Ipsilateral cortico-cortical inhibition of the motor cortex in various neurological disorders

Hanajima, Ritsuko; Ugawa, Yoshikazu; Terao, Yasuo; Ogata, Katsuhisa; Kanazawa, Ichiro

doi:10.1016/0022-510x(96)00100-1

Cited by 154 publications

(84 citation statements)

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“…The reduction in early ICI without changes in ICF in our JME patients provides further evidence to support the hypothesis that inhibitory mechanisms may be altered in JME (19)(20)(21). This finding is in agreement with previous paired TMS investigations on the excitability of motor areas in epilepsy (15)(16)(17). However, in those studies, paired TMS was performed in progressive, severe myoclonic epilepsy (16,17), whereas paired TMS using short ISIs has been investigated only unilaterally in a small number of JME patients (1 5).…”

Section: Discussionsupporting

confidence: 92%

“…ICI ( 1 4 (15) 1600 (700) 52 (9) 68 (15) 93 (20) 125 (14) 40 (7) 32.2 (12) 126 (18) (16) 1400 (500) RMT, resting motor threshold (percent of maximal stimulator output); AMT, active motor threshold (percent of maximal stimulator output); msec, millisecond; CPS-10, -20, -30, duration of the silent period in msec at stimulus intensities of 10, 20, and 30% of stimulator output over the AMT, ICI ( 1 4 ) and ICI (100-150), intracortical inhibition (conditioned MEPkontrol MEP) averaged across interstimulus intervals of 1 to 4 msec and across interstimulus intervals of I00 to 150 msec; ICF (1 0-23, intracortical facilitation (conditioned MEPkontrol MEP) averaged across interstimulus intervals of 10 to 25 msec; MEP/M, motor evoked potential amplitude at 120% of stimulus intensities over the RMT/peripheral M wave amplitude (ratios in percent).…”

Section: Jme Patientsmentioning

confidence: 99%

“…Intraoperative monitoring has shown that the MEP amplitude at long ISIs (100 to 150 milli-seconds) occurs at the cortical level (13). Paired TMS has been used as a research tool to investigate motor cortex excitability in different forms of epilepsy (14)(15)(16)(17) and in several neurological diseases (1 6,lS). Reduced cortical inhibition was observed in progressive myoclonic epilepsy (15,16) and in partial epilepsy (14).…”

mentioning

confidence: 99%

“…Paired TMS has been used as a research tool to investigate motor cortex excitability in different forms of epilepsy (14)(15)(16)(17) and in several neurological diseases (1 6,lS). Reduced cortical inhibition was observed in progressive myoclonic epilepsy (15,16) and in partial epilepsy (14). There is only one report of decreased motor inhibition in a small number of patients with juvenile myoclonic epilepsy (JME); in that study, the authors used paired TMS in one hemisphere at short ISIs (I 5).…”

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confidence: 99%

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Early and Late Intracortical Inhibition in Juvenile Myoclonic Epilepsy

et al. 2000

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Summary: Purpose:We investigated 15 patients with juvenile myoclonic epilepsy (JME) by subjecting them to single and paired transcranial magnetic stimulation to test the hypothesis that motor cortical inhibition may be abnormal in this form of benign epilepsy.Methods: Different conditioning paradigms of paired transcranial magnetic stimulation were used with interstimulus intervals (ISIS) of varying lengths (1 to 400 milliseconds) to investigate changes in balance between excitatory and inhibitory intracortical circuits.Results: Motor evoked potential (MEP) inhibition at ISIs of 1 to 4 milliseconds was significantly lower in JME patients than in age-matched healthy controls (p < 0.001), whereas no significant differences in MEP inhibition were noted at long ISIs (100 to 150 milliseconds). This pattern was observed in both hemispheres in seven of seven patients studied bilaterally and was present in both treated and untreated patients. There were no group differences between JME patients and controls in intracortical facilitation, motor threshold, MEP amplitude, and cortical silent period.Conclusions: We documented a different pattern of MEP inhibition in JME patients, suggesting impaired functioning of inhibitory interneuronal circuits, which may account for the hyperexcitability of the motor system in this form of epilepsy.

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Section: Discussionsupporting

confidence: 92%

Section: Jme Patientsmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Early and Late Intracortical Inhibition in Juvenile Myoclonic Epilepsy

et al. 2000

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“…Among movement disorders, reduction of SICI (Hanajima et al, 1996;Pierantozzi et al, 2001;Ridding et al, 1995;Strafella et al, 2000), prolongation of silent period, and increases in LICI has been reported in the motor cortex of patients with Parkinson's disease (Berardelli et al, 2008;Berardelli et al, 1996). In another study, impairment of both SICI and ICF was observed in early Parkinson's disease patients not treated with dopamine agonists (Bares et al, 2003).…”

Section: Tms-eeg-emg In Diagnosis and Treatment Of Neuropsychiatric Dmentioning

confidence: 99%

Combination of Transcranial Magnetic Stimulation with Electromyography and Electroencephalography: Application in Diagnosis of Neuropsychiatric Disorders

Farzan

Barr

Fitzgerald³

et al. 2012

EMG Methods for Evaluating Muscle and Nerve Function

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Pathophysiology of chorea and bradykinesia in Huntington's disease

Berardelli¹,

Noth²,

Thompson³

et al. 1999

Mov. Disord.

157

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This article reviews the neurophysiological abnormalities described in Huntington's disease. Among the typical features of choreic movements are variable and random patterns of electromyographic (EMG) activity, including cocontraction of agonist and antagonist muscles. Studies of premotor potentials show that choreic movements are not preceded by a Bereitschaftspotential, therefore demonstrating that choreic movement is involuntary. Early cortical median‐nerve somatosensory‐evoked potentials have reduced amplitudes and the reduction correlates with reduced glucose consumption in the caudate nucleus. Long‐latency stretch reflexes evoked in the small hand muscles are depressed. These findings may reflect failed thalamocortical relay of sensory information. In Huntington's disease, the R2 response of the blink reflex has prolonged latencies, diminished amplitudes, and greater habituation than normal. These abnormalities correlate with the severity of chorea in the face. Patients with Huntington's disease perform simple voluntary movements more slowly than normal subjects and with an abnormal triphasic EMG pattern. Bradykinesia is also present during their performance of simultaneous and sequential movements. Eye movements show abnormalities similar to those seen in arm movements. In Huntington's disease, arm movement execution is associated with reduced PET activation of cortical frontal areas. Studies using transcranial magnetic stimulation show that patients with Huntington's disease have normal corticospinal conduction but some patients have a prolonged cortical silent period. Bradykinesia results from degeneration of the basal ganglia output to the supplementary motor areas concerned with the initiation and maintenance of sequential movements. The coexisting hyperkinetic and hypokinetic movement disorders in patients with Huntington's disease probably reflect the involvement of direct and indirect pathways in the basal ganglia–thalamus–cortical motor circuit.

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Ipsilateral cortico-cortical inhibition of the motor cortex in various neurological disorders

Cited by 154 publications

References 11 publications

Early and Late Intracortical Inhibition in Juvenile Myoclonic Epilepsy

Early and Late Intracortical Inhibition in Juvenile Myoclonic Epilepsy

Combination of Transcranial Magnetic Stimulation with Electromyography and Electroencephalography: Application in Diagnosis of Neuropsychiatric Disorders

Pathophysiology of chorea and bradykinesia in Huntington's disease

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