Ocular Smooth Pursuit Research Articles

Adaptive Response Behavior in the Pursuit of Unpredictably Moving Sounds.

Although moving sound-sources abound in natural auditory scenes, it is not clear how the human brain processes auditory motion. Previous studies have indicated that, although ocular localization responses to stationary sounds are quite accurate, ocular smooth pursuit of moving sounds is very poor. We here demonstrate that human subjects faithfully track a sound’s unpredictable movements in the horizontal plane with smooth-pursuit responses of the head. Our analysis revealed that the stimulus–response relation was well described by an under-damped passive, second-order low-pass filter in series with an idiosyncratic, fixed, pure delay. The model contained only two free parameters: the system’s damping coefficient, and its central (resonance) frequency. We found that the latter remained constant at ∼0.6 Hz throughout the experiment for all subjects. Interestingly, the damping coefficient systematically increased with trial number, suggesting the presence of an adaptive mechanism in the auditory pursuit system (APS). This mechanism functions even for unpredictable sound-motion trajectories endowed with fixed, but covert, frequency characteristics in open-loop tracking conditions. We conjecture that the APS optimizes a trade-off between response speed and effort. Taken together, our data support the existence of a pursuit system for auditory head-tracking, which would suggest the presence of a neural representation of a spatial auditory fovea (AF).

The Role of Neuronal Oscillations in Visual Active Sensing.

Visual perception is most often studied as a “passive” process in which an observer fixates steadily at point in space so that stimuli can be delivered to the system with spatial precision. Analysis of neuronal signals related to vision is generally keyed to stimulus onset, stimulus movement, etc.; i.e., events external to the observer. In natural “active” vision, however, information is systematically acquired by using eye movements including rapid (saccadic) eye movements, as well as smooth ocular pursuit of moving objects and slower drifts. Here we consider the use of alternating saccades and fixations to gather information from a visual scene. The underlying motor sampling plan contains highly reliable information regarding “where” and “when” the eyes will land, this information can be used predictively to modify firing properties of neurons precisely at the time when this “contextual” information is most useful – when a volley of retinal input enters the system at the onset of each fixation. Analyses focusing on neural events leading to and resulting from shifts in fixation, as well as visual events external to the observer, can provide a more complete and mechanistic understanding of visual information processing. Studies thus far suggest that active vision may be a fundamentally different from that process we usually study with more traditional passive viewing paradigms. In this Perspective we note that active saccadic sampling behavior imposes robust temporal patterning on the activity of neuron ensembles and large-scale neural dynamics throughout the brain’s visual pathways whose mechanistic effects on information processing are not yet fully understood. The spatio-temporal sequence of eye movements elicits a succession of temporally predictable quasi-rhythmic sensory inputs, whose encoding is enhanced by entrainment of low frequency oscillations to the rate of eye movements. Review of the pertinent findings underscores the fact that temporal coordination between motor and visual cortices is critical for understanding neural dynamics of active vision and posits that phase entrainment of neuronal oscillations plays a mechanistic role in this process.

Comparable rates of simulator sickness in Huntington’s disease and healthy individuals

ObjectiveInvestigating driving competence with a simulator provides a controlled setting and has a high reproducibility. In addition, there is less risk of physical harm compared to on-road tests. A disadvantage of using simulators is the occurrence of simulator sickness, which is comparable to symptoms of motion sickness.The aim of this study was to examine whether patients with Huntington’s disease (HD) are more susceptible to develop simulator sickness compared to healthy individuals. Further, we investigated if the clinical symptoms of HD, such as motor disabilities and cognitive deterioration, might increase the occurrence of simulator sickness. MethodsEighty-three participants (54 HD, 29 controls) drove in a driving simulator that included urban and motorway scenarios. All participants were still active drivers. Motor, cognitive, and oculomotor assessments were administered. Participants completed a questionnaire after the driving session to report possible symptoms of simulator sickness. ResultsFifty-eight (70%) participants completed the driving session, while 25 (30%) participants dropped out due to simulator sickness. The most reported symptoms of simulator sickness by dropouts were difficulties concentrating, dizziness, nausea, sweating, and vomiting. Dropouts were significantly older and more often female compared to completers. Decreased smooth ocular pursuit was predictive of dropout due to simulator sickness. The number of HD participants and controls in the dropout group was comparable. There was no significant difference in cognitive performance and motor functioning between completers and dropouts. ConclusionsHD participants did not have a higher chance of developing simulator sickness while driving in a simulator compared to controls. Female gender, older age, and smooth ocular pursuit were associated with increased simulator sickness, whereas cognitive and motor functioning were unrelated to dropout due to simulator sickness.

A Subconscious Interaction between Fixation and Anticipatory Pursuit.

Ocular smooth pursuit and fixation are typically viewed as separate systems, yet there is evidence that the brainstem fixation system inhibits pursuit. Here we present behavioral evidence that the fixation system modulates pursuit behavior outside of conscious awareness. Human observers (male and female) either pursued a small spot that translated across a screen, or fixated it as it remained stationary. As shown previously, pursuit trials potentiated the oculomotor system, producing anticipatory eye velocity on the next trial before the target moved that mimicked the stimulus-driven velocity. Randomly interleaving fixation trials reduced anticipatory pursuit, suggesting that a potentiated fixation system interacted with pursuit to suppress eye velocity in upcoming pursuit trials. The reduction was not due to passive decay of the potentiated pursuit signal because interleaving "blank" trials in which no target appeared did not reduce anticipatory pursuit. Interspersed short fixation trials reduced anticipation on long pursuit trials, suggesting that fixation potentiation was stronger than pursuit potentiation. Furthermore, adding more pursuit trials to a block did not restore anticipatory pursuit, suggesting that fixation potentiation was not overridden by certainty of an imminent pursuit trial but rather was immune to conscious intervention. To directly test whether cognition can override fixation suppression, we alternated pursuit and fixation trials to perfectly specify trial identity. Still, anticipatory pursuit did not rise above that observed with an equal number of random fixation trials. The results suggest that potentiated fixation circuitry interacts with pursuit circuitry at a subconscious level to inhibit pursuit.SIGNIFICANCE STATEMENT When an object moves, we view it with smooth pursuit eye movements. When an object is stationary, we view it with fixational eye movements. Pursuit and fixation are historically regarded as controlled by different neural circuitry, and alternating between invoking them is thought to be guided by a conscious decision. However, our results show that pursuit is actively suppressed by prior fixation of a stationary object. This suppression is involuntary, and cannot be avoided even if observers are certain that the object will move. The results suggest that the neural fixation circuitry is potentiated by engaging stationary objects, and interacts with pursuit outside of conscious awareness.

Neuro-otological Studies of Patients Suffering from Dizziness with Cerebrospinal Fluid Hypovolemia after Traffic Accident-associated Whiplash Injuries

Vertigo and dizziness are common clinical manifestations after traffic accident-associated whiplash injury. Recently, Shinonaga et al. (2001) suggested that more than 80% of patients with whiplash injury complaining of these symptoms showed cerebrospinal (CSF) hypovolemia on radioisotope (RI) cisternography (111In-DTPA). However, neuro-otological studies to investigate the pathophysiological mechanisms underlying these symptoms have been insufficient. In the present study, patients complaining of these symptoms with CSF hypovolemia after traffic accidents were investigated with posturography and electronystagmography (ENG). Fourteen patients (4 men, 10 women; 24-52 yr) were examined with posturography and showed parameters (tracking distance & area) significantly (p<0.01) larger than those of healthy subjects. Among them, five cases (1 man, 4 women; 31-52 yr) were further investigated with ENG. The slow phase peak velocities of optokinetic nystagmus (OKN) and optokinetic-after nystagmus (OKAN) were significantly (p<0.01) reduced (62.64±6.9 SD deg/sec, 60.76±10.74 SD deg/sec, respectively) and frequencies of OKN were reduced (139.7±10.75 SD), while the ocular smooth pursuit was relatively preserved. Magnetic resonance images (sagittal view) of these five patients demonstrated the downward displacement of the cerebellar tonsils and flattening of the pons, which are characteristic features of CSF hypovolemia, called "brain sagging." Our results suggest that brain sagging due to CSF hypovolemia impairs vestibular and vestibulocerebellar functions, which may cause dizziness and vertigo.

Smooth pursuit eye and gaze movements to moving auditory targets: Evidence for velocity-specific processing in the auditory system

Auditory motion perception remains poorly understood, in contrast with its well-established visual counterpart. Visual smooth pursuit (SP), a velocity-specific behavior, has been well-quantified during both head-fixed (ocular SP) and head-free (eye + head, or gaze SP) conditions. In contrast, auditory SP tracking has received little attention, despite its potential for demonstrating a motion-specific process in audition. We presented constant-velocity (10–40°/s), free-field auditory (0.2–20 kHz white noise), and visual (LED) targets to head-fixed or head-free subjects while recording ocular and gaze SP responses, respectively. To control for possible SP in the absence of a target, subjects were asked to recreate auditory trajectories after priming with a set of auditory ramps (practiced SP). We found that ocular auditory SP is consistently higher in gain than practiced SP, but variable and lower than visual SP. Further, the gain of auditory gaze SP exceeds ocular auditory SP. Finally, SP of periodic (triangular) motion trajectories revealed that auditory, like visual, SP improves rapidly over time, indicating predictive behavior. In sum, auditory SP closely mimics visual SP but with reduced gain. We propose that auditory motion processing exists, is robust, and recruits a velocity-dependent neural process shared with vision.

Infantile-onset saccade initiation delay (congenital ocular motor apraxia).

Infantile-onset saccade initiation delay, also known as congenital ocular motor apraxia, typically presents in early infancy with horizontal head thrusts once head control is achieved. Defective initiation of horizontal saccades and saccade hypometria with normal saccadic velocity are characteristic findings. Isolated impairment of vertical saccades is rare. Impaired smooth ocular pursuit may be seen. Other relatively common features include developmental delay, hypotonia, ataxia, or clumsiness. Brain MRI may be normal or show a diverse range of abnormalities, most commonly involving the cerebellum. Defective slow phases of the optokinetic response are commonly associated with brain MRI abnormalities. Isolated defect of vertical saccade initiation may indicate supratentorial brain abnormalities on MRI. Joubert syndrome, a developmental midbrain-hindbrain malformation, and ataxia telangiectasia are both commonly associated with defective volitional and reflexive saccade initiation, saccade hypometria, and head thrusts. Both horizontal and vertical saccades are impaired in these two disorders.

Do the Clinical Features in Infantile-Onset Saccade Initiation Delay (Congenital Ocular Motor Apraxia) Correlate With Brain Magnetic Resonance Imaging Findings?

Infantile-onset saccade initiation delay (ISID) is a defect in saccade initiation. Other features may include impaired smooth ocular pursuit, developmental delay, hypotonia, and ataxia. Brain magnetic resonance imaging (MRI) can be normal or show supratentorial or infratentorial abnormalities. Our aim was to correlate the clinical features of ISID with brain MRI findings. Detailed review of the English medical literature between 1952 and 2012 revealed 67 studies with possible ISID. Patients without a brain MRI or with inadequate information, Joubert syndrome, neurodegenerative disorders, and acquired saccade initiation delay were excluded. Ninety-one patients (age range, 3 months to 45 years) met the inclusion criteria and were divided into 3 groups based on their brain MRI findings: normal (n = 55), supratentorial abnormalities (n = 17), and infratentorial abnormalities (n = 19). The patients' clinical features including the direction of head thrusts, smooth pursuit, optokinetic response (OKR), tone, development, and coordination were compared and analyzed among the MRI groups using χ test. Horizontal head thrusts were significantly more common in patients with infratentorial abnormalities or normal brain MRI, whereas vertical head thrusts were more common among patients with supratentorial abnormalities (P < 0.0001). The slow phases of the OKR were significantly more likely to be impaired in patients with supratentorial or infratentorial abnormalities than in those with a normal MRI (P = 0.011). Other neuro-ophthalmological, neurological, and developmental features were similar among patients in the 3 neuroimaging groups. The direction of head thrust and the integrity of the slow phases of the OKR are useful clinical indicators of possible sites of abnormality on brain MRI in patients with ISID.

The Syndrome of Infantile-Onset Saccade Initiation Delay

Infantile-onset saccade initiation delay (ISID), also known as congenital ocular motor apraxia, is characterized by the inability to initiate volitional horizontal saccades. Other abnormalities including developmental delay and ataxia have been reported. The frequency of these abnormalities is unknown. We performed a detailed review of the medical literature to quantify features of ISID. We searched the English medical literature for articles related to ISID from 1952 to 2010. Whenever possible, patients were excluded if they had acquired SID, Joubert syndrome or neurodegenerative conditions. The minimum prevalence was calculated for each abnormality. Sixty-six articles with information on 288 patients were included in the analysis. Head thrusts were reported in 84.7%. Blinks without head thrusts were used to initiate saccades in 41%. The fast phases of the optokinetic response and vestibulo-ocular reflex were impaired in 69.8% and 34.4% respectively. Smooth ocular pursuit was abnormal in 33%. Global developmental delay occurred in 41.3%, speech or language delay in 36.5%, cognitive delay in 17%, hypotonia in 35.8%, motor delay in 48.6%, and ataxia/clumsiness in 49.3% of patients. Neuroimaging was performed on 197 patients and was normal in 39.1%. Abnormalities involved the cerebellum (24.9%), cerebrum (15.7%), other infratentorial structures (11.7%), and corpus callosum (6.1%). Infantile-onset saccade initiation delay is frequently associated with deficits in reflexive saccades and less frequently with impaired smooth ocular pursuit. Developmental delay, hypotonia, and ataxia occur frequently in ISID, suggesting more global brain impairment and not just a saccadic disorder.

A family with atypical CADASIL

Dear Sirs, Patients with CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) typically manifest migraine with aura, subcortical ischemic events, mood disturbances, apathy and cognitive impairment [1–3]. We report three of four siblings with atypical CADASIL manifestations, namely progressive ataxia and spastic paraparesis. Patient 1 (female b. 1953) complained of tension type headache, reduced concentration and memory, and fatigue after a moderate whiplash injury in 1998. Neurological examination at that time was normal, but Wechsler memory scale test showed reduced visuospatial memory. CSF and evoked potentials were normal, but MRI showed hyperintense white matter lesions. When re-examined in 2009 (Fig. 1a, b) her cognitive complaints were unchanged and neurological examination remained normal. MRI showed minor progression of the white matter disease. Fig. 1 All four patients had characteristic MRI findings of CADASIL. Coronar (FLAIR) and axial (T2) MRIs of patients 1 (a, b), 2 (c, d), 3 (e, f) and 4 (g, h) show hyperintense signals of white matter. Figure e and f also shows subcortical lacunar infarcts Patient 2 (male b. 1940) was diagnosed as having possible multiple sclerosis in 1993 because of spastic paraparesis and internuclear ophthalmoplegia. CSF and evoked potentials at that time were normal, but MRI showed hyperintense signals in white matter (examination no longer available). Re-examination in 2001 and 2009 still showed a spastic paraparesis, but also the presence of a truncal ataxia. MRI in 2009 showed hyperintense white matter lesions (Fig. 1c, d). Patient 3 (male b.1943) complained of slowly progressive unsteadiness from 1998. Neurological examination in 2001 and 2008 showed bilateral dysdiadochokinesis, truncal ataxia and mild spasticity in the lower limbs with hypereflexia. MRI in 2008 showed hyperintense white matter signals and subcortical infarcts in both hemispheres and basal ganglia (Fig. 1e, f). Patient 4 (male b. 1937) complained of unsteadiness from 2008. Neurological examination in 2009 showed pathological ocular smooth pursuit and bilateral dysdiadochokinesis. MRI in 2009 showed similar hyperintense white matter lesions as seen in the other siblings (Fig. 1e, f). Molecular genetic testing showed that all four siblings had the NOTCH3 gene mutation c.3065G>T that changes a cysteine to phenylalanine at position 1022. Three of our patients had features of slowly progressive cerebellar disease combined in two with pyramidal tract signs. No MRI lesions or atrophy involving the cerebellum were seen in our patients, but subcortical lacunar infarcts were present in patient 3. Patient 2, who was initially diagnosed with possible multiple sclerosis, had a transient diplopia and the finding of an internuclear ophthalmoplegia, was probably caused by a brain stem infarction. Ischemic episodes or transient ischemic attacks occur in 60–85% of the patients with CADASIL, and most of these are subcortical ischemic events [1–3]. Our patients had slowly progressive cognitive, cerebellar and/or pyramidal signs most likely due to the cerebral arteriopathy NOTCH3 mutations, which affects vascular smooth muscle cells [4]. The main mechanism of the progressive symptoms in our patients is probably chronic hypoperfusion due to the arteriopathy which is characterised by a failure of arteries to dilate properly [4]. We have no information on the siblings' children and only little information concerning their parents who are both dead. The father was apparently healthy, but the mother had progressive visual impairment said to be due to retinitis pigmentosa. Of her six siblings, one also had progressive blindness and two had cerebrovascular attacks. We have no MRI or biological material available for genetic testing from any of these individuals. Retinal abnormalities with axonal loss have been described in CADASIL while no visual symptoms were present in these patients [5, 6]. It therefore remains possible that the mother of our patients was a carrier of the NOTCH3 mutation. We present a family with CADASIL in which cerebellar disease including ataxia was a major feature in three of four siblings and two of these also had pyramidal tract signs. Only one of the siblings presented with a feature typical for CADASIL, namely cognitive impairment. This family confirms the intrafamilial variation in CADASIL and demonstrates that ataxia and spastic paraparesis can be presenting features.

Saccadic Compensation for Smooth Eye and Head Movements During Head-Unrestrained Two-Dimensional Tracking

Spatial updating is the ability to keep track of the position of world-fixed objects while we move. In the case of vision, this phenomenon is called spatial constancy and has been studied in head-restraint conditions. During head-restrained smooth pursuit, it has been shown that the saccadic system has access to extraretinal information from the pursuit system to update the objects' position in the surrounding environment. However, during head-unrestrained smooth pursuit, the saccadic system needs to keep track of three different motor commands: the ocular smooth pursuit command, the vestibuloocular reflex (VOR), and the head movement command. The question then arises whether saccades compensate for these movements. To address this question, we briefly presented a target during sinusoidal head-unrestrained smooth pursuit in darkness. Subjects were instructed to look at the flash as soon as they saw it. We observed that subjects were able to orient their gaze to the memorized (and spatially updated) position of the flashed target generally using one to three successive saccades. Similar to the behavior in the head-restrained condition, we found that the longer the gaze saccade latency, the better the compensation for intervening smooth gaze displacements; after about 400 ms, 62% of the smooth gaze displacement had been compensated for. This compensation depended on two independent parameters: the latency of the saccade and the eye contribution to the gaze displacement during this latency period. Separating gaze into eye and head contributions, we show that the larger the eye contribution to the gaze displacement, the better the overall compensation. Finally, we found that the compensation was a function of the head oscillation frequency and we suggest that this relationship is linked to the modulation of VOR gain. We conclude that the general mechanisms of compensation for smooth gaze displacements are similar to those observed in the head-restrained condition.

Smooth ocular pursuit in Chiari type II malformation

Chiari type II malformation (CII) is a congenital anomaly of the cerebellum and brainstem, both important structures for processing smooth ocular pursuit. CII is associated with myelomeningocele and hydrocephalus. We investigated the effects of CII on smooth pursuit (SP) eye movements, and determined the effects of spinal lesion level, number of shunt revisions, nystagmus, and brain dysmorphology on SP. SP was recorded using an infrared eye tracker in 21 participants with CII (11 males, 10 females; age range 8-19y, mean 14y 3mo [SD 3y 2mo]). Thirty-eight healthy children (21 males, 17 females) constituted the comparison group. Participants followed a visual target moving sinusoidally at +/- 10 degrees amplitude, horizontally and vertically at 0.25 or 0.5Hz. SP gains, the ratio of eye to target velocities, were abnormal in the CII group with nystagmus (n= 8). The number of shunt revisions (range 0-10), brain dysmorphology, or spinal lesion level (n= 15 for lower and n= 6 for upper spinal lesion level) did not correlate with SP gains. SP is impaired in children with CII and nystagmus. Abnormal pursuit might be related to the CII dysgenesis or to effects of hydrocephalus. The lack of effect of shunt revisions and abnormal tracking in participants with nystagmus provide evidence that it is related primarily to the cerebellar and brainstem malformation.

Smooth ocular pursuit during the transient disappearance of an accelerating visual target: the role of reflexive and voluntary control

This study examined the extent to which human subjects predict future target motion for the control of smooth ocular pursuit. Subjects were required to pursue an accelerating target (0, 4 or 8 degrees/s2) that underwent a transient occlusion, and consequently reappeared with the same or increased velocity. Presentations were received in a random or blocked order. Subjects exhibited anticipatory smooth pursuit prior to target motion onset, which in blocked presentations was scaled to the velocity generated by the target acceleration. In random presentations subjects also exhibited anticipatory smooth pursuit, but this was reflected in a more generalized response. During the transient occlusion all subjects exhibited a reduction in eye velocity, which was followed in the majority by a recovery prior to target reappearance. In random presentations, eye velocity decayed and recovered to a level that followed on from the response to the initial ramp. In blocked presentations, there was evidence of improved scaling throughout, which culminated in a significant increase in eye velocity between the start and end of the transient occlusion (8 degrees/s2 only). These findings are difficult to reconcile with reflexive accounts of oculomotor control that perpetuate current eye motion, and hence generate a simple form of prediction using a direct efference copy ("eye-velocity memory"). Rather, they are more consistent with the scaling of smooth pursuit eye movements by means of a more-persistent velocity-based representation, which plays a significant role in both random and blocked stimulus presentations.

Timing the anticipatory recovery in smooth ocular pursuit during the transient disappearance of a visual target

After the disappearance of a moving target and the loss of visual feedback regarding image motion, smooth pursuit eye velocity decays rapidly. If, however, there is an expectation the target will reappear further along its trajectory, there is a scaled recovery in eye velocity before target reappearance. The aim of this study was to examine whether the timing of the anticipatory recovery is influenced by the duration of transient target disappearance. We found that subjects (N=6) did not maintain eye velocity close to target velocity throughout the inter-stimulus interval (ISI). In general, after an initial reduction in eye velocity a significant increase was observed for most subjects before target reappearance, or a recovery that halted the decay. The timing of the recovery was not influenced by ISI even when this was predictable. There was, however, a significant effect of the initial visible ramp duration, indicating that the recovery was a consequence of the previous eye velocity trajectory and subsequent reacceleration. We suggest, therefore, that the recovery was timed to the moment of target disappearance rather than reappearance, and was the result of reactivation of a variable gain mechanism that acts on the visuomotor drive to ocular pursuit.

Sequence learning in human ocular smooth pursuit

It has been established that repeated presentation of a transient target motion stimulus such as a constant-velocity ramp leads to the build up of steady state (SS), anticipatory smooth pursuit eye movements after two or three presentations. Each SS response is then composed of the anticipatory component of nonvisual origin, a visual component associated with the stimulus presentation and another nonvisual component that represents the decay of the response after extinction of the stimulus. Here we investigated the interactions that occur when each motion stimulus was itself a sequence containing more than one ramp component. Ramp components had a velocity of 15 degrees /s or 30 degrees /s to left or right and were separated by gaps of 200 ms duration. In an initial experiment, responses to 2-ramp stimuli were examined and compared with responses to the single-ramp stimuli from which they were constituted. We present evidence that the anticipatory, nonvisual components of the double-ramp response result from the linear summation of the nonvisual components of the responses to the constituent single-ramp components. In a 2nd experiment, we examined responses to a wide variety of 4-ramp sequences and again found evidence that, in the SS, the responses were formed from the linear summation of the constituent single-ramp components. Regression analysis performed on the velocity at onset of each ramp component indicated that this nonvisual part of the response was predictive of the upcoming ramp component. To confirm this, unexpected changes were introduced into single ramp components of the 4-ramp sequence after at least five prior presentations of the sequence had allowed a SS response to be established. Subjects continued to initiate a response to the modified component that was appropriate in velocity and direction for the corresponding part of the previous sequence and inappropriate for the newly modified stimulus. This preprogrammed response persisted unmodified for more than 170 ms after onset of the modified ramp component. In contrast, in the second presentation of the new sequence, the anticipatory component of the response was highly correlated with the SS response of the new sequence, but not with that of the prior sequence, showing that the preprogrammed response had been modified very rapidly. Similar behaviour was observed whichever of the 4-ramp components was modified, indicating that the velocity and direction of the anticipatory response to each component had been preprogrammed. The results suggest that velocity information related to at least four elements of a sequence can be temporarily stored and subsequently released with appropriate temporal order to form an anticipatory response throughout the whole sequence.

Oculocentric frames of reference for limb movement.

We have reviewed evidence that suggests that the target for limb motion is encoded in a retinocentric frame of reference. Errors in pointing that are elicited by an illusion that distorts the perceived motion of a target are strongly correlated with errors in gaze position. The modulations in the direction and speed of ocular smooth pursuit and of the hand show remarkable similarities, even though the inertia of the arm is much larger than that of the eye. We have suggested that ocular motion is constrained so that gaze provides an appropriate target signal for the hand. Finally, ocular and manual tracking deficits in patients with cerebellar ataxia are very similar. These deficits are also consistent with the idea that a gaze signal provides the target for hand motion; in some cases limb ataxia would be a consequence of optic ataxia rather than reflecting a deficit in the control of limb motion per se. These results, as well as neurophysiological data summarized here, have led us to revise a hypothesis we have previously put forth to account for the initial stages of sensorimotor transformations underlying targeted limb motions. In the original hypothesis, target location and initial arm posture were ultimately encoded in a common frame of reference tied to somatosensation, i.e. a body-centered frame of reference, and a desired change in posture was derived from the difference between the two. In our new scheme, a movement vector is derived from the difference between variables encoded in a retinocentric frame of reference. Accordingly, gaze, with its exquisite ability to stabilize a target image even under dynamic conditions, would be used as a reference signal. Consequently, this scheme would facilitate the processing of information under conditions in which the body and the target are moving relative to each other.

Volitional selection of direction in the generation of anticipatory ocular smooth pursuit in humans

Anticipatory smooth pursuit eye movements cannot normally be generated in the absence of a moving target. However, repeated presentation of identical target motion stimuli, preceded by warning cues, leads to the build up of anticipatory smooth pursuit prior to target onset. These anticipatory responses arguably depend more on motor habit than cognitive expectations. Here, we show that directional cues, concomitant with a timing cue, may be used to initiate predictive (velocity scaled) movements in response to target stimuli of random direction. Furthermore, we show stored velocity and timing information may be directionally transferred, thus allowing predictive movements in a novel direction. This demonstrates the internal origin of these movements and their volitional as opposed to reflexive nature.

Progressive bradykinesia and hypokinesia of ocular pursuit in Parkinson’s disease

OBJECTIVESPatients with Parkinson’s disease characteristically have difficulty in sustaining repetitive motor actions. The purpose of this study was to establish if parkinsonian difficulty with sustaining repetitive limb movements also applies...

Effects of dual task demands on the accuracy of smooth pursuit eye movements

The effect of attention allocation on smooth pursuit eye movements (SPEM) was investigated. Eye movements were electrooculographically recorded in 27 healthy subjects who tracked a visual target that moved horizontally with constant or unpredictably varying velocity. In some trials, subjects performed additional auditory discrimination tasks varying in difficulty. Pursuit error decreased when attention was divided between both tasks. The pattern of results is incompatible with the assumption made in previous research that attention enhancement improves SPEM accuracy. Rather, ocular smooth pursuit appears to be executed in the automatic mode, although intentional and selective processes must contribute. Moreover, controlled attention directed to the tracking task interfered with smooth pursuit. A reinterpretation of earlier studies in which visual monitoring tasks were used to improve eye tracking is needed.

Autosomal recessive spastic ataxia of Charlevoix–Saguenay

A form of autosomal recessive spastic ataxia unique to the Charlevoix–Saguenay area was clinically identified 20 years ago in patients from that region. This region of Québec, Canada, was once considered a genetic isolate. First noted at gait initiation, signs of ataxia slowly progress along with spasticity of the four limbs, slurred speech, and followed by distal amyotrophy. Early diagnosis relies on the presence of prominent myelinated fibers embedding retinal blood vessels at funduscopy and marked saccadic alteration of ocular smooth pursuit. Imaging of the posterior fossa shows cerebellar vermis atrophy and nerve conduction studies reveal loss of sensory and reduced motor conduction velocities. The clinical features are consistent with a developmental defect in myelination of both retinal and peripheral nerve fibers. The cause of this defect and the progressive axonal degeneration in the corticospinal and spinocerebellar tracts, as well as in the peripheral nerves is still unknown. Results of recent molecular genetic linkage analysis have located the gene locus to chromosome 13q12. Further research is needed to define where this hereditary spastic ataxia stands in the classification of the early onset spinocerebellar degenerations.