PubMed Health⌕ Search

Biomedical subjects

R W Buchanan

Publications and source records attributed to R W Buchanan.

At least 91 records · Page 5Linked to original sources
PubMed1992

The effects of metabolic stress on plasma progesterone in healthy volunteers and schizophrenic patients.

A number of preclinical studies suggest that progesterone may play an important role in the stress response, however, the effects of stress on progesterone in humans has not been established. Also, several lines of evidence indicate that schizophrenia may be associated with abnormal neurobiological responses to stress, but the effects of stress on progesterone in schizophrenia has not been investigated. The purpose of the present study was to examine the effects of stress on plasma progesterone and cortisol in healthy subjects and to determine if schizophrenic patients have altered stress-induced plasma progesterone levels compared to normal controls. Stress was induced through administration of 2-deoxyglucose (2DG), a glucose analog that impairs glucose metabolism resulting in a clinical state comparable to hypoglycemia. There were significant increases in plasma progesterone and cortisol levels following 2DG-induced glucoprivic stress in healthy controls. There was no relationship between stress related progesterone and cortisol elevations. Schizophrenic patients, in comparison to controls, had significantly greater 2DG-induced elevations in progesterone levels but no differences in stress-related cortisol levels. There was evidence that basal progesterone and cortisol levels were elevated in the schizophrenic patients. The implications of these data are discussed.

Adaptation, Physiological↗
PubMed1992

The concept of supersensitivity psychosis.

The hypothesis that chronic neuroleptic treatment may induce relapse in some schizophrenic patients has received considerable attention. This effect, usually called supersensitivity psychosis, has been attributed to neuroleptic-induced changes in mesolimbic or mesocortical dopaminergic receptors. However, research has not established that neuroleptics cause the proposed effect, and considerations of mechanism have not been separated from those of causation. The focus of research in this area should be the establishment or refutation of a causal relationship between chronic neuroleptic use and psychotic relapse.

Antipsychotic Agents↗
PubMed1991

Carbamazepine maintenance treatment in outpatient schizophrenics.

A double-blind crossover trial was used to evaluate carbamazepine as the sole maintenance treatment of chronic, nonmanic schizophrenic outpatients whose conditions had been stabilized with the use of neuroleptics prior to study. Criteria of treatment effectiveness included the number of patients relapsing and time to relapse over a 95-day neuroleptic-free period during which either carbamazepine or placebo was administered. Relapse was determined by the concordance of psychiatric ratings and independent clinical judgements indicating significant worsening. Results for 27 patients (13 receiving carbamazepine and 14 receiving placebo) involved in the first phase of this treatment comparison were nondifferentiating. Corroborating descriptive findings in the second phase were available for 14 of these patients. There was no evidence supporting the existence of a treatment-relevant subgroup defined by episodic dyscontrol phenomena.

Adult↗
PubMed1991

Alprazolam attenuates metabolic stress-induced neuroendocrine and behavioral effects in humans.

The effects of benzodiazepine drugs and the role of their recognition site, the GABAA/benzodiazepine receptor, in acute glucoprivic stress are not known. In the present study, the effects of acute glucoprivation were examined in ten healthy human subjects. Glucoprivation was induced by infusion of the glucose analog, 2-deoxyglucose (2DG), at doses sufficient (50 mg/kg) to competitively inhibit glucose metabolism. In addition, the effects of the triazolobenzodiazepine alprazolam (1.5 mg) on the 2DG-induced stress response was assessed. 2DG produced significant elevations in plasma cortisol (P = 0.0001) and glucose (P = 0.0003) levels. Alprazolam pretreatment attenuated the 2DG-related cortisol elevations (P = 0.05) but did not effect 2DG-induced glucose increases. In addition, 2DG caused significant increases in hunger (P = 0.01) and thirst (P = 0.001), and alprazolam significantly blunted both of these responses. Lastly, 2DG had significant effects on heart rate, diastolic blood pressure and body temperature (P less than 0.05). Alprazolam did not effect these physiologic indices. The significance of these data for the mechanisms involved in acute glucoprivic stress are examined and the implications of the data for the pathophysiology of affective illness and eating disorders are discussed.

Adult↗
PubMed1990

Anhedonia and the deficit syndrome of schizophrenia.

Schizophrenic outpatients with and without the deficit syndrome were administered Chapman's "psychosis proneness" scales. As hypothesized, deficit syndrome patients had higher scores on Social Anhedonia and Physical Anhedonia, but did not differ from nondeficit patients on Perceptual Aberration, Magical Ideation, or Impulsive Nonconformity. The differences between the two groups were not related to race, gender, age, socioeconomic status of family of origin, or drug treatment. These results support the validity of the deficit syndrome, and suggest that the Social Anhedonia and Physical Anhedonia scales may be useful in future studies of schizophrenia.

Adult↗
PubMed1990

The neural basis of the deficit syndrome of schizophrenia.

The deficit syndrome is a domain of schizophrenic psychopathology defined by the presence of primary negative symptoms that are enduring features of a patient's function between periods of relapse. Lesions of the putative neural circuit underlying social affiliation and social behavioral cues in nonhuman primates and other mammals cause behavioral impairments in animals that model the diminished social drive, poverty of speech, and blunted affect of the deficit syndrome. Components of this circuit include the amygdala, periamygdalar cortex, and part of the prefrontal cortex. Abnormal function of this functional circuit may underlie the deficit syndrome.

Amygdala↗
PubMed1990

Clinical correlates of the deficit syndrome of schizophrenia.

The authors propose using primary and enduring negative or deficit symptoms for dichotomizing schizophrenic patients into two groups, deficit and nondeficit. The validity of this approach was examined by comparing 17 deficit and 17 nondeficit patients for differences in premorbid adjustment and degree of neurological impairment. Deficit patients were characterized by poorer premorbid adjustment and greater neurological impairment. Neurological impairment was not related to premorbid adjustment in either group or in the total patient population. These findings support the utility of deficit symptoms for defining a more homogeneous subgroup of schizophrenia.

Adult↗
PubMed1990

Continuous versus targeted medication in schizophrenic outpatients: outcome results.

The authors report on the outcome of treatment of 116 outpatients with chronic schizophrenia who were assigned to a 2-year, single-blind course of treatment with either targeted or continuous medication. These patients were not restricted to those who were good candidates for a medication reduction strategy. Continuous medication was superior to targeted medication in preventing decompensations and hospitalizations and in extent of employment at 2 years. Other measures of psychopathology and functioning at 1 and 2 years did not differentiate the two groups of patients. The targeted approach achieved a substantial reduction in total medication through a reduction in the number of days of medication administration.

Adult↗
PubMed1989

Effect of neuroleptic withdrawal on plasma prolactin: a possible marker of receptor adaptation.

Stable schizophrenic and schizoaffective outpatients underwent abrupt withdrawal from a fixed dose of neuroleptic. Prolactin concentrations were determined preceding and following drug withdrawal. Basal prolactin concentrations were significantly lower 3, 4, or 5 days following drug withdrawal than on subsequent days. This rebound effect may be related to dopaminergic receptor changes in the tuberoinfundibular system that are induced by chronic neuroleptic administration.

Adult↗
PubMed1989

The Neurological Evaluation Scale (NES): a structured instrument for the assessment of neurological signs in schizophrenia.

The significance of neurological signs in schizophrenia is poorly understood. In part, this may reflect the marked variability in the methods of ascertainment in previous studies. The Neurological Evaluation Scale (NES) is designed to standardize the assessment of neurological impairment in schizophrenia. The battery consists of 26 items. Data on the interrater reliability for total score, functional areas of interest, and individual items are presented. Preliminary validity data demonstrate the ability of the battery to discriminate patients with schizophrenia from nonpsychiatric controls.

Brain Damage, Chronic↗
PubMed1989

The Schedule for the Deficit syndrome: an instrument for research in schizophrenia.

The Schedule for the Deficit Syndrome (SDS) is an instrument for categorizing schizophrenic patients into those with and those without the deficit syndrome. In a study of 40 schizophrenic patients diagnosed by DSM-III criteria, raters using the SDS demonstrated good interrater reliability for this categorization, as well as for individual negative symptoms and a rating of global severity.

Affective Symptoms↗
PubMed1989

Diazepam treatment of early symptoms of schizophrenic relapse.

In an open trial, nine drug-free schizophrenic patients received oral diazepam, 10 to 40 mg/day, for the treatment of early symptoms of relapse. Diazepam treatment led to a return of the patient's usual condition in seven of 11 episodes.

Administration, Oral↗
PubMed1989

Oculomotor abnormalities and their clinical correlates in schizophrenia.

Smooth pursuit eye movements (SPEMs) have been consistently found to be abnormal in the majority of schizophrenic patients. The traditional SPEM measurement technique, however, fails to inform us about the underlying oculomotor deficit in these patients, since it remains a non-specific and a global oculomotor measure. A number of diverse clinical features such as tardive dyskinesia (TD) or negative symptoms correlate with the SPEM abnormality. Other eye movement abnormalities such as fixation difficulties, increased "volitional" saccadic latency and saccadic distractibility in anti-saccade paradigm have also been noted in schizophrenic patients. Still, it remains unclear how these different eye movement measures relate with each other and with the traditional SPEM measure, the presence of which is so widely described in schizophrenia. The advantage of some newer oculomotor paradigms is their functional specificity and the degree to which their biology is known. To further address these issues and to search for clinical correlates of various eye movement abnormalities found in schizophrenia, we have developed a battery of oculomotor measures to be administered to a large number of clinically well described schizophrenic patients and normal controls. The results from a preliminary analysis of a relatively small number of subjects are presented here, thus limiting the scope of possible conclusions. But, these results do indicate that this technique of studying multiple paradigms for oculomotor control in schizophrenia may prove to be fruitful.

Eye Movements↗
PubMed1988

Significance and meaning of neurological signs in schizophrenia.

The authors review studies of abnormal signs on clinical neurological examination of schizophrenic patients. In spite of a number of methodologic limitations, the cumulative evidence strongly argues that there are more neurological signs in schizophrenic patients than in nonpsychiatric control subjects. Although less consistent, there is considerable evidence of more neurological signs in schizophrenic patients than in patients with affective disorders or with mixed, nonpsychotic disorders. The existing literature suggests several preliminary hypotheses with respect to neuroanatomical localization of neurological signs, subtyping of schizophrenia, and utility of studies of relatives at high risk and family history studies. Directions for future research in these areas are described.

Depressive Disorder↗