Correlation of N30 somatosensory evoked potentials with spasticity and neurological function after stroke: A cross-sectional study
DOI:
https://doi.org/10.2340/16501977-2867Keywords:
stroke, hemiparesis, spasticity, N30 somatosensory evoked potential, motor evoked potential, function recoveryAbstract
Objective: To test whether the presence of N30 somatosensory evoked potentials, generated from the supplementary motor area and premotor cortex, correlate with post-stroke spasticity, motor deficits, or motor recovery stage.
Design: A cross-sectional study.
Patients: A total of 43 patients with stroke hospitalized at Maoming People’s Hospital, Maoming, China.
Methods: Forty-three stroke patients underwent neurofunctional tests, including Modified Ashworth Scale (MAS), Brunnstrom stage, manual muscle test and neurophysiological tests, including N30 somatosensory evoked potentials, N20 somatosensory evoked potentials, motor evoked potentials, H-reflex. The results were compared between groups. Correlation and regression analyses were performed as well.
Results: Patients with absence of N30 somatosensory evoked potential exhibited stronger flexor carpi radialis muscle spasticity (r = –0.50, p < 0.05) and worse motor function (r = 0.57, p < 0.05) than patients with presence of N30 somatosensory evoked potential. The generalized linear model (GLM) including both N30 somatosensory evoked potentials and motor evoked potentials (Akaike Information Criterion (AIC) = 121.99) better reflected the recovery stage of the affected proximal upper limb than the models including N30 somatosensory evoked potentials (AIC = 125.06) or motor evoked potentials alone (AIC = 127.45).
Conclusion: N30 somatosensory evoked potential status correlates with the degrees of spasticity and motor function of stroke patients. The results showed that N30 somatosensory evoked potentials hold promise as a biomarker for the development of spasticity and the recovery of proximal limbs.
Lay abstract
Impair motor function and spasticity adversely affect the ability to conduct the activities of daily life. Somatosensory evoked potentials and motor evoked potentials are essential to differential evaluation of degree of post-stroke spasticity and stage of motor recovery. This is the first study of the correlations between somatosensory evoked potentials N30, components of somatosensory evoked potentials related to the supplementary motor area and dorsolateral premotor cortex combined with motor evoked potentials and motor function. The results indicate that the N30 somatosensory evoked potential status is correlated with the degrees of spasticity and motor function of stroke patients. The conclusion showed that N30 Somatosensory evoked potentials hold promise as a biomarker for the development of spasticity and the recovery of proximal limbs
Downloads
References
Paul S, Candelario-Jalil E. Emerging neuroprotective strategies for the treatment of ischemic stroke: an overview of clinical and preclinical studies. Exp Neurol 2021; 335: 113518.
Urban PP, Wolf T, Uebele M, Marx JJ, Vogt T, Stoeter P, et al. Occurence and clinical predictors of spasticity after ischemic stroke. Stroke 2010; 41: 2016–2020.
Wieters F, Lucas CW, Gruhn M, Büschges A, Fink GR, Aswendt M. Introduction to spasticity and related mouse models. Exp Neurol 2021; 335: 113491.
Li S, Chen YT, Francisco GE, Zhou P, Rymer WZ. A unifying pathophysiological account for post-stroke spasticity and disordered motor control. Front Neurol 2019; 10: 468.
Cassidy JM, Cramer SC. Spontaneous and therapeutic-induced mechanisms of functional recovery after stroke. Transl Stroke Res 2017; 8: 33–46.
Cebolla AM, Palmero-Soler E, Dan B, Cheron G. Frontal phasic and oscillatory generators of the N30 somatosensory evoked potential. NeuroImage 2011; 54: 1297–1306.
Macerollo A, Brown MJN, Kilner JM, Chen R. Neurophysiological changes measured using somatosensory evoked potentials. Trends Neurosci 2018; 41: 294–310.
Cebolla AM, De Saedeleer C, Bengoetxea A, Leurs F, Balestra C, d’Alcantara P, et al. Movement gating of beta/gamma oscillations involved in the N30 somatosensory evoked potential. Hum Brain Mapp 2009; 30: 1568–1579.
Darling WG, Ge J, Stilwell-Morecraft KS, Rotella DL, Pizzimenti MA, Morecraft RJ. Hand motor recovery following extensive frontoparietal cortical injury is accompanied by upregulated corticoreticular projections in monkey. J Neurosci 2018; 38: 6323–6339.
Jang SH, Lee SJ. Corticoreticular tract in the human brain: a mini review. Front Neurol 2019; 10: 1188.
Frasson E, Priori A, Bertolasi L, Mauguière F, Fiaschi A, Tinazzi M. Somatosensory disinhibition in dystonia. Mov Disord 2001; 16: 674–682.
Legon W, Dionne JK, Staines WR. Continuous theta burst stimulation of the supplementary motor area: effect upon perception and somatosensory and motor evoked potentials. Brain Stimul 2013; 6: 877–883.
Mohebi N, Arab M, Moghaddasi M, Ghader BB, Emamikhah M. Stroke in supplementary motor area mimicking functional disorder: a case report. J Neurol 2019; 266: 2584–2586.
Liu J, Wang C, Qin W, Ding H, Guo J, Han T, et al. Corticospinal fibers with different origins impact motor outcome and brain after subcortical stroke. Stroke 2020; 51: 2170–2178.
Schambra HM, Xu J, Branscheidt M, Lindquist M, Uddin J, Steiner L, et al. Differential poststroke motor recovery in an arm versus hand muscle in the absence of motor evoked potentials. Neurorehabil Neural Repair. 2019; 33: 568–580.
Sangari S, Perez MA. Imbalanced corticospinal and reticulospinal contributions to spasticity in humans with spinal cord injury. J Neurosci 2019; 39: 7872–7881.
Yu S, Chen Y, Cai Q, Ma K, Zheng H, Xie L. A novel quantitative spasticity evaluation method based on surface electromyogram signals and adaptive neuro fuzzy inference system. Front Neurosci 2020; 14: 462.
Pundik S, McCabe J, Skelly M, Tatsuoka C, Daly JJ. Association of spasticity and motor dysfunction in chronic stroke. Ann Phys Rehabil Med 2019; 62: 397–402.
Riddle CN, Edgley SA, Baker SN. Direct and indirect connections with upper limb motoneurons from the primate reticulospinal tract. J Neurosci 2009; 29: 4993–4999.
O’Brien S, Andrew D, Zabihhosseinian M, Yielder P, Murphy B. Proximal upper limb sensorimotor integration in response to novel motor skill acquisition. Brain Sci 2020; 10: 581.
Zhang Y, Su YY, Xiao SY, Liu YF. Somatosensory and brainstem auditory evoked potentials assessed between 4 and 7 days after severe stroke onset predict unfavorable outcome. Biomed Res Int. 2015; 2015: 196148.
Hassanzahraee M, Zoghi M, Jaberzadeh S. Longer transcranial magnetic stimulation intertrial interval increases size, reduces variability, and improves the reliability of motor evoked potentials. Brain Connect 2019; 9: 770–776.
Aguiar SA, Choudhury S, Kumar H, Perez MA, Baker SN. Effect of central lesions on a spinal circuit facilitating human wrist flexors. Sci Rep 2018; 8: 14821.
Diedenhofen B, Musch J. Cocor: a comprehensive solution for the statistical comparison of correlations. PLoS One 2015; 10: e0121945.
Buda A, Jarynowski A. Life time of correlations and its applications. Głogo: Andrzej Buda Wydawnictwo NiezaleĹĽne; 2010.
Waberski TD, Buchner H, Perkuhn M, Gobbelé R, Wagner M, Kücker W, et al. N30 and the effect of explorative finger movements: a model of the contribution of the motor cortex to early somatosensory potentials. Clin Neurophysiol 1999; 110: 1589–1600.
Kaňovský P, Bareš M, Rektor I. The selective gating of the N30 cortical component of the somatosensory evoked potentials of median nerve is different in the mesial and dorsolateral frontal cortex: evidence from intracerebral recordings. Clin Neurophysiol 2003; 114: 981–991.
Rossini PM, Bassetti MA, Pasqualetti P. Median nerve somatosensory evoked potentials. apomorphine-induced transient potentiation of frontal components in Parkinson’s disease and in parkinsonism. Electroencephalogr Clin Neurophysiol 1995; 96: 236–247.
Kang SY, Ma HI. N30 somatosensory evoked potential is negatively correlated with motor function in Parkinson’s disease. J Mov Disord 2016; 9: 35–39.
Ulivelli M, Rossi S, Pasqualetti P, Rossini PM, Ghiglieri O, Passero S, et al. Time course of frontal somatosensory evoked potentials. Relation to L-dopa plasma levels and motor performance in PD. Neurology 1999; 53: 1451–1457.
Chung JW, Burciu RG, Ofori E, Coombes SA, Christou EA, Okun MS, et al. Beta-band oscillations in the supplementary motor cortex are modulated by levodopa and associated with functional activity in the basal ganglia. Neuroimage Clin 2018; 19: 559–571.
Allison T, McCarthy G, Wood CC, Jones SJ. Potentials evoked in human and monkey cerebral cortex by stimulation of the median nerve. A review of scalp and intracranial recordings. Brain 1991; 114 (Pt 6): 2465–2503.
Kreitzer AC, Malenka RC. Striatal plasticity and basal ganglia circuit function. Neuron 2008; 60: 543–554.
Nachev P, Kennard C, Husain M. Functional role of the supplementary and pre-supplementary motor areas. Nat Rev Neurosci 2008; 9: 856–869.
Shadmehr R, Smith MA, Krakauer JW. Error correction, sensory prediction, and adaptation in motor control. Annu Rev Neurosci 2010; 33: 89–108.
Tang Q, Li G, Liu T, Wang A, Feng S, Liao X, et al. Modulation of interhemispheric activation balance in motor-related areas of stroke patients with motor recovery: systematic review and meta-analysis of fMRI studies. Neurosci Biobehav Rev 2015; 57: 392–400.
Baker SN, Zaaimi B, Fisher KM, Edgley SA, Soteropoulos DS. Pathways mediating functional recovery. Prog Brain Res 2015; 218: 389–412.
Welniarz Q, Dusart I, Roze E. The corticospinal tract: evolution, development, and human disorders. Dev Neurobiol 2017; 77: 810–829.
Lee D, Song J, Kim JW, Ahn TB. Spasticity secondary to isolated involvement of the pyramidal tract. J Neurol Sci 2016; 368: 130–131.
Stinear CM, Byblow WD, Ackerley SJ, Barber PA, Smith MC. Predicting recovery potential for individual stroke patients increases rehabilitation efficiency. Stroke 2017; 48: 1011–1101.
Published
How to Cite
License
Copyright (c) 2021 Lilin Chen, Weijie Li, Shimei Cheng, Shouyi Liang, Mudan Huang, Tingting Lei, Xiquan Hu, Zhenhong Liang, Haiqing Zheng
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
All digitalized JRM contents is available freely online. The Foundation for Rehabilitation Medicine owns the copyright for all material published until volume 40 (2008), as from volume 41 (2009) authors retain copyright to their work and as from volume 49 (2017) the journal has been published Open Access, under CC-BY-NC licences (unless otherwise specified). The CC-BY-NC licenses allow third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material for non-commercial purposes, provided proper attribution to the original work.
From 2024, articles are published under the CC-BY licence. This license permits sharing, adapting, and using the material for any purpose, including commercial use, with the condition of providing full attribution to the original publication.
