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1/4. Medial vestibular nucleus lesions in Wallenberg's syndrome cause decreased activity of the contralateral vestibular cortex.

    Three patients with the clinical diagnosis of Wallenberg's syndrome caused by acute unilateral ischemic infarctions, which included the vestibular nucleus in the medullary brain stem and afferent vestibular pathways, were examined by positron emission tomography (PET) during caloric vestibular stimulation. They all had typical signs of vestibular dysfunction such as transient rotatory vertigo with vomiting at the onset, ipsiversive body and ocular lateropulsion, and a complete ocular tilt reaction with tilts of the subjective visual vertical. Compared with healthy volunteers, who show activation in a network of temporoparietal vestibular areas within both hemispheres, especially in the posterior insula and retroinsular region that contains the human homologue of the parietoinsular vestibular cortex (PIVC) in monkeys, the activation pattern of the patients with Wallenberg's syndrome was typically changed. During caloric irrigation of the ear ipsilateral to the side of the lesion, they showed no or significantly reduced activation in the contralateral hemisphere, whereas the activation pattern in the ipsilateral hemisphere appeared "normal." These results are compatible with bilateral ascending vestibular pathways from the vestibular nuclei to the vestibular cortex. The novel finding in all three patients was that the activation patterns were compatible with the assumption that only the crossing fibers from the medial vestibular subnucleus to the contralateral medial longitudinal fascicle were affected, but the ipsilateral vestibular thalamocortical projections via the superior vestibular subnucleus were spared. Thus, the activation pattern in the PET study may reflect the vestibular tonic imbalance within the vestibular nuclei circuitry at the cortical level.
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2/4. Vestibular assessment in a patient with confirmed lateral medullary syndrome.

    The results of vestibular investigations in a patient with confirmed lateral medullary syndrome are presented. This patient showed a unilateral weakness on caloric testing which has not been reported previously in a patient with lateral medullary syndrome. The case for the possibility of a 'central' canal paresis on caloric testing is presented.
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3/4. Mapping of brainstem lesions by the combined use of tests of visually-induced eye movements.

    To determine the diagnostic value of visually-induced eye movements for indicating the lateralization of the lesion, optokinetic nystagmus (OKN), fixation-suppression of caloric nystagmus and pursuit eye movements were investigated in 28 patients who showed discrete unilateral brainstem lesions. In all patients, pursuit gains decreased in parallel with the direction of the impairment of slow-phase OKN velocity with a significant left/right difference. Decreases of gains were predominantly towards the affected side in 22 patients, whereas they were predominantly towards the contralateral side in 2 patients with dorsal tegmental pontine lesions and in 4 out of 8 patients with Wallenberg's syndrome. The relationship of pursuit gains to percentage reduction of fixation-suppression of caloric nystagmus (%FS) showed no correlation. The following four groups were classified. In group A, which was the largest, pursuit gains and %FS decreased predominantly towards the lesioned side. This group consisted of 5 patients with lesions in the midbrain, 6 patients with lesions in the ventral pons and 4 out of 8 patients with Wallenberg's syndrome. The opposite of group A was group D, showing reverse electro-oculographic (EOG) patterns to those in group A in relation to the lesioned side. Group D consisted of 2 patients with lesions in the dorsal pontine tegmentum. This observation, taken together with the decreases of pursuit and OKN gains in relation to the lesioned side, might indicate that lesions of ascending fibres are responsible for pursuit and OKN abnormalities. Group B, consisting of 7 patients with lesions either in the superior or middle cerebellar peduncles, showed decreased pursuit gains predominantly towards the lesioned side and %FS reduced predominantly towards the side contralateral to the lesion. EOGs of these patients were consistent with the results of floccular ablation in the monkey. In group C, these two parameters showed patterns opposite to those in group B in relation to the lesioned side and this group consisted of the other 4 patients with Wallenberg's syndrome. In patients of this group, the inferior cerebellar peduncle might be involved. The combined use of these tests is thus useful for lateralizing the lesion in the brainstem.
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4/4. Visually guided eye movements in patients with Wallenberg's syndrome.

    To determine the lesions and the lateralization in patients with Wallenberg's syndrome, visually-guided eye movements were quantitatively analysed and these findings were compared with a lesioned site as revealed by magnetic resonance imaging (MRI). The 8 patients could be clearly classified into two subgroups based on the functional test of eye movements. In 4 patients, optokinetic nystagmus (OKN), pursuit eye movements and fixation-suppression of caloric nystagmus (FS), utilizing the slow phase velocity as a parameter, were impaired toward the lesioned side in the medulla. In the remaining 4 patients, OKN and pursuit eye movements were impaired toward the side contralateral to the lesion, whereas FS toward the lesioned side, indicating a lesion affecting not only the medulla but also the inferior peduncle and/or the cerebellum. Therefore, the functional visually-guided eye movements can provide a useful test battery with which to detect the lesion site in Wallenberg's syndrome.
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