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Biomedical subjects

J Volavka

Publications and source records attributed to J Volavka.

At least 55 records · Page 3Linked to original sources
PubMed1994

Does the change of psychopathology during the placebo period predict the response to subsequent treatment with active medication.

We examined whether deterioration in psychiatric symptoms during the placebo period predicted short-term response to subsequent treatment. Acutely exacerbated chronic schizophrenic or schizoaffective patients (n = 123) received placebo for 6.2 days on average. Afterwards, fixed haloperidol plasma levels were maintained for 6 weeks. Psychopathology was evaluated on the basis of the Brief Psychiatric Rating Scale (BPRS), which was administered weekly by trained raters. The global BPRS score at the beginning of the active treatment accounted for 11% of the end-point variance of the global BPRS score (p < 0.0002) and the change of psychopathology during the preceding placebo period explained additional 3.1% (p < 0.053) of it. The change in most of the BPRS factor scores contributed significantly to the prediction of the end-point BPRS score. The patients who had low scores on admission to the study and high scores at the end of the placebo period showed the greatest improvement. The results suggest that in addition to the baseline severity of psychopathology, the change of psychopathology that occurs during the pretreatment placebo period can partially account for treatment response.

Adult↗
PubMed1994

BMY 14802, a sigma receptor ligand for the treatment of schizophrenia.

The theoretical role of sigma receptors in psychosis has led to the development of selective sigma receptor ligands as potential antipsychotic agents. BMY 14802 has its most potent binding at the sigma binding site, with some degree of serotonin subtype 1A and negligible dopamine receptor binding. It is atypical of standard neuroleptics in that it does not induce catalepsy in rats. It has been shown to have efficacy in animal models of psychosis. It was hypothesized that the drug would have antipsychotic effects in humans without producing the extrapyramidal side effects typical of standard neuroleptics. We report here the results of an uncontrolled, multicenter safety and efficacy study of patients with acute exacerbations of schizophrenia treated with BMY 14802. After 1 week of single-blind placebo treatment, 28 patients were treated with BMY 14802 (up to 3000 mg/day) for up to 4 weeks. There was no significant improvement in psychiatric symptoms, as measured by the total Brief Psychiatric Rating Scale scores or Clinical Global Improvement. There were no changes in involuntary movements, as measured by the Abnormal Involuntary Movement Scale, or in extrapyramidal symptoms as measured by the Simpson-Angus Scale.

Adult↗
PubMed1994

Effect of subtle neurological dysfunction on response to haloperidol treatment in schizophrenia.

OBJECTIVE: The primary purpose of this study was to assess whether an interaction between subtle neurological impairment and haloperidol plasma level affects treatment response and, if so, the impact on negative symptoms in particular. METHOD: Forty-three schizophrenic and two schizoaffective inpatients diagnosed according to Research Diagnostic Criteria were given, at the end of a 1-week placebo period, a baseline evaluation consisting of the Brief Psychiatric Rating Scale (BPRS), Scales for the Assessment of Positive and Negative Symptoms, Quantified Neurological Scale, and the Simpson-Angus Scale for extrapyramidal side effects. Subjects were randomly assigned to one of three haloperidol plasma ranges and treated for 6 weeks. At the end point the BPRS, Scales for the Assessment of Positive and Negative Symptoms, and Simpson-Angus Scale were readministered. Multiple linear regressions were used to assess the extent to which the interaction between neurological abnormality and haloperidol plasma level predicted the end-point symptoms once the baseline symptoms, neurological abnormality, and haloperidol plasma level were accounted for. RESULTS: Those patients with higher levels of overall abnormality on the Quantified Neurological Scale at baseline and with frontal dysfunction in particular, had, with increasing haloperidol plasma levels, more severe negative symptoms at end point. Neurological dysfunction was not related to end-point positive symptoms. The effect was specific to end-point negative symptoms and was independent of extrapyramidal side effects. CONCLUSIONS: If confirmed, these findings may indicate that relatively intact frontal function is needed for improvement in negative symptoms and that those patients with schizophrenia who have subtle neurological dysfunction should be treated with lower doses of neuroleptics.

Adult↗
PubMed1993

Long-term high-dose neuroleptic treatment: who gets it and why?

OBJECTIVE: High doses of neuroleptic medication are still administered to many patients, although many studies have shown the effectiveness of low-dose strategies. The purposes of the study were to determine whether and in what ways high-dose patients differed from patients on regular dosages and whether the higher dosages were more effective. METHODS: In a case-control study at two large state hospitals, 38 high-dose patients were compared with 29 regular-dose patients. RESULTS: The high-dose patients had a persistent course of illness, with severe chronic symptoms resulting in hospitalizations of much longer duration than those of the regular-dose patients. The high-dose patients evidenced more regressed functioning and were more violent. To control these behaviors, clinicians increased neuroleptic dosages. CONCLUSIONS: The high-dose patients represented a subgroup of chronic regressed and violent patients. Clinicians prescribed high dosages and continued to use them despite a lack of clear evidence that such treatment is effective.

Affective Disorders, Psychotic↗
PubMed1993

Pharmacoepidemiology of clozapine in 202 inpatients with schizophrenia.

OBJECTIVE: To evaluate clozapine in a field trial for hospitalized patients with treatment-resistant schizophrenia. METHOD: The setting consisted of a large, state-operated, public psychiatric system. The protocol called for the treating psychiatrist to provide symptom- and adverse-effect ratings at four times following the start of drug therapy. The outcome criteria included the Sandoz study outcome measure of symptom improvement as well as discharge status for one year of follow-up. To assess the validity of the ratings, several measures of internal consistency were determined. Clozapine therapy was started in 227 patients, and symptom data are available for 202. RESULTS: Overall, 33 percent (n = 66) of the patients were improved at the end of one year of treatment; 12 percent (n = 24) maintained symptom improvement at all three evaluation times. Modest, statistically significant improvement after 12 weeks compared with baseline Brief Psychiatric Rating Scale (BPRS) total scores was observed for the patients continuing medication (n = 152); the emergence of a previously unimproved group (n = 26) explains this modest improvement. However, in the analysis of all patients (n = 202), (including dropouts), there was no significant symptom improvement after 12 weeks. Lower baseline BPRS scores predicted significant symptom improvement after 12 weeks of treatment. Among those medicated for one year, the pattern of symptom improvement showed that the probability of late improvement was 0.26 for those previously unimproved, and the probability of a 12-week responder losing improvement was 0.23, resulting in a net group gain of 3 cases in 100. By the end of one year, 8 percent (n = 17) of the cohort was discharged, and 3 percent (n = 7) was transferred to another facility while continuing to receive clozapine. Of the 227 original patients started on clozapine therapy, medication was discontinued for adverse effects in 11 percent (n = 25): white blood cell count (WBC) decrease (but no agranulocytosis) in 5 percent (n = 12), seizures in 1 percent (n = 3), one patient with seizures and decreased WBC count, and other events (e.g., cardiovascular changes, fever, or possible neuroleptic malignant syndrome) in 4 percent (n = 9). Patient refusal was reported for 6 percent (n = 13) of those starting treatment. CONCLUSIONS: Although only 19 percent of the patients exhibited improvement at 6 weeks, the response rate at 12 weeks (29 percent) for this naturalistic study cohort was similar to that in the major, double-blind, six-week, controlled, clinical trial of clozapine. The impersistence of response as symptoms were followed for up to one year is a finding that deserves rigorous evaluation.

Adult↗
PubMed1993

Quantitative electroencephalogram examination of effects of risperidone in schizophrenic patients.

The objective of this study was twofold: (1) to describe the effects of risperidone on the quantitative electroencephalogram (EEG) in schizophrenic patients and (2) to explore the relationships between EEG changes and clinical improvement. The subjects were nine male schizophrenic patients participating in a placebo-controlled, double-blind clinical trial (duration, 9 weeks) aimed to assess the effects of risperidone. The EEG effects of risperidone were compared with those of haloperidol. Nine haloperidol patients were selected from a separate treatment study that had a similar design and selection criteria and used identical EEG methods. We found that risperidone treatment induced widespread changes in interhemispheric power asymmetry. Furthermore, overall clinical improvement was related to two EEG measures: (1) absolute power changes in the beta frequency band and (2) power asymmetry in the theta and delta bands. Both relationships were most expressed in the anterior areas. The first relationship could not be linked to any specific cluster of behavioral symptoms. The second relationship was linked to improvements of affective symptoms and hostility-suspiciousness. The relationships observed in the risperidone group could not be detected in the haloperidol-treated patients. We hypothesized that the first relationship is attributable to an interaction between the serotonergic and dopaminergic system; the second relationship was associated with serotonergic mechanisms.

Adolescent↗
PubMed1992

Haloperidol blood levels and clinical effects.

This study explored the relationships between plasma levels and the clinical effects of haloperidol in 176 acutely exacerbated schizophrenic or schizoaffective patients. After a single-blind placebo period of 1 week (period 1), they entered the double-blind period 2 randomly assigned to one of three plasma levels of haloperidol: low (2 to 13 ng/mL), medium (13.1 to 24 ng/mL), or high (24.1 to 35 ng/mL). Patients whose conditions did not improve in period 2 continued on one of the three haloperidol levels (period 3). Periods 2 and 3 lasted 6 weeks each. Only minor differences in clinical responses were noted among the three levels of haloperidol. These results imply that low or moderate doses of neuroleptics are appropriate for many acutely psychotic patients.

Acute Disease↗
PubMed1992

Level of haloperidol in plasma is related to electroencephalographic findings in patients who improve.

This study analyzed interrelationships among plasma level of haloperidol (HAL), electroencephalographic (EEG) changes, and clinical response in 37 acutely exacerbated schizophrenic patients after a 6-week period of treatment. Two hypotheses were tested: (1) EEG theta response to HAL depends on levels of HAL in plasma, and this relationship is expressed in patients showing a clear clinical response (responders). (2) Responders and nonresponders are characterized by a different neuroleptic EEG profile. EEG examinations (resting, waking EEG) were performed at study entry, end point of the placebo period ("baseline"), and weekly during the entire HAL treatment period. EEG response was measured by power spectral changes in four frequency bands (delta, theta, alpha, and beta); clinical response was assessed by the Brief Psychiatric Rating Scale. There was a significant relationship between HAL plasma levels and EEG theta activity for treatment responders, whereas no relationship was detected for the nonresponders. Furthermore, there were EEG changes (in the delta and alpha bands) that depended on clinical response but did not show any relationship, either in responders or nonresponders, to HAL plasma levels. These results supported both hypotheses.

Adult↗
PubMed1992

Brief pulse ECT in melancholia. EEG and clinical effects.

In a visual analysis of electroencephalograms (EEGs) obtained in 33 melancholic men before and after six brief pulse right unilateral, left unilateral, or bilateral electroconvulsive therapy (ECT) treatments, the authors were unable to detect the relation between therapeutic outcome and differential hemispheric lateralization of ECT-induced EEG slowing that had been reported previously for sine wave ECT at the same clinical site. These results may be related to differences in neurophysiologic effects between sine wave and brief pulse ECT, and do not support the hypothesis that lateralization of ECT-induced EEG slowing is central to the antidepressant effects of ECT.

Adult↗
PubMed1992

Assessment of risk behaviors for HIV infection among psychiatric inpatients.

A 13-item questionnaire was constructed to assess risk factors for HIV infection among 476 patients newly admitted over a one-year period to a state psychiatric hospital in New York City. Because psychopathology can affect patients' self-reports, the validity of the instrument was established by HIV antibody tests in a subset of 352 patients. Results of the questionnaire indicated that the 352 patients were almost equally divided between the high-risk and low-risk categories. HIV seroprevalence was .6 percent among the low-risk patients, but 14.4 percent among the high-risk patients. The findings suggest that a screening program to detect HIV-positive patients should be undertaken in this population, that it should be focused on the high-risk subgroup, and that the questionnaire can be used to define that subgroup. However, results of the study may not generalize to other geographic areas.

AIDS Serodiagnosis↗
PubMed1992

Psychobiology of the violent offender.

The antecedents of violent crime may include childhood victimization, head injuries, and alcohol and drug abuse. Neuropsychological and neuropsychiatric findings suggest temporal and frontal lobe dysfunctions in violent offenders; these dysfunctions appear to be more pronounced in the dominant hemisphere. Recent studies implicate disturbances of central serotonergic functions in impulsive homicide and arson. These results provide an adequate rationale for larger interdisciplinary studies using neurochemical, neuropsychiatric/neuropsychological, and psychosocial methods on the same subjects.

Alcohol Drinking↗
PubMed1991

Pretreatment EEG predicts short-term response to haloperidol treatment.

This study analyzed the relationship between pretreatment electroencephalogram (EEG) and response to haloperidol medication in a group of acutely exacerbated schizophrenic patients (n = 34). Improvement was assessed after 3 and 6 weeks of treatment; it was measured globally, as decrease in the total score on the Brief Psychiatric Rating Scale (BPRS), as well as multidimensionally through the individual BPRS factors. Relative powers from four clinical EEG frequency bands were employed as predictor variables. Baseline alpha activity was significantly related to clinical response. Higher alpha values were associated with poorer response to treatment. Specifically, improvements on the "thought disturbance" and "hostility-suspiciousness" factors underlied the relationship between the pretreatment EEG and outcome.

Adult↗
PubMed1991

Lateralized abnormality in the EEG of persistently violent psychiatric inpatients.

Twenty-one consecutive right-handed male psychiatric inpatients treated on a unit designed for the management of violent behavior were given computerized EEGs. We recorded their violent behaviors, the number of staff interventions needed to control their behavior, and their medications. The number of instances of violence as well as the number of staff interventions were related to increased delta band activity and to decreased alpha band activity in the temporal and the parietooccipital areas. These relationships were independent of the current medications and of the length of stay on the special unit. Furthermore, our results demonstrate that violence is very significantly related to the hemispheric asymmetry in EEG for the frontotemporal derivations. With increased levels of violence there was a greater level of delta power in the left compared with the right.

Adult↗