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

into the healthy hemispheric field, vision improved or normalized. Finally, the possibility of changes in the modality-specific attention, a special type of attention that is not necessarily spatially distributed, was raised. Changes in this subtype of attention on lateral gazing may therefore help in overcoming visual field deficit as a compensatory mechanism. 5 We would like to comment upon the tendency of our patient to bisect a horizontal line ipsilaterally to the side of hemianopia, that is, contralaterally to the side of occipital lesion. Patients with complete hemianopia can see only the line on the side of the normal hemifield and would thus be expected to bisect the line ipsilaterally to the brain lesion. However, this is true only in patients with hemianopia and hemispatial neglect, whereas patients with pure hemianopia, as in our case, show a tendency to bisect the line contralaterally to the side of the lesion, toward the hemianopic visual field. 6,7 This is explained by a change in atten-tional distribution when a patient with hemianopia tends to search for the end of the line in the direction of the blind hemis-pace 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 lateropul-sion. 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 olivo-cerebellar 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. Despite the fact that the mechanism responsible for improvement of vision is unknown, it seems that …