Chris Heh

High potency neuroleptics and violence in schizophrenics

In a controlled study, inpatient violence was measured during placebo, high-potency (haloperidol) and low-potency (chlorpromazine or clozapine) neuroleptics. Some patients had a marked increase in violent behavior with the moderately high-dose haloperidol, but not with low-potency neuroleptics. The authors discuss reasons for the increased violence with haloperidol, including akathisia and drug-induced behavioral toxicity.

Neuroleptic-induced hypothermia associated with amelioration of psychosis in schizophrenia

Body temperature is a regulatory function of the hypothalamus. Recently, DeMet et al. (Society for Neuroscience Abstracts Vol 12, 1986) reported that apomorphine stimulation of dopamine autoreceptors caused a significant decrease in metabolic rate in the posterior heat-conserving area of the hypothalamus. The logical hypothesis to follow is that apomorphine administration should induce a decrement in body temperature; this in fact was demonstrated by Cutler et al. (Commun Psychopharmacol 3:375-382, 1979) in humans. It is well known that neuroleptics also disrupt thermoregulation (Clark: Neurosci Biobehav Rev 3:179-231, 1979) and affect dopamine autoreceptors. Therefore, eight chronic treatment-resistant schizophrenics underwent a 6-week single-blind trial of haloperidol and then a subsequent 6-week double-blind trial of clozapine. Both haloperidol and clozapine significantly lowered oral body temperatures relative to baseline washout temperatures. More interestingly, clozapine relative to haloperidol was found to induce a greater decrement in body temperature and was associated with greater clinical improvement. Possible confounding variables are discussed, as is the possible neurochemical basis for the amelioration of psychosis associated with hypothermia.

Subjective neuroleptic response and treatment outcome under open and double-blind conditions — A preliminary report

1. A patients early subjective response to a neuroleptic was recorded in 17 schizophrenic patients following a fixed dose of neuroleptic under both open and double-blind placebo-controlled conditions. 2. High correlations were found between a patients subjective response at 2.5, 24 and 48 hours after the initial dose, suggesting that the timing of the initial subjective response rating is not critical. 3. The relationship between the psychiatric improvement and subjective response was not significant under double-blind conditions (r = 0.004), while the relationship under the open condition showed a trend towards significance comparable to earlier reports (r = 0.32). 4. The findings question the usefulness of applying early subjective response to a neuroleptic to predict clinical improvement.

Serum homovanillic acid concentrations in carbamazepine-treated chronic schizophrenics

Carbamazepine (CBZ) is clinically efficacious for the treatment of acute mania (Ballenger and Post 1980)) schizoaffective and schizophreniform disorders (Placidi et al. 1986), and excited psychotic states, including violent and aggressive schizophrenic patients (Hakola and Laulumaa 1982; Klein et al. 1984). However, there have been no well-controlled studies investigating the clinical efficacy of CBZ as the sole antipsychotic for the treatment of chronic schizophrenia. We report a preliminary, singleblind, 4-week trial of carbamazepine in a group of nonviolent chronic schizophrenic patients. In addition to the performance of routine clinical ratings, serum homovanillic acid (HVA) concentrations were measured to examine the presynaptic dopaminergic effects of CBZ.

Predicting the Posttreatment Depressive State of an Alcoholic Patient

Seventy-eight patients admitted to an alcohol treatment program were studied to identify variables capable of forecasting a patients posttreatment depressive state. Factor analysis reduced a large number of items to 12 factors. Pearson correlations showed that Factor VII--Physical and Neurological Complaints and the pretreatment depressive state were both significantly (p = .002) correlated to the posttreatment depressive state. Multiple regression yielded a significant equation (p = .001) confirming that an alcoholic patient who has a high level of pretreatment depression and physical/neurological complaints, and who exhibits little or no irritability or agitation will tend to sustain a high level of posttreatment depression.