1991
DOI: 10.1002/ana.410300214
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Asymmetrical ocular pursuit with posterior fossa tumors

Abstract: We report two patients with posterior fossa neoplasms who demonstrated asymmetrically impaired horizontal ocular pursuit documented with electrooculography. One patient had impaired pursuit contralateral to a pontomedullary lesion, whereas the second patient had impaired pursuit ipsilateral to a pontocerebellar lesion. These patients demonstrate that posterior fossa lesions may impair ocular pursuit either contralaterally or ipsilaterally unlike cerebral hemispheric lesions, which impair ocular pursuit ipsilat… Show more

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Cited by 5 publications
(1 citation statement)
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“…Defective contralateral smooth pursuit with pontine tegmentum lesions may be associated with several possible mechanisms: (1) disruption of afferent projections to the flocculus/paraflocculus after their decussation; (2) ipsilateral central vestibular damage; and (3) disruption of the ipsilateral vestibular fibers to the abducens nucleus before their decussation. 8,24 As for ipsilateral smooth pursuit impairment by the pontine tegmentum lesion as seen in our pontine sensory stroke patients, 4 mechanisms have been postulated: (1) involvement of corticopontine pathways 9 ; (2) disruption of the pontocerebellar mossy fibers to the flocculus/paraflocculus before their decussation across the midline 8 ; (3) impairment of inhibitory projections from the flocculus/paraflocculus to the vestibular nucleus 25 ; and (4) damage to "pursuit neurons," which lie inferior to the abducens nucleus, outside the PPRF, and which are modulated in response to ipsilateral smooth pursuit eye movements. 26 A rostral lesion in the pons can destroy the corticopontine pathways that mediate the smooth pursuit, but this is unlikely in our patients because, as verified by MRI/CT, our patients' lesions did not involve the corticopontine pathway that descends through the cerebral peduncle and passes through the ventrolateral pons to terminate pontine nuclei in the pontine base.…”
Section: Discussionmentioning
confidence: 99%
“…Defective contralateral smooth pursuit with pontine tegmentum lesions may be associated with several possible mechanisms: (1) disruption of afferent projections to the flocculus/paraflocculus after their decussation; (2) ipsilateral central vestibular damage; and (3) disruption of the ipsilateral vestibular fibers to the abducens nucleus before their decussation. 8,24 As for ipsilateral smooth pursuit impairment by the pontine tegmentum lesion as seen in our pontine sensory stroke patients, 4 mechanisms have been postulated: (1) involvement of corticopontine pathways 9 ; (2) disruption of the pontocerebellar mossy fibers to the flocculus/paraflocculus before their decussation across the midline 8 ; (3) impairment of inhibitory projections from the flocculus/paraflocculus to the vestibular nucleus 25 ; and (4) damage to "pursuit neurons," which lie inferior to the abducens nucleus, outside the PPRF, and which are modulated in response to ipsilateral smooth pursuit eye movements. 26 A rostral lesion in the pons can destroy the corticopontine pathways that mediate the smooth pursuit, but this is unlikely in our patients because, as verified by MRI/CT, our patients' lesions did not involve the corticopontine pathway that descends through the cerebral peduncle and passes through the ventrolateral pons to terminate pontine nuclei in the pontine base.…”
Section: Discussionmentioning
confidence: 99%