作者: T.M. Jenkins
DOI:
关键词: Multiple sclerosis 、 Vision restoration therapy 、 Neuroscience 、 Visual field 、 Visual system 、 Optic neuritis 、 Optic nerve 、 Psychology 、 Optic radiation 、 Demyelinating disease
摘要: In this thesis, the mechanisms of damage and repair in clinically isolated optic neuritis (ON) were investigated vivo, by combining magnetic resonance imaging (MRI), electrophysiology optical coherence tomography (OCT). ON is a demyelinating, inflammatory condition nerve, which may be first presentation of multiple sclerosis. The visual prognosis generally good, despite nerve demyelination axonal loss, but some patients fail to recover. aim thesis was determine reasons underlying recovery. hypothesis was that neuroplastic grey matter reorganisation might contribute outcome. Structural MRI, electrophysiology OCT used quantify nerve oedema, inflammation, myelination neuroaxonal radiation and visual cortical pathology, cohort with acute ON, followed up over the following year. Visual functional MRI (fMRI) employed investigate neuroplasticity. Acutely, measures nerve inflammation conduction block associated with severity inform an fMRI analysis, in order dissect complex structure-function interactions. Evidence found for neuroplasticity dorsal higher areas, act modulate visual dysfunction. Subsequent longitudinal analyses identified associations between early fMRI activation lateral occipital complexes, ventral stream area, and longer term outcome, evident on stimulation either eye, and independent loss pathways. A quadrant-specific paradigm investigate recovery from visual field defects, finding no evidence for defect-specific neuroplastic responses. It concluded that neuroplasticity appears more important recovery from than previously thought, its contribution independent measures of tissue damage. This provide target future therapeutic approaches in demyelinating disease.