Short- and long-latency afferent inhibition; uses, mechanisms and influencing factors

Turco, Claudia V.; El-Sayes, Jenin; Savoie, Mitchell J.; Fassett, Hunter J.; Locke, Mitchell B.; Nelson, Aimee J.

doi:10.1016/j.brs.2017.09.009

Cited by 132 publications

(145 citation statements)

References 201 publications

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“…SAI is suggested to be generated by the thalamocortical output from cholinergic paramedian thalamic nuclei to the primary motor cortex (M1) or by the direct output from primary somatosensory cortex (S1) to inhibitor M1 interneurons . Since no abnormalities in SEP latency or amplitude have been reported in migraine patients, SAI abnormality that we detected in migraine patients probably was not associated with impaired afferent input.…”

Section: Discussionmentioning

confidence: 58%

“…SEP was not assessed in order to set individualized ISI and SAI was not evaluated at different ISI. However, in most studies, researchers used predetermined ISI values and it is unclear whether N20 latency measurement for each subject and adjusting ISI according to it provides any additional precision or reliability . We aimed to shorten the procedure as much as possible to avoid any discomfort in ictal migraineurs.…”

Section: Discussionmentioning

confidence: 99%

“…SAI was obtained as reported previously . Conditioning electrical stimulus set at twofold of sensory threshold.…”

Section: Methodsmentioning

confidence: 99%

“…SAI is observed in the first few milliseconds after the latency of the N20 component of the somatosensory evoked potential. Therefore, most researchers use an ISI of 20‐22 milliseconds assuming that the afferent conduction time from the median nerve at the wrist to the sensorimotor cortex is 20 milliseconds . In this study, ISI between electrical and magnetic stimulation was set at 21 milliseconds and 20 MEPs were obtained in the SAI paradigm.…”

Section: Methodsmentioning

confidence: 99%

“…SAI was obtained as reported previously. 26,27 Conditioning electrical stimulus set at twofold of sensory threshold. The stimulus intensity of the magnetic stimulation over the motor cortex was adjusted to elicit MEPs of approximately 1 millivolt in amplitude and 20 MEPs were obtained at this stimulus intensity.…”

Section: Transcranial Magnetic Stimulation and Short-latency Afferentmentioning

confidence: 99%

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Reduced Short‐Latency Afferent Inhibition Indicates Impaired Sensorimotor Integrity During Migraine Attacks

et al. 2019

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Background and Objective Migraine attacks disrupt sensory information processing and may also disturb sensorimotor integration. This prospective pilot study aimed to assess the sensorimotor integration and inhibitory circuitry in the sensorimotor cortex using short‐latency afferent inhibition (SAI) paradigm in migraine. Methods Twenty‐five migraine without aura patients (10 interictal, 5 preictal, 10 ictal) and 16 healthy controls were enrolled. SAI was elicited by combining the right median nerve electrical stimulation and left motor cortical magnetic stimulation at the 21‐millisecond interval. Mean motor evoked potential (MEP) amplitude ratio, recorded from right abductor pollicis muscle after single and conditioned stimulations, was calculated as SAI. Results Average MEP inhibition ratio after single and conditioned stimuli in healthy controls was not significantly different from interictal patients (45.1% ± 20.3% vs 44.5% ± 14.75% [P = .93]). However, SAI was significantly reduced during preictal/prodromal (−14.6% ± 42.8% [P = .002]) and ictal/headache (−7.4% ± 31.1% [P = .0001]) periods of migraine compared to healthy controls. Conclusion Pronounced decrease in SAI during preictal and ictal periods in migraine was shown for the first time. Instead of inhibition to a conditioned stimulus, facilitation in the sensorimotor cortex was detected both ictally and preictally. Preictal SAI results suggest the presence of increased excitability state several hours prior to the headache phase. This phenomenon could be related to the cortical hyperresponsivity to sensory stimuli and cognitive disturbances accompanying migraine attacks as SAI is modulated by cholinergic activity.

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Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 99%

“…SAI was obtained as reported previously . Conditioning electrical stimulus set at twofold of sensory threshold.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Transcranial Magnetic Stimulation and Short-latency Afferentmentioning

confidence: 99%

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Reduced Short‐Latency Afferent Inhibition Indicates Impaired Sensorimotor Integrity During Migraine Attacks

et al. 2019

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Motor learning enhanced by combined motor imagery and noninvasive brain stimulation is associated with reduced short‐interval intracortical inhibition

et al. 2019

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Background Motor imagery (MI) improves motor skill learning, which is further enhanced when MI is paired with primary motor cortex transcranial brain stimulation or with electrical stimulation of the peripheral median nerve. Applying both stimulation types (here with 25 ms intervals) is called paired associative stimulation (PAS25). The final primary motor cortex output is determined by combined excitatory and intracortical inhibitory circuits, and reducing the latter is associated with enhanced synaptic transmission and efficacy. Indeed, short‐interval intracortical inhibition (SICI) inhibits motor evoked potentials (MEPs), and motor learning has been associated with decreased SICI and increased cortical excitability. Here, we investigated whether cortical excitability and SICI are altered by PAS25 applied after MI‐induced modulation of motor learning. Methods Peak acceleration of a hand‐grasping movement and MEPs and SICI were measured before and after MI alone, PAS25 alone, and MI followed by PAS25 in 16 healthy participants to evaluate changes in motor learning, corticospinal excitability, and intracortical inhibition. Results After PAS25 alone, MEP amplitude increased while peak acceleration was unchanged. However, PAS25 applied following MI not only significantly enhanced both peak acceleration (p = 0.011) and MEP amplitude (p = 0.004) but also decreased SICI (p = 0.011). Moreover, we found that this decrease in SICI was significantly correlated with both the peak acceleration (r = 0.49, p = 0.029) and the MEP amplitude (r = 0.56, p = 0.013). Conclusions These results indicate that brain function altered by PAS25 of the motor cortex enhances MI‐induced motor learning and corticospinal excitability and decreases SICI, suggesting that SICI underlies, at least in part, PAS25 modulation of motor learning.

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The Cholinergic Brain in Parkinson's Disease

Pasquini

Brooks

Pavese

2021

Movement Disord Clin Pract

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The central cholinergic system includes the basal forebrain nuclei, mainly projecting to the cortex, the mesopontine tegmental nuclei, mainly projecting to the thalamus and subcortical structures, and other groups of projecting neurons and interneurons. This system regulates many functions of human behavior such as cognition, locomotion, and sleep. In Parkinson's disease (PD), disruption of central cholinergic transmission has been associated with cognitive decline, gait problems, freezing of gait (FOG), falls, REM sleep behavior disorder (RBD), neuropsychiatric manifestations, and olfactory dysfunction. Neuropathological and neuroimaging evidence suggests that basal forebrain pathology occurs simultaneously with nigrostriatal denervation, whereas pathology in the pontine nuclei may occur before the onset of motor symptoms. These studies have also detailed the clinical implications of cholinergic dysfunction in PD. Degeneration of basal forebrain nuclei and consequential cortical cholinergic denervation are associated with and may predict the subsequent development of cognitive decline and neuropsychiatric symptoms. Gait problems, FOG, and falls are associated with a complex dysfunction of both pontine and basal forebrain nuclei. Olfactory impairment is associated with cholinergic denervation of the limbic archicortex, specifically hippocampus and amygdala. Available evidence suggests that cholinergic dysfunction, alongside failure of the dopaminergic and other neurotransmitters systems, contributes to the generation of a specific set of clinical manifestations. Therefore, a “cholinergic phenotype” can be identified in people presenting with cognitive decline, falls, and RBD. In this review, we will summarize the organization of the central cholinergic system and the clinical correlates of cholinergic dysfunction in PD.

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Short- and long-latency afferent inhibition; uses, mechanisms and influencing factors

Cited by 132 publications

References 201 publications

Reduced Short‐Latency Afferent Inhibition Indicates Impaired Sensorimotor Integrity During Migraine Attacks

Reduced Short‐Latency Afferent Inhibition Indicates Impaired Sensorimotor Integrity During Migraine Attacks

Motor learning enhanced by combined motor imagery and noninvasive brain stimulation is associated with reduced short‐interval intracortical inhibition

The Cholinergic Brain in Parkinson's Disease

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