Alprazolam-neuroleptic combination in schizophrenia.
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Biomedical subjects
Publications and source records attributed to J F Lipinski.
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Six patients with akathisia were treated with clonidine in an open, on-drug/off-drug trial. All six patients demonstrated substantial improvement of their akathisia, with four of the six obtaining complete remission. The dose of clonidine used to treat the remaining two patients was limited by the development of symptomatic hypotension. Daily doses ranged from 0.2 to 0.8 mg, and maximal response to a particular dose occurred within 24 to 48 hours. Although no effects on lithium tremor, parkinsonism, or tardive dyskinesia were observed, two bipolar patients exhibited considerable improvement in their manic and psychotic symptoms during treatment with clonidine.
Metoprolol was compared to propranolol in the treatment of neuroleptic-induced akathisia by means of an on-drug/off-drug crossover study. Both beta-blockers were effective, but the usefulness of metoprolol was limited by side effects due to the high dose of this medication required to produce a therapeutic effect. The mechanism of action of beta-blockers in the treatment of akathisia is discussed in light of the different pharmacologic properties of metoprolol and propranolol. The study results suggest that these agents are effective in reducing akathisia through a central mechanism of action requiring beta-2 blockade.
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The symptoms of three bipolar patients remitted after clonidine treatment. One patient presented with mixed bipolar disorder, two were manic, and all were psychotic. One patient's akathisia also appeared to respond to clonidine. Clonidine's thymoleptic effect paralleled resulting cardiovascular changes.
Fourteen patients with neuroleptic-induced akathisia were treated with propranolol in an open trial. All patients demonstrated substantial improvement of their akathisia; nine of the 14 obtained complete remission. Response was quite rapid, occurring within 24 hours in most cases. Doses required for improvement were low (30-80 mg/day), and side effects were few. Lithium-induced tremor improved considerably, but symptoms of parkinsonism and tardive dyskinesia showed little change. Preliminary results with certain other beta blockers suggest that they are less effective than propranolol in the treatment of akathisia.
Nine depressed inpatients completed trials with S-adenosylmethionine. Seven showed improvement or remission of their symptoms. As in European studies, no side effects were seen except the apparent induction of mania in two patients with bipolar disorder.
Four patients with akathisia as a result of neuroleptic administration were treated with amantadine. Although substantial improvement occurred initially, all four patients developed tolerance to this therapeutic effect within 1 week. An increase in dosage also had only a transient effect. The rapid development of tolerance significantly limits the usefulness of amantadine in the treatment of akathisia. One patient who suffered from akathisia and drug-induced parkinsonism experienced significant attenuation of both movement disorders in response to treatment with amantadine. Although she became tolerant to the effect of amantadine on her akathisia within the first week of treatment, her parkinsonism did not recur. The possibility that these two neuroleptic-induced extrapyramidal syndromes are pharmacologically separable is discussed.
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Dexamethasone suppression tests were given to 69 consecutively admitted psychiatric patients. Nonsuppression rates for depression with or without melancholia and for schizophrenia were similar to those previously reported, but for mania and other psychoses the frequencies were higher than expected.
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The first-degree relatives (N = 199) of DSM-III schizophrenic probands (N = 39) were diagnosed from chart data by a rater who was blind to proband diagnosis. No cases of even "possible" schizophrenia were found. This augments the growing evidence that the genetic component in schizophrenia may be less than was formerly suspected.
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The authors report double-blind, placebo-controlled trials of pure lecithin in the treatment of mania. As in preliminary trials, lecithin appeared to be nontoxic and effective. Improvement with lecithin was significantly greater than improvement with placebo in five of the six patients studied. The concurrent use of anticholinergic agents did not prevent the antimanic effect of lecithin. The authors discuss the possible mechanism of action of lecithin, including cholinergic and membrane-altering effects.
The CT scans of 11 schizophrenics and 26 controls were evaluated for both linear (Evan's and cella media ratios) and volume (planimetry and grid ratios) measurements of ventricular size. There were no differences between the two groups on any of the measures obtained. These results are discussed in relation to previous reports showing ventricular enlargement in schizophrenics. The relatively younger age and briefer period of hospitalization in this present sample are suggested as variables possibly associated with these findings.
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