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Bruce H. Peters, MD; Harvey S. Levin, PhD

Arch Neurol. 1977;34(4):215-219.

Abstract
• Central anticholinergic agents (eg, scopolamine) are known to produce transient memory deficits in human and animal subjects. Damage to the limbic system frequently results from herpes simplex encephalitis (HSE) and produces a memory deficit. If this deficit is due to limbic cholinergic pathway destruction, it might improve with central cholinergic agonists (eg, physostigmine). In a double-blind study over a three-week period, we compared memory performance on three days after 0.8-mg subcutaneous physostigmine therapy (three sessions) to baseline performance and that obtained in three randomly interspersed control sessions. Serial assessment of memory by the Selective Reminding Test showed reproducible enhancement of long-term storage and retrieval with physostigmine treatment. Performance after control injections did not exceed baseline levels. Our findings encourage the hypothesis that cholinergic mechanisms subserve memory and that their pharmacological potentiation might favorably influence some amnesic conditions.

Author Affiliations
From the Departments of Neurology (Dr Peters) and Neurosurgery (Dr Levin) and the Marine Biomedical Institute (Dr Peters), the University of Texas Medical Branch, Galveston, Tex.

Footnotes
Accepted for publication Dec 14, 1976.

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