Rebound Nystagmus

Hood, J. D.; Kayan, A; Leech, John

doi:10.1093/brain/96.3.507

Cited by 82 publications

(21 citation statements)

References 1 publication

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“…cerebellar atrophy, disturbances in the pyrami dal tract and ambilateral optic atrophy were found. General impairment of the central ner vous system could be proven on the basis of the CT-scan (distinct internal hydrocephalus) and the nystagmographic findings with signs of the brainstem and cerebellum (7,16). According to the literature, cerebellar degeneration was only observed to be the outstanding neurological symptom of the basal cell nevus syndrome in the case of Codisli et al (5) and again for our patient.…”

Section: Discussionsupporting

confidence: 62%

Neurologic Symptoms of Basal Cell Nevus Syndrome

Esser¹,

Bohnert²

1980

Eur Neurol

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The neurological symptomatology of the basal cell nevus syndrome (Gorlin-Goltz syndrome) is described based on a personal observation and previously published cases. The case presented here, with dominant cerebellar symptomatology, optic atrophy and pyramidal signs, is discussed pathophysiologically either as a primary central nervous manifestation of the basic disturbance or as a secondary cerebral paraneoplastic process.

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Section: Discussionsupporting

confidence: 62%

Neurologic Symptoms of Basal Cell Nevus Syndrome

Esser¹,

Bohnert²

1980

Eur Neurol

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“…8). The notion of such a set point adapting to changes in eye position may be exemplified in the clinical phenomenon of rebound nystagmus (Hood et al, 1973;Hood, 1981;Leigh and Zee, 1999). This phenomenon consists of nystagmus induced by an eccentric saccade, beating in the direction of eye position, which declines gradually and stabilizes over time.…”

Section: Implications Of Auditory Spatial Adaptation To Eye Movementsmentioning

confidence: 99%

Auditory Spatial Perception Dynamically Realigns with Changing Eye Position

Razavi¹,

O’Neill²,

Paige³

2007

J. Neurosci.

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Audition and vision both form spatial maps of the environment in the brain, and their congruency requires alignment and calibration. Because audition is referenced to the head and vision is referenced to movable eyes, the brain must accurately account for eye position to maintain alignment between the two modalities as well as perceptual space constancy. Changes in eye position are known to variably, but inconsistently, shift sound localization, suggesting subtle shortcomings in the accuracy or use of eye position signals. We systematically and directly quantified sound localization across a broad spatial range and over time after changes in eye position. A sustained fixation task addressed the spatial (steady-state) attributes of eye position-dependent effects on sound localization. Subjects continuously fixated visual reference spots straight ahead (center), to the left (20°), or to the right (20°) of the midline in separate sessions while localizing auditory targets using a laser pointer guided by peripheral vision. An alternating fixation task focused on the temporal (dynamic) aspects of auditory spatial shifts after changes in eye position. Localization proceeded as in sustained fixation, except that eye position alternated between the three fixation references over multiple epochs, each lasting minutes. Auditory space shifted by ϳ40% toward the new eye position and dynamically over several minutes. We propose that this spatial shift reflects an adaptation mechanism for aligning the "straight-ahead" of perceived sensory-motor maps, particularly during early childhood when normal ocular alignment is achieved, but also resolving challenges to normal spatial perception throughout life.

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“…Robinson proposed that the neural velocity-to-position integrator is inherently "leaky" and as a result requires cerebellar input to calibrate its output precisely in proportion to eye position [5]. Impaired gaze holding secondary to such "leaky" integration has been demonstrated in humans with acute [7,8] and chronic [9][10][11][12] cerebellar disease and in primates after flocculectomy [13] or (hemi-)cerebellectomy [14][15][16]. Centripetal eye-drift therefore is considered an essential clinical sign of a deficient brainstem neural velocity-to-position integrator or its cerebellar modulatory structures.…”

Section: Introductionmentioning

confidence: 99%

Gaze holding deficits discriminate early from late onset cerebellar degeneration

Tarnutzer

Weber

Schuknecht³

et al. 2015

J Neurol

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The vestibulo-cerebellum calibrates the output of the inherently leaky brainstem neural velocityto-position integrator to provide stable gaze holding. In healthy humans small-amplitude centrifugal nystagmus is present at extreme gaze-angles, with a non-linear relationship between eye-drift velocity and eye eccentricity. In cerebellar degeneration this calibration is impaired, resulting in pathological gaze-evoked nystagmus (GEN). For cerebellar dysfunction, increased eye drift may be present at any gaze angle (reflecting pure scaling of eye drift found in controls) or restricted to far-lateral gaze (reflecting changes in shape of the non-linear relationship) and resulting eyed-drift patterns could be related to specific disorders. We recorded horizontal eye positions in 21 patients with cerebellar neurodegeneration (gaze-angle = ±40°) and clinically confirmed GEN. Eye-drift velocity, linearity and symmetry of drift were determined. MR-images were assessed for cerebellar atrophy. In our patients, the relation between eye-drift velocity and gaze eccentricity was non-linear, yielding (compared to controls) significant GEN at gaze-eccentricities 20°. Pure scaling was most frequently observed (n = 10/18), followed by pure shape-changing (n = 4/18) and a mixed pattern (n = 4/18). Pure shape-changing patients were significantly (p = 0.001) younger at disease-onset compared to pure scaling patients. Atrophy centered around the superior/dorsal vermis, flocculus/paraflocculus and dentate nucleus and did not correlate with the specific drift behaviors observed. Eye drift in cerebellar degeneration varies in magnitude; however, it retains its non-linear properties. With different drift patterns being linked to age at disease-onset, we propose that the gaze-holding pattern (scaling vs. shape-changing) may discriminate early-from late-onset cerebellar degeneration. Whether this allows a distinction among specific cerebellar disorders remains to be determined.

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Rebound Nystagmus

Cited by 82 publications

References 1 publication

Neurologic Symptoms of Basal Cell Nevus Syndrome

Neurologic Symptoms of Basal Cell Nevus Syndrome

Auditory Spatial Perception Dynamically Realigns with Changing Eye Position

Gaze holding deficits discriminate early from late onset cerebellar degeneration

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