by the pines

Definition

Rivastigmine is a drug used to treat symptoms of Alzheimer’s disease. In the United States, rivastigmine is sold as the brand name drug Exelon.

Purpose

Rivastigmine is used to treat symptoms of Alzeheimer’s disease in individuals with mild to moderate illness. It has also been used to treat dementia caused by other conditions such as Lewy-body disease or following strokes. The drug may produce mild improvements in symptoms of thinking for a short period of time, but rivastigmine does not cure or stop progression of underlying diseases.

Description

The Food and Drug Administration approved rivastigmine in 2000 specifically for treating Alzheimer’s disease. In Alzheimer’s disease, some cells in specific regions of the brain die. Because of this cell death, these brain cells lose their ability to transmit nerve impulses. Brain cells normally transmit nerve impulses another by secreting various chemicals known as neurotransmitters.

Brain cells that make and secrete a neurotransmitter called acetylcholine are affected early in the course of Alzheimer’s disease. Rivastigmine prevents the breakdown of acetylcholine in the brain, thus temporarily increasing its concentration. In doing so, rivastigmine may improve the thinking process by facilitating nerve impulse transmission within the brain.

Rivastigmine is available as capsules in four different strengths and as an oral solution for use by people who have difficulty swallowing. Unlike some other drugs used to treat Alzheimer’s disease, the liver does not break down rivastigmine. As a result, it may be preferred in the treatment of people with Alzeheimer’s disease who have liver disease.

Recommended dosage

The initial dosage of rivastigmine is 1.5 mg taken two times per day. If this dose is tolerated without difficulty, the dosage may be increased to 3 mg twice a day after at least two weeks at the lower dosage. Some people are unable to tolerate nausea, vomiting, anorexia, and weight loss that occur with higher dosages. If the drug does not cause significant adverse effects, the dose may be increased to 4.5 mg two times per day, followed by 6 mg two times per day. The dosage should be increased slowly, at two-week intervals. If side effects occur and cannot be tolerated, the drug may be stopped for several doses. When the drug is started again, the same dosage or the next lower dosage may be tried. The maximum daily dosage is 6 mg two times per day.

Precautions

Rivastigmine may slow heart rates, increase acid in the stomach, make urination difficult, cause breathing difficulties, and may possibly contribute to seizures. As a result, it should be used with close physician supervision and monitoring in people with certain heart conditions, those who are prone to stomach ulcers, people with bladder obstruction, individuals with asthma or chronic obstructive pulmonary disease, and people with a history of seizures disorders.

Individuals taking rivastigmine should be reassessed periodically to determine whether the drug is providing any benefits. If caregivers feel the drug is no longer beneficial, it may be stopped.

Side effects

The most frequent side effects associated with rivastigmine involve stomach upset. Nausea, vomiting, anorexia, heartburn, and weakness occur in more than 5% of people and at twice the rate of placebo pills. Dizziness and headaches also occur in more than 10% of people taking rivastigmine.

Other, less common, side effects are difficulty sleeping, confusion, depression, anxiety, sleepiness, hallucinations, tremors, fainting, aggression, constipation, gas, overwhelming fatigue, weight loss, increased sweating, and infections.

Interactions

Drugs such as dicyclomine may inhibit the effects of rivastigmine. Other drugs like bethanechol may possibly increase some of the side effects of rivastigmine. Rivastigmine may interact with some of the drugs used to relax muscles during surgery. The interaction increases the effects of both drugs.

Definition

Risperidone is classified as an atypical antipsychotic drug. It is sold in the United States under the brand name of Risperdal.

Purpose

Risperidone is used for the management of symptoms of psychotic disorders such as schizophrenia.

Description

Risperidone is an atypical antipsychotic agent for two reasons. First, it is chemically unrelated to the older antipsychotic drugs. Second, unlike older antipsychotic drugs that primarily inhibit the actions of dopamine, a chemical in the brain, risperidone may also have some action against another brain chemical, serotonin. The proper level of both dopamine and serotonin are influential in maintaining mental well-being.

An advantage of using risperidone over one of the older antipsychotic drugs is a lower incidence of parkinsonian-like side effects. These side effects may be sufficiently troublesome to cause patients to discontinue treatment for their schizophrenia. For this reason, patients who have had negative experiences with older antipsychotics may benefit from risperidone. Also, some patients who showed little improvement with older antipsychotic drugs respond better to risperidone.

Risperidone is available in 0.25-mg, 0.5-mg, 1-mg, 2-mg, 3-mg, and 4-mg tablets and a solution containing 1 mg of drug in each milliliter of solution.

Recommended dosage

For treating psychotic disorders in adults, the usual starting dose of risperidone is 1 mg twice daily. Dosage is increased gradually until a target dose of 3 mg twice daily is reached. Some patients do just as well with a single daily dose (6 mg once a day, for example). There is little clinical evidence to indicate that increasing the daily dose beyond 8 mg offers additional benefit. However, higher doses may contribute to additional side effects. If the dose needs to be adjusted, the changes should made no more often than once per week.

In older patients (over age 60), starting dosage should not exceed 1 mg daily. Most patients should not take more than 3 mg daily. People with low blood pressure and those who have kidney disease should take a similarly reduced dose.

Precautions

Patients with a history of cardiovascular disease or low blood pressure should take risperidone only after discussing the risks and benefits with their physician, and then with close physician monitoring.

Risperidone has occasionally been associated with seizures. People with a past history of seizures should discuss with their doctor whether risperidone is the right antipsychotic for them to use.

People taking risperidone should avoid operating a motor vehicle or other dangerous machinery until they see how risperidone affects them. Some people have trouble regulating their body temperature while taking risperidone. Patients receiving this drug should be aware of this and avoid extremes in outdoor temperatures.

Side effects

The most common and bothersome side effect associated with risperidone is decreased blood pressure while standing up (known as orthostatic hypotension). This can cause dizziness or fainting. A decrease in blood pressure usually occurs early in therapy, while the proper dose is being established. It is more common in older patients than in younger ones. Usually, this side effect disappears entirely with time. If it continues, the physician may decrease the dose. Meanwhile, people taking risperidone should be aware of this side effect and get up slowly if they have been sitting for an extended time.

The most common nervous system side effects of risperidone include insomnia, agitation, anxiety, and headache. Early in therapy, patients may experience an inability to think clearly or perform certain tasks that require mental alertness. High doses of risperidone can cause unwanted sleepiness in about 40% of patients.

Antipsychotic drugs, including risperidone, can cause side effects that are similar to the symptoms of Parkinson’s disease. The patient does not have Parkinson’s disease, but may have shaking in muscles at rest, difficulty with voluntary movements, and poor muscle tone. These symptoms normally disappear if the drug is stopped.

The most common gastrointestinal side effects include nausea, vomiting, constipation, and difficulty digesting food.

Up to 10% of patients taking risperidone experience rhinitis (runny nose).

Interactions

There is very little information about how risperidone interacts with other drugs. However, because some patients receiving risperidone experience lowered blood pressure while standing, it is expected that other drugs that lower blood pressure may increase the incidence and severity of this side effect when taken with risperidone.

Definition

In the course of illness, relapse is a return of symptoms after a period of time when no symptoms are present. Any strategies or treatments applied in advance to prevent future symptoms are known as relapse prevention.

Purpose

When people seek help for mental disorders, they receive treatment that, hopefully, reduces or eliminates symptoms. However, once they leave treatment, they may gradually revert to old habits and ways of living. This results in a return of symptoms known as relapse. Relapse prevention aims to teach people strategies that will maintain the wellness skills they learned while in treatment.

Prevention of relapse in mental disorders is crucial—not only because symptoms are detrimental to quality of life but also because the occurrence of relapse increases chances for future relapses. In addition, with each relapse, symptoms tend to be more severe and have more serious consequences.

Description

Relapse is a concern with any disorder, whether physical or psychological. Cancer is a prime example of a physical condition where relapse is common, either after a short period or many years of remission (being symptom-free). Psychological disorders can follow a similar pattern, and certain psychological disorders tend to have a higher rate of relapse than others. Addictive disorders, such as alcohol and drug abuse, smoking, overeating, and pathological gambling, are well known for high levels of relapse. Many addictions involve a lifestyle centered around the addictive behavior. In such cases, individuals must not only discontinue the addictive habit, they must also restructure their entire lives in order for changes to last. Such vast changes are difficult at best, approaching impossible in the worst scenarios. For example, an individual with a drug addiction may live in a neighborhood where drugs are prevalent but may lack the resources to move. According to recent statistics, relapse rates are approximately 33% for people who gamble pathologically (within three months of treatment), 90% for people who quit smoking, and 50% for people who abuse alcohol. Within one year of treatment, people struggling with obesity typically regain 30% to 50% of the weight they lost.

Affective disorders, such as depression and anxiety, also have high rates of relapse. People with affective disorders are thought to engage in self-defeating, negative thought patterns that occur more or less automatically. These thought patterns affect behavior, resulting in unproductive or negative consequences. Negative consequences are regarded by such individuals as proof that their original self-defeating thoughts must be correct. The thought-behavior pattern becomes a repetitive cycle, with negative thoughts resulting in negative behavioral outcomes, and consequences of negative behavior encouraging more self-defeating thoughts. This cycle is extremely difficult to break because it becomes a habitual way of responding to the world that occurs almost without awareness. Relapse rates for depression are reportedly as high as 80%.

Relapse among people who commit sex offenses is a constant safety concern for those in the community. However, some statistics show that this population has a very low rate of relapse. A recent report by Robin J. Wilson and colleagues indicated rates as low as 3.7% to 6.3%. This same report stated that, among various criminal offenses, those who commit sex offenses relapse at lower rates than those who commit general offenses. Other professionals may not necessarily agree with this study, however. Those who commit sex offenses are considered at a higher risk for relapse if they display little insight into the impact of their crime. Those at high risk of committing a sex offense are not typically released back into the community.

For many types of disorders, initial treatment is often effective at eliminating the unwanted behavior. However, these effects are rarely maintained long-term without some type of preventive planning. Results of medications are similar; symptoms are alleviated, but once the medication is discontinued, symptoms return unless the individual has had some type of training in coping with his or her disorder and that training has been effective. There are various forms of relapse prevention training. Most follow a similar pattern with and employ the following common elements:

• Identifying high-risk situations: Symptoms are often initiated by particular times, places, people, or events. For example, a person with agoraphobia is more likely to experience symptoms of panic in a crowded building. An essential key to preventing relapse is to be aware of the specific situations where one feels vulnerable. These situations are called “triggers,” because they trigger the onset of symptoms. While people with the same mental disorder may share similar triggers, triggers can also be highly individual. People tend to react—sometimes unknowingly—to negative experiences in their past. For example, a woman who was sexually abused as a child may have negative emotions when in the presence of men who resemble her abuser. Because some triggers occur without conscious awareness, individuals may not know all their triggers. Many prevention programs encourage individuals to monitor their behavior closely, reflecting on situations where symptoms occurred and determining what was happening immediately before the onset of symptoms. With this kind of analysis, a pattern often emerges that gives clues about the trigger.
• Learning alternate ways to respond to high-risk situations: Once triggers have been identified, one must find new ways of coping with those situations. The easiest coping mechanism for high-risk situations is to avoid them altogether. This may include avoiding certain people who have a negative influence or avoiding locations where the symptom is likely to occur. In some instances, avoidance is a good strategy. For example, individuals who abuse alcohol may successfully reduce their risk by avoiding bars or parties. In other instances, avoidance is not possible or advisable. For example, individuals attempting to lose weight may notice that they are more likely to binge at certain times during the day. One cannot avoid a time of day. Rather, by being aware of this trigger, one can purposely engage in alternate activities during that time. Strategies for coping with unavoidable triggers are generally skills that need to be learned and practiced in order to be effective. Strategies include—but are not limited to—discussion of feelings, whether with a friend, counselor, or via a hotline; distraction, such as music, exercise, or engaging in a hobby; refocusing techniques, such as meditation, deep-breathing exercises, progressive muscle relaxation (focusing on each muscle group separately, and routinely tensing then relaxing that muscle), prayer, or journaling; and cognitive restructuring, such as positive affirmation statements (such as, “I am worthwhile”), active problem solving (defining the problem, generating possible solutions, identifying the consequences of those solutions, choosing the best solution), challenging the validity of negative thoughts, or guided imagery (imagining oneself in a different place or handling a situation appropriately).
• Creating a plan for healthy living: Besides being prepared for high-risk situations, relapse prevention also focuses on general principles of mental health that, if followed, greatly reduce the likelihood of symptoms. These include factors such as balanced nutrition, regular exercise, sufficient sleep, health education, reciprocally caring relationships, productive and recreational interests, and spiritual development.
• Developing a support system: Many research studies have demonstrated the importance of social support in maintaining a healthy lifestyle. Individuals who are socially isolated tend to display more symptoms of mental disorders. Conversely, individuals with mental disorders tend to have more difficultly initiating and maintaining relationships due to inappropriate social behavior. For such people, a support system may be nonexistent. Research suggests that support systems are most effective when they are naturally occurring—in other words, when a circle of family and friends who genuinely care about the individual is already in place. However, artificially created support systems are certainly better than none at all. For this reason, relapse prevention programs strive to involve family members and other significant persons in the treatment program. Everyone in the support system should be knowledgeable about the person’s goals, what that person is like when he or she is doing well, and warning signs that the person may be on a path toward relapse. The support system agrees on who will take what role in encouraging, confronting, or otherwise caring for that person. Self-help groups such as Alcoholics Anonymous or Moderation Management are often examples of artificially created support systems.
• Preparing for possible relapse: Although the ultimate goal of relapse prevention is to avoid relapse altogether, statistics demonstrate that relapse potential is very real. Individuals need to be aware that, even when exerting their best efforts, they may occasionally experience lapses (one occurrence of a symptom or behavior) or relapses (return to a previous, undesirable level of symptoms or behavior). Acknowledging the potential for relapse is important, because many people consider a lapse or relapse as evidence of personal failure and give up completely. In their widely acclaimed book for professionals, Motivational Interviewing, William R. Miller and Stephen Rollnick cite a study by Prochaska and DiClemente that found that smokers typically relapse between three and seven times before quitting for good. From the perspective of Miller and Rollnick, each relapse can be a step closer to full recovery if relapse is used as a learning experience to improve prevention strategies. Although some argue that such a tolerant attitude invites relapse, general consensus is that individuals need to forgive themselves if relapse occurs and then move on. Some prevention programs include designing a crisis plan to be put into effect if a relapse occurs. The crisis plan involves specific actions to be taken by the individual or members of the support system.

These elements are common to all relapse prevention programs, but programs can be further customized to meet the particular characteristics of a disorder. For example, prevention of depression or anxiety may focus on becoming aware of thoughts as passing mental events rather than facts about self or reality. Learning to identify bodily sensations that accompany maladaptive thoughts is also important for preventing depression and anxiety. Addictive disorders concentrate on reactions to social pressure, interpersonal conflicts, and negative emotional states as part of a relapse prevention plan.

Preparation

As with any type of therapeutic treatment, success of relapse prevention programs depend heavily on motivation. If an individual is not interested in making life changes, he or she is not likely to follow a prevention plan. Individuals low in motivation may need to participate in group or individual psychotherapy before deciding whether to enter a relapse prevention program.

Aftercare

Aftercare typically consists of participation in support groups. For addictions, 12-step groups (such as Alcoholics Anonymous) are most commonly recommended. These types of groups can be attended daily. Support groups exist for other types of mental disorders, and may be run by peers or a professional facilitator. Aftercare groups, usually run in treatment facilities by professional staff, may be used to continue practicing skills and to trouble-shoot problems individuals are experiencing with their prevention plans in everyday life. Aftercare groups usually meet less frequently (once a week or month) and may gradually taper off. Some relapse-prevention programs may use telephone contacts or individual therapy sessions to help individuals continue to use prevention skills effectively.

Normal results

Successful relapse prevention programs will empower individuals to make choices about how they respond in stressful, high-risk situations (triggers) rather than responding in habitual, unhealthy ways. Individuals should be aware of their personal triggers, use positive strategies for coping with stress, practice healthy lifestyle choices, involve others in their efforts, and have a realistic attitude regarding relapse. Use of these prevention skills should reduce symptoms and increase the time span between occurrences of lapses or relapses.

Abnormal results

If an individual is unmotivated to make life changes, or a relapse prevention program has been ineffective, that individual will demonstrate few (if any) of the prevention skills learned. The individual will show little improvement in symptomatic or problematic behavior. Periods of remission (symptom-free behavior) will be short and relapses will occur frequently.

Definition

A reinforcer is a stimulus that follows some behavior and increases the probability that the behavior will occur. For example, when a dog’s owner is trying to teach the dog to sit on command, the owner may give the dog a treat every time the dog sits when commanded to do so. The treat reinforces the desired behavior.

Description

In operant conditioning (as developed by B. F. Skinner), positive reinforcers are rewards that strengthen a conditioned response after it has occurred, such as feeding a hungry pigeon after it has pecked a key. Negative reinforcers are stimuli that are removed when the desired response has been obtained. For example, when a rat is receiving an electric shock and presses a bar that stops the shock, the shock is a negative reinforcer— it is an aversive stimulus that reinforces the bar-pressing behavior. The application of negative reinforcement may be divided into two types: escape and avoidance conditioning. In escape conditioning, the subject learns to escape an unpleasant or aversive stimulus (a dog jumps over a barrier to escape electric shock). In avoidance conditioning, the subject is presented with a warning stimulus, such as a buzzer, just before the aversive stimulus occurs and learns to act on it in order to avoid the stimulus altogether.

Punishment can be used to decrease unwanted behaviors. Punishment is the application of an aversive stimulus in reaction to a particular behavior. For children, a punishment could be the removal of television privileges when they disobey their parents or teacher. The removal of the privileges follows the undesired behavior and decreases its likelihood of occurring again.

Reinforcement may be administered according to various schedules. A particular behavior may be reinforced every time it occurs, which is referred to as continuous reinforcement. In many cases, however, behaviors are reinforced only some of the time, which is termed partial or intermittent reinforcement. Reinforcement may also be based on the number of responses or scheduled at particular time intervals. In addition, it may be delivered in regularly or irregularly. These variables combine to produce four basic types of partial reinforcement. In fixed-ratio (FR) schedules, reinforcement is provided following a set number of responses (a factory worker is paid for every garment he assembles). With variable-ratio (VR) schedules, reinforcement is provided after a variable number of responses (a slot machine pays off after varying numbers of attempts). Fixed-interval (FI) schedules provide for reinforcement of the first response made within a given interval since the previous one (contest entrants are not eligible for a prize if they have won one within the past 30 days). Finally, with variable-interval (VI) schedules, first responses are rewarded at varying intervals from the previous one.

Definition

Reading disorder is a learning disorder that involves significant impairment of reading accuracy, speed, or comprehension to the extent that the impairment interferes with academic achievement or activities of daily life. People with reading disorder perform reading tasks well below the level one would expect on the basis of their general intelligence, educational opportunities, and physical health. Reading disorder is most commonly called dyslexia. Dyslexia, however, usually includes deficits in spelling and writing as well as reading.

Description

Reading disorder is a learning disorder characterized by a significant disparity between an individual’s general intelligence and his or her reading skills. Learning disorders, formerly called academic skills disorders, are disorders that account for difficulty learning and poor academic performance when low performance cannot be attributed to mental retardation, low intelligence, lack of learning opportunities, or such specific physical problems as vision or hearing deficits. Common learning disabilities include reading disorder (often called dyslexia), mathematics disorder, disorder of written expression, and some language processing disorders.

Reading disorder can cause severe problems in reading, and consequently in academic work, even in people with normal intelligence, educational opportunities, motivation to learn to read, and emotional self-control. Reading disorder is different from slowness in learning or mental retardation. In reading disorder, there is a significant gap between the expected level of performance and actual achievement. Difficulties in reading can occur on many levels, and reading disorder may have several causes that manifest in different ways. Common problems in people with reading disorder include:

• slow reading speed
• poor comprehension when reading material either aloud or silently
• omission of words while reading
• reversal of words or letters while reading
• difficulty decoding syllables or single words and associating them with specific sounds (phonics)
• limited sight word vocabulary

Causes and symptoms

Causes

Reading disorder was first recognized in the late nineteenth century, when it was called pure word blindness, then developmental alexia. Starting in the 1960s, educators commonly referred to reading disorder as dyslexia, from the Greek word dys, meaning poor or inadequate, and the word lexismeaning words or language. Despite the long history of reading disorder, its cause is not known.

Learning to read is a complex task. It requires coordination of the eye muscles to follow a line of print, spatial orientation to interpret letters and words, visual memory to retain the meaning of letters and sight words, sequencing ability, a grasp of sentence structure and grammar, and the ability to categorize and analyze. In addition, the brain must integrate visual cues with memory and associate them with specific sounds. The sounds must then be associated with specific meanings. For comprehension, the meanings must be retained while a sentence or passage is read. Reading disorder occurs when any of these processes are disrupted. For that reason, the roots of reading disorder have proved difficult to isolate, and may be different in different individuals.

Despite the complexity of reading disorder, researchers have found that the condition is at least partially inherited. In 1999, the Centre for Reading Research in Norway studied a large family with reading problems. By evaluating the reading and writing abilities of about 80 family members across four generations, the researchers were able to pinpoint mutations in specific genes that are associated with reading and writing deficits.

It appears that reading disorder may also have causes other than genetic inheritance, as about half the people with this learning disability do not come from families with a history of the problem. Many theories suggest that functional problems in specific areas of the brain underlie reading disorder. Given the complicated demands on the human nervous system involved in reading, it is entirely possible that there are several different problems in brain function related to difficulty in learning to read. What is known is that 90% of children diagnosed with reading disorder have other language deficits. Still other research suggests a possible link with a subtle visual problem that affects the speed with which affected people can read.

• difficulty identifying single words
• problems understanding the sounds in words, sound order, or rhymes
• problems with spelling
• transposing letters in words
• omitting or substituting words
• poor reading comprehension
• slow reading speed (oral or silent)

Diagnosis

Evaluation of children’s reading ability must be done on an individual basis in order to make a diagnosis of reading disorder and distinguish it from slow learning or low intelligence. The examiner must take into account the child’s age, intelligence, educational opportunities, and such cultural factors as whether the language spoken at home is different from the language taught and used at school. Reading disorder is diagnosed when a child’s reading achievement is substantially below what would be expected after taking these factors into account.

In addition, the reading problems must interfere in significant ways with the person’s schoolwork or daily life. If a physical condition is present (for example, mental retardation, poor eyesight, or hearing loss), the reading deficit must be in excess of what one would normally associate with the physical handicap.

Diagnosis is complicated by the fact that 20%–55% of children with reading disorder have attention-deficit/hyperactivity disorder(ADHD), a behavioral disorder that aggravates learning difficulties. In addition, about one-quarter of children with reading disorder have conduct disorder. Oppositional defiant disorder and depression also occur in higher-than-average rates in children with reading disorder. Almost all people with reading disorder have difficulties spelling, and about 80% of them have other language problems.

Anyone who is suspected of having reading disorder or any other learning disability should have a comprehensive evaluation, including hearing, vision, and intelligence testing. The test should include all areas of learning and learning processes, not just reading. In school-age children, this evaluation often involves a team of educators, educational psychologists, and child psychiatrists.

Demographics

Estimates by the National Institutes of Health of the number of people with learning disorders range from 5%–15% of the general population. About 80% of people with a learning disorder have reading disorder. Other studies suggest that about 4% of school-age children have reading disorder. People with reading disorder are more likely to have a parent or sibling with the disorder.

Between 60% and 80% of children diagnosed with reading disorder are boys. For various reasons often related to behavior, boys tend to be referred more frequently to special education classes, which suggests that girls with reading disorder may be underdiagnosed. Some experts think that this disparity comes about because boys are more often disruptive in class.

Treatments

Reading disorder, like other learning disorders, falls under the federal Individuals with Disabilities Education Act (IDEA). Definitions of learning disabilities vary among the states, and some school districts are more willing than others to recognize specific learning disabilities. Any child, however, who has a diagnosed learning disability, including reading disorder or dyslexia, should be eligible for an Individual Education Program (IEP) that provides customized instruction at school designed to address the disability.

Treatment approaches vary from visual stimulation to special diets to enhanced reading instruction. However, it is generally agreed that customized education is the only successful remedy. The American Academy of Ophthalmology, the American Academy of Pediatrics, and the American Association for Pediatric Ophthalmology and Strabismus have issued a policy statement warning against visual treatments and recommending a cross-disciplinary educational approach.

The first researcher to identify and study dyslexia, Samuel Torrey Orton, developed the core principles of such an approach in the 1920s. The work of three of his followers—teachers Bessie Stillman, Anna Gillingham, and Beth Slingerland—underlies many of the programs in use today, including Project READ, the Wilson Reading System, and programs based on the Herman method. There are many successful programs to address individual reading needs. In general, all good programs are:

• Sound/symbol (phonics)-based. They break words down into their smallest visual components: letters and the sounds associated with them.
• Multisensory. Good programs attempt to form and strengthen mental associations among visual, auditory, and kinesthetic channels of stimulation. The student simultaneously sees, feels, and says the sound-symbol association. For example, a student may trace the letter or letter combination with his or her finger while pronouncing a word out loud.
• Highly structured. Remediation begins at the level of the single letter-sound; works up to digraphs (a pair of letters representing a single speech sound); then syllables; then into words and sentences in a systematic fashion. Repetitive drill and practice serve to form necessary associations between sounds and written symbols.

Prognosis

Many famous and successful people have suffered from reading disorders, including at least two Presidents of the United States. How well a person compensates for this disorder depends on the severity of the impairment and the type of educational remediation that he or she receives. Generally, people who are identified as having a reading disorder before grade three and who receive intensive reading education can do well. There is, however, a great deal of variation among people in intelligence, educational opportunities, and the will to overcome a reading disorder, as well as in the type and severity of the problem. All these factors combine to determine the ultimate outcome of this disorder. The prognosis is usually good if the condition is diagnosed early and the person is enrolled in a good remedial program. Strong self-esteem, together with supportive family, friends, and teachers also improve a person’s chances of overcoming this disorder.

Prevention

There is no known way to prevent reading disorder. Early intervention is the key to preventing the associated symptoms of low self-esteem, lack of interest in school, and poor behavior that often accompany low academic achievement.

Definition

Rett’s disorder, which is also known as Rett’s syndrome or RS, belongs to a group of childhood disorders known as pervasive developmental disorders(PDDs) or autistic spectrum disorders. It is classified by the mental health professional’s handbook (the Diagnostic and Statistical Manual of Mental Disordersor the DSM-IV-TR) as a developmental disorder of childhood. Rett’s disorder is characterized by an early-onset slowing of the infant’s head growth and a reduction in brain size, as much as 30%.

Description

RS was first described by an Austrian physician, Andreas Rett, in 1966; prior to 1983, however, little was known about the syndrome because its occurrence is quite rare. Although RS was thought at first to result from the destruction or degeneration of brain tissue, genetic research has indicated that it is caused by the failure of the infant’s brain to develop normally. This developmental failure is in turn caused by a genetic mutation affecting production of a key protein that regulates brain development.

Rett’s disorder has a distinctive onset and course. The child— almost always a girl— develops normally during the first five months of life. After the fifth month, head growth slows down and the child loses whatever purposeful hand movements she had developed during her first five months. After 30 months, the child frequently develops repetitive hand-washing or hand-wringing gestures; 50%–80% of children with the disorder will eventually develop epilepsy. Rett’s disorder is also associated with severe or profound mental retardation.

Causes and symptoms

Causes

The cause of Rett’s disorder is a genetic mutation on the long arm of the X chromosome (Xq28) at a locus known as MECP2. The gene was discovered in 1999, and it produces a protein known as MeCP2, which is essential to life and crucial to the normal development of the human brain. The mutation that causes Rett’s disorder allows other genes to become or remain active at inappropriate points in the brain’s development. These activated genes interfere with the normal pattern of development and maturation of the brain’s functions. Although Rett’s disorder was previously thought to result from degeneration or deterioration of brain tissue, the discovery of the Rett’s gene provides evidence that the disorder may be due to a failure of normal brain development. The sensory, motor, and emotional functions of the brain are not integrated in Rett’s patients as they are in persons without the mutation. Certain regions of the brain in Rett’s patients essentially remain at an infantile stage of development.

RS is classified by geneticists as an X-linked dominant disorder with a high rate of new mutations. Most of these mutations (99.5%) occur while the fetus is developing in the mother’s womb; only 0.5% of cases of Rett’s disorder are recurrences within families. One of the most important aspects of the discovery of the Rett gene is that RS is the first disorder in humans to be traced to defects in a protein (MeCP2) that controls the expression of other genes through its interaction with methylated DNA. The discovery uncovered a new class of genetic disease that might extend far beyond RS in its applications to other disorders related to developmental failures of the nervous system.

Symptoms

The symptoms of Rett’s disorder have been described in terms of four stages in the child’s development.

STAGE ONE, EARLY-ONSET (SIX–18 MONTHS OF AGE). The early symptoms of RS are not always noticeable in Stage 1. The infant may not make eye contact with family members and may not show much interest in toys. She may be considered a “good baby” because she is so calm and quiet. On the other hand, there may be noticeable hand-wringing and slowing of head growth.

STAGE TWO, RAPID DETERIORATION (ONE–FOUR YEARS). This stage may be either rapid or gradual in onset. The child loses her ability to speak and to make purposeful hand movements. Hand-to-mouth movements may appear, as well as hand-wringing or hand-clapping gestures. These movements may be nearly constant while the child is awake but disappear during sleep. There may be noticeable episodes of breath holding and hyperventilating (rapid shallow breathing). The child may have trouble sleeping, and may become irritable. If she is able to walk, she will start to look unsteady on her feet and may have periods of trembling or shaking. Slowed growth of the head is usually most noticeable during this stage.

STAGE THREE, PLATEAU (TWO–10 YEARS). Motor problems and seizures often appear during this stage. The child’s behavior, however, often shows some improvement, with less irritability and crying. She may show greater interest in her surroundings, and her attention span and communication skills often improve. Many patients with RS remain in stage 3 for most of their lives.

STAGE FOUR, LATE DETERIORATION OF MOTOR SKILLS (USUALLY AFTER 10 YEARS OF AGE). In stage 4, patients with RS gradually lose their mobility; some stop walking while others have never learned to walk. There is, however, no loss of cognitive or communication skills, and the repetitive hand movements may decrease. The spine begins to develop an abnormal sideways curvature (scoliosis), and the patient may develop muscle rigidity. Puberty begins at the same age as in most girls.

Demographics

RS is less common than the other PDDs. Recent estimates of its prevalence range between 1:10,000 births and 1:15,000 births. As of 2002, little is known about its prevalence across different racial and ethnic groups.

Until 2000, Rett’s disorder was thought to occur only in girls, but at least two cases have been reported in boys as well. Since RS is caused by a mutation on the X chromosome that affects the production of a protein essential to life, and the Y chromosome that determines male sex cannot compensate for a damaged X chromosome, a male fetus with a defective X chromosome does not usually survive. The two known cases of RS in boys involve one child who has two X chromosomes as well as a Y, and a child whose X chromosome is faulty in some of the cells in his body but not all. This condition is known as mosaicism.

Diagnosis

The diagnosis of Rett’s disorder is made on the basis of observation of the child—usually over a period of several hours or days—and interviews with the parents. There are no laboratory or diagnostic imaging tests for RS. The diagnosis can be made by a pediatrician or primary care physician, but should be confirmed by a pediatric neurologist (specialist in disorders of the nervous system in children) or developmental pediatrician. After the examiner has excluded the possibility of other developmental disorders, there are six criteria that must be met for a diagnosis of Rett’s disorder, and a secondary group of supportive criteria that are frequently observed in RS patients but are not necessary to make the diagnosis.

Diagnostic criteria

The diagnostic criteria for RS include the following:

• a period of apparently normal development before six–18 months of age
• a normal-sized head at birth followed by slowing of head growth between five months and four years
• severe impairment in the use of language and loss of purposeful hand motion
• repetitive hand movements that include one or more of the following: hand washing, hand wringing, or hand clapping
• shaking of the chest or torso, particularly when the child is agitated or upset
• in children able to walk, an unsteady, stiff-legged, wide-based gait

Supportive criteria

Supportive criteria are criteria that are not essential to the diagnosis of a particular disorder (because some people with the disorder do not have them). Supportive criteria are nonetheless strong evidence that a person who exhibits these criteria does in fact have the disorder. Supportive criteria for Rett’s disorder include:

• dysfunctional breathing, which may include hyperventilation, breath holding, and air swallowing
• abnormal electroencephalogram (EEG) patterns
• seizures
• difficulties in chewing and swallowing
• constipation
• muscle rigidity and contracting of the joints that increase with age
• scoliosis (curvature of the spine from side to side)
• teeth grinding
• small feet in relation to overall height
• slow overall growth
• loss of body fat and muscle mass
• abnormal sleeping patterns combined with irritability or agitation
• poor circulation in the feet and legs

These supportive criteria do not always appear in young children with RS but are often observed as the child grows older.

Treatments

There is no single treatment regimen that is applicable to all patients with Rett’s disorder. Some patients benefit from medications for muscular rigidity or for specific mood or behavioral problems, such as anxiety or irritability. A child psychiatrist should be consulted in regard to medications.

The degree of mental retardation associated with RS means that patients with this disorder will not benefit from psychotherapy. Parents of children with RS, however, are often helped by supportive therapy groups for parents of children with PDDs. Another type of program that is helpful for parents is learning skills for coping with the behaviors of RS children. These programs are usually led by a behavioral psychologist.

The U. S. National Institute of Mental Health (NIMH) is presently conducting research studies of psychosocial approaches to treatment of Rett’s and other PDDs as well as studies of medications given for these disorders. Readers who would like more information about this research may contact NIMH Public Inquiries at 6001 Executive Boulevard, Rm. 8184, MSC 9663, Bethesda, MD 20892-9663. (301) 443-4513; Fax (301) 443-4279; TTY (301) 443-8431.

Prognosis

It is important to note that current information about the prognoses of children with Rett’s syndrome is derived from treatments given to patients in the 1970s or 1980s. As knowledge of effective treatments continues to accumulate, children with RS are receiving treatment earlier than they did two decades ago. It is likely that future prognoses for the disorder will reflect these improvements.

As of 2002, the prognosis for RS patients is poor. In most cases, there is a steady loss of cognition, movement-related, social, and behavioral skills throughout the patient’s lifetime. Some patients, however, make modest developmental gains in adolescence. The average life expectancy of patients with RS has not yet been determined, although some are presently middle-aged.

Prevention

As of 2002, there are no effective strategies for preventing Rett’s disorder, since most cases result from new mutations of the MECP2 gene rather than transmission of a defective gene from the parents.

Definition

In reactive attachment disorder, the normal bond between infant and parent is not established or is broken. Infants normally “bond” or form an emotional attachment, to a parent or other caregiver by the eighth month of life. From about the second through the eighth month, most infants will respond to attention from a variety of caregivers, if the caregivers are familiar. By the eighth month, however, normal infants have established a strong emotional preference for one or two primary caregivers. They are distressed if separated from these caregivers for even a few hours, even if another familiar person is present. If this bonding process is interfered with, it can have severe emotional and physical consequences for the child.

Reactive attachment disorder is sometimes called a post-traumatic disorder.

Description

In reactive attachment disorder, an infant or young child has not formed an emotional bond with a parent or other caregiver. This affects the child’s ability to interact normally with others. The child may have severe emotional and social problems that extend into adulthood. There may be learning problems and physical problems such as slow growth and failure to develop as expected.

Causes and symptoms

Causes

An infant does not know how to form an emotional attachment to another person, any more than it knows how to feed or clean itself. Bonding is a necessary developmental step in a baby’s growth. It occurs as the infant is cared for, talked to, played with, and comforted consistently. This helps the infant feel like it knows what will happen every time it sees a certain person. When this process is interfered with, the infant may never learn how to trust or love.

Many things can interfere with the bonding process:

• Loss of parents. The most common cause of reactive attachment disorder is being orphaned or put in foster care at a very early age. The infant may receive care from many people or be moved from place to place often. A bond to a single consistent caregiver cannot be formed.
• Neglect or impaired caregiving. If the infant is not cared for consistently, it will not learn to trust. This includes emotional neglect, where the caregivers may keep the baby clean and fed, but do not allow time for play and bonding. Very often this occurs when the parent or caregiver has a problem that prevents him or her from giving adequate, consistent attention to the infant. Such problems include major depression, psychosis, drug or alcohol abuse, mental retardation, physical illness, and poverty. The parent may also have been a neglected child or may be very young themselves and simply not know how to parent adequately.
• Abuse or pain. Even if an infant is getting love and attention some of the time, it may not learn to attach if it comes to expect pain on occasion from the caregiver. Illness or pain that the caregiver cannot ease can have the same effect.

In disrupted families with more than one child, one child may have reactive attachment disorder while others do not. It is not clear what role personality plays in this problem.

Symptoms

Infants with this problem often resist being held or touched. They may seem sleepy or “slow.” They may not seem aware of what’s going on around them. They may be slow to gain weight. On the other hand, some appear to be overly aware and nervous.

Young children may seem withdrawn and passive. They may ignore others or respond to others in odd ways. Some may seem overly familiar with strangers and touch or cling to people they’ve just met. However, they lack empathy for others. Their behavior comes across to others as needy and strange, unlike the normal friendliness of children.

Other symptoms of reactive attachment disorder in children can include the following:

• inability to learn from mistakes (poor cause-and-effect thinking)
• learning problems or delays in learning
• impulsive behavior
• abnormal speech patterns
• destructive or cruel behavior

Demographics

The prevalence of reactive attachment disorder has been estimated at 1% of all children under the age of five. Children orphaned at a young age have a much higher likelihood of this problem.

Diagnosis

The standard manual for mental health professionals in the United States is the Diagnostic and Statistical Manual of Mental Disorders.This manual lists criteria for diagnosing various mental disorders. The most recent edition, the fourth edition text revised, is also known as the DSM-IV-TR.According to the DSM-IV-TR,reactive attachment disorder is diagnosed when the following criteria are met:

• Presence of strange and developmentally inappropriate social interactions, beginning before age five years. The child does not respond to or initiate social interactions in a way that would be developmentally appropriate; instead, the child is either inhibited or is disinhibited in his or her interactions. Inhibited reactions may be excessively vigilant, restrained or ambivalent. (The child may respond to caregivers with a mixtures of approach, avoidance, and resistance to comforting, as an example from the manual.) Disinhibited reactions occur in a variety of social interactions and the child does not discriminate among people he or she chooses as attachment figures. This child will treat near strangers with inappropriate familiarity.
• The child’s inappropriate social skills are not due exclusively to developmental delay (as in mental retardation) and the child’s symptoms do not meet criteria for a pervasive developmental disorder.
• The child has received care in which his or her basic needs—either emotional or physical— are often unmet, or in which stable attachments have not been able to form (such as when primary caregivers change often).

An infant is diagnosed as having reactive attachment disorder when he or she fails to show signs of bonding to a parent or caregiver by the age of eight months. Infants normally start to follow the parent or caregiver with their eyes and smile in response to attention by about two months. By about five months, the child should reach out to be picked up and obviously enjoy simple interactive games like “peekaboo.”

Treatments

First, the child’s safety and physical health must be attended to. A child that is being abused or has been physically neglected may need to be hospitalized. This is done to separate the child from the harmful situation and take care of any medical problems resulting from neglect or abuse.

The next step is to either make the child’s home environment stable, or place the child in a more stable home. Child protective services may be brought in at this point. The home situation must be evaluated, and the parents or caregivers assessed for emotional fitness to care for the child. The parents or caregivers may be given training in proper childcare and emotional nurturing. Family therapy may be needed in some cases to help the parents or caregivers and other children in the family.

With a young infant, the parents or caregivers will be encouraged to have a regular schedule for the infant and to spend time each day simply holding and playing with the infant.

Treatment of children who are past infancy is difficult. It is important to find a therapist experienced in the treatment of children with reactive attachment disorder. Most therapists use a mix of techniques. The therapist may seek to help the child relive and work through grief and anger from a prior trauma or loss. Cognitive therapy may be used to help an older child understand and reframe negative thoughts about himself or herself, or about parents or caregivers. If the child is too young to verbalize or think rationally, techniques such as play therapy or art therapy may be used to help bring out and work through feelings. Behavioral therapy may be used to help guide development of wanted behaviors.

Prognosis

There has not been much research to date on the course of this problem. It appears that children who are identified and treated early have a better chance of learning how to form appropriate bonds with other people.

Children who are not treated or who are treated later in life have a greater chance of having permanent problems relating to other people.

Prevention

Prevention of reactive attachment disorder begins with good parenting. As far as possible, health care providers and families should be on the lookout for any problem that may prevent parents from giving children the structure and attention they need. If a child loses its primary caregivers, a stable environment with consistent attention from one or two caregivers should be provided as soon as possible.

Early identification of reactive attachment disorder is necessary to get help to the child and family as soon as possible. The earlier this problem is identified and treated, the more likely it is that the child will be able to develop healthy patterns of relating to others.

Definition

Rational emotive therapy (RET) is a psychotherapeutic approach which proposes that unrealistic and irrational beliefs cause many emotional problems.

Purpose

RET is a form of cognitive-behavioral therapy (CBT). The primary focus of this treatment approach is to suggest changes in thinking that will lead to changes in behavior, thereby alleviating or improving symptoms. The therapy emphasizes changing irrational thinking patterns that cause emotional distress into thoughts that are more reasonable and rational. RET can be used to treat people affected from disorders such as anxiety, depression and stess.

Precautions

There are no major precautions, except that persons entering treatment must be willing to change behaviors that promote symptoms.

Description

Rational emotive therapy was developed by Albert Ellis in the mid-1950s. Ellis proposed that people become unhappy and develop self-defeating habits because of unrealistic or faulty beliefs. In research reports from Ellis in 1979 and 1987 he introduced the model that most irrational beliefs originate from three core ideas, each one of which is unrealistic. These three core and unrealistic views include: 1) I must perform well to be approved of by others who are perceived significant; 2) you must treat me fairly—if not, then it is horrible and I cannot bear it; 3) conditions must be my way and if not I cannot stand to live in such a terrible and awful world. These irrational thoughts can lead to grief and needless suffering.

As a therapy, RET is active. The RET therapist strives to change irrational beliefs, challenge thinking, and promote rational self-talk, and various strategies are used to achieve these goals. These strategies may include: disputing irrational beliefs (the therapist points out how irrational it would be for a client to believe he or she had to be good at everything to be considered a worthwhile person), reframing (situations are viewed from a more positive angle), problem solving, role-playing, modeling, and the use of humor. The client may also be requested to complete certain exercises at home, and bibliotherapy (reading about the disorder) may also be used as components of RET.

Preparation

Before a client begins RET, he or she may undergo an assessment with the therapist. This assessment is called a biopsychosocial assessment, consisting of a structured interview. The questions and information-gathering during this assessment typically cover areas such as past medical and psychological history, family and social history, sex and drug history, employment and education history and criminal history. The interview provides information for a diagnosis or a tentative diagnosis that requires further testing or consultation.

Aftercare

Aftercare may or may not be indicated. This is usually decided on between the patient and mental health practitioner. Aftercare follow-up may be recommended if the affected person is at risk of relapse behaviors (returning to old behaviors that the client had sought to change).

Risks

There are no real risks associated with RET. There is a possibility that treatment may not benefit the affected person. This possibility becomes more likely for patients who have multiple psychological disorders.

Normal results

The person undergoing RET will begin to understand the repetitive patterns of irrational thoughts and disruption caused by symptoms. The individual in therapy will develop skills to improve his or her specific problems, and usual results include improved self-esteem and the development of a sense that life events change and that outcomes may not always be favorable.

Abnormal results

There are no abnormal results per se, but persons who are unwilling to change and adhere to treatment recommendations may not gain any new beneficial behaviors.

Definition

Quetiapine is an atypical antipsychotic drug used to treat symptoms of schizophrenia. It is available with a prescription under the trade name Seroquel.

Purpose

Quetiapine is classified as an atypical antipsychotic. It is used to treat psychotic disorders such as schizophrenia.

Description

Quetiapine is thought to modify the actions of several chemicals in the brain. It is chemically related to another atypical antipsychotic agent, clozapine, but differs both chemically and pharmacologically from the earlier phenothiazine antipsychotics.

It is available 25-mg, 100-mg, and 200-mg tablets.

Recommended dosage

Initially, a dosage of 25 mg should be taken twice a day. Each dose should be increased by 25-50 mg increments every three to four days until a target dose of 300-400 mg per day, administered in two or three divided doses, is achieved. It is not known whether doses higher than 800 mg per day are safe.

Precautions

Caution should be used in patients with heart disease because the drug may cause blood pressure to fall too low resulting in dizziness, rapid heartbeat, or fainting.

Quetiapine may cause liver damage. As a result, patients should notify their health care provider if they experience flu-like symptoms, notice yellowing of their skin or eyes, or experience abdominal pain. Liver function should be assessed periodically. The drug should be used cautiously in people with a history of liver disease or alcoholic cirrhosis.

Quetiapine may alter the function of the thyroid gland. Those taking supplements for low thyroid function may require dosage adjustments in their thyroid medication.

Quetiapine may increase cholesterol levels and contribute to the formation of cataracts. Because of this possibility, cholesterol levels should be checked periodically and yearly eye exams should be performed.

Quetiapine should be used carefully in those with a history of seizure disorders because it may increase the tendency to have seizures.

Quetiapine may cause extreme drowsiness and should be used carefully by people who need to be mentally alert.

Quetiapine should not be taken while pregnant or breast-feeding.

Side effects

Relatively common side effects that accompany quetiapine include drowsiness, dizziness, rash, dry mouth, insomnia, fatigue, muscular weakness, anorexia, blurred vision, some loss of muscular control, and amenorrhea (lack of menstruation) in women.

Dystonia (difficulty walking or moving) may occur with quetiapine use. This condition may subside in 24 to 48 hours even when the person continues taking the drug and usually disappears when quetiapine is discontinued.

Quetiapine use may lead to the development of symptoms that resemble Parkinson’s disease. These symptoms may include a tight or mask-like expression on the face, drooling, tremors, pill-rolling motions in the hands, cogwheel rigidity (abnormal rigidity in muscles characterized by jerky movements when the muscle is passively stretched), and a shuffling gait. Taking anti-Parkinson drugs benztropine mesylate or trihexyphenidyl hydrochloride along with the quetiapine usually controls these symptoms.

Quetiapine has the potential to produce a serious side effect called tardive dyskinesia. This syndrome consists of involuntary, uncoordinated movements that may appear late in therapy and may not disappear even after the drug is stopped. Tardive dyskinesia involves involuntary movements of the tongue, jaw, mouth or face or other groups of skeletal muscles. The incidence of tardive dyskinesia increases with increasing age and with increasing dosage of quetiapine. Women are at greater risk than men for developing tardive dyskinesia. There is no known effective treatment for tardive dyskinesia, although gradual (but rarely complete) improvement may occur over a long period.

An occasionally reported side effect of quetiapine is neuroleptic malignant syndrome. This is a complicated and potentially fatal condition characterized by muscle rigidity, high fever, alterations in mental status, and cardiac symptoms such as irregular pulse or blood pressure, sweating, tachycardia (fast heartbeat), and arrhythmias (irregular heartbeat). People who think they may be experiencing any side effects from this or any other medication should talk to their physician promptly.

Interactions

Quetiapine may be less effective when it is taken with drugs like carbamazepine (Tegretol), phenytoin (Dilantin), rifampin (Rifadin), barbiturates, thioridazine (Mellaril), or corticosteroids such as prednisolone, methlylprednisolone, prednisone, and dexamethasone because these drugs increase the breakdown of quetiapine in the liver causing lower-than-normal levels of the drug.

Antifungal drugs such as fluconazole (Diflucan) or ketoconazole (Nizerol), antibiotics such as erythromycin or clarithromycin (Biaxin), and cimetidine (Tagamet), because these drugs may decrease the breakdown of quetiapine in the liver causing higher-than-normal levels of the drug.

Any drug that causes drowsiness may lead to decreased mental alertness and impaired motor skills when taken with Quetiapine. Some examples include alcohol, antidepressants such as imipramine (Tofranil) or paroxetine (Paxil), antipsychotics such as thioridazine (Mellaril), and some antihistamines.

Definition

Quazepam belongs to a class of drugs called benzodiazepines. These drugs ease anxiety and slow the central nervous system. In the United States quazepam is sold under brand name Doral.

Purpose

Quazepam is approved by the United States Food and Drug Administration for the treatment of insomnia.

Description

Quazepam is unique in its drug properties in two ways. Several medications from the same class of drugs have an effect called rebound insomnia. This means that the insomnia becomes worse than the original insomnia when the drug is used for extended periods. Quazepam has a minimal tendency to cause rebound insomnia. Secondly, quazepam is eliminated from the body slowly. This gives quazepam advantage over certain other medications in the benzodiazepine class, such as alprazolam or halazepam, in that patients do not experience earlymorning insomnia, since there is still enough medication to induce sleep in the very early morning hours.

Quazepam’s sedating effect that reduces insomnia lasts only for about four weeks of continuous use. The medication is most effective for an intermediate-term treatment of insomnia (two weeks), rather than a long duration of treatment of over four weeks. Hence, long-term treatment for insomnia with quazepam should be avoided.

Quazepam comes in 7.5-mg and 15-mg tablets.

Recommended dosage

Effective doses of quazepam for the treatment of insomnia range from 7.5 mg to 30 mg at bedtime. Most patients start by taking 15 mg at bedtime. Adjustments from this dosage can be made as determined by individual. In some patients, a dosage as low as 7.5 mg is sufficient to reduce insomnia.

Elderly patients (over age 65) should receive a reduced dosage of 7.5 mg, because it takes a longer time to eliminate the drug from their bodies. Because quazepam is eliminated by the liver, dosage reduction may be necessary in patients with liver problems.

Precautions

Patients who have a condition known as sleep apnea should not use quazepam. This condition involves episodes of breathing difficulty and oxygen deficiency that occur throughout the night. Patients who are pregnant or who had an allergic reaction to quazepam should not take quazepam

People who need to remain mentally alert such as those who are driving or operating dangerous machinery, need to take quazepam with caution as it may cause drowsiness. This effect is intensified when quazepam is taken with alcohol. It is best not to drink alcoholic beverages while taking quazepam. Patients with compromised respiratory function (breathing problems), as well as patients with a history of drug or alcohol abuse, should closely be monitored during the short-term treatment with quazepam.

Side effects

The effects of quazepam taken at bedtime may last, or hang over, into the next day. This is the most common side effect of quazepam. The symptoms of this condition include drowsiness, daytime sleepiness, slurred speech, and mental sluggishness. This effect is dose related, and seems to occur most frequently in patients taking 30-mg doses. These effects are experienced less commonly with the 15-mg dose, but this dose may not be effective in eliminating insomnia some patients. Some people experience headache and dizziness when taking quazepam.

A small number of patients experience dry mouth, weight loss, abnormal taste perception, abdominal pain, nausea, vomiting, and either diarrhea or constipation due to quazepam. These effects occur in about 1% to 10% of people taking the drug.

Side effects that occur in less than 1% of patients include skin problems, such as rash or skin inflammation, muscle cramps, rigidity, and blurred vision.

Interactions

Cimetidine (Tagamet) and ketoconazole increase the levels of quazepam in the body, potentially causing toxicity or increased side effects.

Theophylline decreases the effectiveness of quazepam. Valerian, kava kava, and alcohol cause increased central nervous depression, which may increase sedation, drowsiness, and slowed reflexes if used while taking quazepam.