Diaschisis and Neuropsychological Performance after Cerebellar Stroke

Abstract

The cerebellum has been implicated in higher-order behavior. Blood flow studies (SPECT) have shown that cerebral diaschisis can appear after cerebellar lesions and this phenomenon could serve as a basis for a potential neuropsychological derangement after cerebellar insults. Our objectives in this study were to delineate the neuropsychological profile after cerebellar stroke, to evaluate cerebral diaschisis as measured by SPECT and to correlate the findings. We prospectively studied 26 patients with cerebellar stroke and 16 subjects matched for age, sex and educational level as a control group. A neuropsychological battery test, MRI and cerebral SPECT were performed in both groups. We found that cerebellar stroke results in motor control impairment and mild naming deficit, whereas no dysfunction in declarative memory, language, visuospatial or executive abilities is evident. The anatomical distribution of the lesion does not seem relevant in terms of neuropsychological impairment or diaschisis. Both ipsilateral and contralateral diaschisis as a result of a cerebellar stroke are found, but this phenomenon does not seem to result in overt neuropsychological derangement.

Children and Adolescents With Chronic Cerebellar Lesions Show No Clinically Relevant Signs of Aphasia or Neglect

“…There is also evidence for nonlateralized visuospatial deficits in cerebellar patients (Malm et al 1998;Molinari et al 2004;Neau et al 2000;Schmahmann and Sherman 1998), but impairments of visuospatial functions were not confirmed in other studies (Dimitrov et al 1996;Gomez Beldarrain et al 1997).…”

Visual Motion Perception Deficits Due to Cerebellar Lesions Are Paralleled by Specific Changes in Cerebro-Cortical Activity

“…Although cerebellar damage or inactivation induces changes in cerebro-cortical metabolism, a phenomenon referred to as (crossed) cerebello-cerebral diaschisis (Broich et al, 1987;Gó mez Beldarrain et al, 1997;Tecco et al, 1998;Gasparini et al, 1999;Gold and Lauritzen, 2002;Vokaer et al, 2002;Enager et al, 2004), a thorough description of cerebral activity after loss of cerebellar input is missing to date. The goal of this study was to provide a detailed description of cerebro-cortical functioning after cerebellar lesions and to correlate cognitive performance with neurophysiological properties of cerebral cortex such as recorded by magnetoencephalography (MEG).…”

Language Disorders Subsequent to Left Cerebellar Lesions: A Case for Bilateral Cerebellar Involvement in Language?

“…Neurophysiologically, this form of diaschisis translates as the functional deactivation of a disconnected contralateral cerebral region, as a consequence of impeded excitatory neural transmission via cerebello-thalamocortical pathways [6] . Reports of ipsilateral cortical diaschisis subsequent to cerebellar lesions [8] support a possible left cerebellar hemisphere contribution to the mediation of linguistic processes, presumably via ipsilateral cerebellar-basal ganglia-cortical pathways [10] .…”

“…Studies based on neuroimaging techniques such as single-photon emission computed tomography (SPECT), positron emission tomography and magnetic resonance imaging have consistently revealed regions of contralateral cortical hypoperfusion in relation to the orientation of the cerebellar lesion [8,9] , a phenomenon called crossed cerebello-cerebral diaschisis. Neurophysiologically, this form of diaschisis translates as the functional deactivation of a disconnected contralateral cerebral region, as a consequence of impeded excitatory neural transmission via cerebello-thalamocortical pathways [6] .…”

“…Previously, linguistic functioning in individuals with cerebellar lesions has largely been investigated using tests derived from neuropsychological test batteries, predominantly incorporating verbal fluency measures and more general language assessments such as confrontation naming [8,11,12] . Unfortunately it has been reported that assessments of general language function often fail to identify or adequately characterize the nature of language pathology resulting from cerebellar lesions [13] .…”