[The diagnosis of cerebral contusion in head-injured children: results of a systematic clinical and -EG-follow-up study (author's transl)].
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Biomedical subjects
Publications and source records attributed to J Gerlach.
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Twenty patients with paralysis agitans took part in a double-blind, cross-over investigation of CB 154 (2-bromo-alpha-ergocryptine) and Madopar (L-Dopa + benserazid (a peripheral decarboxylase inhibitor), dose ratio 4:1). Each treatment phase lasted for 8 weeks. Modapar was found to be significantly superior to CB 154 in the treatment of the Parkinson state as a whole (Webster total score) and the individual symptoms of hypokinesia, rigidity and tremor. Compared with pretreatment score, CB 154 had a weak, but significant effect on tremor, but not on the Webster total score, hypokinesia and rigidity. The effect of CB 154, however, varied: four patients preferred CB 154 to Madopar on account of its satisfactory therapeutic effect and fewer side-effects ("on-off" phenomena, hyperkinesia, psychiatric complications); other patients showed neither therapeutic effect nor side-effects of CB 154, which in some cases may be related to too low a dose-level of CB 154 (median 30 mg daily, range 20-60 mg). In the four cases first mentioned which showed a good effect of CB 154, the ratio between the dose of CB 154 and the dose of L-Dopa (in Madopar) was 3.5-10 mg/100 mg, i.e. in certain cases it must be assumed that the maximum dose of CB 154 lies around 120 mg daily.
24 hospitalized psychiatric patients with neuroleptic-induced tardive dyskinesia were treated with alpha-methyl-para-tyrosine (AMPT), 4 g daily for 3 days, and biperiden, 12 mg daily for 3 weeks. The results were evaluated blindly by means of videotape technique. The frequency of tardive dyskinesia was significantly reduced by AMPT and significantly increased by biperiden. The amplitude was reduced by AMPT in ten cases, unchanged in 12 cases and increased in two cases. Biperiden significantly increased the amplitude. The duration of each separate tongue protrusion and/or mouth opening was significantly increased by AMPT and reduced or unchanged by biperiden. It is concluded that a reduced dopaminergic activity (pharmacological or organic) may constitute the primary pathogenetic background for tardive dyskinesia, but that dopaminergic hypersensitivity and/or cholinergic hypofunction is necessary before the hyperkinetic element of the movement disturbances can minifest itself.
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Thirteen out of 18 young out-patients with simple schizophrenia under neuroleptic treatment completed a double-blind cross-over trial with Madopar [L-Dopa + benserazid (a peripheral decarboxylase inhibitor)] and placebo. Nine patients were given 900 mg L-Dopa + 225 mg benserazid daily, 1 patient received 600 mg L-Dopa + 150 mg benserazid, and 3 patients, 300 mg L-Dopa + 75 mg benserazid. In these doses, L-Dopa was effective against emotional withdrawal, blunted affect, tendency to isolation and apathy, without inducing or aggravating productive, accessory symptoms. The activity score, according to the specific activity-withdrawal scale, was significantly increased (P less than 0.05), whereas the total BPRS score (Brief Psychiatric Rating Scale) was slightly, but significantly reduced (P less than 0.05). In cases where L-Dopa had to be limited to 600 and 300 mg daily, a tendency to anxiety, distortion of thinking, and a sense of unreality were observed, depending on the dose of L-Dopa. In no case were gastrointestinal, cardiovascular or neurological side-effects observed.
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8 male schizophrenic patients participated in a double-blind, cross over study of the extrapyramidal side-effects of haloperidol and clozapine (acute dystonis, Parkinsonism and tardive dyskinesia), together with their effect on homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) in the cerebrospinal fluid (CSF). Haloperidol (9 mg/day) caused Parkinsonism, reduced tardive dyskinesias and increased the HVA concentration in the CSF. Clozapine (225 mg/day) had no effect on the neurological phenomena but reduced HVA and 5-HIAA concentrations in the CSF. During the discontinuation phase following the administration of haloperidol, tardive dyskinesia occurred or was aggravated; this did not occur after administration of clozapine. Accordingly, it is suggested that clozapine does not induce dopaminergic hypersensibility and, therefore, will not induce tardive dyskinesias.
By means of a four colour device for measuring continuous reaction sequences the mental blockings of brain damaged patients in comparison with patients suffering from skin disease were determined. Differences due to age were also investigated. The analysis of frequency distribution of reaction times (dissection method according to Daeves and Beckel) yielded the following results: a) Brain damaged patients show a higher percentage of blockings (23%) than patients suffering from skin-disease (10%). "Normal" reaction times as well as "blockings" are not prolonged significantly. b) Older patients show prolonged normal reaction times and prolonged blockings without increase in the percentage of blockings. c) Patients with left hemisphere lesions show longer normal reaction times than those who undergo right hemisphere operations. The results are discussed with regard to their significance for theory and practice (road accidents).
15 hospitalized patients suffering from neuroleptic-induced tardive dyskinesias participated in a double-blind cross-over study of lithium sulphate and placebo. Each drug was given for 3 weeks. The results were evaluated by means of the video-tape technique. Lithium sulphate induced a slight, but significant reduction in the tardive dyskinesia. Lithium had, in addition, a suppressive effect on psychomotor agitation and aggression. The concentrations of homovanillic acid and 5-hydroxyindoleacetic acid were determined in the cerebro-spinal fluid from five patients. It is concluded that lithium can be used with advantage in the treatment of tardive dyskinesia with only moderate intensity, particularly when the movement disturbances are accompanied by psychomotor restlessness. Finally, the effect of lithium on the central aminergic transmitter substances is discussed in relation to the existing hypotheses on the pathophysiology of tardive dyskinesia.
Fifty-six out of 60 schizophrenic patients completed a double-blind study of two long-acting neuroleptics, penfluridol (peroral) and flupenthixol decanoate (parenteral). Half of the patients were on maintenance therapy of flupenthixol prior to the study, the other half on penfluridol. The actual double-blind study (12 weeks) was commenced after a preliminary period of 4 weeks, the patients in the two main groups being randomly divided into two further groups, one continuing the medication unchanged, the other changing to the alternative drug. It was found possible to make a sudden switch from penfluridol to flupenthixol decanoate and vice versa without any significant change in the condition of the patient. The same dosage (in 70% of the patients from 40 to 80 mg) of penfluridol was used per week as was employed for flupenthixol decanoate per fortnight. Changes in the intensity of the symptoms (total Brief Psychiatric Rating Scale (BPRS) score) were moe pronounced in the preliminary period (during unchanged treatment) than on changed medication in the blind period. Both drugs induced approximately the same degree of akathisia, Parkinsonism and autonomic side effects. The practical consequences of equipotent therapeutical effect of a peroral and parenteral long-acting neuroleptic are briefly discussed.
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