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A pharmacologic study of the stiff-man syndrome

Correlation of clinical symptoms with urinary 3-methoxy-4-hydroxy-phenyl glycol excretion

Department of Neurology, Northwestern University Medical School, and the Neurology Service, Veterans Administration Research Hospital, Chicago.

We have investigated hypotheses that link the stiff-man syndrome to an imbalance of neurotransmitter systems. No evidence was found to support the concept of defective synaptic transmission at either cholinergic input to Renshaw inhibitory elements or at glycinergic inhibitory input to motoneurons from spinal interneurons, since neither physostigmine nor glycine altered symptomatology. Urinary excretion of the norepinephrine metabolite 3-methoxy-4-hydroxy-phenyl glycol showed a high correlation with clinical status. This suggests the involvement in the stiff-man syndrome of a central norepinephrine neuronal system that has net excitatory effects upon motoneurons, a system whose activity can be increased slightly by levodopa and decreased markedly by diazepam, with corresponding changes in stiffness.

This study was supported in part by National Institute of General Medical Sciences medical scientist research fellowship award GM56040 to Dr. Stahl.

This paper was read at the twenty-seventh annual meeting of the American Academy of Neurology, Miami, May 1975.

Received for publication November 18, 1974.

Reprint requests should be addressed to Dr. Spehlmann at Veterans Administration Research Hospital, 333 East Huron Street, Chicago, IL 60611. Dr. Schmidt's present address is Department of Pathology, Boston City Hospital, Boston, MA. Dr. Stahl's present address is Departments of Pharmacological and Physiological Sciences and Psychiatry, University of Chicago, Chicago, IL.

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