Impaired short- and long-latency afferent inhibition in amyotrophic lateral sclerosis.


CENGİZ B., Fidanci H., Keceli Y. K., BALTACI H., Kuruoglu R.

Muscle & nerve, vol.59, no.6, pp.699-704, 2019 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 59 Issue: 6
  • Publication Date: 2019
  • Doi Number: 10.1002/mus.26464
  • Journal Name: Muscle & nerve
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.699-704
  • Keywords: amyotrophic lateral sclerosis, cortical excitability, long afferent inhibition, short afferent inhibition, sensorimotor integration, transcranial magnetic stimulation, TRANSCRANIAL MAGNETIC STIMULATION, SOMATOSENSORY EVOKED-POTENTIALS, RAT HYPOGLOSSAL MOTONEURONS, CENTRAL CHOLINERGIC CIRCUITS, HUMAN MOTOR CORTEX, CORTICAL EXCITABILITY, INTRACORTICAL INHIBITION, HYPEREXCITABILITY, DISEASE, ALS
  • Gazi University Affiliated: Yes

Abstract

Introduction: To test the hypothesis of impaired cholinergic activity in amyotrophic lateral sclerosis (ALS), we studied short- and long-latency afferent inhibition (SAI and LAI). Methods: The ulnar nerve was stimulated at the wrist preceding transcranial magnetic stimulation (TMS), 21 ms for SAI and 200 ms for LAI, in 21 patients and 17 control subjects. Short-interval intracortical inhibition (SICI) and cognitive function was assessed in ALS patients using automatic threshold tracking and the Montreal Cognitive Assessment (MoCA). Results: The SAI paradigm resulted in inhibition in all control subjects, whereas inhibition was observed in 13 of 21 (62%) patients. Mean SAI and LAI values were significantly reduced in ALS. No significant correlation existed between afferent inhibition and other neurophysiological data. The MoCA was normal in all but 1 patient. Discussion: LAI and SAI are both impaired in ALS, probably unrelated to increased cortical excitability or cognitive dysfunction. Muscle Nerve 59:699-704, 2019