Role of the flocculus and paraflocculus in optokinetic nystagmus and visual-vestibular interactions: Effects of lesions

Waespe, W.; Cohen, Bernard; Raphan, Theodore

doi:10.1007/bf00238229

Cited by 251 publications

(75 citation statements)

References 44 publications

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“…It seems likely that the floccular complex is far enough downstream in the visual tracking circuits so that its function is independent of the exact stimulus used: this is supported by recordings from floccular Purkinje cells during pursuit (Stone and Lisberger 1990), ocular following (Shidara and Kawano 1993), and optokinetic nystagmus (Büttner and Waespe 1984). Further, lesions of the floccular complex in monkeys cause a deficit in the rapid component of optokinetic nystagmus (Waespe et al 1983) that parallels the deficit in pursuit.…”

Section: Comparison With Results Of Lesions In Other Speciesmentioning

confidence: 98%

Partial Ablations of the Flocculus and Ventral Paraflocculus in Monkeys Cause Linked Deficits in Smooth Pursuit Eye Movements and Adaptive Modification of the VOR

Rambold

Churchland

Selig

et al. 2002

Journal of Neurophysiology

200

124

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The vestibuloocular reflex (VOR) generates compensatory eye movements to stabilize visual images on the retina during head movements. The amplitude of the reflex is calibrated continuously throughout life and undergoes adaptation, also called motor learning, when head movements are persistently associated with image motion. Although the floccular-complex of the cerebellum is necessary for VOR adaptation, it is not known whether this function is localized in its anterior or posterior portions, which comprise the ventral paraflocculus and flocculus, respectively. The present paper reports the effects of partial lesions of the floccular-complex in five macaque monkeys, made either surgically or with stereotaxic injection of 3-nitropropionic acid (3-NP). Before and after the lesions, smooth pursuit eye movements were tested during sinusoidal and step-ramp target motion. Cancellation of the VOR was tested by moving a target exactly with the monkey during sinusoidal head rotation. The control VOR was tested during sinusoidal head rotation in the dark and during 30°/s pulses of head velocity. VOR adaptation was studied by having the monkeys wear ×2 or ×0.25 optics for 4–7 days. In two monkeys, bilateral lesions removed all of the flocculus except for parts of folia 1 and 2 but did not produce any deficits in smooth pursuit, VOR adaptation, or VOR cancellation. We conclude that the flocculus alone probably is not necessary for either pursuit or VOR learning. In two monkeys, unilateral lesions including a large fraction of the ventral paraflocculus produced small deficits in horizontal and vertical smooth pursuit, and mild impairments of VOR adaptation and VOR cancellation. We conclude that the ventral paraflocculus contributes to both behaviors. In one monkey, a bilateral lesion of the flocculus and ventral paraflocculus produced severe deficits smooth pursuit and VOR cancellation, and a complete loss of VOR adaptation. Considering all five cases together, there was a strong correlation between the size of the deficits in VOR learning and pursuit. We found the strongest correlation between the behavior deficits and the size of the lesion of the ventral paraflocculus, a weaker but significant correlation for the full floccular complex, and no correlation with the size of the lesion of the flocculus. We conclude that 1) lesions of the floccular complex cause linked deficits in smooth pursuit and VOR adaptation, and 2) the relevant portions of the structure are primarily in the ventral paraflocculus, although the flocculus may participate.

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Section: Comparison With Results Of Lesions In Other Speciesmentioning

confidence: 98%

Partial Ablations of the Flocculus and Ventral Paraflocculus in Monkeys Cause Linked Deficits in Smooth Pursuit Eye Movements and Adaptive Modification of the VOR

Rambold

Churchland

Selig

et al. 2002

Journal of Neurophysiology

200

124

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“…The rapid rise in slow-phase velocity and the slower rise to a steady state are thought to be generated by separate neural processes. Patients with deficits in slow pursuit of visual targets and monkeys with lesions of the cerebellar flocculus (Waespe et al, 1983;Yee et al, 1979;Zee et al, 1981) display a gradual buildup of the slow phase of OKN. A velocity-storage mechanism shared with the vestibular system is hypothesized to be responsible for the slow buildup of slow-phase velocity and OKAN.…”

Section: Informal Testingmentioning

confidence: 99%

Long- and short-term monocular deprivation in the rhesus monkey: effects on visual fields and optokinetic nystagmus

Sparks¹,

Le²,

Gurski³

et al. 1986

J. Neurosci.

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Monkeys with 1 eyelid sutured within 2 weeks of birth for 7 or 14 d (short-term monocular deprivation, n = 5) or for 18-26 months (long-term monocular deprivation, I = 5) were tested for visual and oculomotor function at approximately 2 years of age. Long-term monocularly deprived animals were behaviorally blind when visual inputs were restricted to the deprived eye. There was no sparing of the monocular segment of the visual field, and optokinetic nystagmus could not be elicited even with vertical stripes up to 15" in width. These behavioral deficits could not be accounted for by optical or retinal abnormalities.In contrast, short-term monocularly deprived animals displayed normal visual fields and optokinetic nystagmus was driven by both eyes. Slow-phase gain was reduced and directional asymmetries were observed when optokinetic stimulation was restricted to the deprived eye.

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“…New anatomical tracing techniques also helped to unravel the connectivity of the circuits that showed activity related to eye movements [14][15][16][17]. The effects of microinjections of chemicals that mimic normal neurotransmitters, focal electrical stimulation, and naturally occurring experimental lesions in the brain improved our understanding of brain function [18][19][20][21][22][23][24][25][26][27][28][29][30][31]. Conceptually, bioengineering approaches, using systems analytical techniques, were combined with anatomical and physiological data, to develop biologically plausible models, replacing the Bblack box^approach to neural modeling.…”

mentioning

confidence: 99%

“…Conceptually, bioengineering approaches, using systems analytical techniques, were combined with anatomical and physiological data, to develop biologically plausible models, replacing the Bblack box^approach to neural modeling. The involvement of bioengineers in eye movement research, exemplified by David A Robinson, enticed basic and clinical neuroscientists to adopt the Bengineering approach^to understanding normal brain function and human disease [27,[32][33][34][35][36][37][38][39][40][41][42][43][44][45][46][47].…”

mentioning

confidence: 99%

“…Other types of eye movements also show patterns of abnormality that localize to the cerebellum, gaze-evoked and downbeating nystagmus and impaired pursuit with the head still or moving point to the flocculus/ paraflocculus, and periodic alternating nystagmus and impaired tilt suppression of post rotatory nystagmus to the nodulus [47]. Even finer distinctions can be made between the effects of lesions in small but adjacent structures within the cerebellum, for example, the flocculus versus the paraflocculus (tonsil) [18,19,26,27,29,51,52]. While not as well localized within the cerebellum, certain patterns of ocular misalignment strongly suggest cerebellar dysfunction (e.g., horizontal (eso, convergent) deviations of the eyes for distance viewing and vertical misalignment that alternates sense (which eye is higher) depending on right versus left gaze) [20,[53][54][55][56][57][58][59].…”

mentioning

confidence: 99%

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Eye Movement Research in the Twenty-First Century—a Window to the Brain, Mind, and More

Shaikh

Zee

2017

Cerebellum

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The study of eye movements not only addresses debilitating neuro-ophthalmological problems but has become an essential tool of basic neuroscience research. Eye movements are a classic way to evaluate brain function-traditionally in disorders affecting the brainstem and cerebellum. Abnormalities of eye movements have localizing value and help narrow the differential diagnosis of complex neurological problems. More recently, using sophisticated behavioral paradigms, measurement of eye movements has also been applied to disorders of the thalamus, basal ganglia, and cerebral cortex. Moreover, in contemporary neuroscience, eye movements play a key role in understanding cognition, behavior, and disorders of the mind. Examples include applications to higher-level decision-making processes as in neuroeconomics and psychiatric and cognitive disorders such as schizophrenia and autism. Eye movements have become valued as objective biomarkers to monitor the natural progression of disease and the effects of therapies. As specific genetic defects are identified for many neurological disorders, ocular motor function often becomes the cornerstone of phenotypic classification and differential diagnosis. Here, we introduce other important applications of eye movement research, including understanding movement disorders affecting the head and limbs. We also emphasize the need to develop standardized test batteries for eye movements of all types including the vestibulo-ocular responses. The evaluation and treatment of patients with cerebellar ataxia are particularly amenable to such an approach.Keywords Saccade . Vestibulo-ocular reflex . Pursuit Eye movements are critical for the survival of any animal that sees. Promptly bringing an image to the fovea of an object that suddenly intrudes into one's periphery, and then keeping the image stable on the fovea, allows the cognitive brain to analyze the visual scene in a tenth of a second. In this way, it can generate an immediate, and sometimes life or death, decision whether to flee, fight, embrace, or just do nothing. Neural correlates of eye movements are found in almost every corner of the brain, helping to provide the most reliable information from our visual systems for all aspects of behavior.Using eye movements to understand human disease extends back to at least the mid-nineteenth century when early reports of strabismus [1][2][3][4][5] and nystagmus [4,[6][7][8][9][10][11][12][13] appeared. Nevertheless, in the years following, for almost another century, the literature on eye movements was meager. In the mid1940s, however, the number of publications on nystagmus and strabismus began to grow (https://www.ncbi.nlm.nih. gov/pubmed/?term = nystagmus, https://www.ncbi.nlm.nih. gov/pubmed/?term = strabismus), and in the mid-1960s, there was another growth spurt with more studies reporting various types of dysfunction of eye movements in conditions affecting the brainstem or cerebellum. Topics such as adaptive control of eye movements and the central role of normal and

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Role of the flocculus and paraflocculus in optokinetic nystagmus and visual-vestibular interactions: Effects of lesions

Cited by 251 publications

References 44 publications

Partial Ablations of the Flocculus and Ventral Paraflocculus in Monkeys Cause Linked Deficits in Smooth Pursuit Eye Movements and Adaptive Modification of the VOR

Partial Ablations of the Flocculus and Ventral Paraflocculus in Monkeys Cause Linked Deficits in Smooth Pursuit Eye Movements and Adaptive Modification of the VOR

Long- and short-term monocular deprivation in the rhesus monkey: effects on visual fields and optokinetic nystagmus

Eye Movement Research in the Twenty-First Century—a Window to the Brain, Mind, and More

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