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Biomedical subjects

L J Siever

Publications and source records attributed to L J Siever.

At least 127 records · Page 7Linked to original sources
PubMed1986

Smooth pursuit eye movement disorder and its psychobiologic correlates in unmedicated schizophrenics.

The accuracy of smooth pursuit eye movements (SPEMs) was evaluated electrooculographically in 14 medication-free schizophrenics. Concentrations of monoamine metabolites and gamma-amino-butyric acid (GABA) were measured in their cerebrospinal fluid (CSF). Ventricular-brain ratios (VBR) were determined by computed axial tomography (CT scan). Premorbid adjustment was evaluated by the Phillips Scale. The SPEMs of eight of the patients were reevaluated after 2 weeks of treatment with either prazosin or pimozide. No consistent significant correlations were found between SPEM accuracy and CSF metabolite concentrations, VBR, or premorbid adjustment. SPEM accuracy was not correlated with number of days off medication and was significantly correlated when measured before and during medication.

Adult↗
PubMed1986

Indices of noradrenergic output in depression.

Concentrations of plasma norepinephrine (NE) and plasma-3-methoxy-4-hydroxyphenylglycol (MHPG), blood pressure, and heart rate were measured on 2 days in 25 depressed patients and 25 controls. Comparisons were made between patients and controls, and also between days for both groups, to determine the short-term stability of these measures. The means of the plasma and urinary noradrenergic metabolite measures were not significantly different between groups. The variance of plasma MHPG, plasma NE, and mean blood pressure was greater in the depressed patients than in controls. Blood pressure, plasma MHPG, and plasma NE were relatively stable as suggested by the significant correlations between the 2 days for each of these variables. Plasma NE, plasma MHPG, and the sum of the deaminated urinary metabolites (MHPG and vanillylmandelic acid) were significantly intercorrelated. These results support other data in suggesting that plasma concentrations of NE and MHPG may be useful measures of noradrenergic activity, but may not consistently distinguish depressed patients from controls.

Adult↗
PubMed1986

Clonidine reduces plasma melatonin levels.

Clonidine, an alpha-adrenoceptor agonist, reduces human plasma melatonin levels when administered intravenously at 2-3 micrograms kg-1 to sleeping volunteers. Measurement of plasma melatonin levels after administration of clonidine could be the basis for a clinical in-vivo test of alpha-adrenoceptors.

Adult↗
PubMed1985

Attention dysfunction and psychopathology in college men.

Four hundred college men were screened on a measure of vigilance, the Continuous Performance Test (CPT). The individuals with good and poor attention (the upper and lower 5% of the CPT score distribution) were compared on multiple measures of psychiatric disturbance, cognition, and psycho-physiologic function. The attention dysfunction group (lower 5%) had a higher incidence of symptoms of hyperactivity both in childhood and as adults, but had no higher incidence of other psychopathology as assessed with either the Research Diagnostic Criteria or the Minnesota Multiphasic Personality Inventory. Cognitive differences between the lower and upper CPT groups, including differences on Wechsler Adult Intelligence Scale subtests, the Stroop test, reaction time, and evoked potentials, substantiated an attention dysfunction syndrome. Thus, attentional dysfunction in young adults seems more closely linked to hyperactivity than to current psychopathology.

Adolescent↗
PubMed1985

The effect of clorgyline on noradrenergic function.

A low dosage of the specific MAO-A inhibitor clorgyline (5-10 mg/day) was administered chronically to 10 depressed patients. Peripheral noradrenergic activity, as assessed by measurements of the plasma norepinephrine (NE) concentration, heart rate, and blood pressure, was determined before and after drug treatment. The administration of a low dosage of clorgyline was associated with a decrement in peripheral presynaptic noradrenergic activity. Comparison with the results of similar studies of the effects of desmethylimipramine (DMI) suggests that antidepressant drugs with unrelated primary actions affect peripheral noradrenergic functions differently.

Adult↗
PubMed1985

Therapeutic responses to tricyclic antidepressants and related drugs in non-affective disorder patient populations.

Although therapeutic responsiveness to tricyclic antidepressants has been primarily associated with the affective disorders, clinical investigations in the last decade have suggested that non-affective disorders such as panic disorder, obsessive-compulsive disorder, anxiety disorder, bulimia, enuresis, migraine, and the chronic pain syndrome may also respond to tricyclics and other antidepressants. This therapeutic responsiveness may sometimes be related to improvement in secondary depressive symptoms, but may also clearly occur in the absence of secondary depression; in particular, improvement in the core symptoms of at least some of these disorders may occur without a change in mood. Furthermore, many patients with these disorders display psychobiologic abnormalities that show many similarities, but also some differences, compared to those observed in patients with affective disorders, despite the frequent absence of affective symptoms. While an improvement in subclinical or "masked" depression remains one hypothesis linking tricyclic responsiveness and shared biological abnormalities in this diverse group of diagnostic entities, an alternative hypothesis (the "ven disorder" hypothesis) is presented, suggesting the possibility that tricyclic and other antidepressant-responding patients have a core disorder with common psychobiologic abnormalities but multiple clinical and diagnostic presentations. An alternative hypothesis (the "shotgun" hypothesis) suggests that the multiple actions of tricyclics (e.g. on adrenergic receptors vs. muscarinic receptors vs. serotonin system changes) may each be differentially important in the therapeutic outcome in patients with specific or predominant problems in one or another of these areas. An examination of both the similarities and differences among the non-affective, tricyclic-responsive disorders and the affective disorders may provide clues about the important psychobiologic elements in these disorders, and to the mode of action of tricyclic antidepressants and related drugs across the psychiatric disorder spectrum.

Anorexia Nervosa↗
PubMed1985

Biological alterations in the primary affective disorders and other tricyclic-responsive disorders.

Noradrenergic function was studied in patients with primary affective disorder and other tricyclic-responsive disorders including obsessive-compulsive disorder, anorexia nervosa and panic attack/agoraphobia in medication-free states. Pre-synaptic noradrenergic activity was assessed by assaying plasma concentrations of norepinephrine (NE) and its metabolite 3-methoxy,4-hydroxyphenylglycol (MHPG). Noradrenergic receptor responsiveness was evaluated by measuring plasma growth hormone (GH), MHPG, and NE responses to clonidine. Binding of tritiated dihydroergocriptine (3H-DHE) and biochemical responsiveness of alpha 2-adrenergic receptors were measured in platelet preparations. These studies suggest that noradrenergic activity may be altered in several tricyclic-responsive disorders and are consistent with the possibility that tricyclic antidepressants may serve to stabilize a dysregulated noradrenergic system in patients from several diagnostic categories.

Adult↗
PubMed1985

Tricyclic response in obsessive compulsive disorder.

Therapeutic responses to the tricyclic antidepressant clomipramine have been demonstrated in five double blind studies of patients with obsessive compulsive disorder. Biological alterations in patients with obsessive compulsive disorder resemble those of depressed patients for the dexamethasone suppression test, for some measures of sleep physiology, and in similar neuroendocrine responses to clonidine. Clomipramine's antiobsessional effect does not require high baseline depression ratings or biological abnormalities similar to those seen in depressives. Preliminary results suggest that in contrast to depressives, patients with obsessive compulsive disorder may respond to clomipramine but not to the tricyclic antidepressant desipramine.

Adolescent↗
PubMed1985

Relatedness of schizotypal to schizophrenic disorders: editors' introduction.

The schizotypal personality category introduced in DSM-III reflects an initial effort to organize psychiatric diagnosis on a biogenetic basis. The schizotypal diagnosis is intended to reflect a genetic association with schizophrenia. One result of this inclusion has been to stimulate a growing body of evidence about its validity--evidence that is reviewed in this issue by Kendler, Torgersen, Siever, and Stone. These studies suggest that criteria which emphasize interpersonal and social trait disabilities are more specific to a schizotype than criteria which stress psychotic-like symptoms. As a result, we suggest that future research on this patient group should broaden its criteria base. However, even if revisions increase the biogenetic specificity of this category, we believe its treatment will remain unclear, and models for its pathogenesis and relationship to schizophrenia will need to remain complex.

Diagnosis, Differential↗
PubMed1985

Biological markers in schizotypal personality disorder.

The establishment of the new diagnostic category, Schizotypal Personality Disorder (SPD), has stimulated biological studies of patients with this disorder. Such studies offer the potential of better understanding the diagnosis and treatment of SPD as well as more clearly defining the boundaries of the schizophrenic disorders. SPD has been studied in the clinical setting, in family studies of schizophrenia, and in the biological high-risk paradigm. In most cases, biological variables associated with schizophrenia have been evaluated. Decreased activities of plasma amine oxidase and platelet monoamine oxidase have been associated with SPD in the families of schizophrenics and in "biological high-risk" studies. Smooth pursuit eye movement (SPEM) impairment has also been associated with SPD in a "biological high-risk" study of college students. Inferior backward masking performance has been demonstrated in SPD patients in the clinical setting. Other studies using psychophysiological measures have been applied to subjects with psychological characteristics similar to DSM-III SPD and found biological abnormalities similar to those reported in schizophrenia. These studies are consistent with the possibility that some individuals with SPD may share common psychobiological abnormalities with schizophrenic individuals and may sharpen our understanding of SPD and its relationship to schizophrenia.

Amine Oxidase (Copper-Containing)↗
PubMed1985

Biological markers for schizophrenia and the biological high-risk approach.

This review examines two putative biological markers for schizophrenia: reduced blood platelet monamine oxidase (MAO) activity and impaired smooth pursuit eye movements. Studies of these biological markers among patient samples are presented, including their theoretical background, measurement, genetics, validity, and specificity of the markers for schizophrenia, and the artifacts that might lessen their utility. These results are then compared with those from the biological high-risk research strategy, which selects nonpatient volunteers solely on the basis of a deviant marker, and then examines the clinical, psychological, and biological correlates of the marker. The results of these studies suggest that low platelet MAO activity is not an adequate marker for schizophrenia but is associated with characteristics related to hypomanic behavior and sensation seeking. Smooth pursuit eye tracking impairment, in contrast, seems to be directly associated with schizophrenia-related traits, such as the negative symptoms found among chronic schizophrenics, or with the characteristics observed in the biological relatives of schizophrenics. Finally, the implications of these findings are discussed.

Adult↗
PubMed1985

Overview: toward a dysregulation hypothesis of depression.

The authors suggest that the activity of neurotransmitter systems in the affective disorders and related psychiatric syndromes may be better understood as a reflection of a relative failure in their regulation, rather than as simple increases or decreases in their activity. A model organized around the concept of "dysregulation" posits that persistent impairment in one or more neurotransmitter homeostatic regulatory mechanisms confers a trait vulnerability to unstable or erratic neurotransmitter output. Evidence from clinical and animal model studies for dysregulation of the noradrenergic system in depression is examined with respect to criteria generated by such a general model, and a specific configuration of noradrenergic dysregulation in some forms of depression is proposed.

Animals↗
PubMed1984

Plasma prolactin changes following fenfluramine in depressed patients compared to controls: an evaluation of central serotonergic responsivity in depression.

In an attempt to evaluate the responsiveness of the serotonergic neurotransmitter system in depression, fenfluramine, a serotonin releasing agent, was administered to 18 depressed patients and 10 controls, and placebo was administered to 16 of the depressed patients in a double-blind paradigm. Plasma prolactin levels were measured prior to and for five hours following fenfluramine. Fenfluramine produced a significant increase in prolactin in both patients and controls. However, the prolactin response to fenfluramine whether measured as an absolute increase or percent increase from baseline was significantly less in depressed patients than controls. This difference remained equally statistically significant when age-and-sex-matched pairs of depressed patients and controls were compared. These results suggest that the central serotonergic system is less responsive in depressed patients than controls.

Adult↗
PubMed1984

Plasma cortisol responses to clonidine in depressed patients and controls. Evidence for a possible alteration in noradrenergic-neuroendocrine relationships.

Plasma cortisol responses to the intravenous administration of clonidine hydrochloride and placebo were evaluated in depressed patients and controls. Depressed patients had higher mean baseline cortisol levels than controls. Cortisol levels decreased during the morning study period following both placebo and 2 micrograms/kg of clonidine hydrochloride in the depressed patients, but the cortisol decrease was sixfold greater on the day of clonidine administration; these placebo-clonidine differences were statistically significant, whether calculated on an absolute decrement basis or as a percent change. In contrast, controls responded to clonidine with only a 1.5-fold greater cortisol reduction than that found after placebo, a nonsignificant difference from the day of placebo administration. Reductions in the concentration of plasma 3-methoxy-4-hydroxyphenylglycol following clonidine administration were significantly negatively correlated with baseline plasma cortisol levels, raising the possibility that abnormalities in the responsiveness of the alpha 2-noradrenergic system may be associated with the hypothalamo-pituitary-adrenal (HPA) axis dysfunction found in depressed patients.

Aged↗