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Biomedical subjects

L J Siever

Publications and source records attributed to L J Siever.

At least 109 records · Page 6Linked to original sources
PubMed1989

Eye tracking, schizophrenic symptoms, and schizotypal personality disorder.

Schizophrenic patients and patients with schizotypal personality disorder were significantly more likely than normal controls to demonstrate impaired eye tracking performance. Fifteen of 27 schizophrenics and 15 of 27 schizotypals had impaired eye tracking, compared with 11 of 39 normal controls. In the schizophrenic group, including 10 out-patients in a stable state of relative remission, impaired eye tracking was associated with more severe formal thought disorder and more time spent in psychiatric hospitals. Among stable schizophrenic out-patients, poor eye tracking was related to more severe formal thought disorder and greater overall psychopathology. This pattern of results suggests a possible relation between eye tracking impairment and more severe enduring symptoms across the spectrum of schizophrenic and schizophrenia-related disorders.

Adult↗
PubMed1989

Clinical, psychophysiological, and neurological characteristics of volunteers with impaired smooth pursuit eye movements.

Two hundred eighty-five volunteers from a community college were screened on campus for accuracy of their smooth pursuit eye movements (SPEM) by electrooculograph (EOG). Those volunteers with the least and the most accurate SPEM were recalled to the laboratory for a comprehensive evaluation of clinical and demographic characteristics, family history, neurological status, and psychophysiological and biological measures, including SPEM [repeat EOG test and infrared (IR) test], an electroencephalogram, auditory and visual evoked potentials, reaction time (RT), the continuous performance task (CPT), platelet monoamine oxidase (MAO), plasma amine oxidase, and dopamine-beta-hydroxylase (DBH). Low-accuracy SPEM was associated with social isolation, inadequate rapport, eccentricity, and a variety of related schizotypal or schizophrenia-like characteristics, but not with generalized psychopathology or other demographic/medical/clinical history variables. Low-accuracy SPEM also was associated with neurological and psychophysiological abnormalities frequently observed in schizophrenic patients. These results suggest that impaired SPEM may reflect an underlying central nervous system dysfunction that is specifically associated with clinical and biological characteristics related to schizophrenia, even in the absence of overt schizophrenia.

Adult↗
PubMed1989

The relationship between smooth pursuit eye movement impairment and psychological measures of psychopathology.

Two hundred and eighty-four male college volunteers were screened for smooth pursuit eyetracking deficiencies, a commonly reported concomitant of schizophrenia. A sample of 36 subjects, weighted with poor eyetrackers, was brought into the National Institute of Mental Health laboratory and retested on electro-oculogram and infrared tracking procedures. They were also administered psychological tests which assessed nine dimensions relevant to schizophrenic, neuropsychological, and affective disorders. In the area of schizophrenia-like symptoms, measures of attention deficits, stimulation avoidance, and identity problems predicted poor eyetracking for the whole sample. Using the poor eyetracking subjects alone (N = 24), interpersonal withdrawal was also significantly related to poor performance but not stimulation avoidance. In the neuropsychological area, measures of attention control and perceptual-motor dysfunction for the total sample, and perceptual problems and general intellectual decrements for the poor eyetrackers were significantly related to poor performance. There was no relationship between measures of affective dysfunction and poor eyetracking.

Adult↗
PubMed1988

Memory impairment in schizophrenic patients with tardive dyskinesia.

Memory functioning was contrasted in 40 schizophrenic patients with and without tardive dyskinesia (TD). Visual and verbal memory tests were used to investigate specific types of impairments. The presence of TD was ascertained using the Abnormal Involuntary Movement Scale (AIMS). TD patients scored significantly lower than non-TD patients on two measures of visual learning, though no differences were found for verbal learning or immediate recall. These results are consistent with previous reports that schizophrenic patients with TD demonstrate impaired cognitive functioning. They also raise the possibility that the neurochemical and structural changes underlying TD may produce specific deficits in memory for visual materials. In addition, a significant relationship was found between total score on the Brief Psychiatric Rating Scale (BPRS) and performance on all of the test measures included in the cognitive test battery. This demonstrates the importance of attending to the overall level of schizophrenic symptomatology when evaluating results from experimental learning tasks.

Dyskinesia, Drug-Induced↗
PubMed1988

Platelet alpha 2-adrenergic receptor function in psychiatric disorders.

The inhibitory effects of norepinephrine (NE) on the cyclic adenosine-3',5'-monophosphate (cAMP) response to prostaglandin E1 (PGE1), a measure of alpha 2-adrenergic receptor function, have been compared in platelets from drug-free schizophrenic patients, depressive patients, and normal controls. The absolute value of the inhibition by NE of the cAMP response to PGE1 was smaller in platelets from schizophrenic and depressive patients than in controls. However, this result was secondary to the smaller baseline platelet cAMP response to PGE1 in patients with these disorders. Effects of NE on cAMP production did not discriminate between actively ill and remitted patients with either schizophrenia or depression. Platelet alpha 2-receptor sensitivity, as measured by the effects of NE on cAMP production, does not appear to be altered in these psychiatric disorders.

Adult↗
PubMed1988

Dissociation of norepinephrine turnover from alpha-2 responses after clorgiline.

Responses to intravenous clonidine, a possible central noradrenergic probe, were examined in patients with depression before and after treatment with clorgiline, a selective monoamine oxidase type A inhibitor. Pulse rate, mean arterial blood pressure, plasma norepinephrine, 3-methoxy-4-hydroxyphenylglycol, and growth hormone were measured. Clorgiline treatment (2.5 to 10 mg/day) produced a variable reduction in the hypotensive response to clonidine but did not influence heart rate or plasma norepinephrine responses. Clorgiline markedly reduced the urinary output of norepinephrine and metabolites, indicating a reduced turnover of norepinephrine. None of the measured parameters corresponded with clinical effect. These data suggest that any clorgiline-induced alterations in alpha 2-receptor function as measured by responses to clonidine are modest and highly variable. Furthermore, since the variable and inconsistent changes in alpha 2-receptor function are dissociated from the massive changes in norepinephrine metabolism, regulation of presynaptic alpha 2-receptors appears unlikely to mediate the effects of clorgiline in patients with depression.

Bipolar Disorder↗
PubMed1988

Central serotoninergic stimulation by fenfluramine challenge does not affect plasma thyrotropin-stimulating hormone levels in man.

Thyrotropin-stimulating hormone (TSH) and prolactin (PRL) responses to an acute oral challenge of fenfluramine (60 mg), a central serotoninergic (5-hydroxytryptamine) releasing/uptake inhibiting agent, were examined in 8 healthy males in order to assess the role of central serotoninergic stimulation in the release of TSH. Plasma PRL, but not TSH, was significantly elevated by fenfluramine. These data suggest that central serotoninergic activity does not play an important role in the physiologic release of plasma TSH in man. Further, thyrotropin-releasing hormone is unlikely to be the PRL-releasing factor involved in the fenfluramine-induced stimulation of PRL.

Administration, Oral↗
PubMed1987

Increased growth hormone response to clonidine in 6-hydroxydopamine-treated rats.

Alpha 2-adrenergic receptors mediate adrenergic stimulation of growth hormone (GH) secretion in the rat. The GH response to the alpha 2-adrenergic agonist clonidine has thus been used as an index of alpha 2-adrenergic receptor responsiveness. Pharmacologic manipulations known to upregulate alpha 2-adrenergic receptor sensitivity would then be expected to result in an enhancement of the GH response to clonidine. To test this hypothesis, rats were injected in the lateral ventricle with either 6-hydroxydopamine or sterile saline. One month following the lesion, urethane-anesthetized rats from each group were administered clonidine or saline. Venous samples for plasma GH were drawn prior to or following the clonidine or saline administration. Rats administered clonidine had greater GH responses than those administered saline within either the lesioned or nonlesioned groups. The GH response to clonidine was significantly greater in the lesioned group than in the nonlesioned group. As 6-hydroxydopamine pretreatment upregulates alpha 2-adrenergic receptors, these results support the validity of the use of the GH response to clinidine as an index of alpha 2-adrenergic receptor responsiveness.

Animals↗
PubMed1987

Platelet [3H]imipramine binding in psychiatric disorders.

The Bmax and Kd values for [3H]imipramine binding were measured in platelets from drug-free normal controls and schizophrenic and depressive patients. No differences among groups were found. Exacerbated and remitted patients with either schizophrenia or depression did not differ in platelet [3H]imipramine binding parameters. No correlations were observed between platelet [3H]imipramine binding parameters and measures of symptom severity among actively ill patients with either schizophrenia or depression.

Adult↗
PubMed1987

Eye-tracking, attention and amphetamine challenge.

Smooth pursuit eye movement (SPEM) performance has been linked to nonvoluntary attentional processes. Amphetamine is a psychotropic drug with documented effects on attentional performance. In order to evaluate the relationship between SPEM performance and amphetamine's attentional effects, SPEM performance was measured prior to and following amphetamine administration in five bipolar patients and eight obsessive-compulsive patients. In these 13 patients, amphetamine did not significantly alter the accuracy of SPEM in the two patient groups. However, significant negative correlations were observed in the obsessive-compulsive patients and in the combined patient groups between baseline SPEM impairment and changes in eye-tracking accuracy following amphetamine, i.e. individuals with poorer SPEM accuracy improved while better SPEM performers deteriorated in tracking accuracy during amphetamine treatment.

Attention↗
PubMed1987

L-dopa challenge and relapse in schizophrenia.

Neuroleptic administration has been shown to be superior to placebo in prolonging schizophrenic remission. However, individual patients are able to maintain long periods of remission in the absence of neuroleptic treatment, while others relapse soon after neuroleptic withdrawal. This study attempted to predict time to relapse in 28 schizophrenic patients withdrawn from neuroleptics and challenged with L-dopa for 7 days, then followed until relapse. Time to relapse correlated significantly with L-dopa-induced increase in BPRS score (p = .006). Five of six patients who responded to L-dopa relapsed within 4 weeks after L-dopa administration, while only four of 22 who did not respond relapsed in a comparable period.

Adult↗
PubMed1986

Prostaglandin receptor sensitivity in psychiatric disorders.

The cyclic adenosine monophosphate (cAMP) responses to prostaglandin E1 (PGE1) in platelets and leukocytes from drug-free schizophrenic patients, depressive patients, and normal controls have been compared. Both schizophrenic and depressive patients had a significantly lower platelet cAMP response to PGE1 than controls. The platelet cAMP response to PGE1 did not discriminate among exacerbated, remitted, and poor-prognosis schizophrenic patients, or between exacerbated and remitted depressive patients. The cAMP response to PGE1 was negatively correlated with global symptom severity in actively ill schizophrenic patients, but was not correlated with symptom severity in exacerbated depressive patients. The leukocyte cAMP response to PGE1 did not differ among normal controls, schizophrenic patients, and depressive patients. These data indicate that a diminished platelet cAMP response to PGE1 may be a marker common to both schizophrenia and depression but that this effect does not extend to a cAMP-linked PGE1 receptor on another blood cell type.

Adult↗
PubMed1986

Adrenergic and serotonergic receptor responsiveness in depression.

Preliminary results are presented from a series of studies designed to characterize the regulation of release/metabolism and receptor responsiveness in the noradrenergic and serotonergic systems in acutely depressed patients and depressed patients in remission. Abnormal regulation of noradrenaline release/metabolism might be expected to be associated with the acute state of depression, while abnormalities of adrenoceptor responsiveness were hypothesized to persist in remission. Growth hormone responses to clonidine were measured as indices partially reflecting alpha 2-adrenoceptor responsiveness. Blunted responses to clonidine were found in both acutely depressed patients and patients in remission. The possible implications of these findings for the pathophysiology of the noradrenergic system in depression are discussed. Prolactin responses to the serotonergic agonist and serotonin-releasing agent fenfluramine were evaluated in acutely depressed patients, patients in remission and controls. A subset of the depressed patients appeared to have blunted prolactin responses to fenfluramine. However, very preliminary results do not show any difference in this response between patients who were acutely ill and those in remission, although the variability in both groups was great. These and related findings are discussed in terms of a possible contributory role of the serotonergic system in depression.

Clonidine↗