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Masaharu Takamori, MD; Nobuko Ishii, MD; Masataka Mori, MD

Arch Neurol. 1973;29(6):420-424.

Abstract
The neuromuscular transmission defect of the Eaton-Lambert syndrome in which calcium-dependent acetylcholine release by nerve impulse is defective was partially corrected by epinephrine and methylxanthines. These drugs act on the adenyl cyclase system to increase the content of cyclic 3', 5'-adenosine monophosphate in cells and have effects similar to those of calcium. No meaningful change was seen with these drugs in classical myasthenia patients or in normal subjects. Alpha-adrenergic stimulants showed the same action as epinephrine, while the β-adrenergic stimulants worsened the transmission block. However, the epinephrine-induced relief was potentiated by the β-adrenergic blocker but was eliminated by the -adrenergic blocker. These findings suggest that the presynaptic adrenergic modulation in Eaton-Lambert syndrome is mediated through the a-receptor.

Author Affiliations
Nagasaki, Japan

From the First Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki, Japan.

Footnotes
Accepted for publication July 17, 1973.

Reprint requests to First Department of Internal Medicine, Nagasaki University School of Medicine, 7-1, Sakamoto-cho, Nagasaki, Japan (Dr. Takamori).

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