Brain, Vol. 118, No. 6, 1437-1446, 1995
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research-article |
Inhibition of human motor cortex by ethanol A transcranial magnetic stimulation study
Department of Clinical Neurophysiology, University of Göttingen Germany
Correspondence to:
Correspondence to: Dr Ulf Ziemann, Department of Clinical Neurophysiology, University of Göttingen, Robert-Koch-Straße 40, D-37075 Göttingen, Germany
The non-invasive technique of focal transcranial magnetic stimulation (TMS) was used in six healthy volunteers to evaluate the effect of ethanol on four aspects of human central motor system excitability: (i) threshold intensity for the motor evoked potential (MEP) in the resting and active abductor digiti minimi muscle (ADM): (ii) variation of MEP amplitude with increasing stimulus intensity; (iii) duration of the TMS induced cortical silent period (CSP); (iv) intracortical inhibition and facilitation after paired magnetic stimulation. In addition, the maximum M wave (Mmax) after supra-maximal electrical ulnar nerve stimulation and the peripheral silent period (PSP) have been tested as parameters of peripheral motor excitability. Baseline measurements were compared with data obtained on a mean ethanol blood concentration of 0.8 ml/l. Resting and active motor thresholds remained unchanged. Also, the absolute Mmax values and the MEP/Mmax ratio at various TMS intensities were not affected by ethanol. The mean CSP duration was prolonged by up to 35 ms while the PSP duration showed no change. The principal effect of ethanol was an enhancement of intracortical inhibition and a suppression of intracortical facilitation. These results are discussed in relation to data from animal experiments which have shown a potentiation of r-aminobutyric acid (GABA) receptor-mediated currents as the main mode of action of ethanol in the mammalian cortex. It is suggested that CSP and intracortical inhibition reflect the activation of cortical GABAergic mechanisms by TMS, while motor threshold does not
motor cortex excitability; ethanol; transcranial magnetic brain stimulation; human
Received June 21, 1995. Accepted July 22, 1995.
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