Definition

Encopresis is an elimination disorder that involves repeatedly having bowel movements in inappropriate places after the age when bowel control is normally expected. Encopresis is also called “soiling” or “fecal incontinence.”

Description

By four years of age, most children are toilet trained for bowel movements. After that age, when inappropriate bowel movements occur regularly over a period of several months, a child may be diagnosed with encopresis. Encopresis can be intentional on unintentional. Intentional soiling is associated with several psychiatric disorders. Involuntary or unintentional soiling is often the result of constipation.

Causes and symptoms

The only symptom of encopresis is that a person has bowel movements in inappropriate places, such as in clothing or on the floor. This soiling is not caused by taking laxatives or other medications, and is not due to a disability or physical defect in the bowel. There are two main types of encopresis, and they have different causes.

Involuntary encopresis

With involuntary encopresis, a person has no control over elimination of feces from the bowel. The feces is semi-soft to almost liquid, and it leaks into clothing without the person making any effort to expel it. Leakage usually occurs during the day when the person is active, and ranges from infrequent or almost continuous.

Involuntary soiling usually results from constipation. A hard mass of feces develops in the large intestine and is not completely expelled during a regular bowel movement in the toilet. This mass then stretches the large intestine out of shape, allowing liquid feces behind it to leak out. Up to 95% of encopresis is involuntary.

Although involuntary encopresis, called by the American Psychiatric Association (APA) encopresis with constipation and overflow incontinence, is caused by constipation, the constipation may be the result of psychological factors. Experiencing a stressful life event, harsh toilet training, toilet fear, or emotionally disturbing events can cause a child to withhold bowel movements or become constipated. Historically, children separated from their parents during World War II are reported to have shown a high incidence of encopresis, indicating that psychological factors play a role in this disorder.

Voluntary encopresis

A person with voluntary encopresis has control over when and where bowel movements occur and chooses to have them in inappropriate places. Constipation is not a factor, and the feces is usually a normal consistency. Often feces is smeared in an obvious place, although sometimes it is hidden around the house. The APA classifies voluntary encopresis as encopresis without constipation and overflow incontinence.

In young children, voluntary encopresis may represent a power struggle between the child and the caregiver doing the toilet training. In older children, voluntary encopresis is often associated with oppositional defiant disorder(ODD), conduct disorder, sexual abuse, or high levels of psychological stressors.

Demographics

Encopresis occurs in 1–3% of children and is seen more often in boys than in girls. The frequency of encopresis appears to be independent of social class, and there is no evidence that it runs in families.

Diagnosis

To receive an APAdiagnosis of encopresis, a child must have a bowel movement, either intentional or accidental, in an inappropriate place at least once a month for a minimum of three months. In addition, the child must be chronologically or developmentally at least four years old, and the soiling cannot be caused by illness, medical conditions (such as chronic diarrhea, spina bifida, anal stenosis, etc.), medications, or disabilities. However, it may be caused by constipation.

Treatments

Involuntary encopresis is treated by addressing the cause of the constipation and establishing soft, pain-free stools. This can include:

• increasing the amount of liquids a child drinks
• adding high-fiber foods to the diet
• short-term use of laxatives or stool softeners
• emptying the large intestine by using an enema
• establishing regular bowel habits

Once the constipation is resolved, involuntary encopresis normally stops.

Treatment of voluntary encopresis depends on the cause. When voluntary encopresis results from a power struggle between child and adult, it is treated with behavior modification. In addition to taking the steps listed above to ensure a soft, pain-free stool, the adult should make toileting a pleasant, pressure-free activity. Some experts suggest transferring the initiative for toileting to the child instead of constantly asking him/her to use the toilet. Others recommend toileting at scheduled times, but without pressure to perform. In either case, success should be praised and failure treated in a matter-of-fact manner. If opposition to using the toilet continues, the family may be referred to a child psychiatrist or a pediatric psychologist.

With older children who smear or hide feces, voluntary encopresis is usually a symptom of another more serious disorder. When children are successfully treated for the underlying disorder with psychiatric interventions, behavior modification, and education, the encopresis is often resolved.

Prognosis

Since 80–95% of encopresis is related to constipation, the success rate in resolving involuntary encopresis is high, although it may take time to establish good bowel habits and eliminate a reoccurrence of constipation. The success rate is also good for younger children in a power struggle with adults over toileting, although the results may be slow. The prognosis for older children with associated behavioral disorders is less promising and depends more on the success of resolving those problems than on direct treatment of the symptoms of encopresis.

Prevention

Power struggles during toilet training that lead to encopresis can be reduced by waiting until the child is developmentally ready and interested in using the toilet. Toilet training undertaken kindly, calmly, and with realistic expectations is most likely to lead to success. Successes should be rewarded and failures accepted. Once toilet training has been established, encopresis can be reduced by developing regular bowel habits and encouraging a healthy, high-fiber diet.

Description

The American Psychiatric Association recognizes two elimination disorders, encopresis and enuresis. Encopresis is an elimination disorder that involves repeatedly having bowel movements in inappropriate places after the age when bowel control is normally expected. Encopresis is also called fecal incontinence. Enuresis, more commonly called bed-wetting, is an elimination disorder that involves release of urine into bedding, clothing, or other inappropriate places. Both of these disorders can occur during the day (diurnal) or at night (nocturnal). They may be voluntary or involuntary. Encopresis and enuresis may occur together, although most often they occur separately.

Elimination disorders may be caused by a physical condition, a side effect of a drug, or a psychiatric disorder. It is much more common for elimination disorders to be caused by medical conditions than psychiatric ones. In most cases in which the cause is medical, the soiling is unintentional. When the causes are psychiatric, the soiling may be intentional, but it is not always so.

Encopresis

Medical causes of encopresis are usually related to chronic constipation. As hard feces build up in the large intestine, the bowel is stretched out of shape. This allows liquid feces behind the hard stool to involuntarily leak out and stain clothing. Other medical causes of encopresis include malformations of the bowel and side effects of medication. Laxatives (medications that relieve constipation), drugs that kill some of the good bacteria in the intestines, and drugs that increase contractions in the intestines can all cause involuntary encopresis. Pediatricians or family physicians treat almost all cases of encopresis having medical causes. In cases of prolonged involuntary soiling, children may develop feelings of shame and embarrassment, leading to low self-esteem.

Psychiatric causes of encopresis are not as clear. A few children may experience encopresis because of fear of the toilet or because their toilet training was either overly pressured or irregular and incomplete. Older children may soil intentionally, sometimes smearing the feces on wall or clothing or hiding feces around the house. Children who show this pattern of soiling behavior often have clinical behavior problems such as conduct disorder or oppositional defiant disorder. About one-quarter of children who soil intentionally also have enuresis.

Enuresis

Enuresis also has both medical and psychiatric causes. Primary enuresis occurs when a child has never established bladder control. Medical causes of primary enuresis are often related to malformations of the urinary system, developmental delays, and hormonal imbalances that affect the ability to concentrate urine. There appears to be a genetic component to primary enuresis, since the condition tends to run in families. Primary enuresis may also be caused by psychological stressors such as family instability or erratic toilet training.

Secondary enuresis occurs when a child has established good bladder control for a substantial period, then begins wetting again. Involuntary secondary enuresis is thought to be brought on by life stresses. For example, it is common for young children to begin wetting the bed after moving to a new house or having a new sibling enter the family. Voluntary enuresis is not common. Like voluntary encopresis, it is associated with psychiatric conditions such as conduct disorder and oppositional defiant disorder.

Treatment and prognosis

Most children outgrow their elimination disorders successfully by the time they are teens, with the exception of those children whose elimination disorders are symptoms of other psychiatric disturbances.

Encopresis is treated with stool softeners or laxatives and by instituting regular bowel evacuation patterns. Enuresis is treated by behavior modification including changing nighttime toileting habits. The least expensive and most effective method is by having the child sleep on a special pad that sets off an alarm when the pad becomes wet. This wakes the child and allows him to finish relieving in the toilet. Eventually he awakes without assistance before wetting. Drugs can also help in the treatment of enuresis, although relapse is common after they are stopped. Secondary enuresis caused by stress is treated by resolving the stress. Psychotherapy is usually not needed, although it may be helpful to children who develop feelings of shame associated with their elimination disorders. Adults can help children avoid shame and embarrassment by treating elimination accidents mater-of-factly and kindly.

Children with voluntary elimination disorders are treated for the diagnosed psychiatric problem associated with the elimination disorder using behavior modification, drugs, and other psychiatric interventions.

Purpose

The EEG is an important aid in the diagnosis and management of epilepsy and other seizure disorders, as well as in the diagnosis of brain damage related to trauma and diseases such as strokes, tumors, encephalitis, and drug and alcohol intoxication. The EEG is also useful in monitoring brain wave activity and in the determination of brain death. Research is active in determining the role of EEG in the diagnosis and management of mental retardation, sleep disorders, degenerative diseases such as Alzheimer’s disease and Parkinson’s disease, and in certain mental disorders such as autism and schizophrenia.

Precautions

The EEG should be administered, monitored, and interpreted only by a specially trained health professional. It is important to recognize that diagnosis should not be based on the EEG alone—the EEG represents an adjunct to the neurological history, examination, and other specialized studies. The EEG is an extremely sensitive instrument, and tracings can be greatly influenced by the actions and the physiologic status of the patient. It is important that the patient be properly prepared physically and psychologically in order to obtain an accurate and reliable record. Medications such as anticonvulsants, tranquilizers, stimulants—including coffee, tea, cola drinks—and alcohol should be withheld for at least 24–48 hours prior to the test. Inasmuch as hypoglycemia affects brain wave patterns, the patient is told not to withhold any meals.

Description

Brain function is associated with electrical activity, which is always accompanied by an electrical field. This field consists of two parts, the electrical field and the magnetic field, and is called an electromagnetic field. The electrical field is measured by surface electrodes and is recorded by the electroencephalogram. Prior to the recording session, approximately 16–20 electrodes are attached to the patient’s scalp with a conductive washable paste, or collodion. Depending on the purpose of the EEG, implantable needle electrodes may be utilized, in which case the patient should be informed that there will be mild discomfort.

The patient lies on a bed, padded table, or comfortable reclining chair and is asked to remain quiet and relaxed during the approximately one hour that is usually required. A sleep recording up to three hours in duration is usually obtained if the diagnosis is a seizure disorder. Under certain conditions, various stimuli such as flashing lights or deep breathing may be utilized. In an ambulatory EEG recording, the patient is attached to a portable cassette recorder and goes about regular activities, usually for up to 24 hours.

Magnetoencephalography

Magnetoencephalography, a supplement to EEG, also uses an electroencephalogram to measure the patient’s electrical field. In addition, however, the patient’s magnetic field is also recorded to measure electrical activity. Every electrical current generates a magnetic field. The magnetic field is detected by an instrument called a biomagnetometer and recorded as a magnetoencephalograph (MEG). The information provided by the MEG is entirely different from that provided by computed tomography(CT), topographic encephalography, or magnetic resonance imaging(MRI)—imaging instruments that provide still, structural, and anatomical information. The information recorded by the MEG provides important supplemental information to that recorded by the encephalogram and, used together and conjointly, they both provide a much more complete and comprehensive idea of cerebral events. Using MEG, the brain can be observed “in action” rather than just being viewed as a still image.

Magnetoencephalography has been used to map the sensory and motor cortices of the brain, to determine the organization of the auditory center of the brain, and to study cognitive functions such as speech, memory, attention and consciousness. This information is critical for neurosurgical planning such as the removal of brain lesions. Thus, preoperative MEG is valuable in planning the surgical treatment of tumors and malformations. MEG can provide surgeons with real-time computer-generated images of deep-seated lesions that are essential before surgery. The quantitative EEG is also known by the acronym BEAM (brain electrical activity mapping).

Preparation

Prior to the EEG, the patient is given full instructions in the procedure, particularly about the avoidance of certain medications and food. In cases where a sleep EEG is anticipated, the patient may be requested to minimize sleep or stay awake the night before the procedure. Sedatives to induce sleep should be avoided, if possible.

Aftercare

No specific procedures or aftercare are required. Patients are advised to resume their usual activities, especially the resumption of medications that had been temporarily discontinued.

Risks

The primary risk of EEG is the production of a seizure in an epileptic patient. This may result from the temporary discontinuation of anticonvulsant medication or from the provocation of a seizure by an epileptogenic stimulus such as flashing lights or deep breathing. Although the provocation of a seizure may serve to substantiate the diagnosis, all potential seizure patients should be carefully monitored to avoid injury in case a seizure does result.

 

Purpose

Also known as electroconvulsive shock therapy or electroshock therapy, ECT is used together with anesthesia, muscle relaxants and oxygen to produce a mild generalized seizure or convulsion. With repeated administration, usually over a period of weeks, ECT is highly effective in relieving symptoms of several mental illnesses.

The American Psychiatric Association’s Practice Guidelines for the Treatment of Psychiatric Disordersdiscusses the use of ECT in the treatment of major depressive disorder, bipolar disorder and schizophrenia. Electroconvulsive therapy is administered to provide relief from the signs and symptoms of these and occasionally other mental illnesses. ECT is used routinely to treat patients with major depression, delusional depression, mania, and depression associated with bipolar disorder and schizophrenia. It is most closely associated with the treatment of severe depression, for which it provides the most rapid relief available as of 2002. In addition, patients suffering from catatonia, neuroleptic malignant syndrome, and parkinsonism may also benefit from the procedure.

ECT may become the treatment of first choice for depression if a patient with severe depression or psychotic symptoms is at increased risk of committing suicide and has not responded to other treatments. Although antidepressant medications are effective in many cases, they may take two to six weeks to begin to work. Some patients with mania and schizophrenia may not be able to tolerate the side effects of the antipsychotic medications used to treat these disorders. In addition, some patients may be unable to take their prescribed medications. For these individuals, ECT is an important option. ECT is also indicated when patients need a treatment that brings about rapid improvement because they are refusing to eat or drink, or presenting some other danger to themselves.

ECT is also recommended for certain subgroups of patients diagnosed with depression. Many elderly patients, for example, respond better to ECT than to antidepressant medications. Pregnant women are another subgroup that may benefit from ECT. Because ECT does not harm a fetus as some medications might, pregnant women suffering from severe depression can safely choose ECT for relief of their depressive symptoms.

Precautions

Candidates for ECT must be carefully screened. Prior to receiving this treatment, patients receive a thorough evaluation to identify any medical conditions they may have that might complicate their response to the procedure. This evaluation includes a complete medical history, a physical examination, and routine laboratory tests. In addition to standard blood tests, the patient should receive an electrocardiogram (EKG) to test for heart abnormalities. Evidence of a recent heart attack would disqualify a patient from receiving ECT. Spinal and chest x rays can identify other physical conditions that might complicate a patient’s response. Finally, a computed tomography(CT) scan should be performed to rule out any structural abnormalities in the brain that might be made worse by the electrical stimulation and resulting convulsions associated with ECT. Signs of a recent stroke or a tumor in the brain, for instance, would disqualify a patient as a candidate for ECT therapy.

The doctors who are administering the procedure must receive the informed consent of the patient a day before the first treatment is given. In addition, at least two psychiatrists should confirm that ECT is the proper treatment for a specific patient. One of these physicians should serve as the source of a “second opinion” and not be actively involved in treating the patient on a daily basis. This second, or outside, medical consultant should independently determine that ECT is appropriate for a particular patient after conducting a physical examination. The second physician should also confirm that the patient is mentally sound enough to give informed consent to the procedure.

Patients in any age group are eligible for treatment with ECT; however, informed consent for patients under 18 must be given by a parent or legal guardian.

Description

Early history of ECT

Ugo Cerletti and Lucio Bini, who were two Italian physicians working in the 1930s, were the first to use electroconvulsive therapy to treat patients with severe mental illnesses. Their first patient was a 39-year-old unidentifiable homeless man who had been found wandering through the railroad station in Rome, mumbling incoherently. The doctors were inspired to try the new method by a notion that intrigued psychiatrists in this period, who were desperate for useful therapies— namely, that epilepsy and schizophrenia never appeared in the same person at the same time. (It was later shown, however, that it is possible for the same individual to suffer from both disorders at the same time.) Since epilepsy causes seizures, psychiatrists in the 1930s reasoned that artificially induced seizures might cure schizophrenia. Some in the medical community were receptive to this approach because physicians were already using a variety of chemicals to produce seizures in patients. Unfortunately, many of their patients died or suffered severe injuries because the strength of the convulsions could not be well controlled.

As ECT became more widely used, many members of the general public and some in the psychiatric profession were opposed to its use. To them it seemed barbaric and crude. ECT joined psychosurgery as one of the most intensely distrusted psychiatric and neurological practices. Many people were frightened simply because ECT was called “shock treatment.” Many assumed the procedure would be painful; others thought it was a form of electrocution; and still others believed it would cause brain damage. Unfavorable publicity in newspapers, magazines and movies added to these fears. Indeed, from the 1930s up through the 1960s, doctors and nurses did not explain either ECT or other forms of psychiatric treatment to patients and their families very often. Moreover, many critics had good reasons for opposing the procedure before it was refined. Neither anesthesia nor muscle relaxants were used in the early days of ECT. As a result, patients had violent seizures, and even though they did not remember them, the thought of the procedure itself seemed frightening. Even more unfortunately, this crude, early version of ECT was applied sometimes to patients who could never have benefited from ECT under any conditions.

As the procedures used with ECT became more refined, psychiatrists found that ECT was an effective treatment for schizophrenia and soon after, depression and bipolar disorder. The use of ECT, however, was phased out when antipsychotic and antidepressant drugs were introduced during the 1950s and 1960s. The psychiatric community reintroduced ECT several years later when patients who didn’t respond to the new drugs stimulated a search by mental health professionals for effective, and if necessary, non-drug treatments. While the new psychotropic medications provided relief for untold thousands of patients who suffered greatly from their illnesses and would otherwise have been condemned to mental hospitals, the drugs unfortunately produced a number of side effects, some of which are irreversible. Another drawback is that some medications do not have a noticeable effect on the patient’s mood for two to six weeks. During this time, the patient may be at risk for suicide. In addition, there are patients who do not respond to any medications or who have severe allergic reactions to them. For these individuals, ECT may be the only treatment that will help.

ECT in contemporary practice

Today, with the introduction of improved safety procedures, ECT is a remarkably safe and highly effective procedure. It is performed in both inpatient and outpatient facilities in specially equipped rooms with oxygen, suction, and cardiopulmonary resuscitation equipment readily available to deal with the rare emergency. A team of health care professionals, including a psychiatrist, an anesthesiologist, a respiratory therapist, and other assistants, is present throughout the entire procedure.

As of 2000, the American Psychiatric Association has renewed its set of guidelines, first published in 1990, for determining the appropriate use of ECT in patients suffering from depression. They state that patients qualify for ECT if they:

• cannot tolerate, or receive no significant benefit from, antidepressant medications
• have responded well to ECT treatments during past depressive episodes
• face a greater risk from taking antidepressant drugs than from undergoing ECT
• need treatment without delay to avoid suicide or other self-destructive acts

Administration of ECT

ECT is performed while the patient is unconscious. Unconsciousness is induced by a short-acting barbiturate such as methohexital (Brevital sodium), or another appropriate anesthetic drug. The drug is given intravenously. To prevent the patient from harming themselves during the convulsions or seizures induced by ECT, he or she is given succinylcholine (Anectine) or a similar drug that temporarily paralyzes the muscles. Because the patient’s muscles are relaxed, the seizures will not produce any violent contractions of the limbs and torso. Instead, the patient lies quietly on the operating table. One of the patient’s hands or feet, however, is tied off with a tourniquet before the muscle relaxant is given. The tourniquet prevents the muscles in this limb from being paralyzed like the muscles in other parts of the patient’s body. The hand or foot is used to monitor muscle movement induced by the electrical current applied to the brain.

 

A breathing tube is then inserted into the unconscious patient’s airway and a rubber mouthpiece is inserted into the mouth to prevent him or her from biting down on teeth or tongue during the electrically induced convulsion. As the current is applied, brain activity is monitored using electroencephalography. These brain wave tracings tell the medical team exactly how long the seizure lasts. The contraction of muscles in the arm or leg not affected by the muscle relaxant also provides an indication of the seizure’s duration.

The electrodes for ECT may be placed on both sides of the head (bilateral) or one side (unilateral). Physicians often use bilateral electrode placement during the first week or so of treatments. An electric current is passed through the brain by means of a machine specifically designed for this purpose. The usual dose of electricity is 70–150 volts for 0.1–0.5 seconds. In the first stage of the seizure (tonic phase), the muscles in the body that have not been paralyzed by medication contract for a period of 5–15 seconds. This is followed by the second stage of the seizure (clonic phase) that is characterized by twitching movements, usually visible only in the toes or in a nonparalyzed arm or leg. These are caused by alternating contraction and relaxation of these same muscles. This stage lasts approximately 10–60 seconds. The physician in charge will try to induce a seizure that lasts between one-half and two minutes. If the first application of electricity fails to produce a seizure lasting at least 25 seconds, another attempt is made 60 seconds later. The session is stopped if the patient has no seizures after three attempts. The entire procedure, from beginning to end, lasts about 30 minutes.

The absence of seizures is most commonly caused either by the patient’s physical condition at the time of treatment or by the individual nature of human responses to drugs and other treatment procedures. Just as there are some patients who do not respond to one type of antidepressant medication but do respond to others, some patients do not respond to ECT.

The total number of ECT treatments that will be given depends on such factors as the patient’s age, diagnosis, the history of illness, family support and response to therapy. Treatments are normally given every other day with a total of two to three per week. The ECT treatments are stopped when the patient’s psychiatric symptoms show significant signs of improvement. Depending on the patient’s condition, this improvement may happen in a few weeks or, rarely, over a six-month period. In most cases, patients with depression require between six and twelve ECT sessions.

Only rarely is ECT treatment extended beyond six months. In such infrequent cases, treatments are decreased from two to four per week after the first month to one treatment every month or so.

No one knows for certain why ECT is effective. Because the treatment involves passing an electric current through the brain, which is electrically excitable tissue, it is not surprising that ECT has been shown to affect many neurotransmitter systems. Neurotransmitters are chemical messengers in the nervous system that carry signals from nerve cell to nerve cell. The neurotransmitters affected by ECT include dopamine, norepinephrine, serotonin and GABA (gamma-aminobutyric acid).

Description

Everyone experiences feelings of unhappiness and sadness occasionally. When these depressed feelings start to dominate everyday life and cause physical and mental deterioration, the feelings become known as depressive disorders. Depressive disorders can be categorized as major depressive disorder or dysthymic disorder. Individuals who suffer from dysthymic disorder have had their depressive symptoms for years— they often cannot pinpoint exactly when they started to feel depressed. People suffering from dysthymic disorder may describe to their doctor feelings of hopelessness, lowered self-esteem, poor concentration, indecisiveness, decreased motivation, sleeping too much or too little, or eating too much or too little. Symptoms are present often and for the whole day, and are typically present for at least two years.

Causes and symptoms

Causes

The causes of depression are complex and not yet completely understood. Sleep abnormalities, hormones, neurotransmitters(chemicals that communicate impulses from one nerve cell to another), upbringing, heredity, and stressors (significant life changes or events that cause stress) all have been implicated as causes of depression.

Dysthymic disorder occurs in approximately 25% to 50% of persons who have sleep abnormalities that include reduced rapid eye movement (REM) sleep and impaired sleep continuity. Rapid eye movement sleep is an essential component of the sleep cycle and quality of sleep.

There is some evidence that suggests a correlation with hormonal imbalances of cortisol or thyroid hormones. In many adults, levels of cortisol (a stress hormone) are elevated during acute depressive periods and return to normal when the person is no longer depressed. In children and adolescents, results have been quite inconsistent, although there is some evidence that hypersecretion of cortisol is associated with more severe depressive symptoms and with a higher likelihood of recurrence of depression. A lack of thyroid hormone mimics depression quite well and is routinely checked in patients with recent onset depression.

In depression, there appears to be abnormal excess or inhibition of signals that control mood, thoughts, pain, and other sensations. Some studies suggest an imbalance of the neurotransmitter called serotonin. It is assumed that the reason antidepressants are effective is that they correct these chemical imbalances. For example, the selective serotonin reuptake inhibitors (SSRIs), one class of antidepressant medications that includes fluoxetine(Prozac), appears to establish a normal level of serotonin. As the name implies, the drug inhibits the re-uptake of serotonin neurotransmitter from the gaps between the nerve cells, thus increasing neurotransmitter action, alleviating depressive symptoms.

A child’s upbringing may also be key in the development of dysthymic disorder. For example, it is speculated that if a person is abused and neglected throughout childhood and adolescence, a pattern of low self-esteem and negative thinking may emerge, and, from that, a lifelong pattern of depression may follow.

Heredity seems to play a role in the development of depressive disorders. People with major depression in their immediate family are up to three times more likely to have the disorder themselves. It would seem that biological and genetic factors may make certain individuals more prone to depressive disorders, but that environmental circumstances, or stressors, may then trigger the disorder.

Symptoms

The mental health professional’s handbook to aid patient diagnosis is the Diagnostic and Statistical Manual of Mental Disorders,also called the DSM.The 2000 edition of this manual is known as the DSM-IV-TR(fourth edition, text revised). The DSM-IV-TRhas established a list of criteria that can indicate a diagnosis. These criteria include:

• Depressed mood for most of the day, more days than not.
• When depressed, two (or more) of the following are also present: decreased appetite or overeating, too much or too little sleep, low energy level, low self-esteem, decreased ability to concentrate, difficulty making decisions, and/ or feelings of hopelessness.
• During the two years of the disorder, the patient has never been without symptoms listed for more than two months at a time.
• No major depressive episode (a more severe form of depression) has been present during the first two years of the disorder.
• There has never been a manic disorder, and criteria for a less severe depression called cyclothymic disorder has never been established.
• The disorder does not exclusively occur with psychosis, schizophrenia or delusional illnesses.
• The symptoms of depression cause clinically significant impairment and distress in occupational, social, and general functioning. Dysthymic disorder can be described as “early onset” (onset before age 21 years), “late onset” (onset is age 21 years or older), and “with atypical features” (features that are not commonly observed).

Demographics

The lifetime prevalence has been estimated to be 4.1% for women and 2.2% for men. In adults, dysthymic disorder is more common in women than in men and research suggests that the prevalence in the age group 25 to 64 years is 6% for women. In children, dysthymic disorder can occur equally among both genders.

Diagnosis

To diagnose a patient with this disorder, the DSM-IVTRcriteria must be established, and this is accomplished through an extensive psychological interview and evaluation. The affected person seeking the clinician’s help usually exhibits symptoms of irritability, feelings of worthlessness and hopelessness, crying spells, decreased sex drive, agitation, and thoughts of death. The clinician must rule out any possible medical conditions that can cause depressed affect. (Affect can be defined as the expression of emotion displayed to others through facial expressions, hand gestures, tone of voice, etc.) The diagnosis cannot be made if depression occurs during an active course of psychosis, delusions, schizophrenia, or schizoaffective disorder. If substance abuse is determined as the cause of depression, then a diagnosis of substance-induced mood disorder can be established.

Further psychological tests that can be administered to help in the diagnostic process include the Beck Depression Inventory and the Hamilton Depression Scale.

Treatments

The goals of treatment include remission of symptoms and psychological and social recovery.

Medications

Studies suggest some treatment success with medications such as tricyclic antidepressants (TCAs) or monoaminoxidase inhibitors (MAOIs). Medications can be effective in patients who have depression due to sleep abnormalities. Some tricyclic antidepressants include amitriptyline(Elavil), imipramine(Tofranil), and nortriptyline(Aventyl, Pamelor), and some MAOIs include tranylcypromine(Parnate) and phenelzine(Nardil). Selective serotonin reuptake inhibitors (SSRIs) are recommended during initial treatment planning after a definitive diagnosis is well established. The most commonly prescribed SSRIs are fluoxetine (Prozac), sertraline(Zoloft), paroxetine(Paxil), fluvoxamine(Luvox), and citalopram(Celexa).

Psychological therapies

Clinical reports suggest that cognitive-behavioral therapy, interpersonal psychotherapy, or family therapy can be effective with concurrent antidepressant medication to treat the symptoms of depression. In these therapies, the goal is to help the patient develop healthy problem-solving and coping skills.

Prognosis

Dysthymic disorder often begins in late childhood or adolescence. The disorder follows a chronic (long-term) course. The development of a more major form of clinical depression called major depressive disorder among children with dysthymic disorder is significant. In other words, childhood onset of dysthymic disorder is considered an early indicator for recurrent mood disorder that may even have more severe clinical symptoms in the patient’s future.

Patients with this disorder usually have impaired emotional, social, and physical functioning.

In general, the clinical course of dysthymic disorder is not promising. Causes of a poorer outcome include not completing treatment, noncompliance with medication intake, and lack of willingness to change behaviors that promote a depressed state. However, patients can do very well with a short course of medications if they have a desire to follow psychotherapy treatment recommendations.

If left untreated, dysthymic disorder can result in significant financial and occupational losses. People with this disorder tend to isolate themselves by restricting daily activities and spending days in bed. Patients often complain of poor health and incur more disability days when compared to the general population. Higher rates of successful outcome occur in people who undergo psychotherapy and treatment with appropriate medications.

Prevention

There is no known prevention for dysthymic disorder. Early intervention for children with depression may be effective in arresting the development of more severe problems.

Description

Dyspareunia is any pain experienced any time before, during, or following sexual intercourse. The pain may be located in the genitals or within the pelvis. It is not unusual for women occasionally to experience pain during intercourse. This is not true dyspareunia.

A woman who has dyspareunia often also has vaginismus. This is an involuntary tightening of the vaginal muscles in response to penetration. It can make intercourse painful, or impossible.

Causes and symptoms

Causes

Psychosocial causes of dyspareunia include:

• Prior sexual trauma. Many women who have been raped or sexually abused as children have dyspareunia. Even when a woman wishes to have sex with someone later, the act of intercourse may trigger memories of the trauma and interfere with her enjoyment of the act. Vaginismus also often occurs in such women.
• Guilt, anxiety, or tension about sex. Any of these can cause tense vaginal muscles and also prevent arousal from occurring. People who were raised with the idea that sex is bad may be more prone to have this problem. Fear of pregnancy may make arousal difficult.
• Prior physical trauma to the vaginal area. Women who have had an accidental injury or surgery in the vaginal area may become sensitive to penetration. Vaginismus is common in these cases, as well.
• Depression or anxiety in general. Either of these can lead to loss of interest in sex. This can be experienced by either sex.
• Problems in a relationship. Dyspareunia may occur when a woman feels her sexual partner is abusive or emotionally distant, she is no longer attracted to her partner, or she fears her partner is no longer attracted to her. Men, too, can lose interest in sex because of prior emotional trauma in a relationship; however, the result is usually impotence, rather than dyspareunia.
• Vasocongestion. Vasocongestion can occur when either partner frequently becomes aroused but does not reach orgasm. Vasocongestion is a pooling of blood in dilated blood vessels. Normally, the pelvic area becomes congested with blood when a person becomes sexually aroused. This congestion goes away quickly after orgasm. If there is no orgasm, the congestion takes much longer to resolve.

Any of these factors may cause painful sex. The affected person may then associate pain with sex and find it even harder to relax and become aroused in future.

Symptoms

The DSM-IV-TRdiagnostic criteria for dyspareunia are as follows:

• Recurrent or persistent genital pain related to sexual intercourse that may occur before, during, or after intercourse.
• The affected person is distressed by the pain, or experiences relationship problems as a result of the pain.
• The pain is not caused exclusively by vaginismus or lack of lubrication, is not better accounted for by another disorder, and is not due exclusively to the direct effects of a drug, medication, or a general medical condition. Dyspareunia can occur with other sexual dysfunctions.

The most common symptom of dyspareunia from psychosocial causes is pain at the vaginal opening as the penis enters the vagina. Entry may be difficult, and the pain may be burning, or sharp. The woman may have a sense of being “dry.” Pain may continue or ease as thrusting continues.

Vasocongestion can cause an aching pain in the pelvic area that persists for hours after intercourse. Pain with orgasm, or pain deep in the pelvis with thrusting, is more likely to be a sign of a medical problem, but can result from lack of arousal and tension.

A person who experiences pain during sex may feel embarrassed or ashamed. Dyspareunia can cause problems in relationships or lead to the affected person avoiding relationships altogether.

Demographics

About 15% of women may have pain with intercourse at some point in their lives. About 1–2% have true dyspareunia. The incidence is much higher in women who have been raped or otherwise sexually abused. As stated, dyspareunia in men is rare and is almost always caused by a medical problem.

Diagnosis

About 30% to 40% of all women who seek help from a sexual counselor for dyspareunia turn out to have a medical problem that is causing their pain. A full medical examination is necessary to rule out a possible medical cause. This includes a pelvic exam and may also include an ultrasound, as well as other diagnostic tests. Examples of possible physical causes are infections, sexually transmitted diseases (STDs), estrogen deficiencies, and vulvar vestibulitis.

Once a medical cause is ruled out, a full family and sexual history can help pinpoint possible psychosocial causes. A psychological evaluation can determine the cause of the problem. Women who have been raped or abused may also suffer from post-traumatic stress disorder (PTSD) or generalized anxiety disorder.

There are two types of dyspareunia. Lifelong or primary dyspareunia means that the condition has been present for the entire sexual life of the affected person. This type is usually associated with being raised to believe that sex is bad, sexual abuse, fear of sex, or a painful first sexual experience. Acquired or secondary dyspareunia begins after a period of normal sexual function. It often has a medical cause, but may be a result of some sort of trauma, such as rape.

Treatments

Counseling is often helpful to identify and reframe negative feelings about sex. Couples therapy can help improve communication between partners and resolve problems that may be a factor in the sexual relationship. Women who have been abused or raped may benefit from counseling techniques designed to help overcome fears and issues caused by traumatic experiences.

Sex therapy may be offered to provide information about the physical aspects of arousal and orgasm. A sex therapist will also offer suggestions for how to improve sexual technique. For example, increasing time for foreplay and allowing the woman to control when and how penetration occurs can help her to relax and become aroused more easily.

Women who also have vaginismus may be given a set of devices they can use at home to dilate the opening of the vagina. Affected women start with a very small device and gradually work up to a penis-sized device, proceeding to a larger size only when they can use the smaller one without pain or fear. This retrains the vaginal muscles and helps the involuntary muscle tightening of vaginismus.

Use of a vaginal lubricant, at least temporarily, may be helpful in some women to reduce anxiety about possible pain.

There are no specific medications that treat dyspareunia. Medications that increase blood flow or relax muscles may be helpful in some cases.

Prognosis

With treatment, the chance of overcoming dyspareunia and having an enjoyable sexual life is good. Treatment can take several months, particularly in the case of survivors of a violent trauma such as rape.

Description

The prevalence of people with dual diagnoses became fully apparent to clinicians in the early 1980s. Initially, dual diagnoses were thought to be most likely in young adults with schizophrenia or bipolar disorder who also had extensive histories of drug or alcohol abuse. There was a widespread belief, often shared by family members of affected patients, that a young person’s initiation into illegal drug use actually caused a subsequent mental illness. It is now more commonly thought that symptoms of the mental disorder generally appear first, and that the abuse of drugs or alcohol may represent the patient’s attempt to self-medicate and alleviate the troublesome symptoms that accompany mental health disorders.

Today it is clear that the co-occurrence of mental illness and substance abuse is common: about 50% of individuals with severe mental illnesses are affected by substance abuse. A dual diagnosis is also associated with a host of negative outcomes that may include higher rates of relapse, hospitalization, incarceration, violence, homelessness, and exposure to such serious infections as HIV and hepatitis.

Despite almost twenty years of evidence regarding the prevalence and serious illnesses of people with dual diagnoses, the United States mental health and substance abuse systems continue to operate on parallel tracks, causing additional confusion to those with concurrent disorders. Refusal to combine services to provide better coordinated treatment has meant unnecessary suffering and expense for thousands of patients and their families.

For many people with dual diagnoses, the criminal justice system—juvenile as well as adult— becomes their de facto treatment system. Nearly two-thirds of incarcerated youth with substance abuse disorders have at least one other mental health disorder. The common association between conduct disorder or attention-deficit/hyperactivity disorder and substance abuse are two examples of combinations of serious and disabling disorders. A person in need of treatment for dual diagnoses who is in the current criminal justice system may not be evaluated or assessed, let alone provided with appropriate treatment.

Demographics

Children of alcohol or other drug-addicted parents are at increased risk for developing substance abuse and mental health problems. Disruptive behavior disorders coexist with adolescent substance abuse problems more often than not. Other special groups that may be affected include older adults with mood or anxiety disorders, especially those who are grieving numerous losses. They may drink or misuse or abuse prescription drugs to cope with their lowered quality of life. These factors can often complicate treatment of hypertension, diabetes, arthritis, and other health-related problems that affect the elderly as well.

Abuse of alcohol or other drugs may occur in persons with eating disorders in an effort to deal with guilt, shame, anxiety, or feelings of self-loathing as a result of bingeing and purging food. Many military veterans suffer from anxiety, depression or post-traumatic stress disorder and have histories of substance abuse. Services for veterans are woefully inadequate, adding to the chronic nature of dual diagnosis among them.

Treatment

One of the difficulties in treating patients with dual diagnoses is that most treatments for mental illness are usually developed for and validated by studies of patients with single diagnoses; therefore, many cases of comorbidity may not be well treated by these approaches. Recent research on services provided to people with dual diagnoses, however, indicates that treatment can be successful, provided certain specific components are included in the treatment process. The critical elements identified as part of treatment programs with the most successful outcomes are:

• • Staged interventions that begin with engaging the client; persuading him or her to become involved in recovery-focused activities; acquiring skills and support to control the illnesses; and then helping the patient with relapse prevention.
• • Assertive outreach that may involve intensive case management and meetings in the person’s home.
• • Motivational interventions to help the client become committed to self-management of their illnesses.
• • Counseling that includes cognitive and behavioral skills.
• • Social network support and/or family interventions.
• • An understanding of the long-term nature of recovery.
• • Comprehensive scope to treatment that includes personal habits, stress management, friendship networks, housing, and many other aspects of a person’s life.
• • Cultural sensitivity and competence.

The success of 12-step programs in the treatment of substance abuse is well-established. Nevertheless, the level of confrontation sometimes found in a traditional 12-step group may feel overwhelming to people with mental illnesses. In addition, the use of psychotropic (mood- or behavior-altering) medications is controversial in some areas of the substance abuse recovery community. As a result, other models of consumer-led support groups specifically for people with concurrent disorders, such as Dual Recovery Anonymous and Double Trouble, are being developed.

Purpose

Doxepin is used primarily to treat depression and to treat the combination of symptoms of anxiety and depression. Like most antidepressants, doxepin has also been used to treat panic disorder, obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, enuresis (bed-wetting), eating disorders such as bulimia nervosa, cocaine dependency, and the depressive phase of bipolar (manic-depressive) disorder. It has also been used to support smoking cessation programs.

Description

Doxepin acts to change the balance of naturally occurring chemicals in the brain that regulate the transmission of nerve impulses between cells. Its action primarily increases the concentration of norepinephrine and serotonin (both chemicals that stimulate nerve cells) and, to a lesser extent, blocks the action of another brain chemical, acetylcholine. Although not technically a tricyclic antidepressant, doxepin shares most of the properties of these drugs, which include amitriptyline, clomipramine, desipramine, imipramine, nortriptyline, protriptyline, and trimipramine. Studies comparing doxepin with these other drugs have shown that doxepin is no more or less effective than other antidepressants of its type. Its choice for treatment is as much a function of physician preference as any other factor.

The therapeutic effects of doxepin, like other antidepressants, appear slowly. Maximum benefit is often not evident for at least two weeks after starting the drug. People taking doxepin should be aware of this and continue taking the drug as directed even if they do not see immediate improvement.

Recommended dosage

As with any antidepressant, doxepin must be carefully adjusted by the physician to produce the desired therapeutic effect. Doxepin is available as 10-mg, 25-mg, 50-mg, 75-mg, 100-mg, and 150-mg oral capsules as well as an oral concentrate solution containing 10 mg of drug in each milliliter of solution.

Therapy is usually started at 30 to 150 mg per day and gradually increased to 300 mg daily if needed. There is little evidence that doses above 300 mg daily provide any additional benefits. Amounts up to 150 mg may be taken as a single dose at bedtime to decrease daytime sleepiness. Doses of more than 150 mg per day should be divided into two or three doses and taken throughout the day.

In patients over age 60, therapy should be maintained at the low end of the dosing range and increased cautiously and with physician supervision. Patients with organic brain syndrome (psychiatric symptoms of dementia often seen in elderly patients) generally require daily doses of only 25 to 50 mg.

If the oral concentrate of doxepin is used, each dose should be diluted in at least 4 ounces (120 mL) of milk, orange, prune, tomato, pineapple, or grapefruit juice just before administration. Doxepin is not compatible with many carbonated beverages and should not be diluted in them.

Precautions

As with tricyclic antidepressants, doxepin should be used cautiously and with close physician supervision in people, especially the elderly, who have benign prostatic hypertrophy, urinary retention, and glaucoma, especially angle-closure glaucoma (the most severe form). Before starting treatment, people with these conditions should discuss the relative risks and benefits of treatment with their doctors to help determine if doxepin is the right antidepressant for them.

A common problem with antidepressants is sedation (drowsiness, lack of physical and mental alertness). This side effect is especially noticeable early in therapy. In most patients, sedation decreases or disappears entirely with time, but until then, patients taking doxepin should not perform hazardous activities requiring mental alertness or coordination. The sedative effect is increased when doxepin is taken with other central nervous system depressants, such as alcoholic beverages, sleeping medications, other sedatives, or antihistamines. It may be dangerous to take doxepin in combination with these substances. Doxepin may increase the possibility of having seizures. Patients should tell their physician if they have a history of seizures, including seizures brought on by the abuse of drugs or alcohol. These people should use doxepin only with caution and be closely monitored by their physician.

Doxepin may increase heart rate and stress on the heart. It may be dangerous for people with cardiovascular disease, especially those who have recently had a heart attack, to take this drug or other antidepressants in the same pharmacological class. In rare cases where patients with cardiovascular disease must receive doxepin, they should be monitored closely for cardiac rhythm disturbances and signs of cardiac stress or damage.

Doxepin should not be taken by nursing mothers because it is secreted into breast milk and may cause side effects in the nursing infant.

Side effects

Doxepin shares the side effects of tricyclic antidepressants. The most frequent of these are dry mouth, constipation, urinary retention, increased heart rate, sedation, irritability, dizziness, and decreased coordination. As with most side effects associated with tricyclic antidepressants, the intensity is highest at the beginning of therapy and tends to decrease with continued use.

Dry mouth, if severe to the point of causing difficulty speaking or swallowing, may be managed by dosage reduction or temporary discontinuation of the drug. Patients may also chew sugarless gum or suck on sugarless candy in order to increase the flow of saliva. Some artificial saliva products may give temporary relief.

Men with prostate enlargement who take doxepin may be especially likely to have problems with urinary retention. Symptoms include having difficulty starting a urine flow and more difficulty than usual passing urine. In most cases, urinary retention is managed with dose reduction or by switching to another type of antidepressant. In extreme cases, patients may require treatment with bethanechol, a drug that reverses this particular side effect. People who think they may be experiencing any side effects from this or any other medication should tell their physicians.

Interactions

Dangerously high blood pressure has resulted from the combination of antidepressants such as doxepin and members of another class of antidepressants known as monoamine oxidase (MAO) inhibitors. Because of this, doxepin should never be taken in combination with MAO inhibitors. Patients taking any MAO inhibitors, for example Nardil (phenelzine sulfate) or Parmate (tranylcypromine sulfate), should stop the MAO inhibitor then wait at least 14 days before starting doxepin or any tricyclic antidepressant. The same holds true when discontinuing doxepin and starting an MAO inhibitor.

Doxepin may decrease the blood pressure–lowering effects of clonidine. Patients who take both drugs should be monitored for loss of blood-pressure control and the dose of clonidine increased as needed.

The sedative effects of doxepin are increased by other central nervous system depressants such as alcohol, sedatives, sleeping medications, or medications used for other mental disorders such as schizophrenia. The anticholinergic effects of doxepin are additive with other anticholinergic drugs such as benztropine, biperiden, trihexyphenidyl, and antihistamines.

Purpose

Donepezil is used to help treat symptoms of Alzheimer’s disease in individuals with mild to moderate illness. The drug may cause small improvements in dementia for a short period of time, but donepezil does not stop the progression of Alzheimer’s disease.

Description

The Food and Drug Administration has approved donepezil for treatment of the symptoms of 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 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. Donepezil helps prevent the breakdown of acetylcholine in the brain, thus temporarily increasing its concentration. In doing so, donepezil may improve the thinking process by facilitating nerve impulse transmission within the brain.

Donepezil is available as tablets in two different strengths. It is broken down by the liver.

Recommended dosage

The initial dosage of donepezil is 5 mg taken at bedtime. This dose should be continued for four to six weeks. The dosage may then be increased to 10 mg at bedtime, but there is no clear evidence that the higher dosage is more beneficial. However, the higher dosage is likely to cause more side effects.

Precautions

Donepezil may slow heart rate, increase acid in the stomach, make urination difficult, cause breathing difficulties, and may make it more likely for people to have seizures. As a result, it should be used carefully with close physician supervision by 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 seizure disorders.

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

Side effects

More than 5% of people taking donepezil experience difficulty sleeping, dizziness, nausea, diarrhea, muscle cramps, headache, or other pains.

Diarrhea, nausea, and vomiting occur more often with the 10-mg dose than the 5-mg dosage. These adverse effects are usually mild, short-lived, and typically subside when the drug is stopped. Other, less common, side effects are abnormal dreams, depression, drowsiness, fainting, loss of appetite, weight loss, frequent urination, arthritis, and easy bruising.

Interactions

Many drugs may alter the effects of donepezil; likewise, donepezil may alter the action of other drugs. Drugs such as dicylomine, phenytoin, carbamazepine, dexamethasone, rifampin, or phenobarbital may lessen the effects of donepezil. Other drugs such as bethanechol, ketoconazole, or quinidine may increase some of the side effects associated with donepezil. When donepezil and nonsteroidal anti-inflammatory drugs such as ibuprofen (Advil) or naproxen are used together, there may be an increased tendency to develop stomach ulcers. Donepezil may increase the side effects associated with use of fluvoxamine, an antidepressant. If succinylcholine, a drug commonly used during anesthesia, is used with donepezil, prolonged muscle paralysis may result.

Purpose

Divalproex sodium is effective in the treatment of epilepsy, particularly for preventing simple, complex (petit mal), absence, mixed, and tonic-clonic (grand mal) seizures. Divalproex sodium is also used to treat the manic phase of bipolar disorder (also called manic-depressive disorder) in adults, and to prevent migraine headache in adults.

Description

Divalproex sodium is chemically compounded from sodium valproate and valproic acid in a 1:1 ratio.

Divalproex sodium is thought to work by increasing the levels of a brain neurotransmitter called gamma-aminobutyric acid (GABA). GABA is an inhibitory neurotransmitter, which means that its presence makes it harder for nerve cells (neurons) in the brain to become activated (fire). It is believed that increasing GABA’s inhibitory action on brain neurons accounts for the ability of divalproex sodium to decrease seizures, curb manic behaviors, and decrease the frequency of migraine headaches.

Divalproex sodium was discovered to decrease the likelihood of seizure in 1963. In 1978, the United States Food and Drug Administration approved it for this use. Other uses for divalproex sodium were researched and approved subsequently, including use against mania (1995) and use to decrease migraine headache frequency. Divalproex sodium’s 1995 approval as an anti-mania medication was considered an exciting advance, since it represented the first new drug introduced for this use in 25 years.

Recommended dosage

Divalproex sodium is available in tablets of 125 mg, 250 mg, and 500 mg. Divalproex sodium is also available in 125-mg capsules, and in a 500-mg extended release tablet. A syrup is also available, containing 250 mg active drug per 5 mL.

Divalproex sodium therapy is usually started at 10–15 mg per kg of body weight per day. Dosages are then increased until seizures seem to be well controlled. This is usually achieved at averages under 60 mg per kg per day.

To treat mania, divalproex sodium is usually started at a daily dose of about 750 mg.

For migraine prevention, divalproex sodium is started at 250 mg, twice per day. In some patients, this dose will have to be raised to a total of 1,000 mg per day.

Precautions

A greater risk of liver damage exists in patients with kidney disease, known liver disease, Addison’s disease, blood diseases, children under the age of two, patients with organic brain diseases (such as Alzheimer’s, Parkinson’s, slow virus infections, Huntington’s chorea, multiple sclerosis, etc.), patients with metabolic disorders present at birth, patients with severe seizure disorders and accompanying mental retardation, and patients who are taking several other anticonvulsant drugs.

Because divalproex sodium can affect a patient’s blood by dropping the platelet (a type of blood cell that affects clotting) count and interfering with coagulation (clotting) capability, both platelet count and coagulation parameters should be verified before starting the medication and at intervals throughout its use.

Divalproex sodium is known to cause an increased risk of birth defects when taken during pregnancy. An individual and her health care provider must weigh the potential risks and benefits of using this medication during pregnancy. Women who take this medicine should not breast-feed, since a small amount will pass into the breast milk

Divalproex sodium causes drowsiness and impairs alertness in some individuals. Patients just beginning to use the medication should avoid driving and using dangerous machinery until they determine how the drug affects them. The sedative effects are increased in the presence of alcohol, so patients should avoid drinking while taking medicines containing divalproex sodium.

Side effects

Some of the more common side effects of divalproex sodium include mild stomach cramps, change in menstrual cycle, diarrhea, loss of hair, indigestion, decreased appetite, nausea and vomiting, trembling in the hands and arms, and weight loss or weight gain. These side effects usually go away as the patient’s body becomes accustomed to the medication.

Less common side effects include severe stomach cramps or continued nausea and vomiting, changes in mood, behavior, or thinking, double vision or seeing spots, severe fatigue, easy bruising or unusual bleeding, yellow cast to the skin or the whites of the eyes (jaundice), odd eye movements, and increased seizures. Patients who notice these symptoms should check with their doctor to see if their dosage or medication needs to be adjusted.

Rare side effects that should be checked out by a doctor include clumsiness, difficulty with balance, constipation, dizziness, drowsiness, headache, skin rash, agitation, restlessness, or irritability.

Interactions

Divalproex sodium is broken down (metabolized) in the liver. Other drugs that are metabolized in the liver can have too low or too high concentrations in the body when taken with divalproex sodium. Levels of divalproex sodium may be increased when taken with felbamate, isoniazid, salicylates (aspirin-containing medications), clarithromycin, erythromycin, and troleandomycin. Divalproex sodium may increase levels of carbamazepine, phenytoin, lamotrigine, nimodipine, phenobarbital, and zidovudine. Use with clonazepam may cause absence seizures. Cholestyramine and colestipol may reduce the absorption and the blood levels of divalproex sodium.