2015
DOI: 10.1136/bcr-2014-209075
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Periventricular white matter lesion and incomplete MRZ reaction in a male patient with anti-N-methyl-d-aspartate receptor encephalitis presenting with dysphoric mania

Abstract: Several findings suggest that there may be an overlap of anti-N-methyl-d-aspartate receptor (NMDAR) antibody encephalitis with neuromyelitis optica spectrum disorders or acute demyelinating encephalomyelitis (ADEM)-like demyelination. We present a case of a patient with anti-NMDAR antibody encephalitis, who on MRI featured a single prominent T2-hyperintensive white matter lesion in the periventricular region, adjacent to the anterior horn of the left lateral ventricle. In view of the lesion location and the ce… Show more

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Cited by 11 publications
(4 citation statements)
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“…Some are positive for MOG-or AQP4-antibodies, while others remain seronegative. [32][33][34] Other patients have anti-NMDAR encephalitis that overlaps with MS. [35][36][37][38][39][40][41][42][43] In our patient, brain MRI was initially unremarkable and demyelinating lesions were first found 4 years after the onset of NMDAR-encephalitis and showed imaging features more typical of MS than NMOSD or MOG-antibody-associated disease. The mechanisms that trigger overlapping NMDAR-encephalitis and demyelination are unclear and the pathogenesis may be heterogeneous.…”
Section: Discussionmentioning
confidence: 55%
See 1 more Smart Citation
“…Some are positive for MOG-or AQP4-antibodies, while others remain seronegative. [32][33][34] Other patients have anti-NMDAR encephalitis that overlaps with MS. [35][36][37][38][39][40][41][42][43] In our patient, brain MRI was initially unremarkable and demyelinating lesions were first found 4 years after the onset of NMDAR-encephalitis and showed imaging features more typical of MS than NMOSD or MOG-antibody-associated disease. The mechanisms that trigger overlapping NMDAR-encephalitis and demyelination are unclear and the pathogenesis may be heterogeneous.…”
Section: Discussionmentioning
confidence: 55%
“…Some are positive for MOG‐ or AQP4‐antibodies, while others remain seronegative 32–34 . Other patients have anti‐NMDAR encephalitis that overlaps with MS 35–43 . In our patient, brain MRI was initially unremarkable and demyelinating lesions were first found 4 years after the onset of NMDAR‐encephalitis and showed imaging features more typical of MS than NMOSD or MOG‐antibody‐associated disease.…”
Section: Discussionmentioning
confidence: 58%
“…A high number of relapses have been observed in anti-NMDAR encephalitis with white matter changes. 10,11 On the other hand, there have been reports of the presence of anti-NMDAR antibodies in patients who have ADEM, MS, and NMO spectrum disorder (NMOSD) during both initial presentation and relapse episode. [12][13][14][15] Tumor removal is a curative treatment along with reducing the autoimmune antibodies by immunotherapy.…”
Section: Discussionmentioning
confidence: 99%
“…For example, by actively participating in AE progression, inflammatory events can directly cause the damage of nerve cells including neurons and oligodendrocytes (92,93). Patients with AE often present with leukoencephalopathy syndrome (94)(95)(96)(97), which occurs simultaneously or in succession (98). As structural elements of neurons and glial cells, the neurofilament light (Nfl), total tau protein (T-tau), and glial fibrillary acidic protein (GFAP) imply neuronal and glial cell damage and death.…”
Section: Nerve Damage and Glial Activity Markersmentioning
confidence: 99%