Adrenergic responses during physical stress such as cold exposure have been reported to differ from those responses observed during cognitive activity. Both the separate and the combined effects of cold and cognitive activity on catecholamine activity were examined in six male subjects. Alterations in plasma epinephrine and norepinephrine showed different patterns as a function of exposure to a 4 degrees C cold environment, a cognitive performance assessment battery (PAB), and the two conditions combined. Plasma epinephrine was not altered by exposure to cold and only slightly increased by PAB performance when given at 23 degrees C. However, epinephrine was substantially elevated by exposure to combined cold and PAB. Heart rate changes paralleled observed changes in epinephrine. Norepinephrine release was predominantly increased by cold exposure and was not altered by PAB performance.
The vasopressin analog desmopressin (DDAVP) is known to enhance memory in animals and man but its precise mechanism of action is uncertain. We report the case of a patient who experienced chronic memory dysfunction with impaired job performance following transsphenoidal resection of a pituitary adenoma. A prospective double-blind, placebo-controlled trial of the effects of DDAVP was performed. Memory storage and recall improved with DDAVP treatment and declined within 1 week after drug withdrawal both by subjective and objective criteria. The Buschke Selective Reminding Test was clearly the most responsive out of a battery of standard memory testing paradigms employed to track the presence or absence of DDAVP treatment.
Ten subjects were exposed to 3.5K Hz tone pulses of 660 msec duration, presented 24‐hr‐per‐day for 30 days. The interstimulus interval was 22 sec. There were 10 days each at 80, 85, and 90 dB in that order. The average evoked potential (AEP) at C3 referenced to linked mastoids was obtained from contiguous stage 2 and REM sleep segments on the first, second, and last recorded nights of tone‐pulse exposure. The AEP was consistently larger in stage 2 than in REM sleep. In both stage 2 and REM sleep, AEP amplitude on the second recorded night bore no consistent relationship to first or last recorded night AEPs. Only the N2–P3 amplitude yielded consistent decreases, with 9 of 10 subjects in both stage 2 and REM sleep having smaller N2–P3 amplitudes on the last than on the first recorded night. There were no changes in latency of any component. During sleep there is little, if any, habituation of the auditory AEP during long‐duration exposures to nonmeaningful stimuli, and certainly no extinction of the AEP under these conditions.
The authors compared treatment of chronic anxiety with biofeedback-mediated electromyographic (EMG) relaxation to treatment with group psychotherapy in a control group. Feedback patients were given two weeks of EMG relaxation training followed by two weeks of self-practice. Significant decreases were found in the feedback group in electromyogram levels, mood distrubance, trait anxiety, and (to a lesser extent) state anxiety; no such decreases occurred in the control group. The authors suggest that EMG feedback can be an important adjunct therapy for chronic anxiety.
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