Fluoxetine for the prolonged treatment of schizophreniform psychosis.
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Biomedical subjects
Publications and source records attributed to R Wilbur.
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1. This paper proposes that the neuropsychiatric symptoms of tardive dyskinesia, akathisia and pseudoparkinsonian tremor are modulated by a noradrenergic pathway that projects from the locus coeruleus to the limbic system. 2. The proposed pathway is found to the consistent with neuroanatomical and neurochemical data in the literature. 3. The proposed pathway is found to be clinically consistent with observations by ourselves and others on the efficacy of clonidine and beta-adrenoreceptor blockers like propranolol for treating akathisia and pseudoparkinsonian tremor. It is also consistent with reports by ourselves and others that some patients with tardive dyskinesia benefit from treatment with propranolol or clonidine. 4. Noradrenergic modulation of the limbic system by way of the locus coeruleus accounts for a number of clinical observations, such as the worsening of tardive dyskinesia by stress, the greater risk for tardive dyskinesia in patients with affective disorder, the time-of-onset of tardive dyskinesia, and the coexistence of tardive dyskinesia and pseudoparkinsonism. 5. The functional significance of beta-adrenoreceptors in the basal ganglia is considered from an evolutionary perspective. 6. The model proposed in this article appears to have considerable heuristic value because it may further our understanding of Gilles de la Tourette syndrome and attention deficit disorder (hyperkinesis).
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Sixty-three children with ALL in CCR and treated according to a standard therapy protocol were immunized with the 14-valent pneumococcal vaccine. Forty-six children were vaccinated 1, 3, or 6 months following initial induction remission; 15 were vaccinated 4-6 weeks following successful completion of 30 months of antileukemia therapy; and two were vaccinated at the time of diagnosis. Response to the vaccine was suboptimal and by the 6-month follow-up there were only two serotypes for which more than half the patients tested had greater than or equal to 300 ng antibodies N/ml.
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This case report describes a schizophrenic patient who developed akathisia and tremor following neuroleptic pharmacotherapy with fluphenazine decanoate. The patient also suffered from familial (benign essential) tremor. The patient's neuroleptic-induced extrapyramidal side effects were not relieved by anticholinergic antiparkinson drugs or by phenobarbital. The patient was started on propranolol 10 mg b.i.d. She was also started on diazepam 5 mg t.i.d. for anxiety. The diazepam dose was held constant and propranolol was gradually increased to 40 mg q.i.d. The patient's extrapyramidal symptomatology gradually resolved over the course of one month, during which time the propranolol dose was being steadily increased. Propranolol also effectively controlled her familial tremor. After nine months as an outpatient, during which time the patient was neuroleptic-free, she developed psychotic decompensation for which she was treated with thiothixene. Akathisia or tremor did not develop, possibly because the patient was taking propranolol simultaneously. Propranolol may be useful for treating neuroleptic-induced akathisia. This requires systematic investigation with open and controlled trials.
A patient developed severe anxiety, moodswing, depression, and thinking disorder 24 hours after abruptly stopping oxazepam, of which he had taken 30 mg 3 times a day for two months, for anxiety and panic attacks. Oxazepam was restarted and tapered off gradually; nevertheless, a relatively severe abstinence syndrome occurred. Muscular fasciculations and moodswing were very marked. The patient also experienced significant anxiety, depression, moodswing, and muscular fasciculations for two months after detoxication from oxazepam. Subsequently, the patient's panic attacks were treated successfully with propranolol hydrochloride. This report concludes with a brief review of the literature on benzodiazepine withdrawal.
1. This report describes two cases of psychotic syndrome from benztropine (Cogentin), which was used to treat haloperidol-induced extrapyramidal side effects. The patients' symptomatology meets DSM III criteria for delirium. Both patients displayed repetitive motor automatisms (stereotypy). 2. Symptomatology appeared one-to-two days after the start of benztropine 2 mg b.i.d. and subsided one-to-several days after benztropine was stopped. Treatment consisted of administration of sedative hypnotic drugs. 3. The literature on anticholinergic-induced psychotic syndromes is surveyed. Particular attention is drawn to the occurrence of stereotypy. 4. It is proposed, on the basis of a review of animal and clinical data, that stereotypies in delirious patients are related to muscarinic blockade in the central nervous system. This model is used to explain repetitive motor automatisms which are seen in Alzheimer's disease. 5. The paper concludes with brief guidelines for the management of anticholinergic delirium.
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The evidence for the efficacy of anticonvulsant drugs in the control of seizures during alcohol withdrawal is examined. The literature on the use of anticonvulsants to control anxiety, irritability, tension, and other symptoms of abstinence syndrome is reviewed. The data on benzodiazepines, phenobarbital, hydroxyzine, and neuroleptics are discussed briefly. There is no evidence to support the routine use of phenytoin for seizure prophylaxis in detoxication. However, phenytoin may be valuable in patients at a high risk for seizures, such as skid-row alcoholics. Only one retrospective study has been done on primidone; it claimed primidone was an efficacious adjuvant. Carbamazepine and valproic acid may be useful in the treatment of anxiety, dysphoric mood, somatization, and other symptoms of abstinence syndrome, as well as for seizure prophylaxis. The benzodiazepines, diazepam and chlordiazepoxide, are recognized as primary therapeutic agents in the detoxication of alcoholic patients. The major difficulty with the use of phenobarbital is that it cannot be used over as wide a range as the benzodiazepines. Hydroxyzine has been shown to be inferior to chlorazepate dipotassium. Most neuroleptics appear to be inappropriate for detoxication because they lower the seizure threshold; however, haloperidol has been found efficacious in acutely abstinent alcoholics. Carbamazepine, valproic acid, primidone, and phenobarbital should be tested against standard drugs such as chlordiazepoxide and diazepam in the detoxication of alcoholic patients.
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