Attentional dysfunction after cerebellar stroke: a P300 case report

The functional domain of the cerebellum extends beyond its traditional role in motor control. In recent years this structure has increasingly been seen as playing a crucial role also in cognitive processes, supported by observations of cerebellar activation demonstrated by functional imaging studies performed during cognitive tasks, as well as by findings showing that cerebellar lesions produced impairment in cognitive tasks. We investigated the psychophysiological profile of attentional processing of the stimulus in a patient with a cerebellar stroke using P300 component both during the acute phase and during four weeks of follow-up. A 55-year-old man with a history of diabetes mellitus presented with headache in the occipital region and generalized asthenia. At admission, neurological examination revealed a deviation to the left of the index test and of gait star. Diffusion-weighted imaging showed an acute ischemic lesion in the left posterior cerebellar hemispheric cortex, supplied by the posterior inferior cerebellar artery. MMSE, BDI and STAY1-2 and MICARS were administered to assess cognitive, neuropsychiatric and motor status; moreover, patient underwent a psychophysiological evaluation consisting of a classical auditory P300 oddball paradigm at 24 hours from stroke (T0), after two weeks (T1) and after four weeks (T2). The patient correctly performed required tasks during each ERPs recording. Measurements of P300 component at T0 and T1 revealed lower amplitude in the patient than in the group of 10 controls matched for age and gender (T0: Cz p=0.05, Pz p=0.01; T1: Cz p=0.07, Pz p=0.01). Latency and amplitude of P300 component were comparable to the controls only at the third ERPs evaluation (T2). The MICARS score improved after two weeks and then remained stable (T0=11; T1=3; T2=3). The early abnormality of the P300 component after stroke suggests a dysfunction in the attentional processing of the stimulus as a result of a focal cerebellar lesion. This ERP component, in fact, reflects activation of a complex neural network involved in attention and memory processes. P300 amplitude seems to normalize progressively after stroke thus indicating a recovery of the cognitive functioning that was preceded and paralleled by improvement in skilled movements (as indexed by MICARS scores), suggesting that the functional recovery of the cerebellum played a pathophysiological role in both motor and cognitive performances. Reasonably, reduced P300 amplitude results from dysfunction of the cerebellar projections towards prefrontal and posterior-parietal cortices that are crucial for attentional processes. Thus, after a cerebellar stroke, a cerebello-cerebral diaschisis may be the pathophysiological cause transiently inducing a failure in engaging the networks responsible ofthe attentional and discrimination process of the stimuli.