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Biomedical subjects

J F Greden

Publications and source records attributed to J F Greden.

At least 55 records · Page 3Linked to original sources
PubMed1991

Dexamethasone suppression test in schizophrenia: relationship to symptomatology, ventricular enlargement, and outcome.

To relieve confusion about the clinical correlates and prognostic implications of the dexamethasone suppression test (DST) in schizophrenia, we conducted a DST in 44 schizophrenic inpatients at drug-free baseline and approximately 4 weeks after neuroleptic treatment. Patients were rated on positive, negative, and depressive symptoms at both times. A head computed tomography (CT) scan was performed and measures of ventricle-brain ratio (VBR) obtained. Clinical improvement was monitored at four weeks, and longer-term outcome assessed at 1 year. Seventeen of the 44 patients were DST nonsuppressors at baseline, and five of these remained nonsuppressors at 4 weeks posttreatment. Postdexamethasone plasma cortisol levels were correlated with negative symptoms at baseline (r = 0.45; p less than 0.01), but not after 4 weeks of neuroleptic treatment. Postdexamethasone plasma cortisols were not related to global severity, positive, or depressive symptoms at either timepoint or to VBR. Persistent nonsuppression was associated with poor outcome, but baseline postdexamethasone cortisol levels were unrelated to outcome at 4 weeks and 1 year. The literature on DST in schizophrenia is reviewed and attempts are made to reconcile discrepant findings and to discuss pathophysiological implications.

Adolescent↗
PubMed1991

Stability of positive and negative symptom constructs during neuroleptic treatment in schizophrenia.

To assess the structural stability of positive and negative symptom ratings, we rated 40 schizophrenic inpatients on the Brief Psychiatric Rating Scale (BPRS) and the Scale for the Assessment of Negative Symptoms (SANS) at medication-free baseline and after 4 weeks of neuroleptic treatment. Positive symptom variables consisted of six BPRS items, and the negative symptom variables consisted of the five SANS subscale global scores. On principal components analysis, a three-factor, oblique-rotated solution resulted, with a negative symptom factor, a positive symptom factor, and an unstable behavioral agitation factor. The pre- and posttreatment factor loading patterns were similar. The findings suggest that BPRS-positive symptom items and the SANS measure distinct clinical dimensions and that the construct is stable, as demonstrated by minimal structural change with time.

Adult↗
PubMed1990

Multiplicity of depressive episodes: phenomenological and neuroendocrine correlates.

Sixty-four patients with a Research Diagnostic Criteria (RDC) diagnosis of major depressive disorder were categorized into three groups based on their number of depressive episodes (DE): Gr I (1 DE), n = 16, Gr II (2-4 DE), n = 25; and Gr III (5 or more DE), n = 23. All patients were nonsuppressors after 1 mg dexamethasone suppression test (DST) prior to the start of treatment. Patients were monitored during the course of their treatment using serial Hamilton Depression scores and post-DST plasma cortisol levels. A proportionately equal number of patients in the three groups had a favorable outcome, i.e., the number of depressive episodes did not predict recovery. Despite favorable clinical outcome, patients with higher numbers of depressive episodes had significantly higher post-DST plasma cortisol levels that were above the suppressive range (greater than 5 micrograms/dl). Patients with a higher number of depressive episodes had a significantly shorter duration of index episode and were younger at first depressive episode than patients in the other two groups. These results, however, were confounded with polarity, with a higher number of bipolars in Gr III than in the other two groups. Results are discussed in light of phenomenological and psychoendocrine findings of earlier studies.

Adult↗
PubMed1990

Plasma dexamethasone levels in children given the dexamethasone suppression test.

To determine whether children who demonstrate dexamethasone suppression test (DST) nonsuppression have lower plasma dexamethasone levels than DST suppressors, we administered the DST to 73 patients ranging in age from 5-14 years. Plasma dexamethasone levels and postdexamethasone cortisol levels were measured at 4:00 PM on day 2. We found: (1) DST nonsuppressors had significantly lower plasma dexamethasone levels (p less than 0.03) than suppressors; similar trends were observed when the population was divided into depressed and nondepressed patients; (2) mg/m2 dose of dexamethasone was directly correlated with plasma dexamethasone (p less than 0.003) and inversely correlated with postdexamethasone plasma cortisol levels (p less than 0.04); and (3) a statistically significant inverse correlation between plasma dexamethasone levels and postdexamethasone cortisol levels (p less than 0.04). Our findings show that plasma dexamethasone levels are important in evaluating DST results in psychiatrically disturbed children and suggest that dexamethasone dosage for use in the DST in children might be better calculated in terms of body surface area.

Adolescent↗
PubMed1990

Electroconvulsive therapy in delusional and non-delusional depressive disorder.

Major depressive disorder (MDD) patients (n = 66) treated with electroconvulsive therapy were stratified by the presence (n = 30) or absence (n = 36) of delusional symptoms (by Research Diagnostic Criteria) to compare their response to treatment. At discharge from hospital 83% of the MDD with psychosis group and 58% of the MDD without psychosis group were good responders (P = 0.03). The implications of this are discussed.

Adult↗
PubMed1990

Severity of depression and hypothalamic-pituitary-adrenal axis dysregulation: identification of contributing factors.

Severity of depression, as reflected by total scores on depression rating scales, has been established as one of several major sources of variance associated with hypothalamic-pituitary-adrenal axis dysregulation in patients with major depressive disorder. To determine which of the symptoms comprising clinically defined severity of illness contribute most to this relationship, we studied the associations between postdexamethasone plasma cortisol levels and components of the Hamilton Rating Scale for Depression (HRSD) in 114 patients with major depressive disorder. At pretreatment baseline, severity of depression was modestly but significantly correlated with postdexamethasone plasma cortisol; a large part of this relationship was associated with the anxiety components of the HRSD. When relationships between postdexamethasone plasma cortisol and severity measures were studied longitudinally during treatment, this contribution of the anxiety items persisted. The anxiety associated with depression appears to be a major clinical factor associated with the hypothalamic-pituitary-adrenal axis dysregulation in major depressive disorder.

Adult↗
PubMed1989

Cholinergic hyperactivity and negative schizophrenic symptoms. A model of cholinergic/dopaminergic interactions in schizophrenia.

Despite renewed interest in negative schizophrenic symptoms, the pathophysiological mechanisms involved in their development remain obscure. Although the cholinergic system has been implicated in schizophrenia, it has not been accorded a major role in current theories of pathophysiology. We present evidence from several lines of research that suggests that muscarinic hyperactivity may be implicated in the pathogenesis of negative schizophrenic symptoms. Specifically, cholinergic overdrive leads to a behavioral syndrome strikingly similar to the negative schizophrenic syndrome, anticholinergic agents may alleviate negative symptoms, schizophrenic patients with negative symptoms tend to "abuse" anticholinergics, and polysomnographic, neuroendocrine, and other pharmacological findings appear to be generally consistent with this hypothesis. The hypothesis is testable and is presented as a heuristic model that focuses on the dynamic interplay between cholinergic and dopaminergic systems in schizophrenia.

Acetylcholine↗
PubMed1989

Neurophysiologic dysfunction in basal ganglia/limbic striatal and thalamocortical circuits as a pathogenetic mechanism of obsessive-compulsive disorder.

This article is intended to elucidate some of the neuropathogenetic mechanisms possibly operative in obsessive-compulsive disorder (OCD). Relevant literature is reviewed, with attention to psychologic, and pathologic considerations. Anatomy, neurochemistry, and known functional associations with neuropathological and behavioral abnormalities of implicated brain regions are discussed. The authors propose that dysfunction of neuronal circuits interconnecting the orbitofrontal cortex, basal ganglia/limbic striatum, and thalamus serves a critical role in the pathogenesis of OCD and that obsessive-compulsive symptoms occur when an aberrant positive feedback loop develops in the reciprocally excitatory frontothalamic neuronal interchange, which is inadequately integrated or inhibited by the ventromedial (limbic) portions of the striatum; the ventromedial striatum may serve to modulate activity in the frontothalamic circuit through a negative feedback loop.

Antidepressive Agents, Tricyclic↗
PubMed1989

Cholinergic syndrome following anticholinergic withdrawal in a schizophrenic patient abusing marijuana.

A 27-year-old neuroleptic-stabilised schizophrenic patient presented with a three-day history of psychomotor retardation, disturbed sleep, and social and emotional withdrawal following reduction of his anticholinergic dosage; his symptoms had intensified after an increase in neuroleptic dosage, based on a diagnosis of psychotic decompensation. Recognition of a cholinergic syndrome and institution of appropriate anticholinergic treatment resulted in rapid improvement. The clinical distinction between a cholinergic overdrive state and schizophrenic exacerbation, while sometimes difficult, can be critical in selecting appropriate management.

Adult↗