Electrogenesis of Cortical DC Potentials

Caspers, H.; Speckmann, Erwin‐Josef; Lehmenkühler, A.

doi:10.1016/s0079-6123(08)61603-9

Cited by 63 publications

(30 citation statements)

References 10 publications

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“…3 Inhibitory processes in deep cortical layers produce surface-negative potentials. 44 The random sequence of TMS during intertrial intervals and lCNV avoided systematic confounding effects of external conditions on N100 results.…”

Section: Effects Of Attention and Motor Preparation During Late Contimentioning

confidence: 99%

“…To prevent a sudden synchronized discharge from generalization, intracortical, as well as thalamocortical, inhibitory mechanisms are activated via the thalamic reticular nucleus as established in animal models, 53,54 producing typical spike wave complexes in the EEG. 44,55,56 Therefore, TMS-evoked N100 could be interpreted as "wave" response to an externally generated "spike." It might provide an in vivo model to assess thalamocortical inhibitory processes in human subjects.…”

Section: Explicatory Mechanismsmentioning

confidence: 99%

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Electroencephalographic response to transcranial magnetic stimulation in children: Evidence for giant inhibitory potentials

Bender

Basseler

Sebastian

et al. 2005

Annals of Neurology

117

127

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The electroencephalographic response to transcranial magnetic stimulation (TMS) recently has been established as a direct parameter of motor cortex excitability. Its N100 component was suggested to reflect an inhibitory response. We investigated influences of cerebral maturation on TMS-evoked N100 in 6- to 10-year-old healthy children. We used a forewarned reaction time (contingent negative variation) task to test the effects of response preparation and sensory attention on N100 amplitude. Single-pulse TMS of motor cortex at 105% motor threshold intensity evoked N100 amplitudes of more than 100 microV in resting children (visible in single trials), which correlated negatively with age and positively with absolute stimulation intensity. During late contingent negative variation, which involves preactivation of the cortical structures necessary for a fast response, N100 amplitude was significantly reduced. We conclude that (1) N100 amplitude reduction during late contingent negative variation provides further evidence that TMS-evoked N100 reflects inhibitory processes, (2) response preparation and attention modulate N100, and (3) TMS-evoked N100 undergoes maturational changes and could serve to test cortical integrity and inhibitory function in children. Parallels between the inhibitory N100 after TMS (provoking massive synchronous excitation) and the inhibitory wave component of epileptic spike wave complexes are suggested.

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Section: Effects Of Attention and Motor Preparation During Late Contimentioning

confidence: 99%

Section: Explicatory Mechanismsmentioning

confidence: 99%

Electroencephalographic response to transcranial magnetic stimulation in children: Evidence for giant inhibitory potentials

Bender

Basseler

Sebastian

et al. 2005

Annals of Neurology

117

127

View full text Add to dashboard Cite

show abstract

“…However, SCPs in the human EEG are increasingly used to make inferences about regional functional localization and this is because of the well-documented finding that negative SCP shifts recorded at the cortical surface reflect increased activation within underlying neural tissue, e.g. postsynaptic potentials and related activity (Birbaumer et al, 1990;Caton, 1875;Ikeda et al, 1995;Kotchoubey et al, 1997;Lang et al, 1989;Niemann et al, 1992;Speckman & Caspers, 1979Caspers et al, 1980;Speckman et al, 1984;Caspers et al, 1987;Rockstroh 1993;Rockstroh et al, 1989). Indeed, topographic variations of slow potentials within human EEG have been examined during complex and sustained cognitive operations and used for functional localization (e.g., Lang et al, 1993;Rosler et al, 1997;see too Curry & Pleydell-Pearce, 1995;Pleydell-Pearce & Whitecross, 2000).…”

Section: Slow Cortical Potentials and Memory Retrievalmentioning

confidence: 99%

The Neuroanatomy of Autobiographical Memory: A Slow Cortical Potential Study of Autobiographical Memory Retrieval☆

Conway

Pleydell-Pearce

Whitecross

2001

Journal of Memory and Language

153

123

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“…Moreover, excessive calcium influx is thought to be the first step of epileptic neuronal events (3)(4)(5)(6)(7). The effects of several calcium channel blockers have been investigated in different models of epilepsy (8)(9)(10)(11)(12); however, the results obtained show important discrepancies.…”

Section: Intracellularmentioning

confidence: 99%

Calcium channel blocker flunarizine suppresses epileptiform activity induced by penicillin in rats

Bağirici¹,

Gökçe²,

Demi̇r³

et al. 2001

Neuroscience Res Communica

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SUMMARYEpilepsy is a neurological disorder that affects approximately 1% of the world population. It is accepted that calcium influx into the cell is the first step of epileptic neuronal events. In the present study, the effects of flunarizine on epileptiform activity were investigated in an experimental epilepsy model induced by intracortical (i.c.) penicillin administration.The left cerebral cortex was exposed by craniotomy in anaesthetised rats. The epileptic focus was produced by injection of penicillin G potassium (500 units) into the somatomotor cortex. After epileptiform activity reached maximum frequency and amplitude, flunarizine was injected into the same area with a Hamilton microinjector.Before flunarizine administration, the average frequency of spikes was 18.7 k 2

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Electrogenesis of Cortical DC Potentials

Cited by 63 publications

References 10 publications

Electroencephalographic response to transcranial magnetic stimulation in children: Evidence for giant inhibitory potentials

Electroencephalographic response to transcranial magnetic stimulation in children: Evidence for giant inhibitory potentials

The Neuroanatomy of Autobiographical Memory: A Slow Cortical Potential Study of Autobiographical Memory Retrieval☆

Calcium channel blocker flunarizine suppresses epileptiform activity induced by penicillin in rats

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