Epilepsy Information

(Abst. 1.36)

Neuropsychological findings in epilepsy patients with and without cerebellar diaschisis as measured by siscom

Authors: Keren Isaacs-Lebeau, Jeffrey Politsky, Charles Zaroff and G. Lee

Evidence exists that the cerebellum (Cb) plays a role in epilepsy and cognition. In focal epilepsy activation of cerebellar-cortical (Cb-Cx) pathways exerts an inhibitory influence over pathologically hyperexcited cortex. In cognition the cerebellar cognitive affective syndrome refers to patients with strictly cerebellar pathology, whose cognitive deficits closely resemble patients with neocortical pathology. To date, there has been no systematic evaluation of cognitive function in patients with refractory partial epilepsy (RPE) with Cb involvement. Cerebellar diaschisis (CbD) occurs in a substantial percentage of patients with RPE, though the exact reason is unclear: opinions range from insignificant activation of anatomical pathways to compensatory activation. Though efferent inhibitory Cb-Cx connections are more often described with reference to motor cortex, we have observed ipsilateral and crossed CbD in patients with temporal and extra-temporal lobe epilepsy, with and without motor involvement. In an effort to determine whether or not the existence CbD in patients with RPE influenced cognitive function (presumably negatively), we analyzed neuropsychological scores and profiles in patients with RPE comparing those with to those without evidence of CbD.


We evaluated 70 patients with RPE who underwent who underwent SISCOM evaluation as part of their pre-surgical epilepsy evaluation at the Medical College of Georgia. 61 had full neuropsychological assessment. Psychometric assessment was accomplished using the Wechsler Adult Intelligence Scale and Wechsler Memory Scale. We hypothesized that Working Memory, Processing Speed, Perceptual Organization, Visual Memory Immediate, and Visual Memory Delayed indices would discriminate between patients with (n = 39) and without (n = 22) CbD; side of seizure onset was similar in the two groups. Paired t-tests were used to measure possible index differences with significance level set at 0.05. D’Agostino tests of normality were run beforehand on each variable.

Data were normally distributed. No significant differences were observed between the two groups on any of the Wechsler indices, including those theorized to discriminate between patients with and without CbD (p > .05).

There were no significant differences in neuropsychological scores comparing those patients with and without CbD. Contributing factors to the current negative results included methodological factors (the absence of additional measures of specific discrete aspects of cognition/behavior), and the pattern of cerebellar-mediated deficits (potentially obscured by neuropsychological deficits imposed by focal and/or lateralizing cortical dysfunction). The current data may also speak to the lesser likelihood of finding cerebellar-mediated neurobehavioral deficits in cases lacking cerebellar lesions. The current data may also address the lesser likelihood of finding cerebellar-mediated neurobehavioral deficits in cases lacking cerebellar lesions.