Aphasia following cerebellar damage: fact or fallacy?

Abstract

During the past two decades, converging neuroscientific evidence has established the view that the human cerebellum participates in a much wider range of functions than conventionally accepted. As a consequence, the concept of ‘cerebellar cognition’ evolved from a mere afterthought to an exciting new multifaceted area of contemporary cognitive neuroscientific investigations. One of the major avenues of current research is the role of the cerebellum in non-motor language processing. Evidence from both neuroimaging and lesion-behaviour studies indicate that aside from its function in the execution of motor speech the cerebellum is also engaged in the processing of language at a higher level than the articulatory one. In this contribution we focus on this topic by an illustrative case in which an ischaemic lesion in the vascular territory of the right arteria cerebellaris superior induced a prefrontal aphasic syndrome and an agrammatism. In the total absence of any neuroradiological evidence for a structural lesion in the left frontal language areas, the hypothetical causative role of the right cerebellar lesion on the contralateral prefrontal aphasic symptomatology is advocated and supported by positive 99mTc-hexamethylpropyleneamine oxime single-photon emission-computed tomography findings ( 99mTc-HMPAO SPECT), revealing focal hypoperfusions in the clinically suspected areas. During longitudinal follow-up the regression of crossed cortical and subcortical left hemisphere diaschisis demonstrated by SPECT parallelled the changes in the neurolinguistic profile. The presented case adds evidence to the view that the phenomenon of so-called ‘crossed cerebello-cerebral diaschisis’, reflecting the distant functional impact of the right cerebellum on the contralateral prefrontal cortical areas, can be associated with an aphasic substrate. The co-occurrence of a right cerebellar lesion and an aphasic syndrome illustrates the pathophysiological hypothesis of a deactivation of prefrontal left hemisphere language functions due to the loss of excitatory impulses through cerebello-ponto-thalamo-cortical pathways.