (heart). Additionally, recurrent trauma, resulting in bone fractures, fatigue, depression, sexual dysfunction, fluctuating blood pressure, and sleep disorders may prompt the clinician to further assess for alcoholism.

Psychological diagnosis can be accomplished through a clinical interview and history (biopsychosocial assessment), and from a choice of many standardized alcohol use tests. The biopsychosocial assessment is an extensive interview conducted by the clinician. During the interview, the clinician will ask the patient about many areas of life, including childhood, education, and medical history. One very simple tool for beginning the diagnosis of alcoholism is called the CAGE questionnaire. It consists of four questions, with the first letters of each key word spelling out the word CAGE:

• Have you ever tried to Cut down on your drinking?
• Have you ever been Annoyed by anyone’s comments about your drinking?
• Have you ever felt Guilty about your drinking?
• Do you ever need an Eye-opener (a morning drink of alcohol) to start the day?

Other, longer lists of questions exist to help determine the severity and effects of a person’s alcohol use. Given the recent research pointing to a genetic basis for alcoholism, the doctor will also attempt to ascertain whether anyone else in the person’s family has ever suffered from alcoholism.

Diagnosis is sometimes facilitated when family members call the attention of a physician to a loved one’s difficulties with alcohol.

Treatments

Comprehensive treatment for alcohol dependence has two components: detoxification and rehabilitation.

Detoxification

The goal of detoxification is to rid the patient’s body of the toxic effects of alcohol. Because the person’s body has become accustomed to alcohol, the person will need to be supported as he or she goes through withdrawal. Withdrawal will be different for different patients, depending on the severity of the alcoholism, as measured by the quantity of alcohol ingested daily and the length of time the patient has been dependent on alcohol. Withdrawal symptoms can range from mild to life-threatening. Mild withdrawal symptoms include nausea, achiness, diarrhea, difficulty sleeping, sweatiness, anxiety, and trembling. This phase is usually over in about three to five days. More severe effects of withdrawal can include hallucinations (in which a patient sees, hears, or feels something that is not actually real), seizures, a strong craving for alcohol, confusion, fever, fast heart rate, high blood pressure, and delirium (a fluctuating level of consciousness). Patients at highest risk for delirium tremens are those with other medical problems, including malnutrition, liver disease, or Wernicke’s syndrome. Delirium tremens usually begins about three to five days after the patient’s last drink, progressing from the more mild symptoms to the more severe, and may last a number of days.

Patients going through mild withdrawal are simply monitored carefully to make sure that more severe symptoms do not develop. No medications are necessary, however. Treatment of a patient suffering the more severe effects of withdrawal may require the use of sedative medications to relieve the discomfort of withdrawal and to avoid the potentially life-threatening complications of high blood pressure, fast heart rate, and seizures. Benzodiazepines are medications that ease tension by slowing down the central nervous system and may be helpful in those patients suffering from hallucinations. Because of the patient’s nausea, fluids may need to be given through a vein (intravenously), along with some necessary sugars and salts. It is crucial that thiamin be included in the fluids, because thiamin is usually quite low in patients with alcohol dependence, and deficiency of thiamin is responsible for Wernicke-Korsakoff syndrome.

Rehabilitation

After cessation of drinking has been accomplished, the next steps involve helping the patient stay healthy and avoid relapsing. (Relapse occurs when a patient returns to old behaviors that he or she was trying to change.) This phase of treatment is referred to as rehabilitation. The best programs incorporate the family into the therapy, because the family has undoubtedly been severely affected by the patient’s drinking. Some therapists believe that family members, in an effort to deal with their loved one’s drinking problem, sometimes develop patterns of behavior that accidentally support or “enable” the patient’s drinking. This situation is referred to as “co-dependence,” and must be addressed in order to treat a person’s alcoholism successfully.

PSYCHOLOGICAL THERAPIES.Psychotherapy helps affected individuals to anticipate, understand, recognize, and prevent relapse. Behavioral therapy approaches typically include community-centered support groups, meetings such as Alcoholics Anonymous (AA), cognitive-behavioral therapy (CBT), and Motivated Enhancement Therapy (MET). CBT focuses on teaching alcoholics recognition and coping skills for craving states and high-risk situations that precipitate or trigger relapsing behaviors. MET can motivate patients to use their personal resources to initiate changes in behavior. Many people recovering from substance dependence find peerled support groups helpful in helping them avoid relapse.

MEDICATIONS. Two medications called naltrexone (Revia) and acamprosate can help decrease craving states in alcoholics. In combination with psychotherapy, these medications can help reduce relapse. Another medication called disulfiram (Antabuse) affects the metabolism of alcohol and causes unpleasant effects in patients who consume alcohol while taking the medication. Antabuse should only be taken by people who are committed to recovery and understand that they are to avoid all contact with alcohol or alcohol-containing products. People who have alcohol dependence along with other disorders, such as depression, can work with their physician to determine if medication might be a feasible treatment option for them.

ADDITIONAL TREATMENTS. Alternative treatments can be a helpful adjunct for the alcoholic patient, once the medical danger of withdrawal has passed. Because many alcoholics have very stressful lives (whether because of or leading to the alcoholism is sometimes a matter of debate), many of the treatments for alcoholism involve managing and relieving stress. These include massage, meditation, and hypnotherapy. The malnutrition of long-term alcohol use is addressed by nutrition-oriented practitioners and dietitians with careful attention to a healthy diet and the use of nutritional supplements such as vitamins A, B complex, and C, as well as certain fatty acids, amino acids, zinc, magnesium, and selenium. Acupuncture is believed to decrease both withdrawal symptoms and to help improve a patient’s chances for continued recovery from alcoholism.

Prognosis

Most people who use alcohol start to drink during adolescence or early adulthood. Approximately 50% of male drinkers have alcohol-related problems such as fighting, blackouts, or legal problems during their early drinking years, usually late teens or early twenties. People who cannot control their drinking behaviors will tend to accumulate drinking-related problems and become dependent on alcohol. Approximately 30% to 60% of alcoholics maintain about one year of sobriety with psychotherapeutic interventions alone. About 20% of alcoholics can achieve long-term abstinence without any type of active treatment.

Prevention

Good prevention includes education and a knowledge of family (genetic) propensity. If alcohol dependence is present in a close family member, then relatives should know and be discouraged to drink alcohol-containing beverages. Education of older children and young teenagers concerning the negative effects and consequences of drinking alcohol may help to decrease or recognize problems before start or worsen.

Definition

Agoraphobia is an anxiety disorder characterized by intense fear related to being in situations from which escape might be difficult or embarrassing (i.e., being on a bus or train), or in which help might not be available in the event of a panic attack or panic symptoms. Panic is defined as extreme and unreasonable fear and anxiety.

According to the handbook used by mental health professionals to diagnose mental disorders, the Diagnostic and Statistical Manual of Mental Disorders, fourth edition, text revision, also known as the DSM-IV-TR, patients with agoraphobia are typically afraid of such symptoms as feeling dizzy, having an attack of diarrhea, fainting, or “going crazy.”

The word “agoraphobia” comes from two Greek words that mean “fear” and “marketplace.” The anxiety associated with agoraphobia leads to avoidance of situations that involve being outside one’s home alone, being in crowds, being on a bridge, or traveling by car or public transportation. Agoraphobia may intensify to the point that it interferes with a person’s ability to take a job outside the home or to carry out such ordinary errands and activities as picking up groceries or going out to a movie.

Description

The close association in agoraphobia between fear of being outside one’s home and fear of having panic symptoms is reflected in DSM-IV-TR classification of two separate disorders: panic disorder (PD) with agoraphobia, and agoraphobia without PD. PD is essentially characterized by sudden attacks of fear and panic. There may be no known reason for the occurrence of panic attacks; they are frequently triggered by fear-producing events or thoughts, such as driving, or being in an elevator. PD is believed due to an abnormal activation of the body’s hormonal system, causing a sudden “fight-or-flight” response.

The chief distinction between PD with agoraphobia and agoraphobia without PD is that patients who are diagnosed with PD with agoraphobia meet all criteria for PD; in agoraphobia without PD, patients are afraid of panic-like symptoms in public places, rather than full-blown panic attacks.

People with agoraphobia appear to suffer from two distinct types of anxiety— panic, and the anticipatory anxiety related to fear of future panic attacks. Patients with agoraphobia are sometimes able to endure being in the situations they fear by “gritting their teeth,” or by having a friend or relative accompany them.

In the United States’ diagnostic system, the symptoms of agoraphobia can be similar to those of specific phobia and social phobia. In agoraphobia and specific phobia, the focus is fear itself; with social phobia, the person’s focus is on how others are perceiving him/her. Patients diagnosed with agoraphobia tend to be more afraid of their own internal physical sensations and similar cues than of the reactions of others per se. In cases of specific phobia, the person fears very specific situations, whereas in agoraphobia, the person generally fears a variety of situations (being outside of the home alone, or traveling on public transportation including a bus, train, or automobile, for example). An example of a patient diagnosed with a specific phobia rather than agoraphobia would be the person whose fear is triggered only by being in a bus, rather than a car or taxi. The fear of the bus is more specific than the agoraphobic’s fear of traveling on public transportation in general. The DSM-IVTR remarks that the differential diagnosis of agoraphobia “can be difficult because all of these conditions are characterized by avoidance of specific situations.”

Causes and symptoms

Causes

GENETIC. As of 2002, the causes of agoraphobia are complex and not completely understood. It has been known for some years that anxiety disorders tend to run in families. Recent research has confirmed earlier hypotheses that there is a genetic component to agoraphobia, and that it can be separated from susceptibility to PD. In 2001 a team of Yale geneticists reported the discovery of a genetic locus on human chomosome 3 that governs a person’s risk of developing agoraphobia. PD was found to be associated with two loci: one on human chromosome 1 and the other on chromosome 11q. The researchers concluded that agoraphobia and PD are common; they are both inheritable anxiety disorders that share some, but not all, of their genetic loci for susceptibility.

INNATE TEMPERAMENT. A number of researchers have pointed to inborn temperament as a broad vulnerability factor in the development of anxiety and mood disorders. In other words, a person’s natural disposition or temperament may become a factor in developing a number of mood or anxiety disorders. Some people seem more sensitive throughout their lives to events, but upbringing and life history are also important factors in determining who will develop these disorders. Children who manifest what is known as “behavioral inhibition” in early infancy are at increased risk for developing more than one anxiety disorder in adult life—particularly if the inhibition remains over time. (Behavioral inhibition refers to a group of behaviors that are displayed when the child is confronted with a new situation or unfamiliar people.) These behaviors include moving around, crying, and general irritability, followed by withdrawing, seeking comfort from a familiar person, and stopping what one is doing when one notices the new person or situation. Children of depressed or anxious parents are more likely to develop behavioral inhibition.

PHYSIOLOGICAL REACTIONS TO ILLNESS. Another factor in the development of PD and agoraphobia appears to be a history of respiratory disease. Some researchers have hypothesized that repeated episodes of respiratory disease would predispose a child to PD by making breathing difficult and lowering the threshold for feeling suffocated. It is also possible that respiratory diseases could generate fearful beliefs in the child’s mind that would lead him or her to exaggerate the significance of respiratory symptoms.

LIFE EVENTS. About 42% of patients diagnosed with agoraphobia report histories of real or feared separation from their parents or other caretakers in childhood. This statistic has been interpreted to mean that agoraphobia in adults is the aftermath of unresolved childhood separation anxiety. The fact that many patients diagnosed with agoraphobia report that their first episode occurred after the death of a loved one, and the observation that other agoraphobics feel safe in going out as long as someone is with them, have been taken as supportive evidence of the separation anxiety hypothesis.

LEARNED BEHAVIOR. There are also theories about human learning that explain agoraphobia. It is thought that a person’s initial experience of panic-like symptoms in a specific situation— for example, being alone in a subway station— may lead the person to associate physical symptoms of panic with all subway stations. Avoiding all subway stations would then reduce the level of the person’s discomfort. Unfortunately, the avoidance strengthens the phobia because the person is unlikely to have the opportunity to test whether subway stations actually cause uncomfortable physical sensations. One treatment modality—exposure therapy—is based on the premise that phobias can be “unlearned” by reversing the pattern of avoidance.

SOCIAL FACTORS RELATED TO GENDER. Gender role socialization has been suggested as an explanation for the fact that the majority of patients with agoraphobia are women. One form of this hypothesis maintains that some parents still teach girls to be fearful and timid about venturing out in public. Another version relates agoraphobia to the mother-daughter relationship, maintaining that mothers tend to give daughters mixed messages about becoming separate individuals. As a result, girls grow up with a more fragile sense of self, and may stay within the physical boundaries of their home because they lack a firm sense of their internal psychological boundaries.

Symptoms

The symptoms of an episode of agoraphobia may include any or all of the following:

• trembling
• breaking out in a sweat
• heart palpitations
• paresthesias (tingling or “pins and needles” sensations in the hands or feet)
• nausea
• fatigue
• rapid pulse or breathing rate
• a sense of impending doom

In most cases, the person with agoraphobia feels some relief from the symptoms after he or she has left the precipitating situation or returned home.

Demographics

In general, phobias are the most common mental disorders in the general United States population, affecting about 7% of adults, or 6.4 million Americans. Agoraphobia is one of the most common phobias, affecting between 2.7% and 5.8% of American adults. The onset of symptoms is most likely to occur between age 15 and age 35.The lifetime prevalence of agoraphobia is estimated at 5%–12%. Like most phobias, agoraphobia is two to four times more common in women than in men.

The incidence of agoraphobia appears to be similar across races and ethnic groups in the U.S.

Diagnosis

The differential diagnosis of agoraphobia is described differently in DSM-IV-TRand in ICD-10,the European diagnostic manual. The U.S. diagnostic manual specifies that agoraphobia must be defined in relation to PD, and that the diagnoses of specific phobias and social phobias are the next to consider. The DSM-IV-TRalso specifies that the patient’s symptoms must not be related to substance abuse; and if they are related to a general medical condition, they must have excessive symptoms usually associated with that condition. For example, a person with Crohn’s disease has realistic concerns about an attack of diarrhea in a public place and should not be diagnosed with agoraphobia unless the fear of losing bowel control is clearly exaggerated. The DSMIV-TR does not require a person to experience agoraphobia within a set number of circumstances in order to meet the diagnostic criteria.

In contrast, the European diagnostic manual primarily distinguishes between agoraphobia and delusional or obsessive disorders, and depressive episodes. In addition, ICD-10 specifies that the patient’s anxiety must be restricted to or occur primarily within two out of four specific situations: crowds; public places; traveling alone; or traveling away from home. The primary area of agreement between the American and European diagnostic manuals is that both specify avoidance of the feared situation as a diagnostic criterion.

Diagnosis of agoraphobia is usually made by a physician after careful exclusion of other mental disorders and physical conditions or diseases that might be related to the patient’s fears. Head injury, pneumonia, and withdrawal from certain medications can produce some of the symptoms of a panic attack. In addition, the physician may ask about caffeine intake as a possible dietary factor. As of 2002, there are no laboratory tests or diagnostic imaging studies that can be used to diagnose agoraphobia.

Furthermore, there are no widely used diagnostic interviews or screening instruments specifically for agoraphobia. One self-report questionnaire, however, is under development by Dutch researchers who recently reported on its validity. The test is called the Agoraphobic Self-Statements Questionnaire, or ASQ, and is intended to evaluate thinking processes in patients with agoraphobia, as distinct from their emotional responses.

Treatments

Treatment of agoraphobia usually consists of medication plus cognitive-behavioral therapy (CBT). The physician may also recommend an alternative form of treatment for the anxiety symptoms associated with agoraphobia. Some patients may be advised to cut down on or give up coffee or tea, as the caffeine in these beverages can be contribute to their panic symptoms.

Medications

Medications that have been used with patients diagnosed with agoraphobia include the benzodiazepine tranquilizers, the MAO inhibitors (MAOIs), tricyclic antidepressants (TCAs), and the selective serotonin uptake inhibitors, or SSRIs. In the past few years, the SSRIs have come to be regarded as the first-choice medication treatment because they have fewer side effects. The benzodiazepines have the disadvantage of increasing the symptoms of agoraphobia when they are withdrawn, as well as interfering with CBT. (Benzodiazepines can decrease mental sharpness, making it difficult for patients taking these medications to focus in therapy sessions.) The MAO inhibitors require patients to follow certain dietary guidelines. For example, they must exclude aged cheeses, red wine, and certain types of beans. TCAs may produce such side effects as blurred vision, constipation, dry mouth, and drowsiness.

Psychotherapy

CBT is regarded as the most effective psychotherapeutic treatment for agoraphobia. The specific CBT approach that seems to work best with agoraphobia is exposure therapy. Exposure therapy is based on undoing the association that the patient originally formed between the panic symptoms and the feared situation. By being repeatedly exposed to the feared location or situation, the patient gradually learns that he or she is not in danger, and the anxiety symptoms fade away. The therapist typically explains the procedure of exposure therapy to the patient and reassures him or her that the exposure can be stopped at any time that his or her limits of toleration have been reached. The patient is then exposed in the course of a number of treatment sessions to the feared situation, usually for a slightly longer period each time. A typical course of exposure therapy takes about 12 weeks.

On the other hand, one group of German researchers reported good results in treating patients with agoraphobia with individual high-density exposure therapy. The patients were exposed to their respective feared situations for an entire day for two–three weeks. One year later, the patients had maintained their improvement.

Exposure treatment for agoraphobia may be combined with cognitive restructuring. This form of cognitive behavioral therapy teaches patients to observe the thoughts that they have in the feared situation, such as, “I’ll die if I have to go into that railroad station,” and replace these thoughts with positive statements. In this example, the patient with agoraphobia might say to him- or herself, “I’ll be just fine when I go in there to buy my ticket.”

Although insight-oriented therapies have generally been considered relatively ineffective in treating agoraphobia, a recent trial of brief psychodynamic psychotherapy in patients with PD with agoraphobia indicates that this form of treatment may also be beneficial. Of the 21 patients who participated in the 24-session course of treatment (twice weekly for 12 weeks), 16 experienced remission of their agoraphobia. There were no relapses at six-month follow-up.

Alternative and complementary treatments

Patients diagnosed with agoraphobia have reported that alternative therapies, such as hypnotherapy and music therapy, were helpful in relieving symptoms of anxiety and panic. Ayurvedic medicine, yoga, religious practice, and guided imagery meditation have also been helpful.

Prognosis

The prognosis for untreated agoraphobia is considered poor by most European as well as most American physicians. The DSM-IV-TR remarks that little is known about the course of agoraphobia without PD, but that anecdotal evidence indicates that it may persist for years with patients becoming increasingly impaired. The ICD-10 refers to agoraphobia as “the most incapacitating of the phobic disorders,” to the point that some patients become completely housebound. With proper treatment, however, 90% of patients diagnosed with agoraphobia can recover and resume a normal life.

Prevention

As of this writing in 2002, the genetic factors that appear to be implicated in the development of agoraphobia cannot be prevented. On the other hand, recent recognition of the link between anxiety and mood disorders in parents and vulnerability to phobic disorders in their children may help to identify children at risk and to develop appropriate preventive strategies for them.

Definition

Affect is a psychological term for an observable expression of emotion.

Description

A person’s affect is the expression of emotion or feelings displayed to others through facial expressions, hand gestures, voice tone, and other emotional signs such as laughter or tears. Individual affect fluctuates according to emotional state. What is considered a normal range of affect, called the broad affect, varies from culture to culture, and even within a culture. Certain individuals may gesture prolifically while talking, and display dramatic facial expressions in reaction to social situations or other stimuli. Others may show little outward response to social environments or interactions, expressing a narrow range of emotions to the outside world.

People with psychological disorders may display variations in their affect. A restricted or constricted affect describes a mild restriction in the range or intensity of display of feelings. As the reduction in display of emotion becomes more severe, the term blunted affect may be applied. The absence of any exhibition of emotions is described as flat affect where the voice is monotone, the face expressionless, and the body immobile. Labile affect describes emotional instability or dramatic mood swings. When the outward display of emotion is out of context for the situation, such as laughter while describing pain or sadness, the affect is termed “inappropriate.”

Definition

Acute stress disorder (ASD) is an anxiety disorder characterized by a cluster of dissociative and anxiety symptoms that occur within a month of a traumatic stressor. It is a relatively new diagnostic category and was added to the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) in 1994 to distinguish time-limited reactions to trauma from the farther-reaching and longer-lasting post-traumatic stress disorder (PTSD). Published by the American Psychiatric Association, the DSM contains diagnostic criteria, research findings, and treatment information for mental disorders. It is the primary reference for mental health professionals in the United States.

Description

ASD, like PTSD, begins with exposure to an extremely traumatic, horrifying, or terrifying event. Unlike PTSD, however, ASD emerges sooner and abates more quickly; it is also marked by more dissociative symptoms. If left untreated, however, ASD is likely to progress to PTSD. Because the two share many symptoms, some researchers and clinicians question the validity of maintaining separate diagnostic categories. Others explain them as two phases of an extended reaction to traumatic stress.

Causes and symptoms

Causes

The immediate cause of ASD is exposure to trauma—an extreme stressor involving a threat to life or the prospect of serious injury; witnessing an event that involves the death or serious injury of another person; or learning of the violent death or serious injury of a family member or close friend. The trauma’s impact is determined by its cause, scope, and extent. Natural disasters (floods, earthquakes, hurricanes, etc.) or accidents (plane crashes, workplace explosions) are less traumatic than human acts of intentional cruelty or terrorism. Terrorist-inflicted trauma appears to produce particularly high rates of ASD and PTSD in survivors and bystanders.

Although most people define trauma in terms of events such as war, terrorist attacks, and other events that result in vast loss of life, the leading cause of stress-related mental disorders in the United States is motor vehicle accidents. Most Americans will be involved in a traffic accident at some point in their lives, and 25% of the population will be involved in accidents resulting in serious injuries. The National Comorbidity Survey of 1995 found that 9% of survivors of serious motor vehicle accidents developed ASD or PTSD.

Several factors influence a person’s risk of developing ASD after trauma:

• Age—Older adults are less likely to develop ASD, possibly because they have had more experience coping with painful or stressful events.
• Previous exposure—People who were abused or experienced trauma as children are more likely to develop ASD (or PTSD) as adults, because these may produce long-lasting biochemical changes in the central nervous system.
• Biological vulnerability—Twin studies indicate that certain abnormalities in brain hormone levels and brain structure are inherited, and that these increase a person’s susceptibility to ASD following exposure to trauma.
• Support networks—People who have a network of close friends and relatives are less likely to develop ASD.
• Perception and interpretation—People who feel inappropriate responsibility for the trauma, regard the event as punishment for personal wrongdoing, or have generally negative or pessimistic worldviews are more likely to develop ASD than those who do not personalize the trauma or are able to maintain a balanced view of life.

Symptoms

Acute stress disorder may be diagnosed in patients who (A) lived through or witnessed a traumatic event to which they (B) responded with intense fear, horror, or helplessness, and are (C) currently experiencing three or more of the following dissociative symptoms:

• psychic numbing
• being dazed or less aware of surroundings
• derealization
• depersonalization
• dissociative amnesia

Other symptoms that indicate ASD are:

• Reexperiencing the trauma in recurrent dreams, images, thoughts, illusions, or flashbacks; or intense distress when exposed to reminders of the trauma.
• A marked tendency to avoid people, places, objects, conversations, and other stimuli reminiscent of the trauma (many people who develop ASD after a traffic accident, for example, refuse to drive a car for a period of time).
• Hyperarousal or anxiety, including sleep problems, irritability, inability to concentrate, an unusually intense startle response, hypervigilance, and physical restlessness (pacing the floor, fidgeting, etc.).
• Significantly impaired social functions and/or the inability to do necessary tasks, including seeking help.
• Symptoms last for a minimum of two days and a maximum of four weeks, and occur within four weeks of the traumatic event.
• The symptoms are not caused by a substance (medication or drug of abuse) or by a general medical condition; do not meet the criteria of a brief psychotic disorder; and do not represent the worsening of a mental disorder that the person had before the traumatic event.

People with ASD may also show symptoms of depression including difficulty enjoying activities that they previously found pleasurable; difficulty in concentrating; and survivor’s guilt at having survived an accident or escaping serious injury when others did not. The DSM-IV-TR (revised edition published in 2000) notes that people diagnosed with ASD “often perceive themselves to have greater responsibility for the consequences of the trauma than is warranted,” and may feel that they will not live out their normal lifespans. Many symptoms of ASD are also found in patients with PTSD.

Demographics

Acute responses to traumatic stressors are far more widespread in the general United States population than was first thought in 1980, when PTSD was introduced as a diagnostic category in the DSM-III. The National Comorbidity Survey, a major epidemiological study conducted between 1990 and 1992, estimated that the lifetime prevalence among adult Americans is 7.8%, with women (10.4%) twice as likely as men (5%) to be diagnosed with trauma-related stress disorders at some point in their lives. These figures represent only a small proportion of adults who have experienced at least one traumatic event—60.7% of men and 51.2% of women respectively. More than 10% of the men and 6% of the women reported experiencing four or more types of trauma in their lives.

The prevalence of ASD by itself in the general United States population is not known. A few studies of people exposed to traumatic events found rates of ASD between 14% and 33%. Some groups are at greater risk of developing ASD or PTSD, including people living in depressed urban areas or on Native American reservations (23%) and victims of violent crimes (58%).

Diagnosis

ASD symptoms develop within a month after the traumatic event; it is still unknown, however, why some trauma survivors develop symptoms more rapidly than others. Delayed symptoms are often triggered by a situation that resembles the original trauma.

ASD is usually diagnosed by matching the patient’s symptoms to the DSM-IV-TR criteria. The patient may also meet the criteria for a major depressive episode or major depressive disorder. A person who has been exposed to a traumatic stressor and has developed symptoms that do not meet the criteria for ASD may be diagnosed as having an adjustment disorder.

As of 2002, there are no diagnostic interviews or questionnaires in widespread use for diagnosing ASD, although screening instruments specific to the disorder are being developed. A group of Australian clinicians has developed a 19-item Acute Stress Disorder Scale, which appears to be effective in diagnosing ASD but frequently makes false-positive predictions of PTSD. The authors of the scale recommend that its use should be followed by a careful clinical evaluation.

Treatments

Therapy for ASD requires the use of several treatment modalities because the disorder affects systems of belief and meaning, interpersonal relationships, and occupational functioning as well as physical well-being.

Medications

Medications are usually limited to those necessary for treating individual symptoms. Clonidine is given for hyperarousal; propranolol, clonazepam, or alprazolam for anxiety and panic reactions; fluoxetine for avoidance symptoms; and trazodone or topiramate for insomnia and nightmares. Antidepressants may be prescribed if ASD progresses to PTSD. These medications may include selective serotonin reuptake inhibitors (SSRIs), monoamine oxidase inhibitors (MAOIs), or tricyclic antidepressants.

Psychotherapy

Cognitive-behavioral therapy, exposure therapy, therapeutic writing (journaling), and supportive therapy have been found effective in treating ASD. One variant of cognitive-behavioral therapy called psychoeducational therapy appears to be three to four times as effective as supportive therapy in preventing ASD from progressing to PTSD. This treatment combines cognitive restructuring of the traumatic event with exposure to disturbing images and techniques for anxiety management. In addition, it can help patients identify and reinforce positive aspects of their experience. For example, some people find new strengths or talents within themselves in times of crisis, or discover new spiritual resources.

Group and family therapies also appear to help patients with ASD reinforce effective strategies for coping with the trauma, and may reduce the risk of social isolation as a reaction to the trauma. They give patients opportunities to describe what happened and how they responded; they also let patients receive warmth and caring from their listeners, and help put memories of the event into a coherent narrative, allowing them to integrate the trauma into their overall lives.

Critical incident stress management (CISM) is a comprehensive crisis-intervention system in which a team of specially trained practitioners comes to the site of a traumatic event and provides several different forms of assistance, including one-on-one crisis support; crisis management briefing, which is a 45–75-minute intervention for groups of people affected by the traumatic event; and critical incident stress debriefing, which is a structured group discussion of the event. CISM appears to be particularly helpful in preventing burnout and ASD in emergency service personnel, rescue personnel, police, and other caregivers who are involved in treating survivors of a traumatic event.

Definition

Acupuncture, one of the main forms of therapy in traditional Chinese medicine (TCM), has been practiced for at least 2,500 years. In acupuncture, certain points on the body associated with energy channels or meridians are stimulated by the insertion of fine needles. Unlike the hollow hypodermic needles used in mainstream medicine to give injections or draw blood, acupuncture needles are solid. The points can be needled between 15 and 90 degrees in range relative to the skin’s surface, depending on treatment.

Acupuncture is thought to restore health by removing energy imbalances and blockages in the body. Practitioners of TCM believe that there is a vital force or energy called qi(pronounced “chee”) that flows through the body, and between the skin surface and the internal organs, along channels or pathways called meridians. There are 12 major and 8 minor meridians. Qi regulates the spiritual, emotional, mental, and physical harmony of the body by keeping the forces of yin and yang in balance. Yang is a principle of heat, activity, brightness, outwardness, while yin represents coldness, passivity, darkness, interiority, etc. TCM does not try to eliminate either yin or yang, but to keep them in harmonious balance. Acupuncture may be used to raise or lower the level of yin or yang in a specific part of the body in order to restore the energy balance.

Acupuncture was virtually unknown in the United States prior to President Nixon’s trip to China in 1972. A reporter for the New York Timesnamed James Reston wrote a story for the newspaper about the doctors in Beijing who used acupuncture to relieve his pain following abdominal surgery. By 1993, Americans were making 12 million visits per year to acupuncturists, and spending $500 million annually on acupuncture treatments. By 1995, there were an estimated 10,000 certified acupuncturists practicing in the United States; as of 2000, there were 20,000. About a third of the credentialed acupuncturists in the United States as of 2002 are MDs.

Acupuncture’s record of success has been sufficiently impressive to stimulate a number of research projects investigating its mechanisms as well as its efficacy. Research has been funded not only by the National Center for Complementary and Alternative Medicine (NCCAM), but also by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), the National Institute of Dental Research, the National Institute of Neurological Disorders and Stroke (NINDS), and the National Institute on Drug Abuse. In 1997 a consensus panel of the National Institutes of Health (NIH) presented a landmark report in which it described acupuncture as a sufficiently promising form of treatment to merit further study. In 2000, the British Medical Association (BMA) recommended that acupuncture should be made more readily available through the National Health Service (NHS), and that family doctors should be trained in some of its techniques.

Precautions

Although the risk of infection in acupuncture is minimal, patients should make sure that the acupuncturist uses sterile disposable needles. In the United States, the Food and Drug Administration (FDA) mandates the use of sterilized needles made from nontoxic materials. The needles must be clearly labeled as having their use restricted to qualified practitioners.

Patients should also inquire about the practitioner’s credentials. Since acupuncture is now taught in over forty accredited medical schools and osteopathic colleges in the United States, patients who would prefer to be treated by an MD or an osteopath can obtain a list of licensed physicians who practice acupuncture in their area from the American Academy of Medical Acupuncture. With regard to nonphysician acupuncturists, 31 states have established training standards that acupuncturists must meet in order to be licensed in those states. In Great Britain, practitioners must qualify by passing a course offered by the British Acupuncture Accreditation Board.

Patients seeking acupuncture treatment should provide the practitioner with the same information about their health conditions and other forms of treatment that they would give their primary care doctor. This information should include other alternative and complementary therapies, especially herbal remedies.

Acupuncture should not be used to treat severe traumatic injuries and other emergency conditions requiring immediate surgery. In addition, it does not appear to be useful in smoking cessation programs.

As is true with other forms of medical treatment, a minority of patients do not respond to acupuncture. The reasons for nonresponsiveness are not known at the present stage of research.

Description

In traditional Chinese medicine, acupuncture treatment begins with a thorough physical examination in which the practitioner evaluates the patient’s skin color, vocal tone, and tongue color and coating. The practitioner then takes the patient’s pulse at six locations and three depth levels on each wrist. These thirty-six pulse measurements will tell the practitioner where the qi in the patient’s body might be blocked or unbalanced. After collecting this information, the acupuncturist will then identify the patterns of energy disturbance and the acupuncture points that should be stimulated to unblock the qi or restore harmony. Up to ten or twelve acupuncture needles will be inserted at strategic points along the relevant meridians. In traditional Chinese practice, the needles are twirled or rotated as they are inserted. Many patients feel nothing at all during this procedure, although others experience a prickling or mild aching sensation, and still others a feeling of warmth or heaviness.

The practitioner may combine acupuncture with moxibustion to increase the effectiveness of the treatment. Moxibustion is a technique in which the acupuncturist lights a small piece of wormwood, called a moxa, above the acupuncture point above the skin. When the patient begins to feel the warmth from the burning herb, it is removed. Cupping is another technique that is a method of stimulation of acupuncture points by applying suction through a metal, wood, or glass jar, and in which a partial vacuum has been created. Producing blood congestion at the site, the site is thus stimulated. The method is used for lower back pain, sprains, soft tissue injuries, as well as relieving fluid from the lungs in chronic br