Abstract
Dysimmune encephalitis are frequent and disabling pathologies with efficacious treatments (immunotherapy). Evocative clinical signs are: rapid progressive evolution, seizure, movement disorder, psychiatric troubles, memory defect, dysautonomia and hyponatremia. Classical ancillary test: magnetic resonance imaging (MRI) and standard cerebro-spinal fluid (CSF) analysis can be normal. In this context, the cerebral positron emission tomography (PET) is helpful for the diagnosis. More often reported patterns are: association of hyper- and hypo-metabolism; fronto-temporal hyper-metabolism/parieto-occipital hypo-metabolism gradient (anti-N-methyl-D-aspartate receptor [NMDAR] encephalitis); temporal and basal ganglia hyper-metabolism (anti-leucine-rich glioma inactivated protein 1 [LGI1] encephalitis); temporal hyper-metabolism (other limbic encephalitis); parieto-occipital±basal ganglia hypo-metabolism (neurolupus); unihemispheric diffuse hypo-metabolism (Rasmussen encephalitis). The diagnosis could require research of specific antibodies. Finally, the cerebral PET is also useful during the follow-up: treatment's efficacy (improvement of metabolism), relapse (aggravation of metabolism's alteration), and evaluation of possible sequelae.
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