Kaplan + Sadock's Synopsis of Psychiatry, 11e

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Chapter 29: Psychopharmacological Treatment

Table 29.2-3 Treatment of Neuroleptic Malignant Syndrome

Intervention

Dosing

Effectiveness

Amantadine

200 to 400 mg PO/day in divided doses

Beneficial as monotherapy or in combination; decrease in death rate Mortality reduced as a single or combined agent

Bromocriptine

2.5 mg PO bid or tid, may increase to a total of 45 mg/day

Levodopa/carbidopa Electroconvulsive therapy

Levodopa 50 to 100 mg/day IV as continuous infusion Case reports of dramatic improvement

Reports of good outcome with both unilateral and bilateral treatments; response may occur in as few as three treatments 1 mg/kg/day for 8 days, then continue as PO for 7 additional days 1 to 2 mg IM as test dose; if effective, switch to PO; consider use if underlying disorder has catatonic symptoms IV hydration, cooling blankets, ice packs, ice-water enema, oxygenation, antipyretics

Effective when medications have failed; also may treat underlying psychiatric disorder

Dantrolene

Benefits may occur in minutes or hours as a single agent or in combination Has been reported effective when other agents have failed

Benzodiazepines

Supportive measures

Often effective as initial approach early in the episode

PO, orally; bid, twice a day; tid, three times a day; IV, intravenously; IM, intramuscularly. (Adapted from Davis JM, Caroif SN, Mann SC. Treatment of neuroleptic malignant syndrome. Psychiatr Ann. 2000;30:325–331, with permission.)

Medication-Induced Acute Akathisia Diagnosis, Signs, and Symptoms Akathisia is subjective feelings of restlessness, objective signs of restlessness, or both. Examples include a sense of anxiety, inability to relax, jitteriness, pacing, rocking motions while sitting, and rapid alternation of sitting and standing. Akathisia has been associated with the use of a wide range of psychiatric drugs, including antipsychotics, antidepressants, and sympatho- mimetics. Once akathisia is recognized and diagnosed, the anti- psychotic dose should be reduced to the minimal effective level. Akathisia may be associated with a poor treatment outcome. Epidemiology Middle-aged women are at increased risk of akathisia, and the time course is similar to that for neuroleptic-induced parkinsonism. Treatment Three basic steps in the treatment of akathisia are reducing med- ication dosage, attempting treatment with appropriate drugs, and considering changing the neuroleptic. The most efficacious drugs are b -adrenergic receptor antagonists, although anticho- linergic drugs, benzodiazepines, and cyproheptadine (Periactin) may benefit some patients. In some cases of akathisia, no treat- ment seems to be effective.

neuroleptics. There is a higher incidence of acute dystonia in men, in patients younger than age 30 years, and in patients given high dosages of high-potency medications.

Etiology Although it is most common with intramuscular doses of high- potency antipsychotics, dystonia can occur with any antipsy- chotic. The mechanism of action is thought to be dopaminergic hyperactivity in the basal ganglia that occurs when central ner- vous system (CNS) levels of the antipsychotic drug begin to fall between doses. Differential Diagnosis The differential diagnosis includes seizures and tardive dyskinesia. Course and Prognosis Dystonia can fluctuate spontaneously and respond to reassur- ance, so the clinician gets the false impression that the move- ment is hysterical or completely under conscious control. Treatment Prophylaxis with anticholinergics or related drugs (outlined in Table 29.2-2) usually prevents dystonia, although the risks of prophylactic treatment weigh against that benefit. Treatment with intramuscular anticholinergics or intravenous or intra- muscular diphenhydramine (Benadryl) (50 mg) almost always relieves the symptoms. Diazepam (Valium) (10 mg intrave- nously), amobarbital (Amytal), caffeine sodium benzoate, and hypnosis have also been reported to be effective. Although tol- erance for the adverse effects usually develops, it is prudent to change the antipsychotic if the patient is particularly concerned that the reaction may recur.

Tardive Dyskinesia Diagnosis, Signs, and Symptoms

Tardive dyskinesia is a delayed effect of antipsychotics; it rarely occurs until after 6 months of treatment. The disorder consists of abnormal, involuntary, irregular choreoathetoid movements of the muscles of the head, limbs, and trunk. The severity of the movements ranges from minimal—often missed by patients and their families—to grossly incapacitating. Perioral movements