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This study assessed the link between bulimic and depressive cognitions. Twenty-nine bulimics and 16 controls from the general population were first assessed on levels of depression using the Schedule for Affective Disorders and Schizophrenia-Change Version and the Beck Depression Inventory (BDI). Bulimics were significantly more depressed than controls. Bulimics differed significantly from controls on all cognitive measures associated with depression (Automatic Thoughts Questionnaire, Dysfunctional Attitude Scale, and Attributional Style Questionnaire), but differences on these measures were nonsignificant when depression, as measured by the BDI, was controlled. Bulimics differed from controls regardless of level of depression on the three scales of the Restraint Inventory, the Rationalization and All-or-None scales of the Thoughts About Eating Inventory, and most of the eight scales of the Eating Disorders Inventory. Bulimics showed more maladaptive thinking associated with depression, but these differences likely reflect the levels of depression for each group. The differences on the measures of cognitive and behavioral symptoms of bulimia remained when the level of depression was controlled statistically. This suggests that although depression can be frequently diagnosed in a bulimic sample, specific maladaptive cognitions and behaviors reflect a distinct disorder (bulimia) and are not simply the expression of an affective disorder.

Sleep electroencephalograms (EEGs) of subjects with primary panic disorder were compared to those of normal controls matched for age and sex. Significant differences were found between patients and controls in sleep latency, sleep efficiency, and stage 2 sleep duration. No differences were found between the two groups in REM latency. Because depressed patients are known to have reduced latency to REM sleep, these data add support to the hypothesis that panic disorder and depression are distinct disorders.

Five patients who had been diagnosed with panic disorder and irritable bowel syndrome are described. Both panic and gastrointestinal symptoms responded dramatically and rapidly to pharmacologic treatment of panic symptoms in all five patients. The frequent overlap of gastrointestinal symptoms and psychiatric (particularly anxiety) disorders suggests that some patients with functional gastrointestinal complaints may have a primary anxiety disorder.

A 5-week double-blind study compared amoxapine to imipramine (2:1 dosage ratio) in the treatment of depressed outpatients. The two agents were similar in anti-depressant efficacy and rapidity of action. The most common adverse reactions to both drugs were anticholinergic effects and sedation; cardiovascular effects were minimal. A few amoxapine-treated patients developed adverse effects typical of neuroleptic drugs: some experienced extrapyramidal signs, one developed galactorrhea, and most showed elevated plasma prolactin concentrations. Amoxapine was associated with significant neuroleptic activity in plasma. No correlation was found between blood levels of either drug and therapeutic response.

Patients diagnosed as having agoraphobia with panic attacks by DSM-III criteria were evaluated with the dexamethasone suppression test (DST). Depressive symptoms were assessed using the Beck Depression Inventory, the Depression Scale of the Minnesota Multiphasic Personality Inventory, and the Hamilton Rating Scale for Depression. Of 97 patients tested, 12.4% had a positive DST. These findings are consistent with earlier reports that found an incidence of abnormal DSTs between 11% and 15% in agoraphobic patients. Abnormal DSTs did not correlate with levels of depression on any of the depression measures.

Fourteen patients who met DSM-III criteria for agoraphobia with panic attacks received 200 mg desipramine (DMI) per day for 12 to 16 weeks on an open basis. Seven of eight patients who responded had steady state plasma DMI levels greater than 125 ng/ml, while five of six nonresponders had DMI levels less than 125 ng/ml. Following increases in dosage sufficient to raise DMI levels to greater than 150 ng/ml, four nonresponders improved dramatically. Implications of these findings are discussed briefly.

Disturbances in thyroid function can result in symptoms similar to those occurring in patients with anxiety disorders, especially panic disorder. An association between thyroid illness and panic and phobic disorders has been suggested, but few studies have directly investigated this issue. To assess this possible relationship, the authors measured indices of thyroid function in 165 subjects who had a current DSM-III diagnosis of panic disorder, either with or without phobic avoidance. These subjects reported a higher prevalence of thyroid illness by history compared with the prevalence of thyroid illness in the general population; however, less than 1% of all subjects had current thyroid dysfunction. The presence of a major depressive episode (MDE) was unrelated to current thyroid function, although subjects with MDE reported a higher prevalence of thyroid disease by history. Indices of thyroid function were not correlated with the severity of panic attacks or phobias.

The authors relate their clinical experience with 46 panic disorder patients who were receiving 3-10 mg/day of alprazolam. Fifteen (33%) developed symptoms consistent with DSM-III criteria for major depression despite remission of their panic symptoms. Clinicians should be alert to this potentially reversible complication.

This review surveys the literature in the area of predictors of response to antipsychotic drugs. Four general categories are presented and discussed: diagnosis as a predictor, clinical predictors, biological predictors, and pharmacological predictors. No single consistent predictor of response could be discerned; it appears that a variety of factors affect outcome and that several variables must be considered simultaneously. Based on the findings of this review, suggestions for improvements in clinical research design are made.

Earlier reports indicated that phenelzine treatment may result in clinically significant reductions of vitamin B6 in some individuals. Sixteen subjects, ages 21-59 years (seven men, nine women) with panic disorder with or without agoraphobia were treated with an average of phenelzine 53.5 mg/day for an average of 10 weeks in an open treatment study. No significant effects on plasma levels of pyridoxal phosphate, the active form of vitamin B6, were discernible in this group, nor was there any clear relationship between pyridoxal phosphate levels and symptoms in the subgroup of five patients who did develop deficiency-type symptoms. Pyridoxine replacement had unclear effects in symptomatic patients.