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Biomedical subjects

A M Wagman

Publications and source records attributed to A M Wagman.

At least 19 recordsLinked to original sources
PubMed1992

Report of a workshop on issues in brain tissue acquisition.

In the recent past the National Institute of Mental Health (NIMH) has been interested in developing a research initiative to stimulate human brain research on the biological characteristics of schizophrenic brain tissue. The Schizophrenia Research Branch of the Division of Clinical Research of NIMH sponsored a workshop to study the issues of impediments to research on human brain tissue and develop recommendations for solving some of these problems. This article is the first implementation of one of these recommendations, that is, to provide information to the scientific community that brain tissue donations are important and that appropriate means must be taken in order for a donation to proceed.

Brain↗
PubMed1991

Reduction of perseverative errors in patients with schizophrenia using monetary feedback.

The influence of monetary feedback on Wisconsin Card Sort Test (WCST) performance of 14 male schizophrenics was investigated. Patients were administered the test under standard instructions and with monetary feedback in counterbalanced order. Monetary reinforcement reduced perseverative errors and increased correct responses (p less than .05). These findings suggest that the WCST perseverative errors of schizophrenics reflect motivational as well as cognitive factors.

Adult↗
PubMed1991

Commentary: the acquisition and use of human brain tissue in neuropsychiatric research.

Witelson and McCulloch (1991) report on the establishment of a collection of normal human brain tissue that was secured through a unique method of premortem and postmortem assessments. Their work highlights the growing need in neuro-scientific research for carefully characterized collections of human brain tissue from both normal control subjects and patients with specific neuropsychiatric disorders. Brain tissue of this type, however, has not been readily available. Patients with mental disorders may not be competent to consent to a postmortem brain donation; other obstacles include various socioeconomic and legal impediments to autopsies. In addition, a number of methodologic issues exist regarding human brain tissue collections, including the problem of standardized postmortem diagnostic assessment and difficulty in establishing uniform procedures for processing formalin-fixed and frozen tissue. Various proposals to enhance brain-tissue collections are discussed. These include the establishment of networks for tissue donation and use, the linking of ultimate postmortem brain tissue collection to prospective clinical studies, and promulgation of standardized procedures for methods of postmortem diagnosis and tissue handling.

Adult↗
PubMed1990

Sleep polygraphy in schizophrenia: methodological issues.

The findings of sleep studies in schizophrenia have remained inconsistent in the literature as exemplified by the recent controversy regarding reduced rapid eye movements (REM) latency in these patients. These inconsistencies can partly be explained by major methodological shortcomings in studies evaluating sleep in schizophrenia. Lack of standardized scoring and diagnostic methods in the earlier studies and more recently, the effect of neuroleptic treatment or its withdrawal, have confounded the sleep results. Data are presented to illustrate the effect of the presence of tardive dyskinesia or active psychotic symptoms that further skew the sleep polygraphic measurements in these patients. Studies in drug-naive patients can circumvent some of these confounds but then these studies are weakened by sampling bias. Available data suggest that previous duration of neuroleptic treatment, duration of neuroleptic withdrawal, presence of tardive dyskinesia, and severity of psychotic symptoms should be considered when interpreting REM sleep measures in schizophrenic patients.

Antipsychotic Agents↗
PubMed1989

Alterations in sleep polygraphy after neuroleptic withdrawal: a putative supersensitive dopaminergic mechanism.

Although a number of studies have reported sleep disturbances following neuroleptic withdrawal, a full description of such changes in sleep architecture is not available. Polysomnographic, plasma prolactin, and clinical measurements were carried out in a small number of patients on chronic neuroleptic treatment and after drug withdrawal. Preliminary findings show that in these chronically treated schizophrenic patients with and without tardive dyskinesia (TD), abrupt neuroleptic withdrawal induces reductions in total sleep, rapid eye movement (REM) sleep, and plasma prolactin. Furthermore, an increase in delta sleep was observed only in patients without TD. The REM suppression occurred significantly earlier in TD patients compared to the non-TD schizophrenic patients. These changes were transient, and both sleep measures and plasma prolactin stabilized during the 2-4 weeks after withdrawal to levels somewhere between the values observed during chronic treatment and withdrawal (week 1) periods. As the withdrawal-induced exaggerated changes mimicked the dopamine agonist effect on these sleep and hormonal measures, one can hypothesize that the observed changes are due to unmasking of supersensitive dopamine receptors following drug cessation. Normalization of these receptors and/or adaptational changes in other nondopaminergic system(s) can hypothetically explain the eventual stabilization of these measures during the following weeks.

Adult↗
PubMed1988

The embedded set procedure. Comment on Galbraith, MacCrimmon, and Steffy.

The reaction-time crossover phenomenon discovered by Rodnick and Shakow has come to be studied mainly with the embedded isotemporal sets procedure and indexed by the difference in reaction time to regular and irregular trials at a 7-second preparatory interval (PI). A 1983 report in this journal by Galbraith et al. (J Nerv Ment Dis 171:670-675) demonstrated that the magnitude of crossover at this PI was influenced by the duration of the preparatory interval immediately prior (PPI) to the first trial of the 7-second isotemporal blocks. Secondary analyses reported here extend the examination of PPI influences and indicate: a) that the crossover phenomenon as assessed in the embedded sets procedure is due mainly to the very slow reaction time to the first trial of the 1-second isotemporal blocks; and b) that crossover in this paradigm is partially due to uncontrolled PPI influences across the 1-, 3-, and 7-second embedded blocks. These are further reasons for returning to the original Rodnick-Shakow method as Galbraith et al. recommended.

Attention↗
PubMed1988

Deficit and nondeficit forms of schizophrenia: the concept.

The authors provide a rationale for distinguishing the primary, enduring negative symptoms of schizophrenia (termed "deficit symptoms") from the more transient negative symptoms secondary to other factors. They argue that the former are more likely to provide a basis for meaningful subtyping of the schizophrenic syndrome, while the latter are more likely to respond to currently available treatments. They describe their experience in using clinical judgment based on longitudinal observations to identify deficit and nondeficit subtypes of schizophrenic patients and propose criteria for defining schizophrenia with the deficit syndrome.

Adult↗
PubMed1987

Deficit and nondeficit forms of schizophrenia: neuropsychological evaluation.

The neuropsychological function of 15 deficit and 15 matched nondeficit syndrome schizophrenics was compared to that of 15 age- and sex-matched normal subjects. Both schizophrenic groups performed poorly on the Psychomotor factor compared to the normals. Only the deficit group performed more poorly on the General Performance factor. The results were not associated with severity of either positive or negative symptoms at the time of testing. These findings support the usefulness of the deficit syndrome distinction in contradistinction to the cross-sectional positive and negative symptom dichotomy.

Adolescent↗
PubMed1986

Neuronal cholecystokinin and schizophrenia: pathogenic and therapeutic studies.

Neuroleptic-free schizophrenic patients received caerulein, a potent analogue of cholecystokinin octapeptide, in a fixed- and rising-dose schedule. In addition, neuroleptic-treated patients received a single dose of the peptide with a 4-week follow-up. No significant change in mental status was observed after any of these administration schedules. Peak plasma levels of caerulein were noted at 20-30 min after IM administration; at this time no changes in cortical evoked potential were demonstrated. Furthermore, levels of cholecystokinin were not found to be reduced, but were in fact elevated in lumbar cerebrospinal fluid of schizophrenic patients. These data argue against the antipsychotic efficacy of systemic caerulein administration and, because evidence of CNS response to CCK is lacking, suggest that other pharmacologic strategies may be necessary to effectively modify central peptide systems with systemically administered drugs.

Adult↗
PubMed1983

Preparatory interval influences on reaction-time of elderly adults.

The influence of regularity of preparatory interval (PI) on simple reaction-time (RT) in elderly persons was studied in a sample of 25 women between 65 and 88 years of age. RTs to regular and variable PIs of 1, 3, 7, 9, and 13 seconds were compared using Steffy's embedded isotemporal blocks method. The advantage of PI regularity was lost at 13 sec, where performance was faster for irregular trials. The RT-PI functions were similar to those found by Botwinick and his associates who used Shakow's paradigm, even though overall RT was slower in this sample. The similarity of results across the two paradigms suggest that the point of RT function crossover is interval dependent and unrelated to response latency in elderly adults.

Aged↗
PubMed1979

Effects of L-tryptophan on sleep onset insomniacs.

Eighteen female subjects with demonstrated laboratory sleep onset latency greater than 20 minutes for two nights participated in this double blind study of the effectiveness of l-tryptophan as a hypnotic. Standard sleep recordings were made on 10 nights over a 3 month period with lights out occurring 20 minutes after drug administration (placebo, 1 gm. l-tryptophan, 3 gms. l-tryptophan). Neither dose of l-tryptophan differed from placebo as to the amount of REM, SWS or wakefulness, but 3 gms. significantly reduced sleep onset latency on some of the nights. Those subjects with latencies longer than 40 mins. had the greatest reduction in latency with 3 gms. and also evidenced high levels of anxiety on the Taylor Manifest Anxiety Scale initially. Subjects with latency between 20 and 40 minutes appeared to receive the longest lasting hypnotic effect from the higher dose. Adaptation to the sleep lab took place across the entire 10 nights of the study. Therefore, valid comparisons between treatments in a sleep study extending over a number of nights should be made between temporally adjacent samples.

Clinical Trials as Topic↗
PubMed1978

Residual effects of ethanol and chlordiazepoxide treatments for alcohol withdrawal.

Eighteen male alcoholics were randomly assigned to one of two alcohol detoxification treatments. One group received a low dose ethanol treatment while the other group received a chlordiazepoxide treatment. This study compares recovery of sleep EEG and clinical symptomatology following these two detoxification treatments. Sleep EEG and clinical measures were obtained for the final medication day and during a 6-day postmedication "recovery" period. The chlordiazepoxide treatment produced suppression of rapid eye movement (REM) sleep lasting for about 4 days and virtually eliminated delta sleep (stages III and IV) during the recovery period. The low dose ethanol treatment regimen produced less disruption of REM and delta sleep during the recovery period. These findings suggest that under some circumstances an ethanol treatment regimen may prove more beneficial to the healthy alcoholic patient than current regimens which employ other psychoactive medication. In particular, the long lasting suppression of delta sleep during the recovery period in subjects treated with chlordiazepoxide suggests a vulnerability of the slow wave sleep mechanisms during early alcohol abstinence and raises the possibility that this regimen prolongs functional tolerance to alcohol effects. Continued clinical evaluation of low dose ethanol detoxification treatment is suggested.

Adult↗
PubMed1978

EEG measures of functional tolerance to alcohol.

The literature suggests that alcohol ingestion produces characteristic alterations of sleep physiology and evoked response in alcoholics. Studies of alcohol withdrawal indicate that for some alcoholics residual functional tolerance remains apparent for an indefinite period. Low amounts of slow wave sleep (SWS) appear to be one of the physiological concomitants of the residual tolerance. Visual evoked responses were recorded from two small groups of inpatient alcoholics identified as normal or low SWS during a sober period. Alcohol ingestion produced no significant changes of evoked response parameters. Alcohol withdrawal produced significant augmentation of early component amplitude for the low SWS group only. These data suggest that low SWS and augmented primary component amplitude may be physiological correlates of functional tolerance to alcohol.

Adult↗