Crossed cerebellar diaschisis in status epilepticus: A systematic review of the literature

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Abstract

OBJECTIVE: Crossed cerebellar diaschisis is a neuroimaging phenomenon observed in various neurological conditions, including status epilepticus. This systematic review aims to summarize the clinical and radiological characteristics of patients developing crossed cerebellar diaschisis following status epilepticus and to discuss potential pathophysiological mechanisms.

METHODS: A systematic literature search was conducted using MEDLINE/PubMed, Embase, Web of Science, and CENTRAL from inception to October 2025. Studies reporting crossed cerebellar diaschisis in patients with status epilepticus, confirmed by neuroimaging (MRI, PET, or SPECT), were included. Data on demographics, semiology, etiology, imaging findings, EEG, and outcomes were extracted and synthesized. A spatial analysis of supratentorial MRI abnormalities associated with crossed cerebellar diaschisis was performed in 18 cases with suitable imaging.

RESULTS: Sixty patients from 50 studies were included. Mean age was 46.1 years; 50% were female. Convulsive status epilepticus was present in 62% of cases. Etiology was acute in 40%, unknown in 45%. Crossed cerebellar diaschisis was most frequently detected via DWI hyperintensity (55%) and FLAIR/T2 changes (52%). Arterial spin labelling and SPECT often showed hyperperfusion in the acute phase. Spatial mapping of supratentorial MRI abnormalities revealed a predominant involvement of cortical temporo-occipital regions, with minimal subcortical involvement, aligning with known cerebro-cerebellar connectivity patterns. Cerebellar symptoms were rare (5%), but cerebellar atrophy was reported in 7% of cases. Mortality was 10%; 30% recovered completely, while 33% had neurological deficits at discharge.

SIGNIFICANCE: Crossed cerebellar diaschisis is a dynamic phenomenon, presenting with both hyper- and hypoperfusion or metabolism, based on the timing and severity of status epilepticus. It may result from increased inhibitory cerebellar activity during seizures, followed by metabolic exhaustion and Purkinje cell loss. Although often clinically silent, it might lead to long-term cerebellar atrophy and neurological sequelae.

Original languageEnglish
Number of pages13
JournalEPILEPTIC DISORDERS
Early online dateJan 2026
DOIs
Publication statusPublished - 3 Jan 2026

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