Oculomotor and Oculovestibular Functions in a Hemispherectomy Patient

Estañol, B; Romero, Ramon; Viteri, Manuel Sáenz de; Mateos, J.H; Corvera, Jorge

doi:10.1001/archneur.1980.00500550067009

Cited by 21 publications

(15 citation statements)

References 17 publications

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“…Consistent with this observation, humans also showed asymmetry in their VOR during sinusoidal, horizontal whole-body rotation after hemidecortication or hemispherectomy with the basal ganglia and thalamus left intact (Estaaeol et al 1980;Sharpe and Lo 1981): gain (eye velocity/head velocity) of the VOR in complete darkness was lower during rotation toward the side contralateral to the lesion (i.e., the slow phase to the lesioned side) than gain during rotation toward the lesioned side; gain of the VOR tested with a stationary target also had a similar asymmetry (Estaaeol et al 1980;Sharpe and Lo 1981). The patients also had a slow eye drift of 3±8/s toward the side contralateral to the lesion, particularly in darkness (Estaaeol et al 1980;Sharpe and Lo 1981), and this drift may have contributed to the asymmetry in the VOR gain.…”

Section: Decorticationsupporting

confidence: 65%

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Corticovestibular interactions: anatomy, electrophysiology, and functional considerations

Fukushima¹

1997

Exp Brain Res

137

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This review summarizes anatomical and electrophysiological observations related to corticovestibular interactions as a step toward understanding their possible functions. Vestibular information is represented in at least three distinct regions of the cerebral cortex in cats and monkeys: the parietal and somatosensory cortex and the parietoinsular vestibular cortex. In addition, vestibular-related signals are found in more extensive regions, including the motor and premotor regions and frontal eye fields. Most of these regions also project directly to the vestibular nuclei. In monkeys, at least six cortical regions have been identified, including the motor, somatosensory, parietal and temporal areas. Most of these regions receive vestibular projections via the thalamus. Most neurons in those cortical areas respond to head velocity and receive converging vestibular, visual and somatosensory input. Electrical stimulation of some of these cortical areas in anesthetized cats influences the activity of many vestibular nuclear neurons including those projecting to the spinal cord. Lesions of the parietal vestibular regions impair the vestibulo-ocular reflex (VOR) and visual suppression of the VOR as well as vestibular-related cognitive functions such as spatial perception and memory in human subjects. Diffuse cortical damage also results in similar impairment of the VOR and suppression of the VOR and possibly the vestibulo-collic reflex. Such impairments after cortical lesions may well be due in part to interruption of cortico-vestibular connections. Future studies in alert animals should focus on the role of different cortical regions projecting to the vestibular nuclei, specifically on how each affects the processing of vestibular signals that mediate vestibulo-motor reflexes and that are used for vestibular related cognitive processes.

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Section: Decorticationsupporting

confidence: 65%

“…The patients also had a slow eye drift of 3±8/s toward the side contralateral to the lesion, particularly in darkness (Estaaeol et al 1980;Sharpe and Lo 1981), and this drift may have contributed to the asymmetry in the VOR gain.…”

Section: Decorticationmentioning

confidence: 96%

Corticovestibular interactions: anatomy, electrophysiology, and functional considerations

Fukushima¹

1997

Exp Brain Res

137

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“…Third, previous studies in hemispherectomised patients [22,57] disclosed defects of the horizontal VOR that appear directionally opposed to those reported in the present investigation. In many cases, hemispherectomy was performed to bring about relief from seizures with very early onset in the life of patients.…”

Section: Cautions and Conclusioncontrasting

confidence: 98%

“…In hemispherectomised patients, the gain of horizontal slow phases directed ipsilesionally is reduced and the suppression of slow phases directed contralesionally is impaired [22,57]. Patients with temporal or parietal lesions [4,16] can also suffer from this latter deficit.…”

Section: Introductionmentioning

confidence: 99%

Vestibulo-ocular and optokinetic impairments in left unilateral neglect

et al. 2002

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“…Such devia tion is much more often contralateral than ipsilateral to the lesion [80], The mechanisms of these different forms of ocular deviation observed after unilateral cerebral damage are not yet well understood. However, relatively prolonged eye deviation, lasting at least several weeks, suggests preexisting damage to the contralateral frontal region [81], Enduring deficits caused by large chronic unilateral hemispheral lesions include [10,[82][83][84]: usual eye devia tion away from the side of the lesion on forced lid closure or in darkness; saccades with decreased velocity and increased latency, bilaterally; reduced smooth-pursuit gain ipsilateral to the lesion with, on occasion, increased gain away from the side of the lesion; reduced gain of OKN slow phase directed ipsilaterally to the lesion; VOR gain slightly asymmetric and greater for eye movements away from the side of the lesion. and OKN, and severe impairment of visually guided saccades (increased latency and decreased accuracy), with preservation of some intentional saccades, such as saccades made on verbal command.…”

Section: Acute or Large Unilateral Cortical Lesionsmentioning

confidence: 99%

Saccade and Smooth-Pursuit Impairment after Cerebral Hemispheric Lesions

Pierrot‐Deseilligny¹

1994

Eur Neurol

108

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A number of cortical and subcortical areas are involved in the control of sac-cades and smooth pursuit, and lesions affecting these areas result in various ocular motor syndromes. Most of these syndromes are relatively subtle and have to be ascertained using recordings, because other brain areas may largely take over the function of a damaged area. Anterior cortical, posterior cortical, large and bilateral cortical, subcortical and degenerative cerebral lesions are successively reviewed. In the anterior part of the cerebral hemisphere, the frontal eye field (FEF), supplementary eye field (SEF) and prefrontal cortex (PFC), i.e area 46 of Brodmann, control eye movements. The FEF appears to be principally involved in the control of intentional saccades, in particular those made with a retinotopic reference system, and in smooth pursuit. The SEF could control saccades made with a spatiotopic reference system, and sequences of saccades (requiring a temporal working memory). The PFC could control the inhibition of unwanted reflexive saccades, and be involved in spatial memory used for programming all types of memory-guided saccades. In the posterior part of the cerebral hemisphere, the parietal eye field (PEF) is involved in the triggering of reflexive visually guided saccades, and the middle temporal (MT) and medial superior temporal (MST) areas in smooth pursuit. Acute and large unilateral lesions usually result in transitory ipsilateral conjugate eye deviation. Bilateral lesions affecting both the FEF and the PEF result in severe saccade and smooth-pursuit paresis, whereas bilateral posterior temporoparietal lesions result in Balint’s syndrome, consisting of both eye movement and visual-attention abnormalities. Subcortical lesions also result in various eye movement abnormalities, which have been little documented to date. Lastly, degenerative cerebral diseases, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, progressive supranuclear palsy and corti-cobasal degeneration result in more or less severe eye movement disturbances. Eye movement recordings may contribute to early differential diagnosis of some of these degenerative diseases.

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Oculomotor and Oculovestibular Functions in a Hemispherectomy Patient

Cited by 21 publications

References 17 publications

Corticovestibular interactions: anatomy, electrophysiology, and functional considerations

Corticovestibular interactions: anatomy, electrophysiology, and functional considerations

Vestibulo-ocular and optokinetic impairments in left unilateral neglect

Saccade and Smooth-Pursuit Impairment after Cerebral Hemispheric Lesions

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