UPPER LIMB ATAXIC MONOPARESIS AND ASTERIXIS CAUSED BY A PARIETAL INFARCT

A 58-year old right-handed man with chronic non valvular atrial fibril lation developed an acute left upper limb ataxia with transient numbne ss and mild motor impairement Two weeks later, there was a severe degr ee of ataxia of the left upper limb and prominent asterixis of the lef t hand CT scan and MRI showed a small parietal infarct. Initial median nerve somatosensory evoked potentials (SEPs) showed mild impairment o f right parietal responses with absent right frontal SEPs P22 and N30. Two months later, parietal responses were normal but right frontal SE Ps P22 and N30 remained abolished while ataxia of left upper limb pers isted. Electromyographic activity recorded at the same time showed per iodic involvement of the left hand distal tonus. These finding suggest ed that both ataxia and asterixis were due to a single postcentral inf arct. Frontal SEP components are known to convey proprioceptive inputs which could be received by neocerebellar afferent pathways. Generator s of these components are presumably located in premotor cortex and ca n 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 pathwa ys resulting in the emergence of parietal ataxia.