1. B. The question describes the pharmacological profile of a high-potency classical antipsychotic agent, most likely of the butyrophenone or phenothiazine class. Thioridazine is a low-potency piperidine phe-nothiazine agent with significant affinity for a1-adrenergic and muscarinic receptors, having a high potential for sedation as a side effect. Haloperidol is a high-potency butyrophenone with its primary action at the D2 dopaminergic receptor, so it produces a significant incidence of extrapyramidal toxicity and little sedation. Clozapine is a low-potency atypical antipsychotic that binds primarily to D4, 5-HT2, and a1 receptors and possesses very little extrapyramidal toxicity but significant sedative and autonomic side effects. Flumazenil is a benzodi-azepine antagonist, and carbamazepine is an anti-convulsant; neither possesses significant antipsy-chotic properties.

2. D. This question concerns the most important extrapyramidal reaction to long-term antipsychotic administration—tardive dyskinesia—and its generally accepted basis. Although some tolerance to the sedative effects of antipsychotics can occur, there is no evidence linking this to tardive dyskinesia. Antipsychotic agents enhance dopamine synthesis acutely by blocking D2-autoreceptors by which the transmitter normally inhibits dopamine cell firing and synthesis. Long-term treatment with a D2-receptor antagonist causes depolarization inactivation of dopamine neurons with diminished transmitter production and release. However, a decrease in dopamine synthesis has not been linked with tardive dyskinesia. On the contrary, lower dopamine tone would more resemble a parkinsonian state, whereas in tardive dyskinesia, antidopaminergic drugs tend to suppress the dyskinetic symptoms, and dopaminergic agonists worsen the condition. Therefore, it is generally accepted that up-regulated dopamine receptors underlie tardive dyskinesia. There is no evidence that the antipsychotics lead to loss of striatal cholinergic neurons.

3. C. Tardive dyskinesia is an extrapyramidal reaction that occurs most commonly after long-term administration of high-potency butyrophenone, thioxan-thene, or phenothiazine. Thus, thiothixene is not a good choice. Chlorpromazine is a low-potency phe-nothiazine agent with moderate potential to cause extrapyramidal signs. Clozapine is well known to have the lowest potential for producing tardive dyskinesia during chronic therapy. It has other undesirable side effects, but clinical experience with other newer atypical antipsychotics is not sufficient to establish their potential for causing this disorder. Imipramine and fluoxetine are antidepressants.

4. A. The question concerns actions of antipsychotic agents that may have untoward consequences when combined with other coincident or preexisting medical conditions. These drugs have an activating effect on the EEG in epileptic patients and thus may worsen that condition. Generally, the antipsychotics have antiemetic properties but generally are more potent than is necessary to treat motion sickness. The other three conditions listed—C, D, and E—are indications for the use of antipsychotic agents.

5. E. The question concerns the emergence of parkin-sonian signs relatively early in a patient's therapy for schizophrenia and their elimination by switching treatment to a second agent, thioridazine. Haloperidol has high affinity for D2-dopaminergic receptors and is well known to have a high potential for causing these kinds of extrapyramidal signs. The drug has no direct action on GABAergic neurons and does not act presynaptically to affect dopamine release. While thioridazine binds to D2-

dopaminergic receptors with an affinity similar to that of haloperidol, it also has much greater an-timuscarinic activity. This latter action can compensate for dopamine receptor blockade in the nigro-striatal tract, so that extrapyramidal function is more appropriately maintained. Thioridazine has greater ^-adrenergic blocking activity than haloperidol, but this is not thought to play a role in elimination of the parkinsonian signs.

6. D. The neuroleptic malignant syndrome is an infrequent extrapyramidal reaction with a relatively high rate of lethality. It is marked by muscle rigidity, high fever, and autonomic instability. It may result from too-rapid block of dopaminergic receptors in individuals who are highly sensitive to the extrapyramidal effects of antipsychotic drugs. Management consists of control of fever, use of muscle relaxants, and administration of the dopamine agonist bromocrip-tine, which is likely to worsen the psychotic symptoms. Choices A to C are antipsychotics and would likely worsen neuroleptic malignant syndrome. Valproic acid has antimanic, antimigraine, and anti-convulsant properties, but it is not used to treat the syndrome in question.

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