Limbic encephalitis with autoantibodies against the glutamate receptor epsilon 2 mimicking temporal lobe epilepsy

Yoshino, Aihide; Kimura, Yasutoshi; Miyazaki, Masaki; Ogawa, Tetsuo; Matsumoto, Aki; Nomura, Soichiro; Nemoto, Hideaki; Takahashi, Yukitoshi

doi:10.1111/j.1440-1819.2007.01669.x

Cited by 6 publications

(3 citation statements)

References 2 publications

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“…Since unilateral involvement of the medial temporal lobe is considered atypical for autoimmune limbic encephalitis, as long as the specific antibodies are absent, we diagnosed this case as autoimmune encephalitis rather than autoimmune limbic encephalitis (9,(11)(12)(13). In our case, considering the rapid progression of psychiatric symptoms, MRI findings, lack of evi-dence of herpetic infection, elevated CSF IgG index, and detection of antibodies to GluRs (especially against N2B) in the CSF, which is occasionally useful for diagnosing and differentiating encephalitis from epilepsy (14), we diagnosed autoimmune encephalitis concurrent with solitary intracranial plasmacytoma.…”

Section: Discussionmentioning

confidence: 80%

Autoimmune Encephalitis in a Patient with a Solitary Intracranial Plasmacytoma

Mizutani,

Sakurai,

Uchida

et al. 2024

Intern. Med.

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A 65-year-old woman presented with fever and abnormal behavior. Magnetic resonance imaging showed swelling of the left medial temporal lobe and an intracranial extra-axial occipital tumor. While her neurological symptoms improved after the administration of corticosteroid therapy under the suspicion of autoimmune encephalitis, the occipital tumor unexpectedly shrank, and the diagnosis of a solitary plasmacytoma was confirmed by biopsy. Additional examinations revealed elevated anti-glutamate receptor antibodies in the cerebrospinal fluid. The patient was diagnosed with autoimmune encephalitis concurrent with an intracranial solitary plasmacytoma. Central nervous system involvement can be considered a neurological complication in patients with a solitary plasmacytoma.

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Section: Discussionmentioning

confidence: 80%

Autoimmune Encephalitis in a Patient with a Solitary Intracranial Plasmacytoma

Mizutani,

Sakurai,

Uchida

et al. 2024

Intern. Med.

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“…GluN2B is prominent in adult hippocampal synapses as an integral part of GluN1, GluN2A, and GluN2B (Rauner and Köhr, 2011). Anti-GluR antibodies are associated with various neurological conditions, such as limbic encephalitis (Mochizuki et al, 2006), epilepsy (Yoshino et al, 2007), and cerebellitis (Shiihara et al, 2007;Shimokaze et al, 2007). Antibodies against GluN2B have been found in patients with non-herpetic limbic encephalitis (Mochizuki et al, 2006), temporal lobe epilepsy (Yoshino et al, 2007), and epilepsia partialis continua (Takahashi et al, 2005).…”

Section: Epilepsy and Anti-glutamate Receptor Antibodiesmentioning

confidence: 99%

“…Anti‐GluR antibodies are associated with various neurological conditions, such as limbic encephalitis (Mochizuki et al ., ), epilepsy (Yoshino et al ., ), and cerebellitis (Shiihara et al ., ; Shimokaze et al ., ). Antibodies against GluN2B have been found in patients with non‐herpetic limbic encephalitis (Mochizuki et al ., ), temporal lobe epilepsy (Yoshino et al ., ), and epilepsia partialis continua (Takahashi et al ., ). GluD2 is predominantly expressed in cerebellar Purkinje cells (Hirai et al ., ).…”

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confidence: 99%

Epilepsy with myoclonic atonic seizures and chronic cerebellar symptoms associated with antibodies against glutamate receptors N2B and D2 in serum and cerebrospinal fluid

Matsuura

Hamano

Ikemoto

et al. 2017

Epileptic Disorders

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A 3‐year‐old boy with normal development presented with acute cerebellitis at one year and 10 months of age. His truncal ataxia resolved without treatment. He experienced a relapse of truncal ataxia and atonic seizures at 2 years and one month of age. Five months later, he experienced myoclonic atonic seizures. By 3 years of age, the truncal ataxia had become severe, and the frequency of myoclonic atonic seizures increased. Compared to controls, we found higher levels of anti‐C‐terminal GluN2B and anti‐N terminal GluD2 antibodies in the serum, and anti‐N terminal GluN2B and anti‐C terminal GluD2 antibodies in the cerebrospinal fluid (CSF). A cell‐based assay revealed the presence of anti‐NMDA‐type glutamate receptor antibody in the serum, but absence in the CSF. Ictal EEG of myoclonic atonic seizures showed generalized spike and wave complexes. The patient was diagnosed with myoclonic atonic epilepsy. Adrenocorticotrophic hormone therapy resolved the truncal ataxia and myoclonic atonic seizures, along with the decreased serum anti‐C‐terminal GluN2B and anti‐N‐terminal GluD2 antibodies, and CSF anti‐N‐terminal GluN2B and anti‐C‐terminal anti‐GluD2 antibodies. Our results suggest that the anti‐GluN2B and anti‐GluD2 antibodies may be associated with myoclonic atonic epileptic seizures and chronic cerebellitis.

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