Gain Of Smooth Pursuit Eye Movements Research Articles

Elevated Smooth Pursuit Gain in Collegiate Athletes with Sport-related Concussion Immediately Following Injury.

Although there is evidence that sport-related concussion (SRC) affects oculomotor function and perceptual ability, experiments are often poorly controlled and are not replicable. This study aims to test the hypothesis that there are decreased values when assessing oculomotor impairment indicating poorer performance in SRC patients. Fifteen DI athletes presenting with SRC (7 females, 8 males) and 15 student volunteers (CON) (12 females, 3 males) completed a dynamic visual acuity (DVA) task that involved answering the direction of a moving stimulus (Landolt C) while wearing a head-mounted binocular eye tracker. There were 120 trials total with 60 trials presenting at 30º per second and 60 presenting at 90º per second. Various eye movement measurements, including horizontal smooth pursuit eye movements (SPEM) gain and saccadic peak velocity, were analyzed between groups using univariate ANOVAs. Saccade count in SPEM trials, accuracy, and vision were analyzed using Kruskal-Wallis tests. There was no statistical difference in saccadic peak velocity: SRC = 414.7 42º/s, CON = 406.6 40.6º/s. A significant difference was found between SRC patients and healthy controls in horizontal SPEM gain (SRC = 0.9 0.04, CON = 0.86 0.03, F(1,28) = 7.243, P = 0.012) indicating that patients demonstrated compensatory eye movements when tracking the target. There were significantly more saccades in all SPEM trials (P = 0.001). SRCoculomotor deficits manifest as elevated horizontal SPEM gain when assessed within 48 hours of injury and compared to healthy controls within the same age range. SRC demonstrates altered oculomotor ability. While accurate in tracking a stimulus, SRC patients may conduct less controlled eye movements.

Clinical value of video oculomotor evaluation in the differential diagnosis of multiple system atrophy and Parkinson's disease.

Multiple system atrophy (MSA) is a neurodegenerative disease that progresses rapidly and has a poor prognosis. This study aimed to assess the value of video oculomotor evaluation (VOE) in the differential diagnosis of MSA and Parkinson's disease (PD). In total, 28 patients with MSA, 31 patients with PD, and 30 age- and sex-matched healthy controls (HC) were screened and included in this study. The evaluation consisted of a gaze-holding test, smooth pursuit eye movement (SPEM), random saccade, and optokinetic nystagmus (OKN). The MSA and PD groups had more abnormalities and decreased SPEM gain than the HC group (64.29%, 35.48%, 10%, p<.001). The SPEM gain in the MSA group was significantly lower than that in the PD group at specific frequencies. Patients with MSA and PD showed prolonged latencies in all saccade directions compared with those with HC. However, the two diseases had no significant differences in the saccade parameters. The OKN gain gradually decreased from the HC to the PD and the MSA groups (p<.05). Compared with the PD group, the gain in the MSA group was further decreased in the OKN test at 30°/s (Left, p=.010; Right p=.016). Receiver operating characteristic curves showed that the combination of oculomotor parameters with age and course of disease could aid in the differential diagnosis of patients with MSA and PD, with a sensitivity of 89.29% and a specificity of 70.97%. The combination of oculomotor parameters and clinical data may aid in the differential diagnosis of MSA and PD. Furthermore, VOE is vital in the identification of neurodegenerative diseases.

Oculomotor impairments in de novo Parkinson's disease.

Reliable electrophysiological indicators are urgently needed in the precise evaluation of Parkinson's disease (PD). It is still elusive whether oculomotor performance is impaired or has clinical value in early PD. This study aims to explore oculomotor performance in newly diagnosed, drug-naïve PD and its correlation with clinical phenotype. Seventy-five patients with de novo PD, 75 patients with essential tremor (ET), and 46 gender-and age-matched healthy controls (HCs) were included in this cross-sectional study. All subjects underwent oculomotor test via videonystagmography. Visually guided saccade latency, saccadic accuracy and gain in smooth pursuit eye movement (SPEM) at three frequencies of the horizontal axis were compared among the three groups. Patients with PD also received detailed motor and non-motor evaluation by serial scales. The association between key oculomotor parameters and clinical phenotypes were explored in PD patients. Both de novo PD and ET patients showed prolonged saccadic latency and decreased saccadic accuracy relative to HCs. SPEM gain in PD was uniformly reduced at each frequency. SPEM gain at 0.4 Hz was also decreased in ET compared with HCs. However, there was no significant difference of oculomotor parameters between de novo PD and ET patients. Furthermore, prolonged saccadic latency was correlated with long disease duration, whereas decreased SPEM gain was associated with severe motor symptoms in de novo PD patients. Ocular movements are impaired in de novo, drug naïve PD patients; these changes could be indicators for disease progression in PD.

FV 3. Diagnostic value of oculomotor parameters in progressive supranuclear palsy: a monocentric study in 100 patients

Introduction. For progressive supranuclear palsy (PSP), oculomotor function is one of the core features on which the diagnosis is based upon according to the diagnostic criteria by the Movement Disorder Society (MDS) supported PSP-Study-Group from 2017 (“O criterion”). The aim of this study was to analyze the value of specific oculomotor parameters. Material/Method. An analysis of the videooculographic examinations of smooth pursuit eye movements and visually guided reactive saccades in 100 PSP patients and 49 matched control subjects was performed. Group differences as well as correlations were tested at a two-sided level α=0.05. Cut-off values for the development of new subgroups were defined by the fifth or 95th percentile of specific parameters of the control group. ROC-analyses were used to determine sensitivity and specificity. Results. Each of the investigated oculomotor parameters (for smooth pursuit eye movements gain, for saccades latency, gain, peak eye velocity, asymmetry of velocities up- and downwards, rate of saccadic intrusions (SI)) was significantly altered in PSP compared with the control population (p<0.0001 each). The threshold for vertical saccade velocity was approximately 240°/s for both components so that about 70% of the patients could be captured. A cut-off value of 9.60°/s was determined for SI, and approximately 56% of the patients achieved higher values. By combining both parameters, almost 80% of the patients could be classified. With regard to the specifically calculated asymmetry of the vertical saccade velocities, 34% of the patients were abnormal at a threshold of 0.42 (overview in Fig. 1). The majority of patients (63.5%) performed faster downward than upward saccades. The vertical saccade velocity and SI had a high specificity of more than 95%, while sensitivity was maximally 60% for the velocity components and 54.2% for the SI. At similar specificity, the asymmetry reached a sensitivity of 27.1%. Discussion. The results for vertical saccade velocity and SI, respectively, emphasized their relevance as part of the MDS-PSP diagnostic criteria, whereas the significance of the asymmetry of the vertical velocities was limited. With respect to directional tendency, the findings are still heterogeneous. In future evaluations, unbiased quantifications of clinical parameters offer a good possibility to further develop the quality of the diagnostic procedures used for PSP. Fig. 1.

Clinical and Oculomotor Correlates With Freezing of Gait in a Chinese Cohort of Parkinson's Disease Patients.

Accumulating evidence suggests that freezing of gait (FOG) is a unique gait disturbance in Parkinson’s disease (PD), and its pathophysiology is not fully elucidated. The present study aims to investigate the clinical and oculomotor associations with FOG in Chinese PD patients. From Jan 2017 to Dec 2019, a total of 210 PD patients were consecutively registered for FOG evaluation based on item-3 of the Freezing of Gait Questionnaire (FOGQ). We explored the demographic, motor, and non-motor symptom differences in FOG positive (PD+FOG, n = 45) vs. negative (PD-FOG, n = 165) group. In addition, 40 PD patients and 37 healthy controls (HC) also underwent oculomotor test via videonystagmography (VNG). Visually guided saccade (VGS) latency, saccade accuracy and gain in smooth pursuit eye movement (SPEM) at three frequencies of horizontal axis were compared among PD+FOG (n = 20), PD-FOG (n = 20), and HC (n = 37). Compared with PD-FOG, PD+FOG had longer disease duration, more severe motor symptoms, lower cognitive scores, more severe depressive and autonomic impairments, as well as higher daily levodopa equivalent dosage. FOG occurred more frequently in patients with wearing-off. VNG subgroup analysis demonstrated that PD+FOG had prolonged saccade latency and decreased saccade accuracy relative to PD-FOG or HC. SPEM gain at 0.1 and 0.2 Hz was also decreased in PD+FOG compared with HC. Furthermore, prolonged saccade latency was correlated with higher FOGQ scores in PD patients. Our results verify that PD with FOG patients suffer from more severe motor and non-motor symptoms, indicating more extensive neurodegeneration. Prolonged saccade latency could be a practical oculomotor parameter both for identification and progression of FOG in PD.

Smooth Pursuit And Saccadic Eye Movements Following Years Of Contact Collision Sports: A Pilot Study

Repetitive head impacts (RHI) are the result of a blow to the head that does not elicit clinical signs or symptoms of a concussion. Recent evidence suggests that RHI from a single season of collegiate football can lead to a reduction in midbrain white matter integrity. The midbrain carries projecting fibers to the trochlear and oculomotor nerves, which if damaged may impair oculomotor control. PURPOSE: The purpose of this study was to evaluate oculomotor function following multiple years of Division I contact sports during a dynamic visual acuity (DVA) task. METHODS: Two NCAA Division I football defensive backs with no diagnosed concussion history (a first-year freshmen [F1; age=18 years], senior [S1; age=21 years]) and a healthy control (CON; age=23 years), all with lower than 20/20 vision, completed a DVA task at pre-season. For the DVA task (optotype spatial range=1.0 to -0.3), participants were asked to complete 60 randomized trials of smooth pursuit (30°/s) and saccades (150°/s). Participants head were stabilized in a chin rest at a distance of 154cm away from the 26° visual field monitor (165Hz, 2560 x 1440 pixel resolution, 300 cd/m2 luminance) while wearing a head-mounted binocular video oculography eye tracker (Eyelink SR research, 500 Hz, Ottawa, CN). Using a 2-up-1-down staircase method, participants tracked a Landolt-C ring that moved across the screen (horizontally left to right) where the size of the gap in the C along with the orientation (left, right, up or down) adjusted based on the correct/incorrect responses during both smooth pursuit and saccadic trials. Smooth pursuit eye movement (SPEM) velocity gain and saccadic peak velocity were calculated using ternary eye movement classification from the transformed spherical coordinates via a custom MATLAB code (MATLAB 2019a, Natick, MA, USA). No statistical analysis were performed given the single-subject design. RESULTS: SPEMs gain is lower for S1 (0.88) when compared to F1 (0.82) and CON (0.92). Similarly, during the saccadic trials, S1 had slower average saccadic peak velocity (S1=279.75°/s; F1 =392.34°/s; CON=491.96°/s). CONCLUSIONS: These results may indicate that engaging in contact collision sport for 2+ years at the Division 1 level may result in less accurate (lower SPEMs gain) and slower saccadic eye movements. Supported by NIH P20GM103650

Mechanisms of smooth pursuit eye movements in schizotypy

Several studies suggest that highly schizotypal individuals display a deficit in smooth pursuit eye movements (SPEM), which are considered an important biomarker of schizophrenia. In schizophrenia, abnormal SPEM is thought to be driven by impairments in motion perception. In schizotypy, the processes underlying reduced SPEM performance have not been examined so far, and there are no studies on motion perception deficits in schizotypy. Thus, in this registered report, we aimed to investigate whether motion perception is impaired in highly schizotypal individuals, and how it contributes to SPEM performance. On an exploratory basis, we were interested in the association between schizotypy and prediction, another mechanism underlying SPEM. To address this issue, participants with high total scores of the Oxford–Liverpool Inventory of Feelings and Experiences (O-LIFE short form) and control participants with low scores (N = 86 in each group) performed a standard sinusoidal SPEM task, random dot kinematograms to measure motion perception, and a blanking SPEM task to assess prediction abilities. Group comparisons as well as mediator analyses were carried out to identify whether motion perception or prediction are responsible for SPEM performance in schizotypy. We found reduced blanking SPEM performance in schizotypes compared to controls, but no group differences regarding sinusoidal SPEM and motion perception. Although no significant mediators were identified for SPEM performance in schizotypes, an exploratory analysis revealed an association between motion perception and SPEM gain in high, but not in low schizotypy. Our findings imply that despite the schizotypy-related impairment in prediction, motion perception seems to be a more important predictor of SPEM performance in schizotypes. A deficit in prediction that does not relate to SPEM performance suggests that protective factors (e.g., other cognitive processes) might operate in schizotypal individuals to maintain SPEM performance on a healthy level.

Eye movement abnormalities in essential tremor versus tremor dominant Parkinson’s disease

ObjectiveTo show that eye movement abnormalities differ between essential tremor (ET) and tremor dominant Parkinson’s disease (PD-T), and that these abnormalities reflect cerebellar dysfunction in ET and basal ganglia pathology in PD-T. MethodsIn this exploratory study, in 23 patients with ET, 21 age-matched patients with PD-T, and 19 age-matched healthy controls (HCs), we investigated visually guided saccades, antisaccades, and smooth pursuit eye movements (SPEM). ResultsWhile the ET group had a normal gain (saccade amplitude/target amplitude) and latency of saccades, the PD-T group had hypometric visually guided saccades, and a prolonged latency of visually guided saccades and antisaccades. The SPEM gain was similarly low in both ET and PD-T and was significantly lower in both patient groups than in the HC group. ConclusionsIn ET, SPEM gain was reduced in the presence of normal saccades, whereas in PD-T, the reduced SPEM gain was accompanied by delayed saccade initiation and hypometric saccades, in line with cerebellar dysfunction in ET and basal ganglia dysfunction in PD-T. SignificanceThese findings support the presumed cerebellar pathology in ET. In addition, the difference in saccade features may contribute to the groundwork for a quantitative diagnostic test to differentiate between these disorders.

Combining two model systems of psychosis: The effects of schizotypy and sleep deprivation on oculomotor control and psychotomimetic states.

Model systems of psychosis, such as schizotypy or sleep deprivation, are valuable in informing our understanding of the etiology of the disorder and aiding the development of new treatments. Schizophrenia patients, high schizotypes, and sleep-deprived subjects are known to share deficits in oculomotor biomarkers. Here, we aimed to further validate the schizotypy and sleep deprivation models and investigated, for the first time, their interactive effects on smooth pursuit eye movements (SPEM), prosaccades, antisaccades, predictive saccades, and measures of psychotomimetic states, anxiety, depression, and stress. To do so, n = 19 controls and n = 17 high positive schizotypes were examined after both a normal sleep night and 24 h of sleep deprivation. Schizotypes displayed higher SPEM global position error, catch-up saccade amplitude, and increased psychotomimetic states. Sleep deprivation impaired SPEM, prosaccade, antisaccade, and predictive saccade performance and increased levels of psychotomimetic experiences. Additionally, sleep deprivation reduced SPEM gain in schizotypes but not controls. We conclude that oculomotor impairments are observed in relation to schizotypy and following sleep deprivation, supporting their utility as biomarkers in model systems of psychosis. The combination of these models with oculomotor biomarkers may be particularly fruitful in assisting the development of new antipsychotic or pro-cognitive drugs.

The effects of ketamine and risperidone on eye movement control in healthy volunteers.

The non-competitive N-methyl-D-aspartate receptor antagonist ketamine leads to transient psychosis-like symptoms and impairments in oculomotor performance in healthy volunteers. This study examined whether the adverse effects of ketamine on oculomotor performance can be reversed by the atypical antipsychotic risperidone. In this randomized double-blind, placebo-controlled study, 72 healthy participants performed smooth pursuit eye movements (SPEM), prosaccades (PS) and antisaccades (AS) while being randomly assigned to one of four drug groups (intravenous 100 ng ml−1 ketamine, 2 mg oral risperidone, 100 ng ml−1 ketamine plus 2 mg oral risperidone, placebo). Drug administration did not lead to harmful adverse events. Ketamine increased saccadic frequency and decreased velocity gain of SPEM (all P<0.01) but had no significant effects on PS or AS (all P⩾0.07). An effect of risperidone was observed for amplitude gain and peak velocity of PS and AS, indicating hypometric gain and slower velocities compared with placebo (both P⩽0.04). No ketamine by risperidone interactions were found (all P⩾0.26). The results confirm that the administration of ketamine produces oculomotor performance deficits similar in part to those seen in schizophrenia. The atypical antipsychotic risperidone did not reverse ketamine-induced deteriorations. These findings do not support the cognitive enhancing potential of risperidone on oculomotor biomarkers in this model system of schizophrenia and point towards the importance of developing alternative performance-enhancing compounds to optimise pharmacological treatment of schizophrenia.

Eye movement impairments in Parkinson's disease: possible role of extradopaminergic mechanisms

BackgroundThe basal ganglia (BG) are thought to play an important role in the control of eye movements. Accordingly, the broad variety of subtle oculomotor alterations that has been described in Parkinson's disease (PD) are generally attributed to the dysfunction of the BG dopaminergic system. However, the present study suggest that dopamine substitution is much less effective in improving oculomotor performance than it is in restoring skeletomotor abilities.MethodsWe investigated reactive, visually guided saccades (RS), smooth pursuit eye movements (SPEM), and rapidly left-right alternating voluntary gaze shifts (AVGS) by video-oculography in 34 PD patients receiving oral dopaminergic medication (PD-DA), 14 patients with deep brain stimulation of the nucleus subthalamicus (DBS-STN), and 23 control subjects (CTL);In addition, we performed a thorough review of recent literature according therapeuthic effects on oculomotor performance in PD by switching deep brain stimulation off and on in the PD-DBS patients, we achieved swift changes between their therapeutic states without the delays of dopamine withdrawal. In addition, participants underwent neuropsychological testing.ResultsPatients exhibited the well known deficits such as increased saccade latency, reduced SPEM gain, and reduced frequency and amplitude of AVGS. Across patients none of the investigated oculomotor parameters correlated with UPDRS III whereas there was a negative correlation between SPEM gain and susceptibility to interference (Stroop score). Of the observed deficiencies, DBS-STN slightly improved AVGS frequency but neither AVGS amplitude nor SPEM or RS performance.ConclusionsWe conclude that the impairment of SPEM in PD results from a cortical, conceivably non-dopaminergic dysfunction, whereas patients' difficulty to rapidly execute AVGS might be related to their BG dysfunction.

Comparison of smooth pursuit eye movement deficits in multiple system atrophy and Parkinson’s disease

Because of the large overlap and quantitative similarity of eye movement alterations in Parkinson's disease (PD) and multiple system atrophy (MSA), a measurement of eye movement is generally not considered helpful for the differential diagnosis. However, in view of the pathophysiological differences between MSA and PD as well as between the cerebellar (MSA-C) and Parkinsonian (MSA-P) subtypes of MSA, we wondered whether a detailed investigation of oculomotor performance would unravel parameters that could help to differentiate between these entities. We recorded eye movements during sinusoidal pursuit tracking by means of video-oculography in 11 cases of MSA-P, 8 cases of MSA-C and 27 cases of PD and compared them to 23 healthy controls (CTL). The gain of the smooth pursuit eye movement (SPEM) component exhibited significant group differences between each of the three subject groups (MSA, PD, controls) but not between MSA-P and MSA-C. The similarity of pursuit impairment in MSA-P and in MSA-C suggests a commencement of cerebellar pathology in MSA-P despite the lack of clinical signs. Otherwise, SPEM gain was of little use for differential diagnosis between MSA and PD because of wide overlap. However, inspection of the saccadic component of pursuit tracking revealed that in MSA saccades typically correct for position errors accumulated during SPEM epochs ("catch-up saccades"), whereas in PD, saccades were often directed toward future target positions ("anticipatory saccades"). The differences in pursuit tracking between PD and MSA were large enough to warrant their use as ancillary diagnostic criteria for the distinction between these disorders.

Differential diagnostic value of eye movement recording in PSP-parkinsonism, Richardson's syndrome, and idiopathic Parkinson's disease

Vertical gaze palsy is a highly relevant clinical sign in parkinsonian syndromes. As the eponymous sign of progressive supranuclear palsy (PSP), it is one of the core features in the diagnosis of this disease. Recent studies have suggested a further differentiation of PSP in Richardson's syndrome (RS) and PSP-parkinsonism (PSPP). The aim of this study was to search for oculomotor abnormalities in the PSP-P subset of a sample of PSP patients and to compare these findings with those of (i) RS patients, (ii) patients with idiopathic Parkinson's disease (IPD), and (iii) a control group. Twelve cases of RS, 5 cases of PSP-P, and 27 cases of IPD were examined by use of video-oculography (VOG) and compared to 23 healthy normal controls. Both groups of PSP patients (RS, PSP-P) had significantly slower saccades than either IPD patients or controls, whereas no differences in saccadic eye peak velocity were found between the two PSP groups or in the comparison of IPD with controls. RS and PSP-P were also similar to each other with regard to smooth pursuit eye movements (SPEM), with both groups having significantly lower gain than controls (except for downward pursuit); however, SPEM gain exhibited no consistent difference between PSP and IPD. A correlation between eye movement data and clinical data (Hoehn & Yahr scale or disease duration) could not be observed. As PSP-P patients were still in an early stage of the disease when a differentiation from IPD is difficult on clinical grounds, the clear-cut separation between PSP-P and IPD obtained by measuring saccade velocity suggests that VOG could contribute to the early differentiation between these patient groups.

Vergence deficits in cerebellar lesions

The cerebellum is part of the cortico-ponto-cerebellar circuit for conjugate eye movements. Accordingly, cerebellar lesions cause smooth pursuit deficits and saccadic dysmetria. In contrast, the role of the cerebellum for disconjugate, i.e. vergence eye movements in humans is still unknown. The aim of this study was to investigate whether cerebellar lesions affect vergence eye movements. Similar to conjugate eye movements, vergence can be separated into two different components: vergence to step targets (fast vergence) and vergence to ramp and sinusoidal targets (slow vergence). Eye movements (fast and slow vergence, smooth pursuit, saccades) were binocularly recorded with the scleral search coil system in 20 patients with acute cerebellar lesions (ischemic strokes) and age-matched healthy controls. Small dim laser stimuli were presented on an earth horizontal platform at the level of the subject's nose. Smooth pursuit always had a constant vergence angle (iso-vergence). The majority of patients had unilateral lesions in the territory of the posterior inferior cerebellar artery (3 patients with infarctions in the superior cerebellar artery territory, one cavernoma patient). Group analysis revealed impairment of both conjugate and disconjugate eye movements as well as reduced saccadic gain (Table). The gain of slow vergence to sinusoidal targets was reduced in the patients. Patients with vermal lesions (subgroup, n=10) had a significant lower gain compared to controls while the other patients did not differ. In contrast, fast vergence to step targets remained unimpaired (acceleration). Smooth pursuit to step-ramp targets was impaired, with increased latency, decreased initial acceleration and reduced gain. Smooth pursuit eye movement gain to sinusoidal targets was significantly reduced. Similar to vergence eye movements to sinusoidal targets, patients with vermal lesions had a lower smooth pursuit gain while the other patients did not differ from controls. We propose that (1) the cerebellum is involved in the processing of vergence eye movements, (2) the cerebellar vermis plays an important role in executing vergence eye movements and (3) neural control of fast and slow vergence appears to be separated in the cerebellum.

Anterior and superior lateral occipito-temporal cortex responsible for target motion prediction during overt and covert visual pursuit

In smooth-pursuit eye movements (SPEM) with gain close to one, SPEM should be controlled mainly by prediction of target motion because retinal slip is nearly zero. We investigated the neural mechanisms of visual-target prediction by the three fMRI experiments. (1) Overt pursuit task: subjects pursued a sinusoidally moving target which blinked (blink condition) or did not blink (continuous condition). (2) Covert pursuit task: subjects covertly pursued the same target with eyes gazed at fixation point. (3) Attend-to-stationary target task: subjects brought attention on a stationary target with eyes gazed at fixation point. In the overt pursuit task, the SPEM gain and the delay in the blink condition were not very different from the continuous condition, indicating good prediction of the blinking target motion. Activities in the dorsolateral prefrontal, precentral, medial superior frontal, intraparietal, and lateral occipito-temporal cortexes increased in the blink-continuous subtraction. The V1 activity decreased for this contrast. In the covert pursuit task, only the anterior/superior LOTC activity remained in the blink-continuous subtraction. In the attend-to-stationary target task, the blink-continuous subtraction elicited no activation. Consequently, the a/sLOTC activity is responsible for target prediction rather than motor commands for eye movements or just target blinking such as visual saliency.

Smooth pursuit and antisaccade eye movements in siblings discordant for schizophrenia

Smooth pursuit eye movement (SPEM) and antisaccade deficits have been proposed as endophenotypes in the search for schizophrenia genes. We assessed these measures in 24 schizophrenia patients, 24 of their healthy siblings, and 24 healthy controls closely matched to the siblings. Between-group differences were assessed using a random effects regression model taking into account the relatedness between patients and siblings. Patients showed reduced SPEM gain, increased frequency of saccades during pursuit, increased antisaccade error rate, and reduced antisaccade gain compared to controls. Siblings performed intermediate, i.e. between patients and controls, on most measures, but were particularly characterised by reduced antisaccade gain. SPEM gain at one target velocity was significantly correlated between patients and siblings, highlighting the necessity of taking into account within-family correlations in the statistical analysis of between-group differences. It is concluded that subtle SPEM and antisaccade deficits are observed in clinically unaffected siblings of schizophrenia patients; these deficits may be useful markers of genetic liability to schizophrenia.

Poor performance in smooth pursuit and antisaccadic eye-movement tasks in healthy siblings of patients with schizophrenia

This study examines the area of eye movement dysfunctions as an indicator of vulnerability to schizophrenia. Eye movement performance was investigated with three different paradigms: Smooth Pursuit Eye Movements (SPEM); Visually Guided Saccades (VGS); and Antisaccades (AS) in 21 clinically stable patients with schizophrenia, 21 of their healthy, biological full siblings and 21 healthy control subjects. The three groups did not differ on VGS performance, whereas both patients and their siblings showed lower SPEM gain, an increased catch-up Saccades (CUS) rate, reduced AS accuracy and an increased number of AS errors in comparison to control subjects. In addition, patients with schizophrenia exhibited increased AS latency. Among the patients with schizophrenia, eye movement abnormalities did not correlate with age, gender, clinical state or duration of illness. These data suggest that abnormalities of SPEM and AS may represent neurobiological markers of the vulnerability to schizophrenia in individuals at high genetic risk for the disease.

Visual–vestibular interaction in progressive supranuclear palsy

We measured the stability of gaze during horizontal head rotations at 1–3 Hz in four patients with progressive supranuclear palsy (PSP), while they viewed a stationary target. Median gain of compensatory eye movements was 0.94, similar to control subjects. During rotation in darkness, median gain of vestibulo-ocular reflex (VOR) was 0.88, similar to controls. Conversely, the median gain of smooth-pursuit eye movements at 1.0 Hz was 0.23, lower than controls. A simple superposition model of smooth pursuit and the VOR could not account for the observed gaze stability during fixation. Our results are further evidence that a visually mediated mechanism, independent of smooth pursuit, optimizes eye movements to compensate for head rotations.

滑動性追従眼球運動に対する視運動性刺激の加重効果

In seven normal subjects, smooth pursuit eye movements (SPEM), elicited by sinusoidal spot target oscillation, were measured with various backgrounds : the spot target was presented, (1) in darkness (dark), (2) with a stationary textured background (textured), (3) with a moving textured background which was phase-locked to the spot target oscillation at a background/spot velocity ratio of 0.5, 0.75, 1.0 (coupled), 1.25 and 1.5. Spot target oscillation frequencies ranging from 0.2 to 1.6 Hz and peak velocities ranging from 19 to 150 deg/s were employed. Eye movements were measured by a video-based image analyzer (ISCAN system). From the results, compared with the “dark” condition, SPEM gain increased on the “coupled” condition and decreased on the “textured” condition. The influence of background on SPEM gain was significant at higher frequencies and higher peak velocity oscillations, in which the subject failed to continuously keep the target on the fovea because of the low SPEM gain. However, SPEM phase delay were similar for “dark”, “textured” and “coupled” conditions. Since the responses during “coupled” and “textured” conditions are most likely elicited by rapid-rise optokinetic reflex (OKR) interaction, we conclude that the SPEM system is similar to the rapid-rise OKR system. When a phase-locked textured background was presented, “the velocity ratio of 1.0 (coupled)” condition was most prominent in the SPEM gain, i.e. “the velocity ratio of 1.25 and 1.5” conditions never exceeded the “coupled” condition despite the faster background movement. This indicates that optokinetic stimulus (OKS) in the peripheral visual field may be neglected as a driving source of eye movement response when the OKS velocity differed from spot target velocity and only OKS with a velocity equal to the spot target may register in the peripheral visual field.

滑動性追従眼球運動および視運動性眼反射の受動的反応の比較

In 7 healthy subjects, horizontal smooth pursuit eye movements (SPEM) and horizontal optokinetic ocular reflex (OKR) were measured in the dark under the passive attitude which subjects tried to fixate at the center of a screen (passive SPEM and passive OKR). A sinusoidal spot target oscillation and a sinusoidal narrow-band (7 deg bandwidth in vertically) pattern oscillation were employed to elicit passive SPEM and passive OKR, respectively. The pattern consisted of randomly arranged fine dots. For the control, SPEM was elicited by following the spot target actively (active SPEM). Nine sinusoidal oscillations with frequencies ranging from 0.2 to 1.6 Hz and peak velocities ranging from 19 to 150 deg/s were employed. Passive OKR was clearly demonstrated, and the velocity gain of passive OKR was slightly lower than that of active SPEM under frequencies less than 0.8 Hz and was similar at 1.6 Hz. Common frequency-phase profiles were observed between passive OKR and active SPEM. However, the velocity gain of passive SPEM was much lower than that of passive OKR and depended on the amplitude of target oscillation i.e. the lower amplitude provided a higher gain. We concluded that poor response of the passive SPEM and amplitude dependency of the passive SPEM response was caused by the absence of assistance from the voluntary saccade in the passive attitude. The SPEM response for a small moving target may depend on the voluntary saccade function which maintains a target at the fovea while supplementing SPEM.