TY - JOUR
T1 - Electroencephalographic and fluorodeoxyglucose-positron emission tomography correlates in anti-N-methyl-d-aspartate receptor autoimmune encephalitis
AU - Probasco, John C.
AU - Benavides, David R.
AU - Ciarallo, Anthony
AU - Sanin, Beatriz Wills
AU - Wabulya, Angela
AU - Bergey, Gregory K.
AU - Kaplan, Peter W.
N1 - Publisher Copyright:
© 2014.
PY - 2015/2/1
Y1 - 2015/2/1
N2 - Importance: Anti-. N-methyl-. d-aspartate receptor (anti-NMDAR) autoimmune encephalitis is an increasingly recognized cause of limbic encephalitis (LE). Prolonged LE and limbic status epilepticus (LSE) share many features. The ability to distinguish between the two is crucial in directing appropriate therapy because of the potential iatrogenesis associated with immunosuppression and anesthetic-induced coma. Observations: A 34-year-old woman with recurrent LE developed behavioral changes, global aphasia, and repetitive focal and generalized tonic-clonic seizures. Because asymmetric rhythmic delta patterns recurred on electroencephalography (EEG) despite treatment with nonsedating antiepileptic drugs followed by anesthetic-induced coma, an investigation to distinguish LSE from LE was undertaken. Implanted limbic/temporal lobe depth electrodes revealed no epileptiform activity. Brain single-photon emission computerized tomography (SPECT) showed no hyperperfusion, and brain fluorodeoxyglucose-positron emission tomography (FDG-PET) showed hypermetabolism in the left frontal, temporal, and parietal cortices. Anti-. N-methyl-. d-aspartate receptor autoimmune encephalitis was diagnosed based detection of anti-NMDAR antibody in the cerebrospinal fluid (CSF). With chronic immunosuppression, the resolution of brain FDG-PET abnormalities paralleled clinical improvement. Conclusions and relevance: This case of anti-NMDAR autoimmune encephalitis illustrates the challenges of distinguishing prolonged LE from LSE. We discuss the parallels between these two conditions and propose a management paradigm to optimize evaluation and treatment.
AB - Importance: Anti-. N-methyl-. d-aspartate receptor (anti-NMDAR) autoimmune encephalitis is an increasingly recognized cause of limbic encephalitis (LE). Prolonged LE and limbic status epilepticus (LSE) share many features. The ability to distinguish between the two is crucial in directing appropriate therapy because of the potential iatrogenesis associated with immunosuppression and anesthetic-induced coma. Observations: A 34-year-old woman with recurrent LE developed behavioral changes, global aphasia, and repetitive focal and generalized tonic-clonic seizures. Because asymmetric rhythmic delta patterns recurred on electroencephalography (EEG) despite treatment with nonsedating antiepileptic drugs followed by anesthetic-induced coma, an investigation to distinguish LSE from LE was undertaken. Implanted limbic/temporal lobe depth electrodes revealed no epileptiform activity. Brain single-photon emission computerized tomography (SPECT) showed no hyperperfusion, and brain fluorodeoxyglucose-positron emission tomography (FDG-PET) showed hypermetabolism in the left frontal, temporal, and parietal cortices. Anti-. N-methyl-. d-aspartate receptor autoimmune encephalitis was diagnosed based detection of anti-NMDAR antibody in the cerebrospinal fluid (CSF). With chronic immunosuppression, the resolution of brain FDG-PET abnormalities paralleled clinical improvement. Conclusions and relevance: This case of anti-NMDAR autoimmune encephalitis illustrates the challenges of distinguishing prolonged LE from LSE. We discuss the parallels between these two conditions and propose a management paradigm to optimize evaluation and treatment.
KW - Anti-NMDA receptor antibodies
KW - Autoimmune encephalitis
KW - Limbic encephalitis
KW - Limbic status epilepticus
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U2 - 10.1016/j.ebcr.2014.09.005
DO - 10.1016/j.ebcr.2014.09.005
M3 - Article
C2 - 25667900
AN - SCOPUS:84924322606
SN - 2213-3232
VL - 2
SP - 174
EP - 178
JO - Epilepsy and Behavior Case Reports
JF - Epilepsy and Behavior Case Reports
ER -