Anti-N-methyl-d-aspartate receptor encephalitis with minimal cortical impairment

Abstract

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis has been recently identified as a fulminant encephalopathy, presenting with a variety of symptoms including behavioral change, amnesia and seizures suggesting cortical gray matter involvement. A 42-year-old woman presented with acute-onset clinical and magnetic resonance imaging (MRI) findings indicating brainstem and diencephalon involvement. Her neuropsychological examination revealed mild frontal dysfunction with no memory impairment. Detailed diagnostic workup proved negative except for serum/cerebrospinal fluid (CSF) NMDAR-antibodies and increased activity in inguinal and pelvic lymph nodes on positron-emission tomography (PET) examination. The symptoms and MRI findings completely resolved following steroid treatment. A 38-year-old woman presented with migraine-type headache and episodes of forgetfulness. Her brain MRI and neuropsychological examination were normal and diagnostic workup was unremarkable. N-methyl-D-aspartate receptor antibodies were identified in her sera and her symptoms spontaneously resolved within few months. Our cases suggest that anti-NMDAR encephalitis might present with minimal cognitive impairment, no apparent cortical gray matter involvement, a mild clinical course and without the classical clinical features of the disease.

Zinc supplementation affects favorably the frequency of migraine attacks: a double-blind randomized placebo-controlled clinical trial

“…This element may inhibit the release of glutamate in the hippocampus [ 36 ]. Glutamate stimulates the N-methyl-D-aspartate (NMDA) receptor that is a key receptor in the initiation of migraine attacks [ 37 , 38 ]. In addition, zinc may be a competitive antagonist for the NMDA receptor [ 39 ].…”

A Unique Shape of Brainstem Lesion that Caused Orthostatic Hypotension in Anti-NMDAR Encephalitis

“…Almost half of the reported cases of anti-NMDAR encephalitis involve abnormal MRI findings in the medial temporal lobes and cerebral cortex; brainstem lesions have been extremely rare (1). Tüzün et al reported a mild clinical case showing midbrain lesions but no findings in the cortex (6). The present patient showed a uniquely shaped brainstem lesion that preserved the longitudinal pontine bundles bilaterally, indicating that her cranial nerve symptoms were related to damage to the transversal fibers and nuclei.…”