PMID- 18496679
OWN - NLM
STAT- MEDLINE
DCOM- 20081212
LR  - 20211020
IS  - 1432-1106 (Electronic)
IS  - 0014-4819 (Linking)
VI  - 189
IP  - 2
DP  - 2008 Aug
TI  - Enhancement of single motor unit inhibitory responses to transcranial magnetic 
      stimulation in amyotrophic lateral sclerosis.
PG  - 229-42
LID - 10.1007/s00221-008-1420-y [doi]
AB  - In healthy human subjects, transcranial magnetic stimulation (TMS) applied to the 
      motor cortex induces concurrent inhibitory and excitatory effects on motoneurone 
      activity. In amyotrophic lateral sclerosis (ALS), a neurodegenerative disease 
      affecting both cortical and spinal motor neurons, paired-pulse studies based on 
      electromyographic (EMG) recording have revealed a decrease in TMS-induced 
      inhibition. This suggested that inhibition loss may promote excito-toxicity in 
      this disease. Against this hypothesis, an abnormally high incidence of inhibitory 
      responses to TMS has been observed in the peristimulus time histograms (PSTHs) in 
      ALS single motor unit studies. The disappearance of cortico-motoneuronal 
      excitatory inputs might, however, have facilitated the detection of single motor 
      unit inhibitory responses in the PSTHs. This question was addressed here using a 
      new approach, where the strength of the excitatory and inhibitory effects of TMS 
      on motoneurone activity was assessed from the duration of inter-spike intervals 
      (ISIs). This analysis was conducted on single motor unit (MU), tested on healthy 
      subjects and patients with ALS or Kennedy's disease (KD), a motor neuron disease 
      which unlike ALS, spares the cortico-spinal pathway. MUs tested on KD patients 
      behaved like those of healthy subjects unlike those tested on ALS patients. The 
      present data reveal that in ALS, the TMS-induced inhibitory effects are truly 
      enhanced during voluntary contractions and not reduced, as observed in 
      paired-pulse TMS studies under resting conditions. The possible contribution of 
      inhibitory loss to the physiopathology of ALS therefore needs to be reconsidered. 
      The present data do not support the idea that inhibition loss may underlie 
      excito-toxicity in ALS.
FAU - Schmied, Annie
AU  - Schmied A
AD  - Plasticity and Physiopathology of Movement, P3M, UMR 6196, CNRS, University 
      Aix-Marseilles II, 31 Chemin Joseph Aiguier, 13402 Marseilles Cedex 20, France. 
      schmied@dpm.cnrs-mrs.fr
FAU - Attarian, Shahram
AU  - Attarian S
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080522
PL  - Germany
TA  - Exp Brain Res
JT  - Experimental brain research
JID - 0043312
SB  - IM
MH  - Action Potentials/physiology
MH  - Adult
MH  - Aged
MH  - Amyotrophic Lateral Sclerosis/*physiopathology
MH  - Evoked Potentials, Motor/*physiology
MH  - Female
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Motor Cortex/physiology
MH  - Neural Inhibition/*physiology
MH  - Recruitment, Neurophysiological/*physiology
MH  - Transcranial Magnetic Stimulation/*methods
EDAT- 2008/05/23 09:00
MHDA- 2008/12/17 09:00
CRDT- 2008/05/23 09:00
PHST- 2007/09/26 00:00 [received]
PHST- 2008/05/02 00:00 [accepted]
PHST- 2008/05/23 09:00 [pubmed]
PHST- 2008/12/17 09:00 [medline]
PHST- 2008/05/23 09:00 [entrez]
AID - 10.1007/s00221-008-1420-y [doi]
PST - ppublish
SO  - Exp Brain Res. 2008 Aug;189(2):229-42. doi: 10.1007/s00221-008-1420-y. Epub 2008 
      May 22.