Steven P. James

Seasonal Affective Disorder and Phototherapy

Recognition that the timing of depressive episodes is related to the seasons goes back at least to Hippocrates (circa 400 B.C.),’ who noted that “melancholia occurs in the spring.” In the last 150 years many researchers have noted seasonal variations in affective episodes and in suicide, an indirect reflection of the incidence of depression. The suicide data, well reviewed by Kevan2 and A ~ c h o f f , ~ show a peak incidence in late spring and early summer. The incidence of depressive episodes is highest in spring and fall, whereas mania seems to occur most frequently in late summer.‘ Several authors have correkted the incidence of these occurrences with climatic variables such as sunshine and temperature and have shown statistically significant relationship^.^*^-^ Such survey studies, however, cannot establish a causal link between environmental influences and psychopathology. In order to probe the mechanisms by means of which these seasonal rhythms might be mediated, we have adopted a different strategy. We have recruited and studied a population of patients who have a history of extreme seasonal vulnerability to changes in mood and behavior. In this paper we summarize our experience with these patients and their condition, and discuss our interventions in their seasonal rhythms, and the extensive animal literature on which these interventions were patterned.

Frequency analysis of the sleep EEG in depression

Eight patients with major depressive disorder (seven bipolar and one unipolar) and matched controls had sleep studies, on which frequency analysis of the electroencephalogram (EEG) was performed. Total sleep and sleep efficiency were decreased in the patients, but there was no significant difference in rapid eye movement (REM) latency between the two groups. Frequency analysis revealed no group differences in power in the delta band (0.23-2.5 Hz) or the whole EEG spectrum (0.23-25 Hz). These findings suggest that mean REM latencies are not always shorter in major depression. The results are discussed in light of a previous report of decreased delta energy in the sleep EEG of unipolar patients.

Deficient nocturnal surge of TSH secretion during sleep and sleep deprivation in rapid-cycling bipolar illness

Rapid-cycling bipolar patients have a high prevalence of hypothyroidism, and this disturbance in their hypothalamic-pituitary-thyroid (HPT) function may provide a model for understanding the less severe thyroid dysfunction present in other forms of affective disorder. For these reasons, we investigated HPT function in eight rapid-cycling bipolar patients and eight normal controls by measuring plasma levels of thyroid-stimulating hormone (TSH) and cortisol every 30 min during a baseline 24-h period and during an additional night of sleep deprivation. Thyrotropin-releasing hormone (TRH) (500 micrograms) challenge tests were also performed in the patients. Controls exhibited a significant circadian variation in TSH with a nocturnal rise that was augmented by sleep deprivation. In the rapid cyclers, the nocturnal rise in TSH was absent, and sleep deprivation failed to raise their TSH levels significantly compared with baseline. Low nocturnal TSH levels were associated with blunted TSH responses to TRH infusions; due to the relatively brief sampling interval used in the TRH challenge tests, however, these results do not reliably discriminate between hypothalamic and pituitary dysfunction as an etiology for low nocturnal TSH levels. Additional studies are needed to determine the precise nature of the HPT disturbance in rapid-cycling patients.

The dexamethasone suppression test in seasonal affective disorder

Abstract Twenty patients with seasonal affective disorder (SAD) were given 1 mg of dexamethasone to evaluate the hypothalamic-pituitary-adrenal (HPA) axis. Two patients were found to have 4 PM plasma cortisol levels greater than 5 μgm/dL, the generally used criterion for nonsuppression, after administration of dexamethasone the previous night. Normal suppression of the hypothalamic-pituitary-adrenal axis by dexamethasone appears to be a feature of SAD, unlike many other psychiatric disorders.

Effects of melatonin on performance testing in patients with seasonal affective disorder

Psychomotor performance and memory were assessed in 6 patients with seasonal affective disorder following one week of daily administration of oral melatonin. No effect was noted on either vigilance or memory testing, but reaction time on a simple visual/tactile task was significantly reduced. Identical testing following a week of placebo administration showed no changes from baseline. Clinical status was monitored by both observer and self ratings; no clinical changes were detected that could account for the performance difference. The reaction time finding is in contrast to a previous report of a reaction time increase following melatonin administration. We discuss the possibility that this discrepancy is due to different dosages of melatonin administered or to the effects of melatonin on circadian rhythms of performance.

Vitamin B12 deficiency and the dexamethasone suppression test.

The authors describe dexamethasone nonsuppression in a depressed patient with a vitamin B12 deficiency. After B12 replacement there was no change in the patients clinical state. However, the dexamethasone suppression test normalized. Thus, dexamethasone nonsuppression in this patient seemed to be more closely related to vitamin B12 deficiency than to affective state.