Prognostic and Mechanistic Factors Characterizing Seizure-Associated Crossed Cerebellar Diaschisis

Crossed cerebellar diaschisis is a rare finding of hemispheric cerebellar depression following contralateral cerebral injury, hypothesized to result from excessive neuronal excitatory synaptic activity along cortico-pontine-cerebellar pathways. The phenomenon is typically observed following ischemic stroke, but has also been characterized during seizure activity—in particular, status epilepticus (SE). Neurological outcome has varied widely in published reports, with some patients achieving full neurologic recovery, while others experience persistent disability.

Case report and literature review.

We present a 54-year-old man found unresponsive with a right hemispheric syndrome several days after discharge following amygdalohippocampectomy for refractory right temporal lobe epilepsy. Prolonged electroencephalogram demonstrated one subclinical right frontal seizure, along with right frontal periodic lateralized epileptiform discharges, presumed to be associated with SE preceding his admission. Initial MRI demonstrated restricted diffusion on diffusion weighted imaging in the right cerebral hemisphere, ipsilateral thalamus, and contralateral cerebellum. A head CT one week later showed diffuse sulcal effacement with loss of gray–white differentiation in the right frontal and insular regions with low attenuation changes of right thalamus. An MRI showed worsened diffusion restriction, despite a corresponding increase in perfusion. The patient remained paretic at discharge and follow-up. Follow-up MRI at 2 months demonstrated pronounced right cerebral and left cerebellar atrophy, loss of gray matter in much of the right cerebrum, and scattered areas of T2 hyperintensity, consistent with permanent right fronto-temporal neuronal loss.

Collectively, these observations indicate that imaging findings of persistent cerebral restricted diffusion and cytotoxic edema in the subacute post-ictal period may predict irreversible neuronal injury and poor long-term outcome—even when accompanied by evidence of cortical hyperperfusion and recovery of second- and third-order neurons along the involved circuit.