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Biomedical subjects

E Peselow

Publications and source records attributed to E Peselow.

At least 19 recordsLinked to original sources
PubMed1990

Disorders of decision in affective disease: an effect of beta-adrenergic dysfunction?

We investigated response bias (defined as the decision rule subjects adopt when uncertain) in two experiments using a variant of Signal Detection Theory (SDT) with the discrimination measure d'L and the bias measure CL, under which it is possible to independently evaluate discrimination and response bias. In the first experiment, manics, depressed subjects, and matched psychiatrically normal controls were tested with a recognition memory task with easier and more difficult components before and after 1 month of appropriate pharmacological treatment. This experiment showed that abnormally conservative bias was characteristic of depression and liberal (yea-saying) bias was found in mania regardless of severity of illness; discrimination deficits were found only when symptoms were severe. After treatment, aspects of discrimination worsened in both hypomanic and depressed nonresponders whereas response bias remained unchanged in these patients. In both groups of responders, improvements in response bias were more dramatic than improvements in discrimination. In the second experiment, psychiatrically normal hypertensives were tested with a Sternberg short-term memory scanning task on and off treatment with the centrally active beta-blocker propranolol. This experiment showed that treatment with propranolol modeled the bias deficit of depression; that is, bias became more conservative. Both sets of results suggest that disorders of decision may be modulated by beta-adrenergic function.

Arousal↗
PubMed1989

A preliminary comparison of flat affect schizophrenics and brain-damaged patients on measures of affective processing.

Flat affect is a major component of schizophrenia and is often also seen in neurological disorders. A preliminary set of comparisons were conducted to delineate neuropsychological mechanisms underlying flat affect in schizophrenia, and new measures are described for the assessment of affective deficits in clinical populations. Subjects were schizophrenic with flat affect (SZs), right brain-damaged (RBD), Parkinson's Disease (PDs), and normal control (NC) right-handed adults. Subjects were administered affective measures of expression and perception in both facial and vocal channels. For both perceptual and expressive tasks the SZs performed significantly less accurately than the NCs and the PDs but did not differ from the RBDs. This was the case for both face and voice. This finding lends support to the speculation that right hemisphere mechanisms, especially cortical ones, may be compromised among schizophrenics with flat affect.

Adult↗
PubMed1989

Neuroleptic augmentation with alprazolam: clinical effects and pharmacokinetic correlates.

Alprazolam added to stable doses of neuroleptics in nine schizophrenic patients was associated with a 20%-30% mean reduction in positive and negative symptoms, although clinical response was variable and in some patients particularly brisk. The authors examined the possibilities of a pharmacokinetic effect of alprazolam on neuroleptic plasma levels and of a clinical effect of alprazolam. The modest increase in mean neuroleptic plasma levels did not correlate with clinical change, but those patients with the highest alprazolam plasma levels tended to show more robust clinical responses.

Adult↗
PubMed1988

Preliminary studies of clonidine in psychotic patients.

Twelve psychotic patients received a mean dose of 3.3 mg/day of clonidine. In four clonidine was the only treatment and in the remaining eight clonidine was superadded to a neuroleptic regimen after symptomatology was stable. Clonidine caused reduction of scores for both productive psychotic symptoms and anxiety. Negative symptoms were unaffected. These findings are discussed with respect to the small magnitude of the effects, questions as to specificity of the effects and methodologic limitations of this pilot study.

Adult↗
PubMed1987

Double blind controlled trials of cholecystokinin octapeptide in neuroleptic-refractory schizophrenia.

A group of 14 schizophrenics who remained symptomatic after neuroleptic treatment received either 0.02 mcg/kg CCK-8 or saline placebo intravenously. Thereafter, 13 received the alternative infusion as a crossover treatment. A second group of 16 such patients received 0.04 mcg/kg CCK-8 or saline intravenously and, thereafter, 14 of these received the alternative infusion as a crossover treatment. Psychopathology was rated prior to, 2-3 h post, and on days 3, 5 and 7 after each infusion. Ratings consisted of the BPRS, the Abrams and Taylor Scale for Emotional Blunting, the Hamilton Anxiety Scale and a Schneiderian "Positive" symptom scale abstracted from the President State Examination. Parallel groups and cross over design analyses failed to show efficacy for CCK-8.

Antipsychotic Agents↗
PubMed1987

Platelet 3H-imipramine binding and familial transmission of affective disorders.

We studied platelet 3H-imipramine binding and family history of affective illness in 26 patients with bipolar affective disorder and 24 patients with unipolar affective disorder. The density of platelet 3H-imipramine binding sites (Bmax) was significantly lower in bipolar patients with family history of affective illness than in healthy controls; however, there was a considerable overlap in Bmax values between the familial cases and the normal controls. A similar trend was observed in familial cases of unipolar disorder but the differences fell short of statistical significance. The nonfamilial cases of affective disorder did not differ from the healthy controls. The possible role of reduced platelet 3H-imipramine binding as a genetic vulnerability 'marker' in affective disorder was discussed.

Adult↗
PubMed1987

Clonidine in neuroleptic-induced akathisia.

Six hospitalized patients with neuroleptic-induced akathisia were treated with clonidine under single-blind conditions. Akathisia and anxiety at maximum clonidine dose were significantly lower than at baseline, although it was difficult to differentiate specific therapeutic effects from sedation.

Adult↗
PubMed1986

Fluoxetine response: endpoint vs pattern analysis.

A 6-week double-blind trial of fluoxetine treatment of unipolar major depressive disorder in 49 patients was evaluated in terms of improvement in the Hamilton Depression Rating Scale (HDRS) and Clinical Global Improvement (CGI) scores. A relationship was found between change in HDRS (absolute and percentage decrease from baseline) and final CGI ratings. However, because of a few placebo-responders, endpoint analysis with both the HDRS and CGI showed no differences between active drug and placebo. Pattern analysis of persistent response did successively separate active drug from placebo (less than 0.05).

Adolescent↗
PubMed1986

Platelet [3H]imipramine binding in affective disorders: trait versus state characteristics.

Platelet [3H]imipramine binding (Bmax) was determined in 67 patients with major affective illness (33 euthymic bipolar, 34 depressed unipolar) and 58 normal control subjects. Bipolar patients had significantly lower Bmax values than did control subjects. The mean Bmax in the unipolar patients was lower than in the control subjects, but the difference was not statistically significant. Dissociation constant (Kd) values did not distinguish patients in either category from control subjects. The significantly lower Bmax in euthymic bipolar patients and the apparent state independence of Bmax in some but not all unipolar patients suggest that platelet imipramine binding may be a trait marker in a subset of affective disorders.

Adult↗
PubMed1986

Essential fatty acid supplementation in tardive dyskinesia.

Preclinical and clinical observations suggest that enhancement of prostaglandin activity inhibits catecholamine release and may have antidyskinetic effects. A double-blind therapeutic trial with prostaglandin precursor essential fatty acids was conducted in 16 patients with tardive dyskinesia. No beneficial effects were seen.

Clinical Trials as Topic↗
PubMed1986

A controlled assessment of propranolol in the treatment of neuroleptic-induced akathisia.

Twelve patients with neuroleptic-induced akathisia were treated in a randomised, double-blind, cross-over design with propranolol and matching placebo. Propranolol caused significant decrements in both subjective and objective ratings of akathisia, but not in anxiety scores. This confirms prior findings of the efficacy of propranolol in akathisia induced by neuroleptic treatment.

Adult↗