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Biomedical subjects

L Grunhaus

Publications and source records attributed to L Grunhaus.

At least 19 recordsLinked to original sources
PubMed1992

EEG sleep in Cushing's disease and Cushing's syndrome: comparison with patients with major depressive disorder.

Because patients with Cushing' syndrome (CS) and Major depressive disorder (MDD) share features of hypercortisolism and the depressive syndrome, we compared electro-encephalographic (EEG) sleep in patients with pituitary-ACTH-dependent Cushing's syndrome (Cushing's disease, CD), patients with ACTH-independent Cushing's syndrome (AICS), patients with major depressive disorder (MDD), and normal subjects. There were substantial similarities in the abnormal polysomnography profiles of patients with CD, AICS, and MDD. All three patient groups demonstrated poorer sleep continuity, shortened rapid eye movement (REM) latency, and increased first REM period density compared with normal subjects. In addition, AICS patients and MDD patients had elevated REM activity and density. These findings are discussed in terms of models of pathophysiology that relate abnormalities in sleep, mood, and hypothalamic-pituitary-adrenal function.

Adenoma↗
PubMed1992

A longitudinal evaluation of dexamethasone pharmacokinetics in depressed patients and normal controls.

Ten depressed patients and eight control subjects received 1 mg of dexamethasone intravenously at two different time points. Depressed patients were studied when they were depressed and following an improvement in their depression. In control subjects the first and second studies were performed approximately 1 month apart. Dexamethasone and cortisol were determined at 0, 5, 15, and 30 minutes, then at 1, 1.2, 2, 3, 4, 5, 6, 7, 9, 12, 17, and 24 hours following dexamethasone administration. Data from each patient was fit using a computer to a two compartment pharmacokinetic model and area under the time versus plasma concentration curve, elimination half-life, and clearance were also determined. Depressed patients exhibited a slower dexamethasone clearance and a larger area under the curve than control subjects at the first time point, but not at the second time point. The groups did not differ significantly in any of the other pharmacokinetic parameters (including distribution half-life, elimination half-life, or volume of distribution) at either time point. The possible causes and implications of these findings are discussed.

Adult↗
PubMed1991

Heterogeneity in the beta-endorphin immunoreactivity response to electroconvulsive therapy.

Electroconvulsive therapy is accompanied by an activation of the hypothalamic-pituitary-adrenal axis, resulting in a release of beta-endorphin from the anterior pituitary corticotrophs of humans. As a group, patients in our study demonstrated similar plasma beta-endorphin immunoreactivity response to their initial and final treatments. However, approximately half of the patients demonstrated greater beta-endorphin immunoreactivity release with their first seizure compared with their last seizure, and half of the patients demonstrated the opposite pattern. This difference was not explained by age, sex, unilateral vs bilateral treatments, sine wave vs brief pulse, or psychotropic or anticholinergic medication. Patients with constant seizure duration during the first and final treatments demonstrated a greater release of beta-endorphin immunoreactivity with the final treatment compared with the first treatment. Individuals with decreasing seizure duration during the course of the electroconvulsive therapy demonstrated a decreased beta-endorphin immunoreactivity response during their final treatment.

Adult↗
PubMed1990

Beta-lipotropin-beta-endorphin response to low-dose ovine corticotropin releasing factor in endogenous depression. Preliminary studies.

Studies in depression using a maximal stimulatory dose of corticotropin releasing factor have concluded that elevated resting cortisol levels in depressed patients exert a negative feedback effect on the corticotroph, resulting in a decreased corticotropin response. In this preliminary report, we examine the effects of a submaximal dose of corticotropin releasing factor on the release of another corticotroph secretory product, beta-lipotropin-beta-endorphin. We observed a decreased beta-lipotropin-beta-endorphin response in depressed subjects, but a normal adrenal cortisol response. Although the total beta-lipotropin-beta-endorphin response was decreased, the initial secretory response did not differ between patients and normal controls. Rather, the patients appeared to turn off secretion faster. This rapid shutoff was seen in all patients regardless of resting cortisol levels, suggesting that resting cortisol levels alone do not explain the decreased response seen in depressed patients.

Adult↗
PubMed1990

A longitudinal evaluation of dexamethasone and cortisol plasma concentrations in the dexamethasone suppression test before and during treatment with antidepressant drugs.

Thirty depressed in- and outpatients received serial dexamethasone suppression tests (DSTs). Plasma dexamethasone and cortisol concentrations were drawn at 1600 on the day following a 1-mg oral dose of dexamethasone. The first DST was performed after patients were drug-free for a period of 1 week; the second, third, and fourth DSTs while patients received antidepressant medication. Dexamethasone and cortisol concentrations drawn in the drug-free period correlated significantly. The cortisol to dexamethasone ratio changed significantly with time in DST nonsuppressors, suggesting that nonsuppression is associated with an altered pharmacodynamic response of the hypothalamopituitary-adrenal axis to dexamethasone during depression. When dexamethasone concentrations from the drug-free period were compared with those drawn during antidepressant treatment, no significant differences were noted.

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

Intravenous yohimbine. Selective enhancer of norepinephrine and cortisol secretion and systolic blood pressure in humans.

Yohimbine hydrochloride was administered intravenously to nine normal volunteers to assess alpha 2-adrenergic receptor function. Plasma catecholamines, cortisol, and psychophysiological parameters (blood pressure, pulse, somatic symptoms checklist, and visual analogue scales assessing mood) were used as dependent variables. Plasma norepinephrine and plasma cortisol increased significantly after yohimbine administration, while epinephrine remained unchanged. Systolic blood pressure and somatic symptoms were also significantly increased by yohimbine. These findings suggest that low-dose intravenous yohimbine is an effective probe for alpha 2-adrenergic receptors and the hypothalamic-pituitary-adrenal axis.

Adult↗
PubMed1989

Panic attacks and agoraphobia: low dose clomipramine treatment.

Seventeen outpatients with panic anxiety and agoraphobia were treated with a low, flexible dose of clomipramine in an 8-week open trial. Panic attacks ceased completely in 13 patients and markedly decreased in the other four without additional therapeutic measures. Avoidance behavior disappeared in five of the seven agoraphobic patients. Overall mean dosage was 45 mg/day, with eight patients receiving clomipramine 25 mg or less. Higher doses were needed when agoraphobia was present. These results are discussed in conjunction with previous findings and lend support to serotonergic involvement in panic anxiety. Further double-blind studies are needed to confirm these results.

Adolescent↗
PubMed1988

Plasma postdexamethasone cortisol levels in schizoaffective disorder.

The degree of hypothalamic-pituitary-adrenal (HPA) axis dysregulation in depressed patients with schizoaffective disorder was compared to that seen in patients with major depressive disorder with and without delusional features. The frequency of nonsuppression to dexamethasone was similar for all three diagnostic groups. Maximum postdexamethasone plasma cortisol was greater for delusional depressives, but did not differ between patients with major depressive and schizoaffective disorders. Modest correlations were found between postdexamethasone plasma cortisol levels, severity of illness, age, and recent weight loss, for patients with both major depressive disorder and delusional depression. For schizoaffective patients, associations between postdexamethasone plasma cortisol levels and various measures of severity of illness, but not age and recent weight loss, were found. Although HPA axis dysregulation occurs more frequently in all three of the studied diagnostic groups than in normal individuals, factors contributing to this dysregulation may be qualitatively different for schizoaffective patients.

Adult↗
PubMed1988

Major depressive disorder and panic disorder. Effects of comorbidity on treatment outcome with antidepressant medications.

Recent studies suggest that major depressive disorder (MDD) and panic disorder (PD) may coexist in a significant number of patients. The relevance of this association may be such that patients with the simultaneous diagnosis are at risk for more severe psychopathology and poorer treatment outcome. To explore this possibility further, we compared treatment outcome of two groups of patients: one with comorbidity of MDD and PD (N = 19) and another with MDD only (N = 22). Patients with comorbidity of MDD and PD scored significantly worse on a number of outcome assessments.

Antidepressive Agents↗
PubMed1988

Clinical and psychobiological characteristics of simultaneous panic disorder and major depression.

Simultaneous major depression and panic disorder appears to be a common occurrence in psychiatric patients. Patients with this condition present with more severe symptoms than patients with major depression only, respond less well to conventional antidepressants, and in general exhibit greater psychopathology over the course of their illness. Evidence suggesting a possible "dual diathesis," depression and panic, in these patients is reviewed from epidemiological, clinical, and biological perspectives. The importance of taking into account the combined symptoms in treatment planning and physiopathological studies is discussed.

Anxiety Disorders↗
PubMed1988

Behavioral and cognitive toxicity related to elevated plasma tricyclic antidepressant levels.

Tricyclic antidepressants (TCAs) have been occasionally reported to cause delirium, probably via a central antimuscarinic action. Nine of 16 patients with plasma TCA levels greater than 450 ng/ml developed cognitive or behavioral toxicity, compared with only one of 15 patients in a control group with plasma TCA levels between 150 and 450 ng/ml. The clinician should be aware of this potential adverse effect of TCA therapy, which may be easily preventable through the combination of careful clinical monitoring and liberal use of plasma TCA levels.

Adult↗
PubMed1987

Postdexamethasone plasma cortisol and beta-endorphin levels in depression: relationship to severity of illness.

The hypothalamic-pituitary-adrenal (HPA) axis is dysregulated in many patients with depression, probably at all levels of the axis. To determine if HPA dysregulation is associated with severity of depression, we studied a group of 66 patients with major depressive disorder. Each patient underwent a pretreatment Dexamethasone Suppression Test, with plasma postdexamethasone cortisol determination at 8:00 AM, 4:00 PM, and 11:00 PM. All three postdexamethasone cortisol levels were significantly correlated with the Hamilton Rating Scale for Depression (HRSD) scores. We also examined the "profile" measures of mean, maximum, and minimum of the three cortisol values; again, all three were significantly correlated with HRSD scores. To evaluate associations between clinical severity and HPA dysregulation at the pituitary level, we studied a second group of 44 patients with major depressive disorder. Each had postdexamethasone cortisol determinations at 4:00 PM and 11:00 PM as well as pre- and postdexamethasone beta-endorphin determinations at 4:00 PM. The cortisol data from this group followed the same pattern as in the first sample, and there was a significant relationship between HRSD score and degree of beta-endorphin nonsuppression as well. These results suggest that severity of depression is one of the determinants of dysregulation at both adrenal and pituitary levels of the HPA axis, accounting for 10%-20% of the observed variance.

Adult↗
PubMed1987

Serial dexamethasone suppression tests in simultaneous panic and depressive disorders.

Recent work suggests that the simultaneous occurrence of major depressive disorder (MDD) and panic disorder (PD) may be of relevance for clinical findings, therapeutic outcome, and prognosis. It is of interest to know whether or not this relevance extends to biological findings. We addressed this question through comparison of serial Dexamethasone Suppression Test (DST) results in patients who had either MDD alone or simultaneous MDD and PD. We were unable to describe differences between the groups.

Adult↗