目的:探讨视觉诱发电位(VEP)的主要成分(P100)与多发性硬化症(MS)的前和后损伤的关系。
方法:31例患者(EDSS中位数:2.5),13患有先前的视神经炎(ON),31名健康对照者有VEP,光学相干层析成像和磁共振成像。我们测试了P100潜伏期与乳头周围视网膜神经纤维层(pRNFL)的关联,神经节细胞/内丛状层(GCIPL),外侧膝状核体积(LGN),视神经辐射(OR-WML)的白质病变,非损伤光学辐射的各向异性分数(NAOR-FA),和初级视觉皮层的平均厚度(V1)。效应大小以边际R2(mR2)给出。
结果:P100延迟,pRNFL,患者的GCIPL和LGN与对照组不同。在患者中,P100潜伏期与GCIPL显著相关(mR2=0.26),与OR-WML(mR2=0.17)的强度较低,NAOR-FA(mR2=0.13)和pRNFL(mR2=0.08)。在多变量分析中,GCIPL和NAOR-FA仍然与P100潜伏期显著相关(mR2=0.41)。在ON患者中,P100潜伏期与LGN体积显著相关(mR2=-0.56)。
结论:P100-潜伏期受前后视觉通路损伤的影响。在ON患者中,突触级(LGN)的损伤可能另外导致延迟。
结论:我们的发现证实了对VEP信号的后交叉贡献,这可能与MS不同的病理生理机制有关。
OBJECTIVE: To explore associations of the main component (P100) of visual evoked potentials (VEP) to pre- and postchiasmatic damage in multiple sclerosis (MS).
METHODS: 31 patients (median EDSS: 2.5), 13 with previous optic neuritis (ON), and 31 healthy controls had VEP, optical coherence tomography and magnetic resonance imaging. We tested associations of P100-latency to the peripapillary retinal nerve fiber layer (pRNFL), ganglion cell/inner plexiform layers (GCIPL), lateral geniculate nucleus volume (
LGN), white matter lesions of the optic radiations (OR-WML), fractional anisotropy of non-lesional optic radiations (NAOR-FA), and to the mean thickness of primary visual cortex (V1). Effect sizes are given as marginal R2 (mR2).
RESULTS: P100-latency, pRNFL, GCIPL and
LGN in patients differed from controls. Within patients, P100-latency was significantly associated with GCIPL (mR2 = 0.26), and less strongly with OR-WML (mR2 = 0.17), NAOR-FA (mR2 = 0.13) and pRNFL (mR2 = 0.08). In multivariate analysis, GCIPL and NAOR-FA remained significantly associated with P100-latency (mR2 = 0.41). In ON-patients, P100-latency was significantly associated with
LGN volume (mR2 = -0.56).
CONCLUSIONS: P100-latency is affected by anterior and posterior visual pathway damage. In ON-patients, damage at the synapse-level (
LGN) may additionally contribute to latency delay.
CONCLUSIONS: Our findings corroborate post-chiasmatic contributions to the VEP-signal, which may relate to distinct pathophysiological mechanisms in MS.