Characteristic of somatosensory evoked potentials in adolescent idiopathic scoliosis and relationship with Cobb angle.
- Author:
Yong QIU
1
;
Zhi-jun CHEN
;
Wei-wei MA
;
Bin WANG
;
Yang YU
;
Ze-zhang ZHU
;
Feng ZHU
;
Bang-ping QIAN
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Case-Control Studies; Child; Evoked Potentials, Somatosensory; physiology; Female; Humans; Male; Retrospective Studies; Scoliosis; pathology; physiopathology; Spine; pathology; Young Adult
- From: Chinese Journal of Surgery 2009;47(13):1010-1013
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the abnormality of somatosensory evoked potentials (SEPs) in adolescent idiopathic scoliosis (AIS) with different curve magnitudes, and to explore its effect on the etiopathogenesis of AIS.
METHODSPosterior tibial nerve SEPs were evaluated on 489 young operative treated AIS patients with a Cobb angle >40 degrees and 45 age-matched healthy control individuals. Absence of SEPs waveforms, prolongation of peek latency or asymmetrical peek latency were defined as pathological change. Base on the control reference, the incidence of pathological SEPs was determined in AIS group. The association of abnormal SEPs and curve severity for AIS patients was also assessed.
RESULTSPeek latency corrected for body height was slightly longer in AIS patients than in controls, however, with no significant difference. Inter side difference of latency was significantly larger in AIS patients. Abnormal SEPs were found in 166 of 489 AIS patients. Among these, 17 (10.2%) showed absent waveforms, 50 (30.1%) had unilateral latency prolongation, 38 (22.9%) had bilateral latency prolongation, and 120 (72.3%) showed significant inter side difference. Statistical analysis failed to show a correlation between abnormal SEPs and the curve severity of spinal deformity.
CONCLUSIONDisorder of somatosensory pathways does exist in a subgroup of AIS patients, and it might be a primary factor other than secondary change, and could play an import role in the etiopathogenesis of AIS.