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To examine patterns of executive and oculomotor control in a group of both boys and girls with attention-deficit/hyperactivity disorder (ADHD).Cross-sectional study of 120 children aged 8 to 12 years, including 60 with ADHD (24 girls) and 60 typically developing controls (29 girls). Oculomotor paradigms included visually guided saccades (VGS), antisaccades, memory-guided saccades, and a go/no-go test, with variables of interest emphasizing response preparation, response inhibition, and working memory.As a group, children with ADHD demonstrated significant deficits in oculomotor response preparation (VGS latency and variability) and response inhibition but not working memory. Girls, but not boys with ADHD, had significantly longer VGS latencies, even after controlling for differences in ADHD symptom severity. The ADHD subtypes did not differ on response preparation or inhibition measures; however, children with the Inattentive subtype were less accurate on the working memory task than those with the Combined subtype.Sex differences in children with ADHD extend beyond symptom presentation to the development of oculomotor control. Saccade latency may represent a specific deficit among girls with ADHD.

Fragile X and Turner syndromes are two X-chromosome-related disorders associated with executive function and visual spatial deficits. In the present study, we used ocular motor paradigms to examine evidence that disruption to different neurological pathways underlies these deficits. We tested 17 females with fragile X, 19 females with Turner syndrome, and 40 females with neither disorder who comprised the comparison group. Group differences emerged for both the fragile X and Turner syndrome groups, each relative to the comparison group: Females with fragile X had deficits in generating memory-guided saccades, predictive saccades, and saccades made in the overlap condition of a gap/overlap task. Females with Turner syndrome showed deficits in generating memory-guided saccades, but not during either the predictive saccade or gap/overlap task. Females with Turner syndrome, but not females with fragile X, showed deficits in visually guided saccades and anti-saccades. These findings indicate that different brain regions are affected in the two disorders, and suggest that different pathways lead to the similar cognitive phenotypes described for fragile X and Turner syndromes.

Torsional eye movements are rotations of the eye around the line of sight. Measuring torsion is essential to understanding how the brain controls eye position and how it creates a veridical perception of object orientation in three dimensions. Torsion is also important for diagnosis of many vestibular, neurological, and ophthalmological disorders. Currently, there are multiple devices and methods that produce reliable measurements of horizontal and vertical eye movements. Measuring torsion, however, noninvasively and reliably has been a longstanding challenge, with previous methods lacking real-time capabilities or suffering from intrusive artifacts. We propose a novel method for measuring eye movements in three dimensions using modern computer vision software (OpenCV) and concepts of iris recognition. To measure torsion, we use template matching of the entire iris and automatically account for occlusion of the iris and pupil by the eyelids. The current setup operates binocularly at 100 Hz with noise

Background: We used ocular motor paradigms to examine whether or not saccades are impaired in individuals with high functioning autism (HFA). Methods: We recorded eye movements in patients with HFA (n=11), and in normal adolescents (n=11) on anti-saccade, memory-guided saccade (MGS), predictive saccade and gap/overlap tasks. Results: Compared with the normal subjects, patients with HFA had (1) a significantly higher percentage of directional errors on the anti-saccade task (63.2% versus 26.6%), (2) a significantly higher percentage of response suppression errors on a MGS task (60.3% versus 29.5%) and (3) a significantly lower percentage of predictive eye movements on a predictive saccade task. They also showed longer latencies on a MGS task and for all conditions tested on a gap/null/overlap task (fixation target extinguished before, simultaneously, or after the new peripheral target appeared). When the latencies during the gap condition were subtracted from the latencies in the overlap condition, there was no difference between patients and normals. Conclusions: Abnormalities in ocular motor function in patients with HFA provide preliminary evidence for involvement of a number of brain regions in HFA including the dorsolateral prefrontal cortex (dlPFC) and the frontal eye fields (FEFs) and possibly the basal ganglia and parietal lobes.

Objective To assess saccadic eye movements in boys with Tourette syndrome (TS) with and without attention-deficit hyperactivity disorder (ADHD), comparing performance with that of an age-matched group of male controls. Method Three different saccade tasks (prosaccades, antisaccades, and memory-guided saccades) were used to examine functions necessary for the planning and execution of eye movements, including motor response preparation, response inhibition, and working memory. The study included 14 boys with TS without ADHD (TS-only), 11 boys with TS and ADHD (TS+ADHD), and 10 male controls. Results Latency of prosaccades was prolonged in boys with TS (both with and without ADHD) compared with controls. Variability in prosaccade latency was greater in the groups of boys with TS+ADHD compared with both the TS-only and control groups. Response inhibition errors on both the antisaccade task (directional errors) and memory-guided saccade task (anticipatory errors) were increased in boys with TS+ADHD compared with those with TS-only. There were no significant differences among the three groups in accuracy of memory-guided saccades. Conclusions Oculomotor findings suggest that TS is associated with delay in initiation of motor response as evidenced by excessive latency on prosaccades. Signs of impaired response inhibition and variability in motor response appear to be associated with the presence of ADHD.

We review here the eye movements in patients with Huntington's disease (HD), concentrating upon saccades as they show the most prominent abnormalities. Inability to suppress reflexive glances to suddenly appearing novel visual stimuli and delayed initiation of voluntary saccades, including predictive saccades, are early and consistent findings. These two abnormalities can be interpreted in the context of a model, based upon the idea that the frontal lobes and basal ganglia contribute more to the control of voluntary than to reflexive types of saccades. Most patients eventually also show slow saccades but they are most prominent when the disease is early-onset. Slowing of saccades may reflect involvement of both the higher-level cerebral centers that trigger saccades and the areas in the brain stem that produce premotor saccade commands. The study of eye movements in HD has led to a fruitful interaction between basic science and clinical investigation, and has served as a paradigm for examining higher-level defects in saccadic eye movement control in patients with various degenerative, neurological diseases or with focal cerebral hemispheral lesions.

Sensory input from the semicircular canals (SCC) and otolith organs is centrally combined with signals from other sensory modalities to continuously update the internal estimate of self-motion. Constant velocity vertical on-axis rotation leads to decay of the nystagmus response from the horizontal SCC and of perceived angular velocity (PAV), and when the rotation stops, a similar oppositely directed post-rotatory response occurs. Case reports and electrical stimulation studies suggest an involvement of the temporo-peri-Sylvian vestibular cortex in generating the PAV. Here, we transiently inhibited the right superior temporal gyrus (STG) by use of continuous theta-burst stimulation (cTBS) and predicted an accelerated decay of PAV compared to controls (n = 5 control session first, n = 1 cTBS session first). Constant velocity (100°/s) vertical on-axis rotations were applied over 75 s before (1 block) and after (3 blocks) cTBS over the right STG in six subjects. Breaks between the rotations (75 s) were initiated by abrupt stops. By use of a rotating potentiometer, subjects indicated the PAV during and after the chair rotations. Simultaneously eye positions were recorded using a scleral search coil. One subject was excluded for per-rotary analysis. Early after cTBS, the post-rotary PAV decay time constant (DTC) was significantly (9.4 ± 5.7 vs. 13.6 ± 5.9 s; p = 0.049) reduced (no directionality to this effect observed). Overall, post-rotary PAV showed a trend toward shortened DTC compared to the control trials (p = 0.086) in the first 25 min after cTBS, while per-rotary PAV was not significantly changed. Per-rotary and post-rotary aVOR DTC were not significantly changed after cTBS (p > 0.05). These findings support the hypothesis that the right STG is involved in mediating self-motion perception and can be modulated by cTBS.

Studies of eye movements in patients with Huntington's disease (HD) have suggested that frontal lobe-basal ganglia structures are more involved in HD than the parietal lobes. To test this hypothesis further we compared the ability of HD patients and normal subjects to direct “covert” visual attention, using saccade latency and thumb press reaction time tasks that have been shown to be sensitive to parietal lobe dysfunction. Subjects were instructed to move their eyes or to press a button when a peripheral target was illuminated. The peripheral stimulus appeared at various intervals after the appearance of a central arrow(s) that pointed in the direction of the target (valid cue), in the opposite direction (invalid cue), or pointed simultaneously in both directions (neutral cue). For both saccade and thumb press paradigms, the difference in the latencies for trials with invalid and valid cues was the same in HD patients and normals. These findings suggest that the ability to direct visual attention is normal in HD and are compatible with the hypothesis that in HD, frontal-basal ganglia circuits are more affected than parietal lobe pathways.

Previously we have shown that repetitive predictive saccades to alternating visual targets are mediated by an internal clock. That is, when subjects track a periodic visual stimulus alternating at a high rate (a small inter-stimulus interval, ISI, of 500 or 833ms), they use an internal estimate of stimulus timing to pre-program the eye movement timing. Auditory pacing tones at the same rate also generate predictive saccades. It is natural to ask if an identical internal clock is used to generate the predictive saccades in each case. We hypothesized that if subjects can use auditory information to establish an internal estimate of stimulus timing—as we demonstrated can be done with visual targets—then the distributions of predictive inter-saccade intervals should demonstrate the well-known “Scalar Property” for either Auditory Cued or Visual Cued stimuli: inter-saccade interval histograms should be almost identical when each is divided by its mean. However, when making reactive saccades to a pacing stimulus (at a low rate), there should be a difference in the timing statistics between Auditory and Visual pacing, due to differences in sensory processing. We report here that the variances of inter-saccade intervals at three predictive pacing rates (ISIs of 500, 833, and 1000ms) are equivalent, whereas the variance for Auditory Cued Pacing was greater than that for Visual Cued Pacing during reactive saccades at two reactive pacing rates (ISIs of 1667 and 2500ms). When the inter-saccade interval histograms at the predictive pacing rates were normalized, the distributions were nearly identical for both Visual and Auditory Cued Pacing, which means that the Scalar Property holds for predictive saccades from either pacing stimulus. These results suggest that (1) an internal timing reference (clock) can be established by either auditory or visual information and (2) during predictive tracking the variability in saccade timing is due to the variability in the internal timing representation, while during reactive tracking the variability in saccade timing depends on the sensory modality used to trigger the saccades.

Predictive saccade tracking (targets stepping back and forth at frequencies of 1.25 = 1.0 Hz) and self-paced saccades between two stationary targets were measured in patients with cerebellar degeneration and in normal subjects. Cerebellar patients produced similar predictive latencies and generated the same percentage of predictive saccades as did normal subjects. Only the variability in the self-paced saccade paradigm was different between the groups.

We have investigated the effects of mental set on predictive capabilities using a saccade square-wave tracking paradigm with ten normal subjects, comparing three amplitudes (10, 20, and 40 degrees ) and five inter-stimulus intervals (ISIs) (400, 500, 625, 1000, and 2000 ms). Subjects were instructed simply to "follow the lights" (passive, reflexive instruction) or explicitly "move your eyes in time with the lights" (active, volitional instruction). Saccades were defined as reflexive (latency100 ms), predictive (-200 mslatency100 ms), or anticipatory (latency-200 ms). We also calculated arrival time (saccade latency+saccade duration). Instructions had a striking effect on predictive performance. The effects were greatest with the longest ISIs (1000 and 2000 ms) and the largest target displacement (40 degrees ). With the active instruction there were more predictive and anticipatory saccades and with the passive instruction more reflexive saccades. Furthermore, with the active instruction subjects could take into account the duration of the impending saccade so that the eyes would arrive closer to the appearance of the target no matter what the amplitude of the required saccade. In sum, cognitive set, as determined by the specific instructions given to the subject, has a striking effect on predictive saccade behavior, which has important implications for interpreting physiological and imaging correlates of predictive behavior in normals and in patients with neurological disease.

For the neurologist, examination of eye movements at the bedside is a traditional mainstay of anatomic localization and often provides diagnostic certainty in complicated clinical problems. For the basic neuroscientist, recording and analysis of eye movements, both in behaving monkeys and in normal humans, have become powerful tools to understand normal ocular motor control and to probe higher-level cerebral mechanisms that underlie attention, memory, and decision making. The antisaccade task is an example of such a useful eye movement paradigm.1–3⇓⇓ In this task, the subject has to cancel willfully a “reflexive” saccade to a suddenly appearing visual stimulus (i.e., …

Background: Prevailing hypotheses suggest that attention deficit hyperactivity disorder (ADHD) is secondary to dysfunction of motor intentional systems mediated by prefrontal circuitry. Oculomotor paradigms provide a mechanism for examining and localizing dysfunction at the interface between movement and cognition.Objective: Three different saccade tasks (reflexive or prosaccades, antisaccades, and memory-guided saccades) were used to examine functions necessary for the planning and the execution of eye movements, including motor response preparation, response inhibition, and working memory.Methods: The study included 19 children with ADHD, divided into two groups: a group of 8 children on methylphenidate at the time of testing and a group of 11 children not taking any psychoactive medication. Results from the two groups were compared with those from 25 age- and gender-matched normal control children.Results: Both groups of children with ADHD made significantly more directional errors than did controls on the antisaccade task and significantly more anticipatory errors than did controls on the memory-guided saccade task, findings that are consistent with deficits in response inhibition. There were no significant differences in prosaccade latency, although unmedicated children with ADHD showed significantly greater variability in latency on the prosaccade task than did controls. On the memory-guided saccade task there were no significant differences in saccade accuracy; however, unmedicated children with ADHD showed longer saccade latency than did either controls or medicated children with ADHD.Conclusions: Oculomotor findings suggest that deficits in prefrontal functions, in particular response inhibition, contribute to behavioral abnormalities observed in ADHD. Findings also suggest that the administration of methylphenidate is associated with improvements in the consistency of motor response. Although there were no observed improvements in response inhibition with methylphenidate, conclusions await a design in which subjects complete testing both on and off medication.

We compared saccadic eye movements in 21 patients with Huntington's disease (HD) and 21 normal subjects. In a predictive tracking task, HD patients were unable to anticipate normally the timing and location of a visual target that alternated its position predictably (+/- 10 degrees, 0.5 Hz; mean latency of +170 msec in HD and -78 msec in normal subjects). HD patients and normal subjects, however, showed comparable decreases in saccade latency (110 msec in HD, 124 msec in normal subjects) when the fixation target was turned off 200 msec before (gap task) versus 200 msec after (overlap task) the appearance of an unexpected peripheral stimulus. Taken together, these findings support the idea that HD patients show greater defects in initiating internally generated than in initiating externally triggered saccades. This dichotomy is likely due to involvement of frontal lobe--basal ganglia structures in HD, with relative sparing of parietal--superior collicular pathways.

Optokinetic nystagmus (OKN), a periodic sawtooth movement of the eyes, is maximally elicited when a subject's entire visual field is moving. The most appropriate stimulus for the generation of OKN is an optokinetic drum that completely surrounds the subject. Such drums tend to be massive and can only be accelerated rapidly with a powerful motor. This report describes construction details of a drum designed especially to minimize moment of inertia and cost as well.

Eye movements induced by head rotation were studied in 6 patients in acute coma, 4 patients in a persistent vegetative state, and 6 healthy, alert control subjects. Results from control subjects suggest that the oculocephalic response in the supine position is principally a vestibulo-ocular reflex. A position-step rotation of the head produced an initial oppositely directed eye movement, followed by a drift of the eyes back toward midline with a negative exponential time course. The time constant of this drift was greater than or equal to 10 seconds in control subjects but less than or equal to 1.5 seconds in unconscious patients and less than or equal to 0.5 seconds in vegetative patients. The rapid drift back of the eyes in unresponsive patients implies dysfunction of reticular and, possibly, cerebellar connections; the rate of this drift may indicate the severity and extent of brain injury. Sinusoidal head rotation produced slow and quick phases of nystagmus in normal subjects. Quick phases were absent in patients in acute coma; although present in vegetative patients, the quick phases did not keep the eyes close to primary position, as was the case in control subjects.

In five normal subjects, we analyzed uncalled for torsion (blips) during and after horizontal and vertical saccades. Torsion was defined as movement out of Listing's plane. During horizontal saccades in downward gaze the abducting eye extorted and the adducting eye intorted. The direction of the blips reversed in upward gaze. Peak torsional amplitudes (up to 1–2 deg) were always reached during saccades; drifts back to Listing's plane outlasted the saccades. Torsion of the extorting eye was larger than that of the intorting eye, producing a transient positive cyclovergence. Torsion and cyclovergence evoked by vertical saccades were also stereotyped in each eye, but showed idiosyncratic differences among subjects. We conclude that Listing's law is violated during saccades. Transient saccade-evoked torsion might reflect properties of the three-dimensional velocity-to-position integrator and/or the ocular plant.

The maximum smooth pursuit eye velocity was determined in five human subjects. Eye movements were recorded with the d.c.-coupled EOG. On each trial the target moved in a ramp, at a constant velocity between 10 and 200 deg/sec. In four subjects eye velocity was approximately 90% of target velocity up to a target velocity of 100 deg/sec. Eye velocity then saturated with a large variability from trial to trial (standard deviation 16 deg/sec). The fifth subject had eye velocities only 60% of these values.

Article abstract-Eye movements were recorded from 20 mildly affected patients with Huntington’s disease (HD) who were divided into two groups, 10 patients with onset of symptoms before age 30 and 10 with onset of symptoms after age 30. In the younger onset group (HD 30) had peak saccade velocities lower than 300 deg/sec. Latencies for volitional saccades were greater than normal in the HD > 30 group, but were normal for the HD 30 group had an affected mother. These findings suggest that the pathophysiology of the slow saccades, initiation deficit, and excessive distractibility in HD are different. NEUROLOGY 1988;38427-431 In a recent study of eye movements in mildly affected patients with Huntington’s disease (HD), we found abnormalities of both the initiation of saccades as well as the ability to hold steady fixation.’ Most patients showed an increase in saccade latencies that was greater for saccades made on command (voluntary saccades) than for saccades made to the sudden appearance of a visual stimulus (reflexive saccades). All patients showed excessive distractibility; they had difficulty in suppressing a saccade to a suddenly appearing visual target even though they were instructed either to maintain straight-ahead fixation or to make a saccade in the direction opposite to the visual target. We attributed these abnormalities to involvement of the frontal eye fields or basal ganglia in HD. In the present study, we report further abnormalities of eye movements-saccade slowing andsaccade dysmetria-in the same group of patients, and compare these findings with their deficits in saccade initiation and in holding steady fixation. Slow saccades have been noted in patients with HD with a reported prevalence of 18% to 100%.2-10 While one study did seem to show a correlation between the age of the patient and the saccade ~elocity,~ few attempts have been made to correlate saccade slowing with other saccade abnormalities in HD or with patient age or severity or duration of illne~s.~J~J~ In contrast to the saccade initiation and the fixation deficits, which have been attributed to involvement of the basal ganglia or cerebral hemispheres, saccade slowing has usually been attributed to direct pathologic involvement of the intrinsic brainstem structures that generate the immediate premotor commands for saccadic eye movement~.~-~ Accordingly, to better understand the eye movement abnormalities in HD, we compared disor

We studied eye movements in 50 patients with Huntington's disease. Fixation was impaired in 73% of patients; such individuals had difficulty in suppressing saccades toward novel visual stimuli. Impaired initiation of saccades was manifest by increased reaction time (89%) and inability to make a saccade without head movement (89%) or blink (35%). Saccades and quick phases of nystagmus were slowed in 62%. Smooth pursuit was abnormal in 60%, and vergence in 33%. The vestibulo-ocular reflex and the ability to hold eccentric gaze were preserved even late in the disease.