Abstract
In addition to reduced nerve conduction velocity, diabetic neuropathic patients often exhibit a reduction in the amplitude of the compound muscle action potential elicited by stimulation of the Ia-afferent-mediated reflex pathway (Hoffman or H wave) that can contribute to diminished or absent tendon reflexes. In contrast to nerve conduction velocity deficits, changes in H-wave amplitudes have not been reproduced in diabetic animal models. Using electrophysiological techniques developed for repeated recordings in individual animals, we report H-wave deficits in streptozotocin (STZ)-treated insulin-dependent diabetic rats. After 4 weeks of diabetes induced by STZ treatment, a 47% reduction in the H-wave amplitude was demonstrated by recording compound muscle action potentials in foot muscles after stimulation of Ia afferents. Interestingly, we also demonstrate that the H-wave amplitude gradually recovers to a 26% deficit after 12 weeks of experimental diabetes. The recovery of the H wave in STZ-treated rats distinguishes this deficit mechanistically from other STZ-induced electrophysiological changes and may model a similar recovery of the H wave reported in diabetic patients.
Original language | English (US) |
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Pages (from-to) | 220-227 |
Number of pages | 8 |
Journal | Experimental Neurology |
Volume | 172 |
Issue number | 1 |
DOIs | |
State | Published - 2001 |
Externally published | Yes |
Keywords
- Diabetes
- Muscle atrophy
- Neuropathy
- Stz
- Tendon reflex
ASJC Scopus subject areas
- Neurology
- Neuroscience(all)