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On the cause of hyporeflexia in the Holmes-Adie syndrome

From the Division of Neurology and the Playfair Neuroscience Unit, Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada.

Electrophysiologic studies were carried out on 11 patients with Holmes-Adie syndrome, 8 of whom had reduced or absent ankle jerks. Conduction velocities and evoked nerve and muscle compound action potentials in the peroneal, posterior tibial, and sural nerves were normal. The H reflex was absent (or virtually absent) in the patients with depressed reflexes. The amplitude of the composite Ia EPSP in single soleus motoneurons was estimated from changes in firing probability of voluntarily activated soleus motor units in response to stimulation of low threshold afferents in the tibial nerve. These amplitudes were used to test the afferent side of the reflex pathway. Composite group Ia EPSPs in Holmes-Adie patients with hyporeflexia were smaller than normal or absent, indicating that the areflexia in the Holmes-Adie syndrome is due to loss of large spindle afferents or reduced effectiveness of their monosynaptic connections to motoneurons.

Address correspondence and reprint requests to Dr. Ashby, 25 Leonard Avenue, Suite 203, Toronto, Ontario, M5T 2R2, Canada.

Received February 3, 1987. Accepted for publication in final form April 23, 1987.

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