Korsholm Kirsten, Madsen Kristoffer H, Frederiksen Jette L, Skimminge Arnold, Lund Torben E
Danish Research Centre for Magnetic Resonance, Copenhagen University Hospital, Hvidovre, 2650 Hvidovre, Denmark.
Brain. 2007 May;130(Pt 5):1244-53. doi: 10.1093/brain/awm045.
Optic neuritis (ON) is the first clinical manifestation in approximately 20% of patients with multiple sclerosis (MS). The inflammation and demyelination of the optic nerve are characterized by symptomatic visual impairment and retrobulbar pain, and associated with decreased visual acuity, decreased colour and contrast sensitivity, delayed visual evoked potentials and visual field defects. Spontaneous recovery of vision typically occurs within weeks or months after onset, depending on the resolution of inflammation, remyelination, restoration of conduction in axons which persist demyelinated and neuronal plasticity in the cortical and subcortical visual pathways. To assess where recovery takes place along the visual pathway, visual activation was studied in the lateral geniculate nucleus (LGN), the main thalamic relay nucleus in the visual pathway and in three areas of the visual cortex: the lateral occipital complexes (LOC), V1 and V2. We conducted a longitudinal functional magnetic resonance imaging (fMRI) study of regions of interest (ROI) of activation in LGN and visual cortex in 19 patients with acute ON at onset, 3 and 6 months from presentation. With fMRI we measured the activation in the ROIs and compared activation during monocular stimulation of the affected and unaffected eye. In the acute phase the activation of LGN during visual stimulation of the affected eye was significantly reduced (P < 0.01) compared to the unaffected eye. This difference in LGN activation between the affected and unaffected eye diminished during recovery, and after 180 days the difference was no longer significant (P = 0.59). The decreased difference during recovery was mainly due to an increase in the fMRI signal when stimulating the affected eye, but included a component of a decreasing fMRI signal from LGN when stimulating the unaffected eye. In LOC, V1 and V2 activation during visual stimulation of the affected eye in the acute phase was significantly reduced (P < 0.01) compared to the unaffected eye, and during recovery the difference diminished with no significant differences left after 180 days. As the pattern of activation in LOC, V1 and V2 resembled the development in LGN we found no evidence of additional cortical adaptive changes. The reduced activation of the LGN to stimulation of the unaffected eye is interpreted as a shift away from early compensatory changes established in the acute phase in LGN and may indicate very early plasticity of the visual pathways.
视神经炎(ON)是约20%的多发性硬化症(MS)患者的首发临床表现。视神经的炎症和脱髓鞘表现为有症状的视力损害和球后疼痛,并伴有视力下降、颜色和对比度敏感度降低、视觉诱发电位延迟以及视野缺损。视力通常在发病后的数周或数月内自发恢复,这取决于炎症的消退、髓鞘再生、持续脱髓鞘轴突传导的恢复以及皮质和皮质下视觉通路中的神经元可塑性。为了评估视觉通路中恢复发生的位置,我们研究了外侧膝状体(LGN)(视觉通路中的主要丘脑中继核)以及视觉皮质的三个区域:枕外侧复合体(LOC)、V1和V2中的视觉激活情况。我们对19例急性视神经炎发病时、就诊后3个月和6个月的患者进行了一项关于LGN和视觉皮质激活感兴趣区域(ROI)的纵向功能磁共振成像(fMRI)研究。通过fMRI,我们测量了ROI中的激活情况,并比较了单眼刺激患眼和未患眼时的激活情况。在急性期,与未患眼相比,患眼视觉刺激期间LGN的激活显著降低(P < 0.01)。在恢复过程中,患眼和未患眼之间LGN激活的这种差异逐渐减小,180天后差异不再显著(P = 0.59)。恢复过程中差异减小主要是由于刺激患眼时fMRI信号增加,但也包括刺激未患眼时LGN的fMRI信号降低的成分。在急性期,与未患眼相比,患眼视觉刺激期间LOC、V1和V2的激活显著降低(P < 0.01),在恢复过程中差异减小,180天后无显著差异。由于LOC、V1和V2中的激活模式与LGN中的发展相似,我们没有发现额外皮质适应性变化的证据。LGN对未患眼刺激的激活降低被解释为从急性期在LGN中建立的早期代偿性变化的转变,这可能表明视觉通路的非常早期的可塑性。