Short latency afferent inhibition associated with cortical compression and memory impairment in patients with chronic subdural hematoma

Kawasaki, Yukari; Fujiki, Minoru; Ooba, Hiroshi; Sakai, Kenji; Hikawa, Takamitsu; Abé, Tatsuya; Ishii, Keisuke; Kobayashi, Hidenori

doi:10.1016/j.clineuro.2012.02.037

“…The difference between ictal and interictal recordings became evident only when the median nerve stimulus was given at N20+8ms before the TMS stimulus. Similar abnormalities with long ISIs, even exceeding N20+8ms, were observed in various pathologies [11,[29][30][31], underlining the fact that short and long afferent inhibitions may be mediated by partially different cortical circuits [11]. This underscores that exploring the sensorimotor system at long ISIs between 200 to 1000 ms (long-latency afferent inhibition, LAI) would be of interest in migraine [11].…”

Section: Discussionmentioning

confidence: 55%

Short-latency afferent inhibition and somato-sensory evoked potentials during the migraine cycle: surrogate markers of a cycling cholinergic thalamo-cortical drive?

Lenola

¹

,

Abagnale

²

,

Ferrandes

³

et al. 2020

Preprint

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Background: Short-latency afferent inhibition (SAI) consists of motor cortex inhibition induced by sensory afferents and depends on the excitatory effect of cholinergic thalamocortical projections on inhibitory GABAergic cortical networks. Given the electrophysiological evidence for thalamo-cortical dysrhythmia in migraine, we studied SAI in migraineurs during and between attacks and searched for correlations with somatosensory habituation, thalamocortical activation, and clinical features. Methods: SAI was obtained by conditioning the transcranial magnetic stimulation-induced motor evoked potential (MEP) with an electric stimulus on the median nerve at the wrist with random stimulus intervals corresponding to the latency of individual somatosensory evoked potentials (SSEP) N20 plus 2, 4, 6, or 8 ms. We recruited 30 migraine without aura patients, 16 between (MO), 14 during an attack (MI), and 16 healthy volunteers (HV). We calculated the slope of the linear regression between the unconditioned MEP amplitude and the 4-conditioned MEPs as a measure of SAI. We also measured SSEP amplitude habituation, and high-frequency oscillations (HFO) as an index of thalamo-cortical activation. Results: Compared to HV, SAI, SSEP habituation and early SSEP HFOs were significantly reduced in MO patients between attacks, but enhanced during an attack. There was a positive correlation between degree of SAI and amplitude of early HFOs in HV, but not in MO or MI. Conclusions: The migraine cycle-dependent variations of SAI and SSEP HFOs are further evidence that facilitatory thalamocortical activation (of GABAergic networks in the motor cortex for SAI), likely to be cholinergic, is reduced in migraine between attacks, but increased ictally.

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“…The difference between ictal and interictal recordings became evident only when the median nerve stimulus was given at N20 + 8 ms before the TMS stimulus. Similar abnormalities with long ISIs, even exceeding N20 + 8 ms, were observed in various pathologies [11,[29][30][31], underlining the fact that short and long afferent inhibitions may be mediated by partially different cortical circuits [11]. This underscores that exploring the sensorimotor system at long ISIs between 200 to 1000 ms (long-latency afferent inhibition, LAI) would be of interest in migraine [11].…”

Section: Discussionmentioning

confidence: 55%

“…For instance, we were not able to record the same patients during and outside the attack, which would have allowed using each patient as its own control and strengthened our conclusions. Regarding the electrophysiological protocol, averaging 5 stimuli per condition might be not enough to obtain stable SAI measure, although in previous studies reliable SAI results were obtained by averaging 3 trials only per condition [29,30,[35][36][37].…”

Section: Discussionmentioning

confidence: 98%

Short-latency afferent inhibition and somato-sensory evoked potentials during the migraine cycle: surrogate markers of a cycling cholinergic thalamo-cortical drive?

Lenola

¹

,

Abagnale

²

,

Ferrandes

³

et al. 2020

View full text Add to dashboard Cite

Background: Short-latency afferent inhibition (SAI) consists of motor cortex inhibition induced by sensory afferents and depends on the excitatory effect of cholinergic thalamocortical projections on inhibitory GABAergic cortical networks. Given the electrophysiological evidence for thalamo-cortical dysrhythmia in migraine, we studied SAI in migraineurs during and between attacks and searched for correlations with somatosensory habituation, thalamocortical activation, and clinical features. Methods: SAI was obtained by conditioning the transcranial magnetic stimulation-induced motor evoked potential (MEP) with an electric stimulus on the median nerve at the wrist with random stimulus intervals corresponding to the latency of individual somatosensory evoked potentials (SSEP) N20 plus 2, 4, 6, or 8 ms. We recruited 30 migraine without aura patients, 16 between (MO), 14 during an attack (MI), and 16 healthy volunteers (HV). We calculated the slope of the linear regression between the unconditioned MEP amplitude and the 4-conditioned MEPs as a measure of SAI. We also measured SSEP amplitude habituation, and high-frequency oscillations (HFO) as an index of thalamo-cortical activation. Results: Compared to HV, SAI, SSEP habituation and early SSEP HFOs were significantly reduced in MO patients between attacks, but enhanced during an attack. There was a positive correlation between degree of SAI and amplitude of early HFOs in HV, but not in MO or MI. Conclusions: The migraine cycle-dependent variations of SAI and SSEP HFOs are further evidence that facilitatory thalamocortical activation (of GABAergic networks in the motor cortex for SAI), likely to be cholinergic, is reduced in migraine between attacks, but increased ictally.

show abstract

“…Similar abnormalities with long ISIs, even exceeding N20 + 8 ms, were observed in various pathologies [11,[29][30][31], underlining the fact that short and long afferent inhibitions may be mediated by partially different cortical circuits [11]. This underscores that exploring the sensorimotor system at long ISIs between 200 to 1000 ms (long-latency afferent inhibition, LAI) would be of interest in migraine [11].…”

Section: Discussionmentioning

confidence: 55%

“…It would have been of interest indeed to search if the same correlation with the MEP and SSEP amplitude slopes would have emerged as for the time elapsed since the last attack. Regarding the electrophysiological protocol, averaging 5 stimuli per condition might be not enough to obtain stable SAI measure, although in previous studies reliable SAI results were obtained by averaging 3 trials only per condition [29,30,[40][41][42].…”

Section: Discussionmentioning

confidence: 98%

Short-latency afferent inhibition and somato-sensory evoked potentials during the migraine cycle: surrogate markers of a cycling cholinergic thalamo-cortical drive?

Lenola

¹

,

Abagnale

²

,

Ferrandes

³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Short-latency afferent inhibition (SAI) consists of motor cortex inhibition induced by sensory afferents and depends on the excitatory effect of cholinergic thalamocortical projections on inhibitory GABAergic cortical networks. Given the electrophysiological evidence for thalamo-cortical dysrhythmia in migraine, we studied SAI in migraineurs during and between attacks and searched for correlations with somatosensory habituation, thalamocortical activation, and clinical features.Methods: SAI was obtained by conditioning the transcranial magnetic stimulation-induced motor evoked potential (MEP) with an electric stimulus on the median nerve at the wrist with random stimulus intervals corresponding to the latency of individual somatosensory evoked potentials (SSEP) N20 plus 2, 4, 6, or 8 ms. We recruited 30 migraine without aura patients, 16 between (MO), 14 during an attack (MI), and 16 healthy volunteers (HV). We calculated the slope of the linear regression between the unconditioned MEP amplitude and the 4-conditioned MEPs as a measure of SAI. We also measured SSEP amplitude habituation, and high-frequency oscillations (HFO) as an index of thalamo-cortical activation.Results: Compared to HV, SAI, SSEP habituation and early SSEP HFOs were significantly reduced in MO patients between attacks, but enhanced during an attack. There was a positive correlation between degree of SAI and amplitude of early HFOs in HV, but not in MO or MI. When the two patient groups were pooled, both the MEP SAI slope and the SSEP habituation slope correlated positively with the number of days elapsed since the last migraine attack.Conclusions: The migraine cycle-dependent variations of SAI and SSEP HFOs are further evidence that facilitatory thalamocortical activation (of GABAergic networks in the motor cortex for SAI), likely to be cholinergic, is reduced in migraine at a distance from an attack, but increased ictally.

show abstract

Short latency afferent inhibition associated with cortical compression and memory impairment in patients with chronic subdural hematoma

Cited by 8 publications

References 14 publications

Short-latency afferent inhibition and somato-sensory evoked potentials during the migraine cycle: surrogate markers of a cycling cholinergic thalamo-cortical drive?

Short-latency afferent inhibition and somato-sensory evoked potentials during the migraine cycle: surrogate markers of a cycling cholinergic thalamo-cortical drive?

Short-latency afferent inhibition and somato-sensory evoked potentials during the migraine cycle: surrogate markers of a cycling cholinergic thalamo-cortical drive?

Short-latency afferent inhibition and somato-sensory evoked potentials during the migraine cycle: surrogate markers of a cycling cholinergic thalamo-cortical drive?

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