Treatment choices when options appear plentiful.
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Biomedical subjects
Publications and source records attributed to Keith E Isenberg.
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Electroconvulsive therapy (ECT) is a safe procedure, infrequently associated with life-threatening complications. Pulmonary embolism (PE) as a complication of ECT has been rarely reported. We describe a nonfatal case of PE that developed during ECT in a 50-year-old man with depression, hypertension, and diabetes. He developed symptoms of PE immediately upon awakening from the eighth right unilateral ECT, which was later confirmed by spiral chest computed tomography. We review the literature, discussing risk factors relevant to the pathophysiology of PE and making suggestions about the management of patients with suspicious symptoms.
Fetal alcohol exposure causes severe neuropsychiatric problems, but mechanisms of the ethanol-associated changes in central nervous system development are unclear. In vivo, ethanol's interaction with N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acid type A (GABA(A)) receptors may cause increased apoptosis in the immature forebrain. We examined whether ethanol affects survival of neonatal hippocampal neurons in primary cultures. A 6-day ethanol exposure killed hippocampal neurons with an LD50 of approximately 25 mM. Elevated extracellular potassium or insulin-related growth factor 1 inhibited cell loss. Although potentiation of GABA(A) receptors or complete block of NMDA receptors also kills hippocampal neurons, pharmacological studies suggest that ethanol's interaction with GABA(A) and NMDA receptors is not sufficient to explain ethanol's effects on neuronal survival. Ca(2+) influx in response to depolarization was depressed >50% by chronic ethanol treatment. We suggest that chronic ethanol may promote neuronal loss through a mechanism affecting Ca(2+) influx in addition to effects on postsynaptic GABA and glutamate receptors.