Soleus H reflex extinction in controls and spastic patients: ordered occlusion or diffuse inhibition?

A.A.J. Hilgevoord*, L.J. Bour, J.H.T.M. Koelman, B.W. Ongerboer de Visser

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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Abstract

Extinction of the soleus H reflex at higher stimulus intensities is commonly attributed to retrograde conduction of action potentials in motor axons. This study was designed to gain further insight into the mechanisms underlying the extinction. The decrease of the H reflex was quantified in a group of controls and spastic patients, with and without depression of the H response by continuous tendon vibration. Response amplitudes were normalized as a percentage of the maximal M wave amplitude. Stimuli were normalized as a multiple of the M wave threshold. After normalization, the mean M recruitment curves, and similarly the fractions of motor axons activated, were equal in each group. In contrast, the mean H reflex amplitudes at the M threshold were different. The mean H reflex decrease, between 1.0 and 1.5 times the M threshold, was found to be the same fraction of the maximal H reflex amplitude in each group. The largest motor fibres, belonging to the largest motoneurones, are traditionally thought to have the lowest threshold for electrical excitation. Collision or retrograde inactivation should therefore preferentially affect the largest motoneurones, employed in only the largest H reflexes, at the lowest stimulus intensities. Our results are contrary to this hypothesis. Renshaw and/or Ib inhibition is likely to play a role in the initial decrease of the H reflex at higher stimulus intensities.

Original languageEnglish
Pages (from-to)402-407
Number of pages6
JournalElectroencephalography and Clinical Neurophysiology. Electromyography and Motor Control
Volume97
Issue number6
DOIs
Publication statusPublished - Dec 1995
Externally publishedYes

Keywords

  • H reflex extinction
  • Normalization
  • Soleus H reflex recruitment
  • Spasticity
  • Vibratory inhibition

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