Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Magnetic resonance imaging (MRI) measures of brain atrophy are often considered to be a marker of axonal loss in multiple sclerosis (MS) but evidence is limited. Optic neuritis is a common manifestation of MS and results in optic nerve atrophy. Retinal nerve fibre layer (RNFL) imaging is a non-invasive way of detecting axonal loss following optic neuritis. We hypothesise that if the optic nerve atrophy that develops following optic neuritis is contributed to by axonal loss, it will correlate with thinning of the RNFL. Twenty-five patients were studied at least 1 year after a single unilateral attack of optic neuritis without recurrence, with a selection bias towards incomplete recovery. They had MR quantification of optic nerve cross-sectional area and optic nerve lesion length, as well as optical coherence tomography (OCT) measurement of mean RNFL thickness and macular volume, quantitative visual testing, and visual evoked potentials (VEPs). Fifteen controls were also studied. Significant optic nerve atrophy (mean decrease 30% versus controls), RNFL thinning (mean decrease 33% versus controls), and macular volume loss occurred in patients' affected eyes when compared with patients' unaffected eyes and healthy controls. The optic nerve atrophy was correlated with the RNFL thinning, macular volume loss, visual acuity, visual field mean deviation, and whole field VEP amplitude but not latency. These findings suggest that axonal loss contributes to optic nerve atrophy following a single attack of optic neuritis. By inference, axonal loss due to other post-inflammatory brain lesions is likely to contribute to the global MRI measure of brain atrophy in multiple sclerosis.
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PMID:Optic nerve atrophy and retinal nerve fibre layer thinning following optic neuritis: evidence that axonal loss is a substrate of MRI-detected atrophy. 1644 3

We aim to evaluate the clinical relevance of MOG-ab in a cohort of Chinese Han adults with CNS inflammatory demyelinating diseases (IDDs). MOG-ab and AQP4-ab were examined through a fixed cell based indirect immune-fluorescence assay in 86 patients with CNS-IDDs. MOG-ab was positive in 12 patients, while AQP4-ab was positive in 31 patients; none double positives. Optic neuritis (ON) was the most frequent symptom at onset (75.0%) or during the whole disease course (83.3%) of MOG-ab associated IDDs (MOG-IDDs); 79.5% of the episodes involved only the optic nerve in MOG-IDDs. MOG-ab related ON (MOG-ON) usually caused severe visual impairment, longitudinally extensive optic nerve lesion with anterior enhancement and perineural soft tissue enhancement, responded well to steroid, but still could leave remarkable thinning of retinal nerve fiber layer (RNFL) and ganglion cell complex (GCC). MOG-IDDs had less spinal cord involvement compared to AQP4-ab mediated NMO/SD. Heterogeneous brain lesions existed in 66.7% of the patients with MOG-IDDs. Large, edematous white matter lesions were observed with the pathological feature of obvious demyelination yet preservation of astrocyte and axon, fundamentally different from the astrocytopathy typically seen in NMO/SD. Our investigations suggest that MOG-ab mediates a distinct disease entity separate from NMO/SD.
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PMID:MOG-antibody associated demyelinating disease of the CNS: A clinical and pathological study in Chinese Han patients. 2828 41