Cortical inhibition at rest and under a focused attention challenge in adults with migraine with and without aura

Objectives: We aimed to further elucidate the functional and attentional regulation of cortical excitability in migraine patients. Methods: We investigated the cortical silent period (CSP) after transcranial magnetic stimulation as a measure of cortical inhibition under three conditions: resting condition, cortical preactivation during reaction preparation, and during the post-processing of a motor response using a visual contingent negative variation paradigm in adults with migraine with aura, migraine without aura and healthy controls. Results: CSP was reduced in individuals with migraine with aura and unaffected in those with migraine without aura under resting conditions. Along with the intensity of transcranial magnetic stimulation, CSP increased equally in all groups (equal slopes). Furthermore, the functional challenge by a contingent negative variation task requiring focused sustained attention led to a comparable reduction of CSP duration in all groups. Discussion: Our data provide further hints towards the conclusion that a specific cortical inhibition deficit in migraine with aura but not migraine without aura is due to a tonic imbalance and not related to increased reactions to phasic stressors. Given that CSP at rest is related to GABA-ergic inhibition whereas the CSP reduction during late contingent negative variation is thought to be related to dopaminergic disinhibition in the basal ganglia, our results point towards reduced GABA-ergic cortical inhibition related to dysfunctional thalamo-cortical loops, especially in migraine with aura.

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Risperidone increases the cortical silent period in drug-naive patients with first-episode schizophrenia: A transcranial magnetic stimulation study

Journal of Psychopharmacology ◽

10.1177/0269881116662650 ◽

2016 ◽

Vol 31 (4) ◽

pp. 500-504 ◽

Cited By ~ 1

Author(s):

Libor Ustohal ◽

Michaela Mayerova ◽

Veronika Hublova ◽

Hana Prikrylova Kucerova ◽

Eva Ceskova ◽

...

Keyword(s):

Transcranial Magnetic Stimulation ◽

Magnetic Stimulation ◽

Silent Period ◽

Cortical Inhibition ◽

First Episode ◽

Gamma Aminobutyric Acid ◽

Cortical Silent Period ◽

Drug Naïve ◽

The Individual ◽

First Episode Schizophrenia

Objectives: Schizophrenia is accompanied by impaired cortical inhibition, as measured by several markers including the cortical silent period (CSP). It is thought that CSP measures gamma-aminobutyric acid receptors B (GABAB) mediated inhibitory activity. But the mutual roles of schizophrenia as a disease and the drugs used for the treatment of psychosis on GABA mediated neurotransmission are not clear. Methods: We recruited 13 drug-naive patients with first-episode schizophrenia. We used transcranial magnetic stimulation to assess CSP prior to initiating risperidone monotherapy and again four weeks later. At the same time, we rated the severity of psychopathology using the Positive and Negative Syndrome Scale (PANSS). Results: We obtained data from 12 patients who showed a significant increase in CSP, from 134.20±41.81 ms to 162.95±61.98 ms ( p=0.041; Cohen’s d=0.544). After the treatment, the PANSS total score was significantly lower, as were the individual subscores ( p<0.05). However, no correlation was found between ΔCSP and ΔPANSS. Conclusion: Our study in patients with first-episode schizophrenia demonstrated an association between risperidone monotherapy and an increase in GABAB mediated inhibitory neurotransmission.

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Electromyographic bursting following the cortical silent period induced by transcranial magnetic stimulation

Brain Research ◽

10.1016/j.brainres.2012.01.041 ◽

2012 ◽

Vol 1446 ◽

pp. 40-45 ◽

Cited By ~ 7

Author(s):

O. Chin ◽

R.F.H. Cash ◽

G.W. Thickbroom

Keyword(s):

Transcranial Magnetic Stimulation ◽

Magnetic Stimulation ◽

Silent Period ◽

Cortical Silent Period

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Interhemispheric Connectivity in Idiopathic Cervical Dystonia and Spinocerebellar Ataxias: A Transcranial Magnetic Stimulation Study

Clinical EEG and Neuroscience ◽

10.1177/1550059420957487 ◽

2020 ◽

pp. 155005942095748 ◽

Cited By ~ 1

Author(s):

Tommaso Bocci ◽

Davide Baloscio ◽

Roberta Ferrucci ◽

Lucia Briscese ◽

Alberto Priori ◽

...

Keyword(s):

Transcranial Magnetic Stimulation ◽

Cervical Dystonia ◽

Magnetic Stimulation ◽

Silent Period ◽

Cortical Inhibition ◽

Common Disease ◽

Conduction Time ◽

Mutational Load ◽

Spinocerebellar Ataxias ◽

Interhemispheric Communication

Background and Rationale Hyperkinetic movement disorders represent a heterogeneous group of diseases, different from a genetic and clinical perspective. In the past, neurophysiological approaches provided different, sometimes contradictory findings, pointing to an impaired cortical inhibition as a common electrophysiological marker. Our aim was to evaluate changes in interhemispheric communication in patients with idiopathic cervical dystonia (ICD) and spinocerebellar ataxias (SCAs). Materials and Methods Eleven patients with ICD, 7 with genetically confirmed SCA2 or SCA3, and 10 healthy volunteers were enrolled. The onset latency and duration of the ipsilateral silent period (iSPOL and iSPD, respectively), as well as the so-called transcallosal conduction time (TCT), were then recorded from the abductor pollicis brevis of the right side using an 8-shaped focal coil with wing diameters of 70 mm; all these parameters were evaluated and compared among groups. In SCAs, changes in neurophysiological measures were also correlated to the mutational load. Results iSPD was significantly shorter in patients with SCA2 and SCA3, when compared both to control and ICD ( P < .0001); iSPOL and TCT were prolonged in SCAs patients ( P < .001). Changes in iSPD, iSPOL, and TCT in SCAs are significantly correlated with the mutational load ( P = .01, P = .02, and P = .002, respectively). Discussion This is the first study to assess changes in interhemispheric communication in patients with SCAs and ICD, using a transcranial magnetic stimulation protocol. Together with previous data in Huntington’s disease, we suggest that these changes may underlie, at least in part, a common disease mechanism of polyglutamine disorders.

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