UPPER LIMB ATAXIC MONOPARESIS AND ASTERIXIS CAUSED BY A PARIETAL INFARCT

A 58-year old right-handed man with chronic non valvular atrial fibrillation developed an acute left upper limb ataxia with transient numbness and mild motor impairement Two weeks later, there was a severe degree of ataxia of the left upper limb and prominent asterixis of the left hand CT scan and MRI showed a small parietal infarct. Initial median nerve somatosensory evoked potentials (SEPs) showed mild impairment of right parietal responses with absent right frontal SEPs P22 and N30. Two months later, parietal responses were normal but right frontal SEPs P22 and N30 remained abolished while ataxia of left upper limb persisted. Electromyographic activity recorded at the same time showed periodic involvement of the left hand distal tonus. These finding suggested that both ataxia and asterixis were due to a single postcentral infarct. Frontal SEP components are known to convey proprioceptive inputs which could be received by neocerebellar afferent pathways. Generators of these components are presumably located in premotor cortex and can be activated through parietofrontal connections. In our case it can be assumed that the parietal infarct involved these connections, which are mainly implied in the regulation of postural tonus of the distal upper limbs, and simultaneously impaired neocerebellar afferent pathways resulting in the emergence of parietal ataxia.