VIDEO Fixed dystonia unresponsive to pallidal stimulation improved by motor cortex stimulation

6,7 This is explained by a change in attentional distribution when a patient with hemianopia tends to search for the end of the line in the direction of the blind hemispace as an adaptive mechanism.7,8 However, this adaptation may occur on cost of accuracy in perception, as the erroneous bisection shows. The onset of ocular lateropulsion in the direction opposite to the direction of adaptation would therefore possibly temper this attentional redistribution and lead to a greater ease in accurately perceiving the visual world. Neck–proprioceptive and caloric–vestibular stimulation have been shown to improve visual neglect.9 It seems possible that even though our patient had no neglect, the acute onset of vestibular imbalance due to infarction of the left vestibular nucleus could have contributed to the reset of his attentional distribution and to the pronounced left ocular lateropulsion as well. The skew deviation resolved earlier than the ocular lateropulsion. This might be due to differences in the neural substrates underlying skew deviation and ocular lateropulsion. Whereas skew deviation in lateral medullary infarcts is related to damage to the otolith pathways at the level of the medial vestibular nucleus, ocular lateropulsion is the result of involvement of the olivocerebellar fibers in the inferior cerebellar peduncle, as described above. A different impact of the ischemia on these two, although anatomically proximate, neural structures might explain the different speed of recovery.