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Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients
Published on: April 14, 2014
Utility of Diffusion-weighted Magnetic Resonance Imaging in Differentiating Connective Tissue Disease–associated
Yanli Hou1, Hang Zhou2, Rui Li3
1Department of Ophthalmology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China.
Introduction:
To evaluate the feasibility of using diffusion-weighted magnetic resonance imaging (DWI) to differentiate connective tissue disease-associated optic neuritis(CTD-ON) from idiopathic optic neuritis (IDON).
Materials And Methods:
and Methods: A retrospective observational study was conducted on 66 acute optic neuritis(ON) patients. Twenty-five patients (36 eyes) were comorbid with CTD, and 41 patients (49 eyes) had idiopathic ON and served as controls. All patients underwent routine magnetic resonance imaging (MRI) of the orbit and DWI. Affected optic nerves were evaluated for laterality, visual acuity, papilledema, visual outcome, and signal characteristics on DWI and conventional MRI. Clinical characteristics were compared using two-sample t-tests and chi-square tests. Spearman’s rank correlation, logistic regression, and receiver operating characteristic (ROC) curve analyses were performed to evaluate the diagnostic value of DWI for CTD-ON.
Results:
Compared with the IDON group, patients with CTD-ON showed significantly more severe visual impairment and worse prognosis (P < 0.05). Optic nerve hyperintensity on DWI (DWI-H) was a significant risk factor for visual acuity at onset and final visual outcome in ON patients [ORs = 1.893 (95% CI: 1.322-2.711, P < 0.001), 1.716 (95% CI: 1.094-2.691, P = 0.019), respectively]. Acute CTD-ON patients were at higher risk of poor visual outcomes [OR = 2.593 (95% CI: 1.384-4.857, P = 0.003)]. ROC analysis showed that the combination of DWI-H and poor visual outcome yielded an AUC of 0.889 (95% CI: 0.820-0.959, P < 0.001), with a sensitivity of 88.9% and specificity of 77.6%.
Discussion:
The pathogenesis of CTD-ON may involve the following mechanisms. First, CTD-related small-vessel vasculopathy, necrosis, and hypercoagulability-induced thrombosis may lead to vasculitic infarction and ischemic injury of the optic nerve, which manifests as hyperintensity on DWI. Second, autoantibodies induced by CTD may cross-react with neuronal cells.
Conclusion:
Patients with CTD-ON demonstrate more severe visual impairment than those with IDON. The presence of DWI hyperintensity and poor prognosis in patients with ON should raise suspicion for CTD-ON in the appropriate clinical setting.
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