Biomedical subjects
Publications and source records attributed to R Balon.
Jitteriness appears to be a specific side effect of tricyclic antidepressant treatment in panic disorder patients. In addition, the patients with jitteriness have lower serum iron levels compared to those that do not develop jitteriness (p = 0.01).
In a prospective study, we have compared R-axis on routine electrocardiograms of panic disorder patients (n = 52) with that of depressed patients (n = 41) and normal controls (n = 65). All subjects were physically healthy and were normotensive. There was a significant leftward shift of R-axis in both depressed and panic disorder patients compared to normal controls. The implications of these findings are discussed.
Recently, heart rate (HR) variability has received considerable attention, and a decreased HR variability has been linked to a significant risk of cardiovascular illness. We have previously reported such a decreased variability in panic disorder patients. In this study, we report on HR variability in 12 depressed and 6 panic disorder patients at baseline and 1 and 3 weeks of treatment with imipramine as measured by the standard deviation, mean consecutive difference and the standard deviation of the mean consecutive difference of the R-R intervals in supine, supine deep breathing and standing postures. In all subjects, imipramine (mean dose: 70 mg/day) produced a significant decrease in heart rate variability at week 3 as measured by the above variables. This decrease in HR variability during imipramine treatment is probably due to its anticholinergic effects.
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We compared the effects of intravenous infusions of clonidine and placebo on heart rate variability in 10 healthy male controls. Clonidine produced a significant decrease in blood pressure and significantly decreased the heart rate variability during quiet standing.
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We have previously reported decreased heart rate variability upon standing in panic disorder patients compared with controls. In this study, we extend our report to include patients with major depression (n = 19). Compared to normal controls (n = 20) and panic disorder patients (n = 30), there was no significant difference in the immediate changes in heart rate upon standing in the depressed group. The standing heart rate variability (R-R variability) was significantly lower in panic disorder patients compared to both normal controls and depressed patients as indicated by the corrected standard deviations, the corrected mean consecutive difference, the corrected standard deviation of the mean consecutive difference of the R-R intervals, and the high frequency variability in successive R-R intervals, suggesting an increased vagal withdrawal in panic disorder patients, especially upon standing. There was no significant difference in any of the heart rate variability measures between depressed patients and normal controls.
1. Because imipramine has lowered T4 in uncontrolled studies we examined the effect of imipramine on serum thyroid levels in panic disorder patients in a double-blind placebo and diazepam treatment controlled study. 2. Treatment with imipramine (10 subjects) was associated with a significant decrease of T4 and FTI and treatment with diazepam (8 subject) was associated with a significant decrease of T4. However, there was no significant difference across treatment groups. 3. This finding suggests that previously reported decreases in thyroid hormones during antidepressant therapy may be due to nonspecific effects of treatment rather than to the drug itself.
Alterations of immunocompetence in various mental disorders have been reported. We studied white blood cell counts and immunoglobulin levels in 59 panic disorder patients and 30 controls. The significantly increased IgA levels and tendency toward increase in other immunoglobulins in panic disorder patients suggest an immune dysfunction.
Fourteen panic disorder patients were infused with isoproterenol both before and after treatment with tricyclic antidepressants. Thirteen patients had panic attacks before treatment, and only 2 after treatment. There was a significant decrease in anxiety as measured by a Panic Description Scale during posttreatment infusions, and patients were able to tolerate longer infusions posttreatment. Isoproterenol increased systolic blood pressure and decreased diastolic blood pressure in both untreated patients and in 10 normal controls. Tricyclic antidepressant treatment of panic disorder patients abolished isoproterenol-induced increases in systolic blood pressure, but did not affect diastolic blood pressure response. These changes are consistent with a decrease in sensitivity to beta-1 receptor stimulation after treatment with tricyclic antidepressants.
Postural and isometric handgrip tests were performed on nine patients with panic disorder and 13 patients with major depression before and after treatment with imipramine for a mean duration of 10 weeks. There were significant increases in resting supine heart rate (HR), systolic, diastolic and mean blood pressures (SBP, DBP, MBP) after treatment. There were significant increases in HR and DBP after standing from supine posture before treatment, and after treatment, there was a significant enhancement of this tachycardia. The decrease of heart rate during the change from standing to supine posture before treatment significantly decreased further after imipramine treatment. Decreases in SBP and DBP during the change from standing to supine posture were significantly smaller during the post treatment condition. Increases in SBP during the standing isometric exercise test were smaller after treatment. These findings suggest abnormal orthostatic reflexes secondary to an altered adrenergic function and/or cholinergic supersensitivity after treatment with imipramine.
To determine which symptoms characterized isoproterenol-induced panic attacks, we analyzed the presence of panic attacks in 54 panic disorder patients who panicked, 24 patients who did not panic, and 37 controls who did not panic during isoproterenol infusions. The increases over the baseline of the symptoms shortness of breath and fear of going crazy were highly associated with panicking patients when compared to nonpanicking patients and nonpanicking controls. The increases of the symptoms trembling and shaking, generally nervous, and fear of going crazy were highly associated with patients when compared to controls. The possibility of a cognitive theory of panic attacks is discussed.
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Sixty-seven patients with panic disorder were treated with single-blind placebo for one week before being randomized to 6 weeks of double-blind treatment with either lorazepam or alprazolam. Both drugs showed significant and comparable antipanic efficacy throughout the course of the study. With the exception of sedative effects, both drugs were well-tolerated at a mean daily dose of 7 mg for lorazepam and 3 mg for alprazolam. Lorazepam appeared to be as effective as alprazolam in the acute treatment of panic disorder.
Thirty normal controls, 30 panic-disorder patients and 19 depressed patients participated in a study involving postural and isometric handgrip tests. Prestimulus values of heart-rate and blood-pressure were correlated with stimulus phasic responses. The law of initial values did not hold during the change from supine to standing posture or during the isometric handgrip test for heart-rate and blood-pressure, but it held for heart-rate during the change from standing to supine posture. The effect of regression toward the mean was accounted for in the analyses.