Silent period measurement revives as a valuable diagnostic tool with transcranial magnetic stimulation

Haug, Bernhard A.; Schönle, P. W.; Knobloch, Christian; Köhne, Martin

doi:10.1016/0168-5597(92)90081-l

Cited by 135 publications

(41 citation statements)

References 13 publications

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“…The SP obtained from the affected side was prolonged in the PL and IC groups. This finding is consistent with earlier reports 16,20,21 and indicates that subcortical lesions increase the activity of inhibitory neuronal circuits. It is assumed that this enhanced intracortical inhibitory activity is because of a deafferentation of the primary motor cortex by different lesions outside M1.…”

Section: Liepert Et Al Excitability Changes In Motor Strokes 2651supporting

confidence: 83%

Motor Strokes

Liepert

Restemeyer

Kucinski

et al. 2005

Stroke

127

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Background and Purpose-The purpose of this research was to investigate the impact of lesion location on motor excitability and motor performance. Methods-We studied patients with pure motor strokes in 4 different brain areas: motor cortex lesions (nϭ7), striatocapsular lesions (nϭ13), lacunar lesions of the internal capsule (nϭ13), and paramedian pontine lesions (nϭ10). Motor performance tests included the 9-hole-peg test and grip strength recordings. Motor excitability was determined by transcranial magnetic stimulation. Motor thresholds, stimulus-response curves, silent periods, motor cortical inhibition, and facilitation were investigated. Results-The 4 groups were clinically similar but showed major differences in motor excitability. Only motor cortex lesions had a loss of intracortical inhibition in the affected hemisphere. In the internal capsule lesion group and the pontine lesion group, stimulus-response curves were depressed on the affected side. All of the subcortical lesions showed a prolongation of the silent period in the paretic side. Motor thresholds were predominantly elevated in the lesioned hemisphere of patients with internal capsule or pontine lesions. Motor performance was correlated with silent period duration in internal capsule lesions and with motor thresholds in internal capsule and pontine lesions. Conclusions-Motor

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Section: Liepert Et Al Excitability Changes In Motor Strokes 2651supporting

confidence: 83%

Motor Strokes

Liepert

Restemeyer

Kucinski

et al. 2005

Stroke

127

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“…This indicates differences in CSP between groups as well as between intensities, and that differences in CSP between groups were independent of intensities used to evoke CSP. Differences between intensities can be explained by a wellknown positive correlation of CSP duration with stimulus intensity (Haug et al, 1992 Intracortical facilitation at interstimulus intervals 9 and 12 ms was found significantly reduced in smokers compared to nonsmokers (ANOVA, post hoc t-test; for details see Results), whereas short-latency intracortical inhibition did not differ between groups.…”

Section: Motor Cortex Excitabilitymentioning

confidence: 87%

Cortical Hypoexcitability in Chronic Smokers? A Transcranial Magnetic Stimulation Study

Lang

Hasan

Sueske

et al. 2007

Neuropsychopharmacol

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Studies in animal models and humans indicate that chronic nicotine intake influences neuronal excitability, resulting in functional and structural CNS changes. The aim of the present study was to explore human primary motor cortex (M1) excitability with transcranial magnetic stimulation (TMS) in chronic smokers. A total of 44 right-handed volunteers, aged 20-30 years, participated in the study. Chronic smokers were compared with age-and sex-matched healthy nonsmokers. We tested cortical excitability with single-and pairedpulse TMS to the left M1 and short-latency afferent inhibition (SAI) by combining median nerve stimulation and motor cortex TMS. Compared with nonsmoking controls, chronic smokers showed a significantly larger amount of SAI, which is thought to depend upon the activity of cholinergic inhibitory circuits produced by somatosensory inputs. Moreover, TMS-evoked inhibitory cortical silent periods were prolonged, whereas paired-pulse intracortical facilitation and motor-evoked potentials during moderate contraction were reduced. The results suggest that chronic nicotine intake may not only strengthen cholinergic inhibitory circuits, but could also be associated with enhanced inhibitory and reduced facilitatory mechanism of specific neuronal circuits in motor cortex. These changes may form a physiological basis for neurobiological and behavioral variations associated with chronic smoking.

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“…With stronger stimuli, however, the inhibitory effects last longer (Haug et al 1992;Cantello et al 1992;Wilson et al 1993) hemisphere delayed the onset of contralateral more than ipsilateral muscle activity.…”

Section: Discussionmentioning

confidence: 99%

The processing of human ballistic movements explored by stimulation over the cortex.

Palmer

Cafarelli

Ashby

1994

The Journal of Physiology

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1. When seated human subjects abducted one arm rapidly in response to a tone there was successively a burst of electromyographic (EMG) activity in the deltoid and latissimus dorsi muscles followed by another burst in the deltoid muscle. This triphasic pattern is typical of a ballistic 'focal movement'. There were also bursts of EMG activity in the contralateral latissimus dorsi, pectoralis major and abdominal muscles, which were assumed to be 'associated postural adjustments'. The same bilateral pattern of muscle activity occurred in a deafferented subject. 2. When subjects abducted the left arm rapidly, magnetic stimulation over the left motor cortex delayed the onset of the EMG burst in the right latissimus dorsi relative to the initial burst in the left deltoid. When subjects abducted the right arm rapidly, magnetic stimulation over the left motor cortex delayed the onset of the initial EMG burst in the right deltoid relative to the burst in the left latissimus. In each case, the delay of an EMG burst was greatest (about 80 ms) when the stimulus was given just before the burst was expected to occur. The inhibition of voluntary movements by transcranial stimulation was not associated with a reduction in the excitability of spinal motoneurons. 3. We conclude that focal ballistic movements and their associated postural adjustments are generated in exactly the same way. We postulate that these movements are preprogrammed, held in a memory until the 'go' signal and then released through both motor cortices to spinal motoneurons.

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Silent period measurement revives as a valuable diagnostic tool with transcranial magnetic stimulation

Cited by 135 publications

References 13 publications

Motor Strokes

Motor Strokes

Cortical Hypoexcitability in Chronic Smokers? A Transcranial Magnetic Stimulation Study

The processing of human ballistic movements explored by stimulation over the cortex.

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