A 50-year-old lady with longstanding epilepsy and worsening seizure control for 6 months was admitted after a prolonged generalised seizure, with depressed consciousness, aphasia and right-sided weakness, which progressed over the next 72 h. MRI revealed T2-hyperintensity and restricted diffusion throughout the cortex of the left hemisphere and in the right cerebellum. MR imaging 3 months earlier had been normal. Subluxation of C1/C2 was evident on neck imaging. CSF was acellular with normal protein. Brain biopsy revealed non-specific reactive changes. Voltage-gated potassium channel antibodies were low-positive (198pM). Repeat imaging 2 weeks later showed progression of left hemisphere abnormalities to involve deep grey matter structures and 2 months after presentation there was marked cortical atrophy and extensive white matter malacic change in the left hemisphere. She received anti-epileptic drug therapy and had no further seizures. High-dose corticosteroids and plasmaphaeresis has led to clinical improvement. She is alert, obeys simple commands, but is aphasic. We hypothesise that the clinical and imaging features are due to post-ictal neuronal damage in the left hemisphere (secondary to cytotoxic oedema and failure of cerebral autoregulation) with crossed cerebellar diaschisis in the context of decreased metabolic reserve due to autoimmune encephalitis.
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