Donald C. Ross

Effects of Antidepressant Medication on Sexual: Function

There has been little systematic study of the types of sexual dysfunction produced by antidepressant medication or of the frequency with which this type of adverse effect occurs. The authors report results of a double-blind study in which the effects of imipramine, phenelzine, and placebo on specific aspects of sexual function were assessed in depressed outpatients before and after 6 weeks of treatment. Both active treatments were associated with a high incidence of adverse changes in sexual function and produced significantly more adverse effects on sexual function than placebo. Orgasm and ejaculation were impaired to a greater extent than erection. Adverse sexual function changes secondary to antidepressant medication occurred frequently in both men and women, although men reported a higher incidence. Antidepressant-related sexual dysfunction may be of clinical importance for medication compliance in view of current recommendations that antidepressants be administered for longer periods as maintenance therapy or for prophylaxis.

Reanalysis of The National Institute of Mental Health Treatment of Depression Collaborative Research Program General Effectiveness Report

The National Institute of Mental Health (NIMH) Treatment of Depression Collaborative Research Program General Effectiveness Report statistical analyses are criticized. Their analyses, which fostered the belief that the active treatments were indistinguishable, were compromised by an inappropriately stringent level of significance with regard to both heterogeneity of slope and pairwise group differences. Once slope heterogeneity is detected, the Johnson-Neyman technique is more appropriate than arbitrary sample subdivision. All of these tactics lowered power substantially.Our reanalysis indicates a reasonable ordering for the treatments with medication superior to the psychotherapies and the psychotherapies somewhat superior to placebo. These effects are particularly marked among the more symptomatic and impaired patients. The lack of dosage by severity analyses renders the severity findings ambiguous.Scientific and public health implications are discussed.

Early separation anxiety and adult agoraphobia

The authors compared 137 adult patients who had agoraphobia with 81 patients who had either simple or social phobia for a history of childhood and adolescent separation anxiety. Female agoraphobics reported significantly more childhood separation anxiety than female combined simple and social phobics; males showed no significant difference between diagnostic groups. The reported prevalence of separation anxiety in adolescence was relatively low, but agoraphobics of both sexes reported significantly more separation anxiety than combined simple and social phobics. There were no significant differences between groups for parental losses or severe family disruption during childhood. The results suggest that childhood separation anxiety is a risk factor in females but not in males for the later development of agoraphobia.

Arterial blood gas changes in panic disorder and lactate- induced panic

Lactate infusions were conducted in 12 male panic patients and 8 male normal controls with arterial catheters in place to reassess previously reported acid-base changes based on venous blood samples. The analysis of arterial pH, carbon dioxide pressure, and bicarbonate concentration confirmed most venous findings. At baseline, before the infusion, venous blood shows evidence of mixed chronic and acute respiratory alkalosis in patients while arterial blood gasses are most consistent with developing acute respiratory alkalosis. During the infusion both bloods are consistent with mixed metabolic and respiratory alkalosis with the patients hyperventilating more than normal controls and panicking patients hyperventilating more than nonpanicking patients. Arterial blood seems more sensitive than venous blood in detecting baseline differences between panicking and nonpanicking patients. A baseline arterial carbon dioxide pressure of 40 mmHg or higher and an arterial pH below 7.40 may predict no subsequent panic to lactate infusion.

Normalization of venous pH, pCO2, and bicarbonate levels after blockade of panic attacks

Recent evidence suggests that hyperventilation may be associated with spontaneous panic attacks in patients with panic disorder. This is reflected in abnormal patterns of blood gas and blood pH levels in these patients. In this study, absolute levels and variances of pH, pCO2, and bicarbonate were compared between controlled patients before and after successful pharmacological treatment. The results indicate that successful treatment of panic disorder results in a normalization of pH, pCO2, and bicarbonate levels.

Hyperventilation occurs during lactate-induced panic

Abstract Previous work has indicated hyperventilation to be an important concomitant of laboratory provoked anxiety in patients with panic disorder and of anxiety disorder in general. This has led to considerable speculation about the role of hyperventilation in the pathogenesis of panic attacks. We studied minute ventilation changes in 32 patients with panic disorder and 9 normal controls during sodium lactate infusion. The group of patients who had acute panic attacks during the infusion had greater increase in minute ventilation over baseline than patients or controls who did not experience panic attacks. This provides further confirmation that hyperventilation occurs during panic attacks.

Exercise tolerance in panic disorder patients

Sixteen panic patients and fifteen normal controls performed submaximal exercise testing on a bicycle ergometer. Only one patient subject panicked. Biochemical, physiological, and psychological data showed similar exercise tolerance in both patients and controls. Exercise-induced distress and lactate increment do not appear to cause panic attacks.

Specific phobia 10–16 years after treatment

Twenty eight participants, initially treated for specific phobia as part of a comparative treatment study, were evaluated 10 to 16 years (X=12 years) later. A comprehensive, in‐person, semi‐structured diagnostic interview was utilized, which also assessed comorbid disorders. Of 21 patients who had been rated as responders (much improved or very much improved) at treatment termination, 13 (62%) had clinically significant avoidance or endurance with dread subsequent to treatment. Among a subgroup of these responders who had been considered completely recovered (n=11), 5 (45%) had clinically significant symptoms following treatment. None of the seven subjects who had been considered unimproved at treatment termination recovered from phobia symptoms in the intervening years. Positive response to treatment was associated with better long term outcome. Clinical characteristics, such as phobia subtype, age of onset, baseline severity, and lifetime comorbidity of other psychiatric disorders were not associated with long term outcome in this sample. Type of treatment was not associated with long term outcome. Results challenge the notion that recovery from specific phobia following treatment is characterized by complete and enduring cessation of symptoms. Depression and Anxiety 10:105–111, 1999.

A typological model for estimation of drug and placebo effects in depression.

One reason for failure to find specific treatment effects in drug versus placebo trials with patients who have depression is an insufficient period of observation. Also, differentiating between early fleeting response and maintained response has been shown relevant to detecting specific drug action. A model in which various types of drug and placebo response are specifically stipulated and which takes advantage of a two-stage experimental design is proposed. Substantive findings when patients who have major depression with atypical features are studied are: 1) about 6% have only a fleeting response to placebo and no response to drug; 2) by week-10 about 28% of the population will respond even if no medication is given; and 3) specific response to imipramine (21%) can be determined by week-4 but specific response to fluoxetine (20%) cannot be determined until later (week-10 in this study).

Testing Patterned Hypotheses in Multi-Way Contingency Tables Using Weighted Kappa and Weighted Chi Square

Cohens weighted Kappa and weighted Chi square techniques are extended to n-way tables. Formulas are provided for calculating the covariance of two weighted Kappas defined for the same table. This allows a joint Chi square test of several sets of weights. The relationship of this joint test to Cochrans test for a linear trend and to Lancasters partition of Chi square is shown. Some examples of the use of the joint test in evaluating hypotheses about contingency tables are given.