Effects of vigabatrin on motor potentials evoked with magnetic stimulation

Mavroudakis, Nicolas; Caroyer, Jean-Marc; Brunko, Eric; Beyl, D. Zegers de

doi:10.1016/s0924-980x(96)96607-2

Cited by 41 publications

(21 citation statements)

References 22 publications

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“…MT reflects neuronal membrane excitability which largely depends on Na + channel conductivity (Mavroudakis et al, 1997). Paired pulse recovery curves used to measure intracortical inhibition at short ISIs (2-5 ms) are thought to reflect the activity of GABA A mediated interneurons, (Boroojerdi, 2002) while inhibition at longer ISIs (100-300 ms) appears to be mediated by changes in GABA B circuits (McDonnell et al, 2007;Florian et al, 2008, Mott andLewis, 1994).…”

Section: Discussionmentioning

confidence: 98%

Does the region of epileptogenicity influence the pattern of change in cortical excitability?

Badawy

Vogrin

Lai

et al. 2015

Clinical Neurophysiology

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Section: Discussionmentioning

confidence: 98%

Does the region of epileptogenicity influence the pattern of change in cortical excitability?

Badawy

Vogrin

Lai

et al. 2015

Clinical Neurophysiology

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“…Although we do not have the serum levels of LTG in patients, we document that the drug has a dosedependent effect on the motor threshold, probably related to the steady-state level of the drug. We note that while 81 (9) 85 (9) 80 (7) 83 (9) 81 (8) CSP 30% 140 (8) 145 (8) 142 (9) 141 (7) 142 ( the relation between drug serum levels has been reported for a single-dose assumption (9), it has not been systematically studied in detail with long-term, loading-dose treatment.…”

Section: Discussionmentioning

confidence: 99%

“…It was documented in experimental conditions with normal subjects that single doses of PHT, CBZ, and LTG produced a significant increase of motor threshold followed by a rapid return to baseline values in a timewindow of a few hours (5,7). In contrast, AEDs vigabatrin (VGB), gubapentin, lorazepam, and baclofen have no effect on motor thresholds (4,5,8) but increase the intracortical inhibition (5). Similarly, single doses of some AEDs given to healthy subjects produced transi-tory changes in the inhibitory effects of the double-shock transcranial stimulation used to test intracortical excitability (5,9).…”

mentioning

confidence: 99%

Cortical Excitability in Patients After Loading Doses of Lamotrigine: A Study with Magnetic Brain Stimulation

et al. 1999

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Summary:Purpose: Transcranial magnetic stimulation (TMS) of the brain allows the pharmacologic effects of anticonvulsant drugs (AEDs) on the excitability of motor corticospinal pathways to be evaluated in patients with epilepsy and normal subjects. However, no study has yet documented the changes in motor excitability in patients treated with lamotrigine (LTG). We aimed to study the effects of loading doses of LTG on TMS recordings in patients with epilepsy at the beginning of their treatment.Methods: We investigated single-pulse TMS in six patients with complex partial seizures. The TMS recordings were performed in five sessions before and during 5 weeks of treatment. Motor threshold, motor-evoked potential (MEP) amplitude, cortical silent period, and peripheral conduction velocity were used as parameters of evaluation. LTG was started with a dosage of 25 mglday until a daily maintenance dosage of 200 mg/day was reached.Results: The motor threshold activation of thenar muscles was significantly increased by LTG after 2 weeks of treatment and was increased in a parallel way to the loading dose of the drug at week 3 and 5 of treatment. The MEP size recorded from the thenar muscles did not show significant changes at high-or low-intensity stimulation. The cortical silent period remained unchanged at low-and high-intensity stimulation. The absolute latency of MEPs after cortical and cervical stimulation was unchanged, as was the central motor conduction time.Conclusions: Our study documents that loading doses of LTG, administered as monotherapy, progressively increases patients' motor thresholds over short periods.

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“…It is elevated by sodium channel blockers like carbamazepine or phenytoin (Mavroudakis et al, 1994;Z iemann et al, 1996b;Chen et al, 1997b) but remains unchanged by GABAergic drugs like benzodiazepines or vigabatrin (Inghilleri et al, 1996;Ziemann et al, 1996a,b;Mavroudakis et al, 1997) and antiglutamatergic drugs like gabapentin or riluzole (Ziemann et al, 1996b;Liepert et al, 1998). Changes in MEP size from muscles immediately proximal to the level of deafferentation reflect changes in the excitability or in the representation of these mus- Figure 4.…”

Section: Measures Of Motor Cortex Plasticitymentioning

confidence: 99%

Modulation of Plasticity in Human Motor Cortex after Forearm Ischemic Nerve Block

1998

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Deafferentation leads to cortical reorganization that may be functionally beneficial or maladaptive. Therefore, we were interested in learning whether it is possible to purposely modulate deafferentation-induced reorganization. Transient forearm deafferentation was induced by ischemic nerve block (INB) in healthy volunteers. The following five interventions were tested: INB alone; INB plus low-frequency (0.1 Hz) repetitive transcranial magnetic stimulation of the motor cortex ipsilateral to INB (INBϩrTMS i ); rTMS i alone; INB plus rTMS of the motor cortex contralateral to INB (INBϩrTMS c ); and rTMS c alone. Plastic changes in the motor cortex contralateral to deafferentation were probed with TMS, measuring motor threshold (MT), motor evoked-potential (MEP) size, and intracortical inhibition (ICI) and facilitation (ICF) to the biceps brachii muscle proximal to the level of deafferentation. INB alone induced a moderate increase in MEP size, which was significantly enhanced by INBϩrTMS c but blocked by INBϩrTMS i . INB alone had no effect on ICI or ICF, whereas INBϩrTMS c reduced ICI and increased ICF, and conversely, INBϩrTMS i deepened ICI and suppressed ICF. rTMS i and rTMS c alone were ineffective in changing any of these parameters. These findings indicate that the deafferented motor cortex becomes modifiable by inputs that are normally subthreshold for inducing changes in excitability. The deafferentation-induced plastic changes can be up-regulated by direct stimulation of the "plastic" cortex and likely via inhibitory projections down-regulated by stimulation of the opposite cortex. This modulation of cortical plasticity by noninvasive means might be used to facilitate plasticity when it is primarily beneficial or to suppress it when it is predominately maladaptive.

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Effects of vigabatrin on motor potentials evoked with magnetic stimulation

Cited by 41 publications

References 22 publications

Does the region of epileptogenicity influence the pattern of change in cortical excitability?

Does the region of epileptogenicity influence the pattern of change in cortical excitability?

Cortical Excitability in Patients After Loading Doses of Lamotrigine: A Study with Magnetic Brain Stimulation

Modulation of Plasticity in Human Motor Cortex after Forearm Ischemic Nerve Block

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