Summary:Intravenous magnesium is reported to be effective in the treatment of ventricular arrhythmias associated with hypomagnesemia, digitalis toxicity, or prolongation of the QT interval. In most previous reports, magnesium was added to conventional antiarrhythmic drugs that had failed. There are few data on the antiarrhythmic efficacy of magnesium as monotherapy in patients without these associated abnormalities. Ten patients with life-threatening ventricular arrhythmia and inducible ventricular tachyarrhythmia by programmed electrophysiologic testing were treated with intravenous magnesium. Following magnesium infusion, all patients still had inducible ventricular tachyarrhythmia. Moreover, magnesium therapy was not associated with significant changes in ventricular refractory period or in the morphology, cycle length, or hemodynamic response to induced ventricular tachycardia. These data suggest that intravenous magnesium has no significant electrophysiologic or antiarrhythmic effects in patients with life-threatening ventricular arrhythmia and inducible ventricular tachyarrhythmia.
Background: Individuals with schizophrenia show impairments in associative learning. One well-studied, quantifiable form of associative learning is Pavlovian fear conditioning. However, to date, studies of fear conditioning in schizophrenia have been inconclusive, possibly because they lacked sufficient power.
Methods: To address this issue, data were pooled from 4 independent fear conditioning studies that included a total of 77 individuals with schizophrenia and 74 control subjects. Skin conductance responses (SCRs) during fear conditioning to stimuli that were paired (the CS+) and not paired (CS-) with an aversive, unconditioned stimulus were measured, and the success of acquisition of differential conditioning (the magnitude of CS+ vs CS- SCRs) and responses to CS+ and CS- separately were assessed.
Results: Acquisition of differential conditioned fear responses was significantly lower in individuals with schizophreania than in healthy controls (Cohen's d = 0.53). This effect was primarily related to a significantly higher response to the CS- stimulus in the schizophrenia compared to the control group. The magnitude of this response to the CS- in the schizophrenia group was correlated with the severity of delusional ideation. Other symptoms or antipsychotic dose were not associated with fear conditioning measures.
Conclusions: Individuals with schizophrenia who endorse delusional beliefs are over-responsive to neutral stimuli during fear conditioning. This finding is consistent with prior models of aberrant learning in psychosis.
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