CORRELATION OF N30 SOMATOSENSORY EVOKED POTENTIALS WITH SPASTICITY AND NEUROLOGICAL FUNCTION AFTER STROKE: A CROSS-SECTIONAL STUDY

ObjectiveTo 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.DesignA cross-sectional study.PatientsA total of 43 patients with stroke hospitalized at Maoming People’s Hospital, Maoming, China.MethodsForty-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).ConclusionN30 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 ABSTRACTImpair 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 limbsKey words: stroke, hemiparesis, spasticity, N30 somatosensory evoked potential, motor evoked potential, function recovery

Stroke is the leading cause of disability worldwide (1). Most patients with stroke experience motor deficits, which impair motor function and adversely affect their ability to perform activities of daily living (ADL). Spasticity, one of the motor deficits that appears after stroke, is accompanied by an increased risk of falling and resulting fractures, and is associated with increased morbidity and mortality (2). Both post-stroke recovery and the development of spasticity are associated with neural plasticity of different anatomical regions, such as the reticulospinal tracts, supplementary motor area (SMA) and dorsolateral premotor cortex (PMC) (3–5).Precise biomarkers of motor function are critical for early intervention. The identification of somatosensory evoked potentials (SEPs) is essential for the accurate diagnosis of patients with focal brain disorders, and SEP components reflect the activities of different neural structures (6). N30 SEPs are somatosensory evoked potential components. Anatomically, N30 SEPs are generated from the SMA and PMC (7), from which the corticoreticular tracts radiate (8–10). Pathophysiologically, N30 SEPs present apparent inhibition in individuals with other myotonic disorders (11). Continuous theta burst stimulation of the SMA reduces the amplitude of the N30 (12). Moreover, SMA impairment leads to myodystonia and is closely associated with motor outcomes (13, 14).Thus, it was hypothesized that the presence of N30 SEPs is related to the degree of spasticity and functional status in people with stroke. The aims of the study were to test: (i) whether the presence of N30 SEPs correlates with post-stroke spasticity (PSS), motor deficits and stage of motor recovery; and (ii) whether the combination of N30 SEPs and motor evoked potentials (MEPs) can be used for the differential evaluation of degree of PSS and stage of motor recovery.