Buspirone: a new treatment for anxiety.
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Biomedical subjects
Publications and source records attributed to R G Kathol.
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Twenty-six females and seven males with newly diagnosed, untreated hyperthyroidism were administered a structured questionnaire designed to identify anxiety and depression using operational criteria. By DSM III criteria, 10 patients were found to have depression and 15 anxiety. The number of anxiety symptoms paralleled the number of hyperthyroid symptoms whereas depressive symptoms did not. Prior history of psychiatric disease and family history of psychiatric disease did not predict anxiety or depression in patients with hyperthyroidism. The number with depression and anxiety was felt to be artificially inflated by the concurrent presence of somatic thyroid symptoms. Psychiatric practitioners should be careful to exclude patients with hyperthyroidism before a primary psychiatric diagnosis is made.
Psychiatric patients presenting with chronic psychogenic polydipsia are often difficult to treat with standard psychiatric interventions. Pharmacologic intervention was attempted in three patients and was successful in one. One patient had a significant and sustained reduction of water intake while on 160 mg of propranolol. One patient did not improve with either propranolol or captopril while a third patient showed no improvement of serum sodium with demeclocycline nor reduction of water intake with propranolol. The potential mechanisms by which these pharmacologic agents might alter thirst in patients with primary polydipsia are discussed.
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Seven male recovered depressive patients who were dexamethasone suppression test (DST) nonsuppressors while ill and eight male controls submitted an average of thirty-six 24-hr urine specimens for analysis during a 12-mo collection period. Recovered depressive patients had a significantly greater mean peak amplitude (mean distance from fitted regression line to the highest point on the peak) when compared to controls. Peak frequency (number of peaks per year) for recovered depressive patients for peaks greater than 30 micrograms/g-cr was three times that found in the control population. The number of collections by each patient did not account for these differences. Only one of seven recovered depressives had a circasemiannual rhythm of cortisol excretion while none demonstrated a seasonal rhythm. These findings suggest that patients with a history of depression and DST nonsuppression have greater variability in cortisol excretion than a control population while in the compensated state.
Depression appears to be a frequent complication of neoplastic disease. Recent surveys suggest that it is not only a common reason for psychiatric referral but that a substantial minority of hospitalized cancer patients suffer from an affective disturbance severe enough to warrant psychiatric intervention. In view of its reported prevalence it is likely that this complication adversely affects the quality of patients' lives and interferes with the management of their disease. Given the nature of this problem it is disturbing that so little systematic research has been done, especially in the area of treatment. In this article we critically review the literature concerned with the relationship of depression to cancer. We begin with comment on the nature of the association between cancer and depression and the question of whether depression is an etiologic factor in neoplastic disease. Before considering the prevalence of affective disorders among cancer patients, we examine the difficulty of diagnosing depression in seriously ill patients. Next, we explore the role of various psychological and biological factors in the etiology of this complication and, finally, we offer recommendations for treatment and suggest directions for future research.
Eleven of 32 newly diagnosed untreated patients with hyperthyroidism met DSM-III criteria for organic affective syndrome. Thirty of these patients submitted 24-hour urine specimens for measurement of urinary free cortisol levels, and 31 were given a 1-mg dexamethasone suppression test (DST) before antihyperthyroidism therapy was started. There was no difference in the mean +/- SD urinary free cortisol excretion levels between depressed and nondepressed hyperthyroid patients. One nondepressed patient demonstrated nonsuppression (greater than 5 micrograms/dl) at 8:00 a.m. These results suggest that cortisol abnormalities as reflected by urinary free cortisol levels and DST findings are uncommon in patients with hyperthyroidism whether they are depressed or nondepressed.
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A circannual rhythm of corticosteroid excretion has been identified in healthy subjects but is lost in patients who have recovered from a depression associated with dexamethasone nonsuppression. The loss of circannual variation as well as the persistent elevation and increased peak frequency of cortisol excretion could be instrumental in the development of depressive symptoms. A model for this phenomenon can be found in the entity known as intermittent Cushing's disease. That hypercortisolemia could be etiologically related to depression is supported by the case reported here in which a rise in UFC preceded the emergence of psychiatric symptomatology on two occasions. Further investigation into this possibility is clearly warranted.
A patient with a 6-year history of bipolar affective disorder who developed cushingoid features during an exacerbation of her psychiatric condition was found to have intermittent hypersecretion of cortisol. Close observation of this patient for 3 years has revealed that her medical and psychiatric symptoms are controlled by suppression of cortisol with bromocriptine.
Twenty-eight patients underwent a series of provocative endocrine tests an average of one year after their last admission for depression. Hypersecretion of cortisol, early escape of cortisol from dexamethasone suppression, diminished growth hormone response to insulin-induced hypoglycemia and altered thyrotropin response to thyrotropin-releasing hormone reported in acute primary depression were not observed after recovery. There were no differences in these measures after recovery between previous suppressors and nonsuppressors to dexamethasone. The cortisol response to insulin-induced hypoglycemia was less than expected in 6 of 16 recovered patients tested. There were significant differences in post-dexamethasone urinary free cortisol and in basal and early post-insulin serum cortisol levels between patients who had been suppressors and those who had been nonsuppressors to dexamethasone during acute depression. Further studies need to be done to substantiate these findings. These data indicate that hormone responses in recovered depressives are largely normal, suggesting that abnormalities during depression are "state" related phenomena.
Forty-two patients with diagnosed functional visual loss were reexamined an average of four years after their initial visit. Twenty-three patients continued to have constricted or spiral visual fields at follow-up. Despite persistent evidence of functional visual defects, few patients were either socially or economically impaired by them. Patients who had other types of visual field loss or loss of visual acuity were more likely to have these signs resolve than were patients with constricted or spiral fields. Concurrent unrelated organic ocular disease was present in 11 patients. In 20 patients, it was not possible to identify psychiatric symptoms either related to the onset of functional eye signs or at follow-up. Treatment did not substantially alter the course.
The glucose response to a standard insulin tolerance test (ITT) has been reported to be blunted in the acute phase of heterogeneous depressive disorders and to be normal in the recovered phase. We studied the glucose response to ITT in the recovered phase depression in patients who had previously been subclassified according to familial and clinical characteristics. All patients with depressive spectrum disease had an adequate glucose response to the ITT, whereas only 40% of patients with familial pure depressive disease and 56% of patients with bipolar illness had an adequate hypoglycemic response. There was also a trend toward a decrease in insulin sensitivity in patients who had been nonsuppressors to dexamethasone when depressed. These findings suggest that the glucose response to ITT may be a useful tool in differentiating among the heterogeneous depressive disorders.
Twenty-eight patients (10 bipolar, 13 depressive spectrum disease, and 5 familial pure depressive), recovered from depression for an average of 1 year, underwent a series of basal and provocative endocrine tests. No significant differences were found among depressive subtypes in thyrotropin, cortisol, or growth hormone measurements either before or after provocative testing with the exception of growth hormone response to insulin-induced hypoglycemia. Patients with depressive spectrum disease showed a significantly different growth hormone response to insulin-induced hypoglycemia than patients with bipolar disorder, a finding which suggests differences in alpha-adrenergic receptor sensitivity between these groups.
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Fifty-three cases of drug overdose requiring admission to a medical intensive care unit were studied. Tricyclic antidepressants were used in nearly 50 per cent of these serious adult overdoses. Barbiturates were involved in only 20 per cent. This may reflect changing patterns of drug usage and emphasizes the potential danger of tricyclics, the use of which is widespread in the general medical community. Unintentional overdoses occurred most often in substance abusers, whereas intentional overdoses occurred in a wider range of psychiatric disorders. A quarter of drug overdoses were free of psychiatric disease. Patients found to have an obvious manipulative intent were as likely to have made medically serious attempts as those who did not.