Enhancement of inhibitory mechanisms in the motor cortex of patients with cerebellar degeneration: a study with transcranial magnetic brain stimulation

Electroencephalogr Clin Neurophysiol. 1996 Aug;101(4):273-80. doi: 10.1016/0924-980x(96)95531-9.

Abstract

The excitatory state of the primary motor cortex can be studied by measuring either the postexcitatory inhibition after transcranial magnetic single stimulation (pI-S) or the refractory period with magnetic double stimulation (rP-D). The cerebellum may influence the excitability of the motor cortex by cerebellar inputs and outputs from side loops of transcortical projections. Therefore, we studied pI-S and rP-D in 24 patients with autosomal dominant cerebellar ataxia or idiopathic cerebellar ataxia, who were allocated to one group (Group A) with mild to moderate ataxia (n = 11) and to another group (Group B) with severe ataxia (n = 13). The results were compared with those obtained in 21 normal age-matched control subjects. The central motor conduction time (CMCT) was delayed in approximately half of the patients, demonstrating that the degenerative process, beyond the cerebellum, also affects the pyramidal tract. Mean CMCT was significantly delayed only in patients of Group B. pI-S was prolonged in 10 of our 24 patients; incidence of pathology in pI-S did not differ between the two patient groups. In 5 patients with normal CMCT, pathological pI-S results were found. Mean pI-S was prolonged in the whole patient group and in both subgroups as well. rP-D was prolonged in two patients of Group B only, but mean rP-D was significantly prolonged in the whole patient group. Prolonged postexcitatory inhibition and refractory period may be a consequence of a transient facilitation of cortical inhibitory interneurons, which results in a decreased excitability of primary motor cortex in patients with cerebellar degeneration.

MeSH terms

  • Adult
  • Aged
  • Cerebellar Ataxia / physiopathology*
  • Female
  • Humans
  • Magnetics*
  • Male
  • Middle Aged
  • Motor Cortex / physiopathology*
  • Nerve Degeneration / physiology*