The business aspects of forensic psychiatry.
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Biomedical subjects
Publications and source records attributed to R P Granacher.
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Two hundred twenty-four outpatients with major depression entered a 6-week, five-center, double-blind trial of bupropion 300 mg/day and placebo. A total of 216 patients were included in the efficacy analysis. In the combined center analysis, greater efficacy for bupropion was found on one or more measures (Hamilton Rating Scale for Depression, Montgomery-Asberg Depression Rating Scale, and Clinical Global Impressions) at treatment Days 21, 28, 35, and 42. Bupropion was well tolerated; only four adverse events were reported at least 5% more often in the bupropion group than in the placebo group. Six bupropion patients versus 5 placebo patients discontinued treatment because of adverse events. This study extends earlier findings of efficacy for higher-dose treatment in an inpatient population to lower-dose treatment in an outpatient population.
Agitation in elderly patients is often caused by acute cerebral failure, more commonly called acute brain syndrome, delirium, or acute confusional state. Defects in cognition, sleep-waking cycles, and psychomotor behavior result. Careful history taking, physical examination, and laboratory testing may reveal a specific, reversible organic factor related to the acute brain syndrome. This article outlines the clues to recognizing agitation due to a cerebral failure and gives guidelines for workup and management.
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The author states that most psychiatrists should be able easily to recognize tardive dyskinesia. However, this disorder is a subset of a large variety of abnormal involuntary movements, some of which may resemble tardive dyskinesia. Others have serious implications if they are misdiagnosed as tardive dyskinesia. The author describes the characteristic features of a wide variety of abnormal involuntary movements, including parkinsonism, the dystonias, choreas and choreoathetosis, tremors, tics, stereotypies and mannerisms, oral-facial dyskinesias, and disorders with varied or complex manifestations. He emphasizes the differential diagnosis of tardive dyskinesia.
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1. The therapeutic efficacy of papaverine for tardive dyskinesia was tested in 23 psychogeriatric and 18 chronic schizophrenic patients. Papaverine was given in slow-release capsules at 150 mg BID for one week followed by 300 mg BID for five weeks. A single blind design was used with blind raters and a 6-week no drug control condition. 2. Oro-facial dyskinesia was significantly reduced by papaverine in the psychogeriatric group during the first six weeks. Only a few patients showed at least 50% improvement of dyskinesia scores. Overall the drug effects were modest. 3. Other findings of interest were a) EEG showed increased per cent time of alpha and reduced beta 1. b) Parkinsonian side effects tended to confirm dopamine antagonism by papaverine. c) No tolerance was seen after six weeks. d) Elderly female patients and those with oro-facial dyskinesia appeared to respond best to papaverine.
The movement disorder may appear after prolonged use of antipsychotic agents. Differential diagnosis includes hereditary, infectious, toxic and drug-induced causes of extrapyramidal dysfunction. Pathophysiology appears to be related to induced changes in dopamine neuronal function and may represent irreversible extrapyramidal synaptic modification. Treatment includes removing the offending agent when possible or using the lowest effective dose if the medication cannot be totally discontinued. Indiscriminate use of antipsychotic agents in nonpsychotic patients should be avoided.
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A typical case of autoerythrocyte sensitization or the Gardner-Diamond syndrome was reviewed with respect to personality factors, hypnotic influence in general, the effect of controlled hypnosis under two variable conditions, and the measurement of certain psychophysiologic responses before and following hypnosis. In this case it was not possible to delineate a clear psychiatric syndrome and hypnotic suggestion induced the classical lesion only during the active phase of the disease. When the lesions were absent or quiescent, no changes in various psychophysiologic measurements taken were observed.
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Medication with anticholinergic properties are used commonly in family practice. Toxic delirium, which may resemble an acute psychosis, can occur as an adverse drug reaction to properly prescribed anticholingeric medication and to recommended doses of many patent medicines. More frequently it is due to overdosage. The key to diagnosis is the presence of peripheral signs of parasympathetic blockade. Delirium induced by anticholinergic drugs can be treated rapidly and effectively with physostigmine salicylate.
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We reviewed the use of physostigmine in the diagnosis and management of acute toxic psychosis due to drugs with anticholinergic properties. The syndrome of agitation and toxic confusional psychosis associated with peripheral signs of cholinergic blockade is produced by several plant toxins, antispasmodics, ophthalmic preparations, and certain proprietary sedatives, as well as antiparkinson medications, antidepressants, and some antipsychotic drugs. Physostigmine, uniquely among the available reversible anticholinesterase agents, can pass the blood-brain barrier to exert central as well as peripheral cholinomimetic actions to reverse this syndrome. Psychiatrists should make more use of this safe, specific, rapid, and effective treatment for anticholinergic drug toxicity, and should particularly be alert to reversible anticholinergic brain syndromes associated with antidepressants and antiparkinson medications, and even with antipsychotic medications.