Abstracts

Rationale: The term “diaschisis“ refers to the pathophysiological phenomenon of transient or permanent loss of function in a brain region distant from the area of the cortical or subcortical primary brain lesion. Crossed cerebellar diaschisis (CCD) has been observed with several supratentorial brain pathologies. In adults with chronic epilepsy, CCD has been rarely reported, and only two case reports deal with CCD after status epilepticus (SE) [1,2]. Diffusion weighted imaging (DWI) allows to detect acute tissue changes by indicating energy metabolism compromise secondary to ictal activity. We report for the first time CCD findings during status epilepticus by means of DWI, although CCD was clinically not detectable because of non-convulsive SE (NCSE). Methods: A 74 year-old woman was found unresponsive and she experienced a generalized-tonic-clonic seizure responding to lorazepam on emergency admission. Examination revealed unresponsiveness and right, but not left, arm movements to painful stimulation. She showed fixed left-upward gaze and right-sided pupillary dilatation. She was transferred to the intensive care unit for monitoring, therapy and further diagnostic work-up (EEG, CT, MRI, lumbar puncture). Results: Her EEG showed right-hemispheric focal NCSE (Fig. 1). Lumbar puncture yielded normal results. The MRI demonstrated widespread cortical DWI hyperintensity and corresponding apparent diffusion coefficient (ADC) reductions in the right hemisphere including the thalamus, hippocampus, head of the caudate, and parts of the occipital areas together with pronounced cortical swelling of affected areas. This pattern of DWI abnormality excluded brain ischemia and the vessels of the circle of Willis were all normal. Contralaterally to the cortical and subcortical right hemisphere abnormalities, the left cerebellar hemisphere too showed DWI hyperintensities and reduced ADC although this was less pronounced (Fig. 2). The NCSE was refractory to maximal anti-convulsive therapy including therapeutic coma. Hemodynamic instability and evolving multi-organ failure led to the death of the patient on day 4 of hospitalization. Conclusions: Status epilepticus may damage the brain by excitotoxicity resulting from glutamate spillover and an increase of intracellular calcium. Membrane peroxidation and energy exhaustion with breakdown of electrolyte and water homeostasis eventually lead to acute cell death. These mechanisms may be visualised by MRI, especially by means of DWI which may show laminar cortical cytotoxic cell swelling. Proposed mechanisms of CCD were glutamatergic propagation of hyperexcitation through the corticopontocerebellar tracts and/or GABAergic disinhibition of these tracts after lesions of the controlling inhibitory interneurons. Our findings based on imaging techniques like DWI may help to visualize the pathophysiological and neuroanatomical understanding of CCD during SE. [1] Ribeiro, et al. Acta Med Port 2006; 19: 439-41.[2] Biaou O, et al. J Radiol 2008; 89: 507-9.