Decreased triiodothyronines in depression: a preliminary report.
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Biomedical subjects
Publications and source records attributed to T W Uhde.
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The pain sensitivity of 18 patients with panic disorder and age- and sex-matched controls was assessed by signal detection analysis. The authors failed to demonstrate any difference in pain sensitivity between the two groups. The relationship between state anxiety, as assessed by the Spielberger scale, and pain in panic patients tended to be in the opposite direction from that in normals.
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.
The longitudinal course of panic disorder and its associated symptoms were investigated in thirty-eight patients. The temporal relationships among panic attacks, generalized anxiety, agoraphobia and depression are described. Similar and different biological alterations in the tricyclic-responsive disorders of primary depression and panic disorder are reviewed and discussed.
The authors present a review of existing literature along with new data regarding the phenomenology, differential diagnosis, course and treatment of panic disorder and agoraphobia. Panic attacks are viewed as central to the development of these disorders, and individual cognitive frameworks contribute to the manner in which a patient's symptoms evolve. An apparent though unclear relation to depressive states is described. Substance abuse may also be a consequence of recurrent panic attacks. A scheme towards differential diagnosis of panic disorder from other psychiatric and medical disorders is proposed. Personality characteristics of these patients vary considerably, but certain factors, such as dependency, are common. Family relations are often strained and assume importance in treatment. Data on the longitudinal course of illness is presented implying a relationship of panic disorder to both depression and stressful life events in many patients. Treatments that thus far seem most effective are pharmacological and behavioural approaches. Imipramine, MAO inhibitors, and alprazolam currently appear to be the most useful medications employed, although other agents may at times be useful alternatives. Dietary interventions, family therapy, and group and individual psychotherapy are also reviewed and discussed as adjunctive therapies in the treatment of panic disorder.
Using data gathered in a naturalistic study of 95 research patients at the NIMH, a retrospective method of documenting the life course of recurrent affective illness is presented, along with a partial prospective validation of this method. In these patients, the severity, frequency, and duration of manic and depressive episodes, as well as their pattern and distribution, are characterized. These variables are examined in different patients subgrouped according to gender and age of onset, polarity, and rapidity of cycling of illness. The findings are compared with data on the life course of affective illness found in studies from the pre-pharmacologic era.
The relationship between CSF somatostatin and peripheral thyroid hormones was assessed in 11 affectively ill patients before and during carbamazepine treatment. A direct relationship between CSF somatostatin and plasma thyroxine and free thyroxine, but not triiodothyronine, was observed both while patients were medication-free and during carbamazepine treatment. These first data in man are consistent with those in animals, suggesting a close interrelationship between somatostatin and thyroid regulation.
The hematological effects of carbamazepine, a drug effective in the acute and prophylactic treatment of manic-depressive disorder, were assessed in 43 subjects with affective disorder. Carbamazepine was found to cause statistically significant, but clinically insubstantial, decreases in white blood cell indexes. The consistent decreases in white cell counts observed with carbamazepine should be differentiated from the extremely rare, idiosyncratic blood dyscrasias reported in the literature.
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The results of a caffeine consumption inventory indicated that patients with panic anxiety disorder, but not affectively ill patients or normal controls, had levels of self-rated anxiety and depression that correlated with their degree of caffeine consumption. In addition, this self-report survey suggested that patients with panic disorder had an increased sensitivity to the effects of one cup of coffee. This apparent sensitivity to caffeine was also documented by the observation that more patients with panic disorder reported the discontinuation of coffee intake due to untoward side effects than controls. These results, based on self-reports, suggest that the hypothesis that patients with panic disorder are more reactive to caffeine should be directly tested using caffeine challenges and that the mechanisms underlying caffeine's effects on anxiety should be further explored.
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.
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