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Clinical Manifestations Hist ory and Ment al St at us Examinat ion People with avoidant personality disorder experience intense feelings of inadequacy. They are painfully sensitive to criticism, so much so that they are compelled to avoid spending time with people.
Their fears of rejection and humiliation are so powerful that to engage in a relationship, they seek strong guarantees of acceptance. The essence of this disorder is inadequacy, hypersensitivity to criticism, and consequent social inhibition. Different ial Diagnosis The major diagnostic distinction is between avoidant personality disorder and social phobia, generalized type.
Because of their extreme dependence on others for emotional support and decision making, they live in great and continual fear of separation from someone they depend on, hence their submissive and clinging behaviors. Different ial Diagnosis People with dependent personality disorder are similar to individuals with borderline personality disorder in their desire to avoid abandonment but do not exhibit the impulsive behavior, unstable affect, and poor self-image of the borderline patient.
Men are diagnosed with obsessive-compulsive personality disorder twice as frequently as women. Etiology The etiology is unknown, but there may be an association with mood and anxiety disorders. Clinical Manifestations Hist ory and Ment al St at us Examinat ion Individuals with obsessive-compulsive personality disorder are perfectionists.
They require order and control in every dimension of their lives. Their attention to minutiae frequently impairs their ability to finish what they start or to maintain sight of their goals.
They are cold and rigid in relationships and make frequent moral judgments; devotion to work often replaces intimacy. They are serious and plodding; even recreation becomes a sober task. Different ial Diagnosis Obsessive-compulsive personality disorder can be differentiated from obsessive-compulsive disorder based on symptom severity.
Management Because personality may have temperamental components and is developed over a lifetime of interacting with the environment, personality disorders are generally resistant to treatment. In general, psychotherapy is recommended for most personality disorders. Psychodynamically based therapies are commonly used, although they must be modified to each individual and each disorder.
Cognitive, behavioral , and family therapies are also used to treat these disorders. Empirical studies validating the efficacy of various therapies are generally lacking. Dialectical behavioral therapy was developed specifically for the treatment of borderline personality disorder and has been validated in empirical studies. Group therapy incorporating various psychotherapeutic modalities is also used. Pharmacotherapy is widely used in personality disorders, although no specific medication has been shown to treat any specific disorder.
Instead, medications are targeted at the various associated symptoms of personality disorders. For example, mood stabilizers may be used for mood instability and impulsiveness. Benzodiazepines are commonly used for anxiety, although the potential for abuse and dependence is too often overlooked.
For depression, obsessive-compulsive symptoms, and eating disturbances, selective serotonin-reuptake inhibitors and other antidepressants have been successfully used. Psychotic or paranoid symptoms are commonly treated with low-dose antipsychotics. Personalit y disorders consist of an enduring pat t ern of experience and behavior. The disorders can produce t ransient psychot ic sym pt om s during st ress.
Treat m ent is wit h psychot herapy and m edicat ions t arget ed at sym pt om relief. Personalit y disorders are resist ant t o t reat m ent. Personalit y disorders m ay have genet ic associat ions wit h Axis 1 disorders. It is etiologic for many medical illnesses and is frequently comorbid with psychiatric illness.
Hence, alcohol abuse and dependence is defined by the same criteria as heroin abuse and dependence. This chapter defines abuse and dependence and provides clinical descriptions of each substance-related disorder. Here the common substance-related disorders are reviewed in sequence.
Tolerance 2. Withdrawal 3. Repeated, unintended, excessive use 4. Persistent failed efforts to cut down 5. Excessive time spent trying to obtain the substance 6. Reduction in important social, occupational, or recreational activities 7.
Continued use despite awareness that substance is the cause of psychological or physical difficulties Although each substance dependence disorder has unique features, these are considered the common features that define substance dependence.
Major substance use disorders are discussed with particular attention to their unique features. Substance use disorders develop through a biopsychosocial interaction whereby genetic effects and environment interact to culminate in a behavioral pattern of repeated drug use.
Although the degree to which genetic factors explain the risk for abuse of or dependence on a particular substance vary, a disorder develops when a person is biologically vulnerable, has access to the substance, and is repeatedly exposed to the substance with ongoing availability. The mesolimbic dopamine system consists of dopaminergic axons arising from the ventral tegmental area VTA that ascend via the medial forebrain bundle to innervate the ventral striatum, prefrontal cortex, and additional limbic structures.
This structure is a target of the mesolimbic dopamine pathway that mediates reward system function Fig. Naturally occurring rewards having high evolutionary adaptive significance such as feeding, sex, and exercise interact with the mesolimbic dopamine pathway to produce associative memories linked to the rewards that reinforce the probability of rewarding behavior. Drugs of abuse bypass the adaptive components of the reward system and, via direct synaptic effects, produce similar powerful associative memories strongly reinforcing behavior associated with drug use Fig.
Drugs of abuse influence neurons of the nucleus accumbens ventral striatum largely through actions on the dopamine neurons of the ventral tegmental area VTA. Adapted from Wise, , p.
Because addiction occurs when repeated exposure to drugs has produced alterations in the brain's reward system and in other brain regions involved in craving, motivation, and attention, there are conscious and nonconscious elements predisposing to continued drug use despite adverse consequences of the drug. Treatment for addiction, therefore, must include an awareness of the nonconscious factors such as stress, exposure to drug cues, hunger, etc.
The alcohol-dependent patient drinks larger amounts over longer periods of time than intended, spends a great P. In alcohol dependence, there is also a persistent desire or unsuccessful efforts to cut down or control alcohol intake. Epidemiology The percentage of Americans who abuse alcohol is thought to be high. The male to female prevalence ratio for alcohol dependence is Etiology The etiology of alcohol dependence is unknown. Adoption studies and monozygotic twin studies demonstrate a partial genetic basis, particularly for men with alcoholism.
Male alcoholics are more likely than female alcoholics to have a family history of alcoholism. Adoption studies also reveal that alcoholism is multidetermined: genetics and environment family rearing both play a role.
Clinical Manifestations Hist ory The alcohol-dependent patient may deny or minimize the extent of drinking, making the early diagnosis of alcoholism difficult. The patient may present with accidents or falls, blackouts, motor vehicle accidents, or after an arrest for driving under the influence.
Because denial is so prominent in the disorder, collateral information from family members is essential to the diagnosis. Early physical findings that suggest alcohol dependence include acne rosacea, palmar erythema, and painless hepatomegaly from fatty infiltration.
Physical Examinat ion Signs of more advanced alcohol dependence include cirrhosis, jaundice, ascites, testicular atrophy, gynecomastia, and Dupuytren contracture. Cirrhosis can lead to complications including variceal bleeding, hepatocellular carcinoma, and hepatic encephalopathy. Medical disorders with an increased incidence in alcohol-dependent patients include pneumonia, tuberculosis, cardiomyopathy, hypertension, and gastrointestinal cancers i.
Ment al St at us Examinat ion There are also numerous neuropsychiatric complications of alcohol dependence. Wernicke-Korsakoff's syndrome may develop in the alcohol-dependent patient because of thiamine deficiency.
The Wernicke's stage of the syndrome is also called Wer ni cke's encephal opat hy note: Wernicke's encephalopathy is a type of neurological syndrome that is not listed among the DSM-IV alcohol-related diagnoses. Management of Wernicke's encephalopathy is covered in the information to follow. Other neuropsychiatric complications of alcoholism include alcoholic hallucinosis, alcohol-induced dementia, peripheral neuropathy, mental status, changes due to subdural hematoma or other intracranial bleeding, substance-induced depression, and suicide.
In the later stages of alcoholism, significant social and occupational impairment is likely: job loss and family estrangement are typical. Laborat ory T est s Various laboratory tests are helpful in making the diagnosis. Blood alcohol levels quantitatively confirm alcohol in the serum. They can also provide a rough measure of tolerance. In general, the higher the blood alcohol level without significant signs of intoxication, P. Alcohol-dependent patients also develop elevated mean corpuscular volume, elevated serum glutamicoxaloacetic transaminase, and elevated serum glutamic-pyruvic transaminase.
Different ial Diagnosis The diagnosis of alcohol dependence is usually clear after careful history, physical and mental status examination, and consultation with family or friends. Management Management is specific to the clinical syndrome. Intensive care may be required in cases of excessive alcohol intake complicated by respiratory compromise. All suspected or known alcohol-dependent patients should receive oral vitamin supplementation with folate 1 mg per day and thiamine mg per day.
If oral intake is not possible, or if there is concern that the patient may have thiamine deficiency, recent malnutrition, malabsorption, or early signs of Wernicke's encephalopathy, then thiamine should be administered intravenously as a slow infusion before any glucose is given because glucose depletes thiamine stores.
These symptoms may remit with the slow intravenous infusion of thiamine at to mg per day for 4 to 5 days. Magnesium repletion is also essential. Without thiamine at sufficiently high dosages and given intravenously, Wernicke's encephalopathy may progress to a chronic condition of alcohol-induced persisting amnestic disorder information to follow.
The diagnosis of alcohol intoxication must be differentiated from other medical or neurologic states that may mimic intoxication, for example, diabetic hypoglycemia; toxicity with various agents, including but not limited to ethylene glycol, lithium, and phenytoin; and intoxication with benzodiazepines or barbiturates. The diagnosis of alcohol intoxication can be confirmed by serum toxicologic screening, including a blood alcohol level. Alcohol withdrawal commonly occurs with a predictable course but may show much individual variation.
The DSM-IV criteria for alcohol withdrawal basically include the cessation of alcohol intake after a period of prolonged heavy use and withdrawal signs. When alcohol withdrawal is complicated by delirium, then alcohol withdrawal delirium is diagnosed. When alcohol withdrawal is complicated by hallucinations or perceptual alterations with intact reality testing and with other signs of delirium, then alcohol withdrawal with perceptual disturbances is diagnosed.
Clinical signs of alcohol withdrawal include tremor especially of the hands , cardiovascular symptoms tachycardia, hypertension, sweating , gastrointestinal symptoms nausea and vomiting , insomnia, sensory disturbances perceptual distortions, hallucinations , psychomotor agitation, and anxiety. Grand mal seizures may also occur. Along with delirium and Wernicke's encephalopathy, grand mal seizures are among the most serious complications of alcohol withdrawal.
As noted, the evolution of alcohol withdrawal can have a variable time course and does not necessarily progress in fixed order. Table summarizes the time course of alcohol withdrawal symptoms.
It is treated with intravenous benzodiazepines and supportive care. Treatment may need to occur in an intensive care unit, particularly if there is significant autonomic instability e.
The syndrome typically lasts 3 days but can persist for weeks. This is more accurately tied to the point at which alcohol blood levels decline. The diagnosis is made when alcohol is determined to be the cause of the cognitive changes. Alcohol-induced persisting amnestic disorder is also called Kor sakof f 's syndr ome and is irreversible in two-thirds of patients.
Alcohol-induced persisting amnestic disorder is diagnosed in an individual with a history of alcohol dependence who develops memory impairment in learning new memories or recalling old information. Confabulation i. These include alcohol intoxication delirium, alcohol-induced psychotic disorder with delusions, alcohol-induced psychotic disorder with hallucinations, alcohol-induced mood disorder, alcohol- induced anxiety disorder, alcohol-induced sexual dysfunction, and alcohol-induced sleep disorder.
To sustain a lasting recovery, the patient must stop denying the illness and accept the diagnosis of alcohol dependence. Alcoholics Anonymous AA , a worldwide self-help group for recovering alcohol-dependent patients, has been shown to be one of the most effective programs for achieving and maintaining sobriety.
The program involves daily-to-weekly meetings that focus on 12 steps toward recovery. Members are expected to pursue the 12 steps with the assistance of a sponsor preferably someone with several years of sobriety.
Alcohol appears to be a potent cause of depression. Intoxicated patients may appear severely depressed and display suicidal behavior or statements, which resolve when sobriety is achieved. Treatment of depression should be geared to patients who remain depressed after 2 to 4 weeks of sobriety. Anxiety is also common in withdrawing or newly sober patients and should be assessed after at least 1 month of sobriety. Inpatient and residential rehabilitation programs use a team approach aimed at focusing the patient on recovery.
Group therapy allows patients to see their own problems mirrored in and confronted by others. Family therapy allows the patient to examine the role of the family in alcoholism. Disulfiram Antabuse can be helpful in maintaining sobriety in some patients. It acts by inhibiting the second enzyme in the pathway of alcohol metabolism, aldehyde dehydrogenase, so that acetaldehyde accumulates in the bloodstream, causing flushing, nausea, vomiting, palpitations, and hypotension.
In theory, disulfiram should inhibit drinking by making it physiologically unpleasant; however, because the effects can be fatal in rare cases, patients must be committed to abstinence P. The usual dose of disulfiram is mg daily. Naltrexone Revia is an opiate antagonist medication.
Naltrexone reduces both the amount of alcohol intake and the frequency of alcohol intake. Naltrexone is usually dosed at 50 mg per day, but higher doses may potentially be more effective. Unlike disulfiram, patients can continue taking naltrexone if they relapse to alcohol intake. Like naltrexone, acamprosate does not produce a disulfiram-like effect and can be continued in persons who relapse to alcohol consumption.
It is important to note that disulfiram, naltrexone, and acamprosate are used for maintenance therapy and do not prevent the potentially life-threatening symptoms of alcohol withdrawal. Many studies have demonstrated benefits from rehabilitation programs, but nearly half of all treated alcohol-dependent patients will relapse, most commonly in the first 6 months. They are all cross-tolerant with each other and with alcohol.
Included in this class are barbiturates and benzodiazepines. Of these, the benzodiazepines are the most widely prescribed and available. It is important to differentiate these drugs from other drugs used for sleep induction and from other medications used in psychiatry to treat anxiety. In particular, serotonin reuptake inhibitor antidepressants and buspirone are first-line treatments for some types of anxiety but are not classified here.
The barbiturate and benzodiazepines can produce a life-threatening withdrawal syndrome. Some patients abuse these drugs. Physical and Mental Status Examinations Sedative, hypnotic, or anxiolytic intoxication can be distinguished from alcohol intoxication by the presence or absence of alcohol on the breath, in the serum, or urine.
Barbiturates, when taken orally, are much more likely than benzodiazepines to cause clinically significant respiratory compromise. Laboratory Tests Intoxication can be confirmed through quantitative or qualitative serum or urine toxicologic analyses. Serum toxicologic screens can identify the presence of benzodiazepines, barbiturates, and their major metabolites. Withdrawal symptoms are listed in Table Withdrawal delirium confusion, disorientation, and visual and somatic hallucinations has an onset as early as 3 to 4 days after abstinence depending on the P.
Dependence requires the presence of three or more of the seven symptoms listed in Table Generally, inpatient detoxification is required when there is comorbid medical or psychiatric illness, prior treatment failures, or lack of support by family or friends. On an inpatient unit, benzodiazepines or barbiturates may be administered and tapered in a controlled manner.
Withdrawal from short-acting substances is generally more severe, whereas withdrawal from longer-acting substances is more prolonged. Withdrawal from barbiturates is more dangerous than from benzodiazepines, as it can much more easily lead to hyperpyrexia, seizure, and death. Withdrawal is managed by scheduled dosing and tapering of a benzodiazepine or barbiturate diazepam or phenobarbital.
This test allows for the quantification of tolerance to perform a controlled taper, thereby reducing the problems of withdrawal. Treatment of sedative-hypnotic dependence resembles that for alcohol dependence.
After detoxification, the patient can enter a residential rehabilitation program or a day or evening treatment program. Referral to AA is appropriate because the addiction issues and recovery process are similar. Families may be referred to Al-Anon, an AA-focused family education and support group. Heroin is available only illegally in the United States. Opiates are commonly used for pain control. Prevalence for heroin dependence is about 0. Many of those who use opiates recreationally become addicted.
Psychomotor retardation, drowsiness, inactivity, and impaired concentration ensue. Nausea, vomiting, and constipation are common after opiate use. Laboratory Tests Opiate use can be confirmed by urine or serum toxicological measurements. Opiate abuse is defined by the criteria for substance abuse previously noted.
In opiate dependence, users develop a tolerance to the effects of opiates. Withdrawal symptoms usually begin 10 hours after the last dose. Withdrawal from opiates can be highly uncomfortable but is rarely medically complicated or life-threatening. Opiate addicts are more prone to commit crimes because of the high cost of opiates. Opiate addiction is also associated with high mortality rates from inadvertent overdoses, accidents, and suicide. In addition, opiate addicts are at higher risk of medical problems because of poor nutrition and use of dirty needles.
Common medical disorders include serum hepatitis, human immunodeficiency virus infection, endocarditis, pneumonia, and cellulitis. Differential Diagnosis The diagnosis of opiate addiction is usually obvious after a careful history as well as mental status and physical examinations. Thus, it causes relatively few intoxicant or withdrawal effects. Generally, the initial dose of methadone typically 5 to 20 mg is based on the profile of withdrawal symptoms.
Withdrawal from short-acting opiates lasts 7 to 10 days; withdrawal from longer-acting meperidine lasts 2 to 3 weeks. Injectable buprenorphine is employed as an off-label use for opiate detoxification.
Buprenorphine tablets as Subutex buprenorphine alone or as Suboxone buprenorphine plus naltrexone are FDA approved for outpatient treatment of opioid dependence by certain qualified physicians. Inclusion of naltrexone with buprenorphine in Suboxone allows the administration of opiate replacement therapy with decreased euphoric and respiratory depressant effects. It is remarkably effective at treating the autonomic symptoms of withdrawal but does little to curb the drug craving.
Risks of sedation and hypotension limit the usefulness of clonidine in outpatient settings. Clonidine does not appear to be as effective as opiate replacement in helping maintain abstinence. Additional medications can be used to relieve uncomfortable symptoms of withdrawal, such as dicyclomine for abdominal cramping, promethazine for nausea, and quinine for muscle aches.
Rehabilitation generally involves referral to an intensive day treatment program and to Narcotics Anonymous, a step program similar to AA. Methadone maintenance, daily administration of 60 to mg of methadone in government-licensed methadone clinics, is used widely for patients with demonstrated physiologic dependence.
Long-term administration of methadone can alleviate drug hunger and minimize drug-seeking behavior. The patterns of use and abuse of and dependence on cocaine and amphetamines are similar because both are central nervous system stimulants with similar psychoactive and sympathomimetic effects.
Amphetamines have a longer half-life than cocaine and hence are taken less frequently. Rates of depression are generally higher in substance-abusing and substance-dependent individuals. Antidepressant medications influencing catecholamine function, such as desipramine and bupropion, are generally superior to the selective serotonin reuptake inhibitors in the treatment of cocaine-related depression.
Maladaptive behavioral changes e. Tachycardia or bradycardia 3. Pupillary dilatation 4. Hyper- or hypotension 5. Perspiration or chills 6. Nausea or vomiting 7. Psychomotor agitation or retardation 8. Muscular weakness, respiratory depression, chest pain, cardiac dysrhythmias 9. Confusion, seizures, dyskinesia, or coma Cocaine intoxication can cause tactile hallucinations coke bugs.
Both cocaine and amphetamine intoxication can lead to agitation, impaired judgment, and transient psychosis e. Cocaine and amphetamine dependence is defined by the criteria outlined above for substance dependence. Withdrawal of cocaine or amphetamines leads to fatigue, depression, nightmares, headache, profuse sweating, muscle cramps, and hunger.
Withdrawal symptoms peak in 2 to 4 days. Psychosis from amphetamine intoxication or withdrawal is generally self-limited, requiring only observation in a safe environment. Antipsychotic medications can be used to treat agitation. Ultimately, the goal is rehabilitation. Narcotics Anonymous, treatment of comorbid psychopathology, administration of drugs to reduce craving, and family therapy are the essential features of cocaine rehabilitation.
The drug is usually smoked and causes a state of euphoria. Complications of cannabis include impaired judgment, poor concentration, and poor memory. Serious complications include delirium and psychosis. Cannabis withdrawal syndromes are self-limited and do not require psychiatric or medical treatment. These drugs are of a wide variety of chemical classes but are linked by their frequent use in social groups and the fact that they are commonly taken together.
Because of their popularity and tendency for users to show up in emergency rooms, the following information reviews some of the more widely used club drugs. It is important to note that drug use trends can change rapidly, and existing drugs may go in or out of fashion. New drugs may also emerge at any time. Ecstasy Ecstasy 3,4-methylenedioxy-N-methylamphetamine [MDMA] is a widely popular drug with mixed stimulant and hallucinogenic properties.
Many users report a stimulant and euphoric effect, and MDMA appears specifically to enhance the user's desire for intimacy with others. As such, its use has been associated with an increased frequency of unsafe sexual activity. Acute use of MDMA has been associated with deaths from various causes. Long-term MDMA use appears to lead to a long-lasting reduction in serotonin transmission throughout the brain.
Methamphetamine Also known as cr yst al or cr ank, methamphetamine is a psychostimulant that is neurotoxic to dopamine and serotonin axons. Methamphetamine is often produced locally in small laboratories and can therefore vary greatly in purity. In higher doses, GHB is used to produce a high and is common among the club and party scene. GHB is easily overdosed and can lead to death from respiratory arrest.
GHB dependence may occur, and withdrawal requires medical management. Ketamine Also known as Speci al K, ketamine is a dissociative anesthetic mostly used in veterinary medicine.
It is used for its hallucinatory, dissociative effect. Rohypnol produces classic benzodiazepine effects of sedation. It has strong amnestic properties, however, and it may be a frequent culprit in drugging others for the purpose of theft or sexual assault.
Acute use can produce a highly euphoric good trip or a highly dysphoric bad trip hallucinatory experience. Long-term LSD use can lead to psychosis or hallucinogen persisting perception disorder. Benzodiazepines are used in acut e det oxificat ion t o prevent life- t hreat ening com plicat ions of wit hdrawal. Peak incidence of alcoholic seizures is wit hin 24 t o 48 hours. Rehabilit at ion, involving AA and t herapy, is aim ed at abst inence and t reat ing com orbid disorders.
Wernicke's t riad consist s of nyst agm us, at axia, and m ent al confusion. Alcohol- induced persist ing am nest ic disorder Korsakoff's sym pt om s result from brain dam age due t o t hiam ine deficiency and include am nesia and confabulat ion.
Sedat ives and hypnot ic drugs are cross- t olerant wit h alcohol, and wit hdrawal st at es are sim ilar t o alcohol. Opiat e addict s are at increased risk of hum an im m unodeficiency virus, pneum onia, endocardit is, hepat it is, and cellulit is wit h high m ort alit y rat es from accident al overdose, suicide, and accident s.
Opiat e wit hdrawal is uncom fort able but not usually m edically com plicat ed. Cocaine and am phet am ines are cent ral nervous syst em st im ulant s and can cause t ransient psychosis e. St im ulant wit hdrawal sym pt om s fat igue, depression, night m ares, et c. Although eating disorders are classified into two discrete diagnostic categories in the Di agnost i c and St at i st i cal Manual of Ment al Di sor der s, 4th edition DSM-IV , many symptoms overlap. The principal diagnostic distinction is based on ideal body weight.
When abnormal eating behavior causes body weight to fall below a defined percentage of expected body weight, a diagnosis of anorexia nervosa is made. If ideal body weight is maintained in the presence of abnormal eating behaviors, a diagnosis of bulimia nervosa is made. Eating disorders likely lie along a continuum of disturbances in eating behavior and often are associated with mood disorders and other psychiatric illnesses Table NEURAL BASIS Although the different types of eating disorders do not share a single neurobiological origin, serotonergic dysfunction is strongly associated with these conditions and with associated symptoms.
Alterations in dopamine, norepinephrine, neuropeptide, and opiate systems are also implicated. Hypothalamic and limbic neural regions, including the reward system likely play a role. High comorbidity with obsessive-compulsive disorder and body image disturbances body dysmorphic disorder suggests overlap with brain regions affected in these conditions.
Regions mediating feeding behavior, such as nucleus accumbens, orbitofrontal cortex, and insula are also likely affected. The weight loss must result from behavior directed at maintaining low weight or achieving a particular body image. The prevalence in men is not clear. The average age of onset is 17, with onset rare before puberty or after age Anorexia nervosa is more common in industrial societies and higher socioeconomic classes.
Psychological theories of anorexia nervosa remain speculative. Although it is not specific to eating disorders, past physical or sexual abuse may be a risk factor. Contemporary theories focus on the need to control one's body. Social theories propose that societal opinions, which equate low body weight with attractiveness, drive women to develop eating disorders. Although this fact may be responsible for some cases e. Family studies reveal an increased incidence of mood disorders and anorexia nervosa in first-degree relatives of patients with anorexia nervosa.
Twin studies show higher concordance for monozygotic versus dizygotic twins. Neuroendocrine evidence supporting a biologic contribution to anorexia includes alterations in corticotropin-releasing factor, reduced central nervous system norepinephrine metabolism, and that amenorrhea caused by decreased luteinizing hormone and follicle-stimulating hormone release sometimes precedes the onset of anorexia nervosa.
Patients with anorexia nervosa generally do not have a loss of appetite; they refuse to eat out of fear of gaining weight. Amenorrhea is also a diagnostic criterion in postmenarchal females delay of menarche may occur in premenarchal girls. In some cases, amenorrhea precedes the development of anorexia nervosa; however, in most cases, it appears to be a consequence of starvation. Individuals with anorexia nervosa commonly exercise intensely to lose weight and alter body shape.
In the restricting type, the major methods of weight control are food restriction and exercise. The natural course of anorexia is not well understood, but many cases become chronic. Differential Diagnosis Conditions that can resemble anorexia should be ruled out. These include major depression with loss of appetite and weight, some psychotic disorders in which nutrition may not be adequate, body dysmorphic disorder, and a variety of general medical especially neuroendocrine conditions.
Anorexia nervosa is differentiated from bulimia nervosa by the presence of low weight in individuals with the former. When medical complications are present, these must be carefully treated and followed.
If ipecac use to induce vomiting is suspected, ipecac toxicity must be ruled out. During starvation, psychotherapy is of little value because of the cognitive impairment produced by starvation. When patients are less medically ill, a therapeutic program including supervised meals; weight and electrolyte monitoring; psychoeducation about the illness, starvation, and nutrition; individual psychotherapy, and family therapy can begin.
Psychopharmacology management often includes antidepressants, especially the selective serotonin reuptake inhibitors to treat comorbid depression. Psychopharmacologic treatments are used principally to treat any comorbid psychiatric illness and have little or no effect on the anorexia per se.
The male:female ratio is This illness occurs disproportionately among whites in the United States. Familial and genetic studies support similar familial linkages in both disorders. Psychological theories for bulimia nervosa stress an addiction or obsessive-compulsive behavioral model. Biologic, neurologic, and endocrine findings are less prominent in theories of causation of bulimia nervosa. Abnormal serotonin metabolism is thought to play more of a role in bulimia nervosa than in anorexia nervosa.
In addition, these are people whose self-evaluation is overly influenced by their body weight and shape. Food binges in bulimia nervosa may be precipitated by stress or altered mood states. Once a binge begins, the individual typically feels out of control and continues to eat large quantities of food, often to the point of physical discomfort.
Purging may follow and most often consists of vomiting, usually induced mechanically by stimulating the gag reflex or using ipecac. Other purging methods used to avoid weight gain include laxative and diuretic abuse and enemas. Individuals with bulimia often exercise and restrict their food intake. Bulimia nervosa is classified into two subtypes: nonpurging type or purging type Table according to whether purging behavior is present.
Differential Diagnosis Bulimia nervosa should be distinguished from the binge eating and purging subtype of anorexia nervosa. Binge eating can occur in major depression and in borderline personality disorder, but it is not tied to a compulsion to reduce weight. Marchlinski, David J. Jianguo Cheng, Richard W. Rosenquist, Eds. John C. Sun, Hylton V. Julia A. Drose — Fetal Echocardiography-W. Saunders Company Pdf Download. Kaplan-Pharmacology Pdf Download. Kenneth M. Shaw, Michael H.
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