Pharmacologic reversal of cortical hyperexcitability in patients with ALS

Neurology. 2000 Jan 11;54(1):58-64. doi: 10.1212/wnl.54.1.58.

Abstract

Objective: To reverse the profile of abnormal intracortical excitability in patients with ALS by administering drugs that promote GABAergic transmission.

Background: Transcranial magnetic stimulation (TMS) has revealed abnormalities of cortical inhibition in ALS, a reduction of the silent period, and the absence of intracortical inhibition normally occurring in response to paired TMS. Impaired inhibitory transmission could play a role in the physiopathology of this illness.

Methods: Using paired TMS with conditioning stimuli from 1-to-6-msec-interstimulus intervals, we investigated 16 patients with ALS. The protocol included: (1) the "drug-free" profile of paired TMS; (2) paired TMS 30 minutes after the intake of diazepam (3.5 mg); (3) paired TMS after 3 weeks' treatment with gabapentin (GBP) (600 mg/day) or riluzole (50 mg/twice a day).

Results: Intracortical inhibition is lost in patients with ALS, and this abnormal profile is reversed by diazepam or sustained treatment with GBP. We also noted that motor-evoked potential amplitudes to single stimuli increased (p<0.01) after diazepam and GBP.

Conclusions: The demonstration of pharmacologic reversal of hyperexcitability in patients with ALS makes a potentially significant contribution toward understanding the pathophysiology of a disease that has so far eluded an effective cure.

Publication types

  • Clinical Trial

MeSH terms

  • Acetates / therapeutic use
  • Amines*
  • Amyotrophic Lateral Sclerosis / drug therapy*
  • Amyotrophic Lateral Sclerosis / physiopathology*
  • Cerebral Cortex / drug effects*
  • Cerebral Cortex / physiopathology*
  • Cyclohexanecarboxylic Acids*
  • Diazepam / therapeutic use
  • Drug Therapy, Combination
  • Evoked Potentials, Motor
  • Female
  • GABA Agonists / therapeutic use
  • GABA Modulators / therapeutic use
  • Gabapentin
  • Humans
  • Magnetics
  • Male
  • Middle Aged
  • Neural Inhibition / drug effects
  • Neuroprotective Agents / therapeutic use
  • Physical Stimulation / methods
  • Riluzole / therapeutic use
  • Synaptic Transmission / drug effects
  • Treatment Outcome
  • gamma-Aminobutyric Acid*

Substances

  • Acetates
  • Amines
  • Cyclohexanecarboxylic Acids
  • GABA Agonists
  • GABA Modulators
  • Neuroprotective Agents
  • gamma-Aminobutyric Acid
  • Gabapentin
  • Riluzole
  • Diazepam