Horizontal Optokinetic Nystagmus Research Articles

Visual fixation suppression of caloric nystagmus in progressive supranuclear palsy - A comparison with Parkinson's disease.

Impairment of visual fixation suppression (VS) in progressive supranuclear palsy (PSP) is not well documented. To evaluate the usefulness of impaired VS of caloric nystagmus as an index for differential diagnosis between PSP and Parkinson's disease (PD), which is often difficult, especially in the early stage. Subjects comprised 26 PSP patients and 26 PD patients clinically diagnosed at Tokyo Metropolitan Neurological Hospital. We retrospectively investigated VS of caloric nystagmus, horizontal pursuit, saccades, and horizontal optokinetic nystagmus recorded on direct-current-electronystagmography, and neuroradiological findings. The median of the average VS% was 0% and 50.0% in PSP and PD patients, respectively. In PSP, VS was impaired even in the early stage of disease. We found a significant correlation between VS and velocity of saccades or maximum slow phase velocity of optokinetic nystagmus only in PSP patients. PSP patients with atrophy of the subthalamic nucleus or with decreased blood flow in the frontal lobe showed significantly more severe impairment of VS. VS may be a useful biomarker to differentiate patients with PSP from those with PD. Cerebellar networks that connect with the cerebral cortex and basal ganglia may contribute to impaired VS of caloric nystagmus in PSP.

上眼瞼向き眼振・小脳萎縮など認めたParkinson病の 1 例

To the best of our knowledge, upbeat nystagmus (UBN) has not been reported before in patients with Parkinson's disease (PD). There are also very few reports of cerebellar atrophy in patients with PD. A-60-year-old woman with a 10-year history of PD visited our hospital for deep brain stimulation therapy for her camptocormia. Neurological examination revealed not only the core signs of PD (rigidity, resting tremor, postural instability), but also UBN. 123I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy revealed markedly diminished uptake of MIBG, strongly supporting the clinical diagnosis of PD. Brain MRI revealed prominent cerebellar atrophy, while the brainstem was preserved. ENG showed that the UBN was observed at the primary eye position and enhanced during upward gaze in the light, but not during downward gaze. In addition to UBN, several other abnormal ENG findings were also observed, including horizontal gaze-evoked nystagmus and rebound nystagmus. Secondly, both horizontal and vertical pursuits were disturbed and horizontal OKN was poorly induced. Lastly, the horizontal saccade was relatively hypometric, while the upward saccades were slight hypermetric. Although the pathogenesis of UBN in this patient still remains unclear, UBN is known to be mainly caused by dysfunction of the velocity-to-position integrator caused by pontomedullary lesions or pontomesencephalic lesions. Alternatively, cerebellar control over this integrator is presumably disrupted by lesions in the cerebellum itself or lesions in the cerebellar neural circuits. As for the pathogenesis of UBN in our case, pontomedullary lesion was first suspected, because, besides the abovementioned ENG findings, most cases of UBN reported in the literature are caused by medullary lesions, including lesions of both the medial vestibular and prepositus hypoglossi nuclei, which play an important role as the velocity-to-position integrator. In addition, dysfunction of the vestibular cerebellum was also suspected as a cause, judging from the cerebellar atrophy and other abnormal ENG findings. In conclusion, it is necessary to consider dysfunction of the vestibular cerebellum as a cause of abnormal eye movements in PD, not to mention dysfunction of the brainstem.

Optokinetic Nystagmus: Five Reasons Why Every Neurologist Should Evaluate It (P3-9.006)

<h3>Objective:</h3> To highlight the clinical utility of optokinetic nystagmus (OKN) through five illustrative video cases. <h3>Background:</h3> Bedside evaluation of OKN allows for rapid assessment of smooth pursuit (slow phase) and saccades (fast phase). Specific abnormalities of OKN have localizing value and may also suggest specific neurologic disorders. <h3>Design/Methods:</h3> We provide five video cases where OKN was helpful in localization and/or diagnosis. Video cases are provided from https://novel.utah.edu/Gold/. <h3>Results:</h3> (1) OKN can be used to make an early diagnosis of progressive supranuclear palsy before there is ophthalmoparesis. Vertical OKN can demonstrate absent or attenuated saccades, particularly when compared to a normal response to horizontal OKN. (2) A subtle sign of internuclear opthalmoparesis, when there is no obvious limitation of adduction, can be demonstrated with horizontal OKN by noting a slow (lagging) adducting saccade. (3) In patients with dorsal midbrain (Parinaud) syndrome, upgaze is often limited or absent, and the characteristic finding of convergence-retraction nystagmus (CRN) can be easily appreciated when an optokinetic stimulus is moved downward (e.g., downward slow phase followed by CRN instead of an upward fast phase). (4) Patients with a homonymous hemianopsia due to an occipital lesion will have normal OKN; whereas, patients with a homonymous hemianopsia due to a parietal lesion will have absent OKN when the stimulus is directed toward the side of the lesion. (5) In patients who claim to have binocular or monocular blindness, the presence of OKN (when monocular, with the good eye covered) is highly suggestive of functional vision loss. Observing OKN does not prove that the patient’s visual function is normal, but does rule out blindness. <h3>Conclusions:</h3> Assessing optokinetic nystagmus with a flag, tape, drum, or the examiner’s fingertips is a portable, inexpensive, and rapid bedside examination to localize and diagnose a variety of neurologic and neuro-ophthalmic disorders. <b>Disclosure:</b> Dr. Hale has nothing to disclose. Dr. Reich has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Best Doctors. Dr. Reich has received personal compensation in the range of $500-$4,999 for serving as a Consultant for UpToDate. Dr. Reich has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Enterin. Dr. Reich has received personal compensation in the range of $0-$499 for serving on a Scientific Advisory or Data Safety Monitoring board for NIH. Dr. Reich has received personal compensation in the range of $10,000-$49,999 for serving as an Expert Witness for Various law firms. The institution of Dr. Reich has received research support from ninds. Dr. Reich has received publishing royalties from a publication relating to health care. Dr. Reich has received publishing royalties from a publication relating to health care. Dr. Gold has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Springer .

Oculomotor abnormalities and its association with sleep stages in progressive supranuclear palsy

BackgroundOculomotor abnormalities are one of the cardinal clinical features of progressive supranuclear palsy (PSP). Vertical saccadic slowing is an early sign of PSP. The association between oculomotor abnormalities and sleep architecture has not been studied so far. ObjectivesTo study the association of oculomotor abnormalities of PSP with the sleep stages by using video polysomnography (vPSG). MethodsThis was a cross-sectional single-center study. Twenty-two patients with PSP and 15 age and gender-matched controls were recruited. Saccades, vestibulo-ocular reflex, and optokinetic nystagmus were assessed and graded clinically in all patients and one overnight vPSG was done in all cases. ResultsVertical saccades, upward more than downwards, were affected in all cases. While horizontal saccades were normal only in 41% of cases. Vertical optokinetic nystagmus (OKN) was affected in all cases. Horizontal OKN was normal in 36% of patients. The vertical upward saccades had a negative correlation with N1% and duration (r = −0.418; p = 0.05, r = −0.457; p = 0.03), N3% and duration (r = −0.486; p = 0.02, r = −0.510; p = 0.01), REM% (r = −0.449; p = 0.04), total sleep time (r = −0.487; p = 0.02) and sleep efficiency (r = −0.444; p = 0.04). There was a positive correlation between horizontal OKN and sleep onset latency (r = 0.432; p = 0.05). ConclusionsVertical saccadic restriction in PSP has significant negative correlation with total sleep time and sleep efficiency. The oculomotor and sleep abnormalities in PSP are probably interlinked and their assessment is useful in determining the characteristics of the disease.

The association of saccadic abnormalities with rem sleep in patients with Huntington's disease

BackgroundHuntington's disease (HD) is a progressive neurodegenerative disorder characterised by chorea, cognitive impairment, psychiatric and behavioral disturbances. Sleep disturbances including reduced REM sleep have been observed in HD. ObjectivesThe aim of the study was to study the polysomnography findings in HD and to assess whether oculomotor abnormalities are associated with poor REM sleep. MethodsTwenty-nine genetically confirmed HD patients underwent clinical evaluation including extraocular movement and OKN examination. Twenty-six patients and 15 controls underwent overnight video polysomnography (VPSG). ResultsVPSG of 23 HD patients and 13 controls were considered for analysis. Compared to controls, HD patients had higher median wake period and higher WASO percentage (p = 0.005). REM sleep percentage was reduced significantly in HD in comparison to controls (p < 0.001). Out of 23 patients, only two patients had REM sleep above 20% while 14 patients had REM sleep percentage less than 15%. Poor horizontal OKN (grades 2 and 3) was associated with the presence of low REM sleep percentage (REM sleep less than 15%) (p = 0.02). Low REM sleep was also associated with severe illness (UHDRS) (p = 0.038). ConclusionAn association between decreased REM sleep and OKN abnormalities indicate that EOM abnormalities seen in HD could lead to errors in scoring REM sleep. To understand the actual degree of decreased REM sleep percentage will require additional parameters in AASM guidelines to score REM sleep in patients with EOM abnormalities like that seen in HD.

A case of Gerstmann-Straussler-Scheinker (GSS) disease with supranuclear gaze palsy

BackgroundGerstmann-Straussler-Scheinker disease (GSS), an autosomal dominant prion disorder, usually presents as a slowly progressive cerebellar ataxia followed by later cognitive decline. We present a member of the GSS Indiana Kindred with supranuclear palsy, a less common feature in GSS.Case presentationA 42-year-old man presented with 12 months of progressive gait and balance difficulty. Exam was notable for ataxia and cerebellar eye movement abnormalities. Genetic testing revealed a F198S variant in the prion protein (PRNP) gene, the pathological variant of GSS associated with his family, the Indiana kindred. Eighteen months after initial presentation supranuclear palsy developed.ConclusionsGSS is a neurodegenerative prion disease with diverse clinical presentations, and exhibits greater variability in disease phenotype compared to other inherited spongiform encephalopathies. GSS should be on the differential for patients with ataxia and supranuclear palsy, and it is important to assess both horizontal and vertical saccades and optokinetic nystagmus in patients with ataxia.

Teaching Video NeuroImages: Cerebellar esotropia

A 17-year-old girl presented with slowly progressive binocular horizontal diplopia, worse for distance viewing. She had distance esotropia (video), gaze-evoked nystagmus, broken smooth pursuit, reduced horizontal optokinetic nystagmus, and impaired vestibulo-ocular reflex suppression (VORS; video), in keeping with cerebellar dysfunction. The patient had full abduction during monocular viewing and head rotations, and normal saccadic velocities, excluding a bilateral sixth nerve palsy. An MRI scan confirmed a type 1 Chiari malformation (figure). A careful oculomotor assessment in patients with esotropia, including bedside VORS,1 may identify cerebellar signs that would suggest the tropia is cerebellar in origin.2 Cerebellar esotropia may arise from dorsal vermis impairment,2 or possibly from floccular and parafloccular dysfunction, explaining the associated abnormalities in smooth pursuit, optokinetic nystagmus, and VORS that share common neural pathways.

Optokinetic nystagmus in patients with SCA: A bedside test for oculomotor dysfunction grading.

To characterize the clinical features in patients with spinocerebellar ataxia (SCA) type 1, SCA2, and SCA3 and to evaluate the oculomotor dysfunction by using optokinetic nystagmus (OKN) testing, which may be a sensitive marker. In this prospective observational study, all patients underwent detailed neurologic examination with special emphasis on eye movements. OKN was evaluated with a tape. Disease severity was measured with the International Co-Operative Ataxia Rating Scale (ICARS). A total of 73 genetically confirmed patients were included, of whom 28, 30, and 15 patients were positive for SCA1, SCA2, and SCA3, respectively. Dystonia was more common in patients with SCA3 (46%), and absent ankle jerk was more common in those with SCA2 (21.4%). Brisk deep tendon reflexes were common in patients with SCA1 (46.6%), followed by patients with SCA3 (26.6%) and SCA2 (7.1%). Vertical OKN was impaired in all patients and absent in 86.6% of patients with SCA1, 96% of those with SCA2, and 80% of those with SCA3. Horizontal OKN was absent in 30% of patients with SCA1, 57% of patients with SCA2, and 33% of those with SCA3. Higher motor disability (posture and gait, kinetic functions [Motor Disability] subscore on the ICARS) was associated with higher oculomotor dysfunction measured by OKN-saccades impairment grading but not with the Ocular Disorder subscore of ICARS (ICARS-OD). OKN-saccades are a better and sensitive bedside clinical tool to quantify oculomotor dysfunction in neurodegenerative ataxias. Its role needs to be tested further in presymptomatic carriers. The current ICARS-OD scale to grade oculomotor dysfunction in degenerative ataxias need to be modified.

頭位性めまいを主訴とした脊髄小脳失調症6型 (SCA6) 例の ENG 検討

A 57-year-old woman presented at our outpatient clinic with the recent and frequent experience of paroxysmal positional vertical vertigo similar to the sensation of a somersault, especially changing position from sitting to lying supine, accompanied with spells of nausea and blackout. On examination, we observed prominent downbeat nystagmus in the primary eye position and lateral gaze. MRI disclosed prominent cerebellar cortical atrophy, especially in the vermal regions. The patient had a family history of spinocerebellar ataxia type 6 (SCA6) and had herself received a definitive diagnosis of the same phenotype disease from genetic studies. The points of the ENG findings were as follows: (1) downbeat nystagmus was prominent in the primary eye position and was combined with gaze nystagmus in the lateral gaze; (2) both horizontal & vertical rebound nystagmus were noted; and (3) impairment of both horizontal & vertical smooth pursuit were seen. In horizontal and upward pursuit, catch-up saccades (lower gain) were intermingled. In contrast, backup-saccades (higher gain) were intermingled in downward pursuit. Furthermore, (4) Horizontal saccades were hypometric, though vertical saccades were hypermetric (overshoot); (5) In both horizontal and vertical OKN, the slow phase of OKN was severely impaired. Finally, (6) vestibular caloric nystagmus was well induced bilaterally. Both sides of visual suppression of caloric nystagmus were severely impaired. Most of present results are well explainable with the pure cerebellar cortical atrophy as the typical pathological finding of SCA6. However, two important findings should be mainly discussed and stressed here. One, the gain of the horizontal smooth pursuit was lower, while the gain of the downward pursuit was higher. It seemed to be inconsistent that a single part of the cerebellum would simultaneously modulate decreasing gain of the horizontal and increasing gain of vertical smooth pursuit systems. Therefore, this finding suggested that several parts, not a single part, of the cerebellum would be simultaneously engaged in the gain modulation of the smooth pursuit system. Second, the severe impairments of both horizontal and vertical OKN implied disturbances of both the pursuit and the velocity storage systems. In Cohen & Raphan's model, the slow phase of OKN is composed of the “direct pathway” and the “indirect pathway.” The “direct pathway” utilizes the ocular pursuit system in the flocculus/paraflocculus, while the “indirect pathway” is mediated through the velocity storage system in the medial vestibular nuclei/prepositus hypoglossi nuclei or the interstitial nuclei of Cajal in the brainstem. Consequently, the present results of OKN strongly suggested that the neural circuits related to the velocity storage integrator in the brainstem would also be perturbed, together with the disturbance of the ocular pursuit system in the cerebellum.

Infantile Nystagmus and Abnormalities of Conjugate Eye Movements in Down Syndrome.

Subjects with Down syndrome (DS) have an anatomical defect within the cerebellum that may impact downstream oculomotor areas. This study characterized gaze holding and gains for smooth pursuit, saccades, and optokinetic nystagmus (OKN) in DS children with infantile nystagmus (IN). Clinical data of 18 DS children with IN were reviewed retrospectively. Subjects with constant strabismus were excluded to remove any contribution of latent nystagmus. Gaze-holding, horizontal and vertical saccades to target steps, horizontal smooth pursuit of drifting targets, OKN in response to vertically or horizontally-oriented square wave gratings drifted at 15°/s, 30°/s, and 45°/s were recorded using binocular video-oculography. Seven subjects had additional optical coherence tomography imaging. Infantile nystagmus was associated with one or more gaze-holding instabilities (GHI) in each subject. The majority of subjects had a combination of conjugate horizontal jerk with constant or exponential slow-phase velocity, asymmetric or symmetric, and either monocular or binocular pendular nystagmus. Six of seven subjects had mild (Grade 0-1) persistence of retinal layers overlying the fovea, similar to that reported in DS children without nystagmus. All subjects had abnormal gains across one or more stimulus conditions (horizontal smooth pursuit, saccades, or OKN). Saccade velocities followed the main sequence. Down syndrome subjects with IN show a wide range of GHI and abnormalities of conjugate eye movements. We propose that these ocular motor abnormalities result from functional abnormalities of the cerebellum and/or downstream oculomotor circuits, perhaps due to extensive miswiring.

Optokinetic nystagmus of Chiari Malfromation. The aim of our study is to determine the special characteristics of disorders of the Optokinetic nystagmus in the early stages of Chiari Malformation

Background Diagnosis and treatment of cochleovestibular dysfunction becomes complicated in case of genetically based combination of pathology. The Chiari Malformation (CM) is a congenital development defect and associated with the caudal displacement of cerebellum and brain stem. The aim of this study is to determine the special characteristics of disorders of the Optokinetic nystagmus in the early stages of CM. At the otorhinolaryngology department of North-West State Medical University named after I.I.Mechnikov (Russia, St Petersburg), 54 cases (patients aged 16–69 ) were studied. All patients showed the symptoms of cochleovestibular dysfunction. Methods The Optokinetic nystagmus was taken in a dark-room using VNGULMAR system manufactured by the German company “Heinemann Medizintechnik GmBH” running software developed by the French company Synapsys. The fixed speed horizontal and vertical Optokinetic stimulus on screen (20 o/s) was applied with distracted and focused attention of the patients. All the studies were conducted before the calloric test (CT) and after CT. The intensity of Optokinetic nystagmus was assessed as per SSC (speed of slow component) of nystagmus. Later on the relative asymmetry in Optokinetic nystagmus was calculated for each same name pair of horizontal and vertical Optokinetic reactions. Results The studies showed that in order to diagnose CM in the early stages it is important not only to identify the asymmetry in horizontal and vertical Optokinetic nystagmus but to mark the value and the sign of asymmetry as well. The sign of asymmetry is especially important after CT. Patients with the low placement of cerebellar tonsil Optokinetic reactions are more susceptible to CT. Conclusions Therefore, in the early stages of CM and “in the risk group”, i.e. the patients with low placement of cerebellar tonsil, before the neurological symptoms have taken place and we have only vestibular dysfunction, the videonystagmography with quantitative evaluation of Optokinetic reaction becomes a voluble source of important diagnostic information and an indication for MRI studies.

Crouzon Syndrome: Relationship of Eye Movements to Pattern Strabismus.

To characterize conjugate eye movements in Crouzon syndrome (CS) patients with and without strabismus. Smooth pursuit, saccades, horizontal optokinetic nystagmus (OKN), and horizontal vestibulo-ocular reflex (VOR) were recorded using binocular video-oculography (VOG) in 10 children with CS (5 orthotropic, 5 strabismic) and 12 age-matched controls. Hess-Lancaster plots were generated from Orbit 1.8 using rectus muscle pulley locations from computed tomography imaging. Two-dimensional eye scan paths from VOG recordings were compared with the Hess-Lancaster plots. Targeted saccades were normometric on average but variable, and followed the main sequence in both CS groups. Smooth pursuit gains were normal for both CS groups; however, SP gains of the fixating eye in subjects with strabismus were significantly lower. Optokinetic nystagmus gains were reduced in both CS groups (P < 0.02) but were lower in subjects with strabismus. Shifting misalignments of binocular eye position in primary and eccentric gazes were associated with reduction in OKN gain in both CS groups. Vestibulo-ocular reflex gains for both CS groups were largely normal despite the presence of an off-axis vertical component. Normal gains for saccades and smooth pursuit in CS patients with strabismus are consistent with accurate execution of both movements despite extorsion of the globe. Vestibulo-ocular reflex in CS patients with strabismus had an off-axis vertical component consistent with extorted muscle pulleys. Optokinetic nystagmus is reduced in CS without strabismus owing to binocular position disparities and in CS with strabismus is likely due to cortical suppression associated with cross-axis orientation and exotropia.

An Optokinetic Nystagmus Detection Method for Use With Young Children.

The detection of vision problems in early childhood can prevent neurodevelopmental disorders such as amblyopia. However, accurate clinical assessment of visual function in young children is challenging. optokinetic nystagmus (OKN) is a reflexive sawtooth motion of the eye that occurs in response to drifting stimuli, that may allow for objective measurement of visual function in young children if appropriate child-friendly eye tracking techniques are available. In this paper, we present offline tools to detect the presence and direction of the optokinetic reflex in children using consumer grade video equipment. Our methods are tested on video footage of children (n}{}N = 5n children and 20 trials) taken as they freely observed visual stimuli that induced horizontal OKN. Using results from an experienced observer as a baseline, we found the sensitivity and specificity of our OKN detection method to be 89.13% and 98.54%, respectively, across all trials. Our OKN detection results also compared well (85%) with results obtained from a clinically trained assessor. In conclusion, our results suggest that OKN presence and direction can be measured objectively in children using consumer grade equipment, and readily implementable algorithms.

Horizontal and vertical optokinetic eye movements in macaque monkeys with infantile strabismus: directional bias and crosstalk

Optokinetic eye movements stabilize gaze by tracking motion of the visual scene during sustained movement of a creature's body. The purpose of this study was to describe vertical and horizontal optokinetic nystagmus (OKN) in nonhuman primates (NHPs) with normal binocular vision, and to compare their responses to NHPs with infantile strabismus.

Saccade-like behavior in the fast-phases of optokinetic nystagmus: an illustration of the emergence of volitional actions from automatic reflexes.

As a potential exemplar for understanding how volitional actions emerged from reflexes, we studied the relationship between an ancient reflexive gaze stabilization mechanism (optokinetic nystagmus [OKN]) and purposeful eye movements (saccades) that target an object. Traditionally, these have been considered distinct (except in the kinematics of their execution) and have been studied independently. We find that the fast-phases of OKN clearly show properties associated with saccade planning: (a) They are characteristically delayed by irrelevant distractors in an indistinguishable way to saccades (the saccadic inhibition effect), and (b) horizontal OKN fast-phases produce curvature in vertical targeting saccades, just like a competing saccade plan. Thus, we argue that the saccade planning network plays a role in the production of OKN fast-phases, and we question the need for a strict distinction between eye movements that appear to be automatic or volitional. We discuss whether our understanding might benefit from shifting perspective and considering the entire "saccade" system to have developed from an increasingly sophisticated OKN system.

Velocity storage mechanism in zebrafish larvae

The optokinetic reflex (OKR) and the angular vestibulo-ocular reflex (aVOR) complement each other to stabilize images on the retina despite self- or world motion, a joint mechanism that is critical for effective vision. It is currently hypothesized that signals from both systems integrate, in a mathematical sense, in a network of neurons operating as a velocity storage mechanism (VSM). When exposed to a rotating visual surround, subjects display the OKR, slow following eye movements frequently interrupted by fast resetting eye movements. Subsequent to light-off during optokinetic stimulation, eye movements do not stop abruptly, but decay slowly, a phenomenon referred to as the optokinetic after-response (OKAR). The OKAR is most likely generated by the VSM. In this study, we observed the OKAR in developing larval zebrafish before the horizontal aVOR emerged. Our results suggest that the VSM develops prior to and without the need for a functional aVOR. It may be critical to ocular motor control in early development as it increases the efficiency of the OKR.

OKN Asymmetry in Human Subjects: A Literature Review

Optokinetic nystagmus (OKN) is a reflex eye movement induced by motion of the whole or a large proportion of the visual field. It can be horizontal, vertical, and torsional in direction and consists of two basic components, a slow tracking movement and a rapid recovery saccade. Two forms of OKN exist: “look” and “stare” OKN. There is strong evidence that horizontal OKN is symmetrical in normal healthy adults and that the OKN gains can be influenced by a variety of different factors including target size, shape, contrast, and velocity. Vertical OKN on the other hand is less well understood, although there is a belief that vertical OKN is asymmetrical with an upward preference. Recent publications contradict this assertion. In this article a comprehensive literature review was carried out to determine whether a vertical OKN asymmetry exists in healthy subjects and to explain any anomalous findings.

Visual Pathway for the Optokinetic Reflex in Infant Macaque Monkeys

The horizontal optokinetic nystagmus (hOKN) in primates is immature at birth. To elucidate the early functional state of the visual pathway for hOKN, retinal slip neurons were recorded in the nucleus of the optic tract and dorsal terminal nucleus (NOT-DTN) of 4 anesthetized infant macaques. These neurons were direction selective for ipsiversive stimulus movement shortly after birth [postnatal day 9 (P9)], although at a lower direction selectivity index (DSI). The DSI in the older infants (P12, P14, P60) was not different from adults. A total of 96% of NOT-DTN neurons in P9, P12, and P14 were binocular, however, significantly more often dominated by the contralateral eye than in adults. Already in the youngest animals, NOT-DTN neurons were well tuned to different stimulus velocities; however, tuning was truncated toward lower stimulus velocities when compared with adults. As early as at P12, electrical stimulation in V1 elicited orthodromic responses in the NOT-DTN. However, the incidence of activated neurons was much lower in infants (40-60% of the tested NOT-DTN neurons) than in adults (97%). Orthodromic latencies from V1 were significantly longer in P12-P14 (x = 12.2 ± 8.9 ms) than in adults (x = 3.51 ± 0.81 ms). At the same age, electrical stimulation in motion-sensitive area MT was more efficient in activating NOT-DTN neurons (80% of the tested cells) and yielded shorter latencies than in V1 (x = 7.8 ± 3.02 ms; adult x = 2.99 ± 0.85 ms). The differences in discharge rate between neurons in the NOT-DTN contra- and ipsilateral to the stimulated eye are equivalent to the gain asymmetry between monocularly elicited OKN in temporonasal and nasotemporal direction at the various ages.

Effect of distance upon horizontal and vertical look and stare OKN

Previous reports suggest that distance influences horizontal stare OKN gains; however, the effect of distance on vertical OKN and look OKN is unknown. Horizontal and vertical look and stare OKN gains were recorded in 16 healthy volunteers (velocity 38.4 degrees /s) at three distances (0.3 m, 1 m, and 2.5 m) and two different stimulus sizes. Asymmetry of responses and correlation of gains in different directions were compared. Measurements at near were compared with and without glasses. Distance did not significantly affect horizontal look and stare OKN or vertical look OKN, however, downward stare OKN gains were reduced at greater distances (p = 0.002). Mean downward stare OKN gains recorded in each individual were strongly correlated to leftward and rightward gains but not upward gains. In contrast, upward OKN gains were not correlated to gains in leftward, rightward, or downward directions. Downward stare OKN responses are significantly sensitive to the effects of distance, whereas stare OKN in other directions and look OKN responses in all directions are not. Individual mean downward stare OKN gains are more closely related to horizontal responses rather than upward responses. This suggests that the downward OKN system is more functionally related to the horizontal system rather than the upward OKN system.

Adaptation of the angular vestibulo-ocular reflex to head movements in rotating frames of reference

Head movements in a rotating frame of reference are commonly encountered, but their long term effects on the angular vestibulo-ocular reflex (aVOR) are not well understood. To study this, monkeys were oscillated about a naso-occipital (roll) axis for several hours while rotating about a spatial vertical axis (roll-while-rotating, RWR). This induced oscillations in roll and pitch eye velocity and continuous horizontal (yaw) nystagmus. For several hours thereafter, simple roll in darkness induced horizontal nystagmus and pitch and roll oscillations. The rising and falling time constants of the horizontal velocity indicated that the nystagmus arose in velocity storage. The continuous nystagmus was correlated with a phase shift of vertical eye velocity from 90 degrees to 0 degrees re head position. As the phases reverted toward pre-adaptive values, the horizontal velocity declined. Similar yaw nystagmus and pitch and roll velocities were produced by oscillation in roll after adaptation with roll and horizontal optokinetic nystagmus (OKN), but not after adaptation with pitch-while-rotating (PWR). Findings were explained by a model that shifted the roll orientation vector of velocity storage toward the pitch axis during adaptation with RWR and Roll & OKN. This shift produced modulation in vertical eye velocity in the post adaptive state, which was approximately in phase with roll head position, generating horizontal nystagmus. Similar orientation changes to prolonged exposure to complex motion environments may be responsible for producing post-stimulus motion sickness and/or mal de debarquement.