Superficial white matter damage in anti-NMDA receptor encephalitis.

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Item Type:	Article
Title:	Superficial white matter damage in anti-NMDA receptor encephalitis.
Creators Name:	Phillips, O. R., Joshi, S.H., Narr, K.L., Shattuck, D.W., Singh, M., Di Paola, M., Ploner, C.J., Prüss, H., Paul, F. and Finke, C.
Abstract:	Background: Clinical brain MRI is normal in the majority of patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis. However, extensive deep white matter damage wasrecently identifiedin these patients using diffusion weighted imaging. Here, our aim was to study a particularly vulnerable brain compartment, the late myelinating superficial white matter. Methods: Forty-six patients with anti-NMDAR encephalitis were included. Ten out of these were considered neurologically recovered (modified Rankin scale of zero), while 36 patients were non-recovered. In addition, 30 healthy controls were studied. MRI data were collected from all subjects and superficial white matter mean diffusivity derived from diffusion tensor imaging was compared between groups in whole brain, lobar and vertex-based analyses. Patients underwent comprehensive cognitive testing, and correlation analyses were performed between cognitive performance and superficial white matter integrity. Results: Non-recovered patients showed widespread superficial white matter damage in comparison to recovered patients and healthy controls. Vertex-based analyses revealed that damage predominated in frontal and temporal lobes. In contrast, the superficial white matter was intact in recovered patients. Importantly, persistent cognitive impairments in working memory, verbal memory, visuospatial memory and attention significantly correlated with damage of the superficial white matter in patients. Conclusions: Anti-NMDAR encephalitis is associated with extensive superficial white matter damage in patients with incomplete recovery. The strong association with impairment in several cognitive domains highlights the clinical relevance of white matter damage in this disorder and warrants investigations of the underlying pathophysiological mechanisms.
Source:	Journal of Neurology Neurosurgery and Psychiatry
ISSN:	0022-3050
Publisher:	BMJ Publishing Group
Volume:	89
Number:	5
Page Range:	518-525
Date:	May 2018
Official Publication:	https://doi.org/10.1136/jnnp-2017-316822
External Fulltext:	View full text on PubMed Central
PubMed:	View item in PubMed

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