Saccadic Abnormalities Research Articles

Perioperative vestibular assessment and testing

Vestibular disorders can be difficult to accurately diagnose and manage. A careful history and focused physical examination are typically adequate to establish a diagnosis and initiate medical treatment. Vestibular testing is an important component of the work-up, but it is particularly essential for patients being considered for surgical intervention for a vestibular disorder, where the testing can be used to more definitively confirm a suspected diagnosis and to determine baseline vestibular organ function. In this article, we will first briefly review key components of the history and physical examination of patients with vestibular complaints. We will then discuss the most commonly used vestibular tests and their role in the preoperative assessment of patients undergoing vestibular surgery, including nystagmography, caloric testing, rotary chair testing, video head impulse testing, and vestibular evoked myogenic potential testing.

Persistent visual disturbances after concussion.

Ocular dysfunction, including eyemovement defects, has been documented in up to 69% of patients with concussion. However, standard sports-related concussion assessment protocols do not typically include any clinical examination of the ocular system. The aim of this article is to inform general practitioners (GPs) about ocular defects associated with concussion, identify test procedures and highlight the important role of GPs within the concussion paradigm. Ocular dysfunction that commonly occurs with concussion includes abnormalities of accommodation, convergence, saccades and smooth pursuits. This may cause blurred vision, double vision, ocular pain and difficulty with close work. Symptoms can severely affect daily work, school or play activities. Patients complaining of extended ocular symptoms following concussion should be referred to an ophthalmologist for a complete ocular assessment.

Saccadic Direction Errors are Associated with Impulsive Compulsive Behaviours in Parkinson's Disease Patients.

Fifteen individuals with Parkinson's disease (PD) and impulsive compulsive behaviours (PD+ICB) were compared to 15 PD patients without ICBs (PD-ICB) and 15 healthy controls (HC) on a pro-saccades and an anti-saccades task to assess if ICBs are associated with distinct saccadic abnormalities. PD+ICB made shorter saccades than HC and more direction errors in the anti-saccades task than PD-ICB and HC, suggesting that patients with ICBs have greater difficulty in suppressing automatic saccades towards a given target. Saccadic assessment has the potential to evolve into a marker to guide therapeutic decisions in patients at risk of developing ICBs.

Saccadic eye movements in different dimensions of schizophrenia and in clinical high-risk state for psychosis

BackgroundOculomotor dysfunction is one of the most replicated findings in schizophrenia. However the association between saccadic abnormalities and particular clinical syndromes remains unclear. The assessment of saccadic movements in schizophrenia patients as well as in clinical high-risk state for psychosis individuals (CHR) as a part of schizophrenia continuum may be useful in validation of saccadic movements as a possible biomarker.MethodsThe study included 156 patients who met the ICD-10 criteria for schizophrenia: 42 individuals at clinical high-risk-state for psychosis and 61 healthy controls. The schizophrenia patients had three subgroups based on the sum of the global SAPS and SANS scores: (1) patients with predominantly negative symptoms (NS, n = 62); (2) patients with predominantly positive symptoms (PS, n = 54) (3) patients with predominantly disorganization symptoms (DS, n = 40). CHR subjects were characterized by the presence of one of the groups of criteria: (1) Ultra High Risk criteria, (2) Basic Symptoms criteria or (3) negative symptoms and formal thought disorders. Horizontal eye movements were recorded by using videonystagmograph. We measured peak velocity, latency and accuracy in prosaccade, antisaccade and predictive saccade tasks as well as error rates in the antisaccade task.ResultsSchizophrenia patients performed worse than controls in predictive, reflexive and antisaccade tasks. Oculomotor parameters of NS were different from the other groups of patients. Latencies of predictive and reflexive saccades were significantly longer than in controls only in the NS group. The accuracy of predictive saccades was also different from controls only in the NS schizophrenia group. More prominent loss of accuracy of reflexive saccades was found in the DS group and it significantly differed from the one in other groups. Participants from DS group made more errors in antisaccade task compared to NS and PS groups. CHR subjects performed worse than controls as measured by the accuracy of reflexive saccades and antisaccades.ConclusionsThe study confirms the existence of different relations between the symptom dimensions of schizophrenia and saccades tasks performances. Saccadic abnormalities were revealed in the clinical (schizophrenia) and pre-clinical (clinical high risk) populations that provide further evidence for assessing saccadic abnormalities as a possible neurobiological marker for schizophrenia.

Saccades in Parkinson's disease: Hypometric, slow, and maladaptive.

Visuomotor impairments, such as hypometria of visually guided saccades, are common in Parkinson's disease (PD). Explaining the mechanistic underpinning of such abnormal voluntary (eye) movements can provide insights into the pathophysiology of limb movement disorders in PD. We measured visually guided saccades in 20 PD patients using quantitative high-resolution oculography. The experiments source to determine whether common motor deficits in PD, such as those affecting visually-guided saccades reflect excessive inhibition of the superior colliculus or rather involvement of brainstem saccade generators. We found slowing, interruptions, and curvatures in the saccade trajectory. The curvature not only reflected the mismatch in the velocity of relatively slower vertical (compared to horizontal) saccades, but could be due to aberrant activation of the superior colliculus. The irregularities in the saccade trajectory and slowing were prominent in the vertical direction. We suggest that abnormal saccades in PD not only reflect abnormal tectal function, but also suggest abnormal oscillatory behavior in the reciprocally innervating circuit of excitatory and inhibitory burst neurons. Impaired function of excitatory and inhibitory burst neurons causing maladaptive feedback and premature activation of the superior colliculus can cause irregularity in saccade trajectory.

The King-Devick test in an outpatient concussion clinic: Assessing the diagnostic and prognostic value of a vision test in conjunction with exercise testing among acutely concussed adolescents

ObjectiveThis study investigated the diagnostic and prognostic value of the King-Devick (K-D) test in conjunction with treadmill testing in adolescents after sport-related concussion (SRC) in an outpatient concussion management clinic without baseline measures. DesignProspective cohort. MethodsThe K-D test was administered pre- and post-exercise on a graded treadmill test to acutely concussed (AC, <10 days from injury, n = 46, 15.4 ± 2.1 years) participants for 2 clinic visits (1 week apart) and to matched controls (MC, n = 30, 15.8 ± 1.4 years) for 2 visits (1 week apart). Initial K-D test times were compared between MC and AC. Changes in times from pre- to post- exercise during a treadmill test were compared for MC and AC and from Visit 1 to Visit 2. Smooth pursuits and repetitive saccades were compared with initial visit K-D test performance. ResultsComparison of pre-exercise K-D test times at Visit 1 distinguished MC from AC (46.1 ± 9.2 s vs. 53.7 ± 13.0 s, p = .007). Comparison of pre- and post-exercise K-D test times revealed significant improvements for MC (46.1 ± 9.2 s vs. 43.1 ± 8.5 s, p < .001) and AC who recovered by Visit 2 (Fast Recovery Group [FRG], n = 23, 50.4 ± 10.0 s vs. 47.3 ± 9.8 s, p = .002). No significant difference was seen in pre- and post-exercise K-D test times on Visit 1 for AC who took longer than 2 weeks to recover (Slow Recovery Group [SRG], n = 23, 57.0 ± 15.0 s vs. 56.0 ± 16.3 s, p = .478). At Visit 1, AC had more abnormal smooth pursuits than MC (17% vs. 3%, non-significant, p = .064). AC, however, had significantly more abnormal repetitive saccades than MC (37% vs. 3%, p = .001) and AC with abnormal repetitive saccades took significantly longer to complete the Visit 1 pre-exercise K-D test than AC with normal repetitive saccades (58.6 ± 16.0 s vs 50.8 ± 10.2 s, p = .049). ConclusionThe study supports utility of the K-D test as part of outpatient concussion assessment. Lack of improvement in K-D test performance after an exercise test may be an indicator of delayed recovery from SRC.

P22. Long-term course of progression of clinical ocular motor signs in progressive supranuclear palsy

Aim To investigate the natural course of progression of ocular motor signs in patients with progressive supranuclear palsy (PSP). Methods 114 patients with a possible or probable PSP following NINDS-SPSP criteria seen at the Department of Neurology and the German Center for Vertigo and Balance Disorders (LMU, Munich) were included in this retrospective study. All patients underwent a structured neuro-ophthalmological testing by a orthoptist at initial diagnostic evaluation, 35 patients several times during their course of disease. The following ocular motor signs were extracted from the charts: Saccadic slowing (with normal range of movement) and saccadic paresis (loss of saccade initiation or severe saccadic hypometria) in vertical and horizontal direction, range of up- and downward as well as horizontal ocular motility during smooth pursuit in mm, presence of square wave jerks, function of the vestibulo-ocular reflex on head impulse testing. Clinical ocular motor signs were analysed in all patients in relation to the duration of disease at the time of examination (based on the medical history of the first sign indicative for PSP) or longitudinally during the course of disease in a subgroup of 35 patients. Results In the whole group of PSP patients saccadic abnormalities showed the following distribution over time: at 1 year of disease duration 10% showed only saccadic slowing on upgaze, 40% on up- and downgaze, 21% saccadic paresis on upgaze and 29% complete vertical saccade paresis; at 2 years the proportion of vertical saccade paresis was 32%, at 3 years 65% and at 4 years 82%. Progression of horizontal saccade paresis was slower (year 1: 6%, year 2: 9%, year 3: 21%, year 4: 41%). The subgroup of patients with longitudinal follow up showed a similar tendency. Ocular motility in this group decrease by a mean of 1.5 mm/a on upgaze, 1.6 mm/a on downgaze and 1.4 mm/a on horizontal gaze. The degree of motility loss on up- and downgaze over time showed a good correlation (R2 = 0.71). Conclusion Ocular motor examination can be used as a robust marker of disease progression. Variability between patients however is considerable. Prospective clinical and apparative quantification of ocular motor markers in well-characterized cohorts of PSP patients is needed.

B-19. What does eye tracking tell us about neurological patients?

Performances of experimental oculomotor (saccade) paradigms have provided insights into the pathophysiology of neurological patients. However, to investigate the behavioral correlates and the physiological significance of these saccade abnormalities in daily life, we need to look into the difficulty patients actually experience in a more ecological setting. We review studies in which the eye tracking methodology was applied to normal subjects, e.g., when they viewed line drawings presented on a monitor screen to memorize them for later recall. In addition, simultaneous recording of hand (finger) movements with gaze movements allows us to evaluate how the eye and hand coordinates in performing daily actions. For example, eye-hand coordination was studied whey subjects wrote letters on a touch panel, and during a trail making test or in a task simulating finger-nose test. Even eye-voice coordination can be studied by recording the voice of subjects as they read aloud a text. Investigations in neurological patients such as Parkinson’s disease and cerebellar ataxia holds promise for giving insights into how saccade abnormalities observed in oculomotor tasks contribute to their clinical symptoms. They can also be used to quantitatively evaluate motor symptoms of neurological patients from a new perspective.

Correlating the King-Devick Test With Vestibular/Ocular Motor Screening in Adolescent Patients With Concussion: A Pilot Study.

Background:The King-Devick (K-D) test is a rapid number-naming task that has been well validated as a sensitive sideline performance measure for concussion detection. Patients with concussion take significantly longer to complete the K-D test than healthy controls. Previous research suggests that ocular motor deficits, specifically saccadic abnormalities, may be an underlying factor for the prolonged time. However, these findings have not been studied at length.Hypothesis:K-D testing time of concussed adolescents at the initial clinical concussion visit will positively correlate with vestibular/ocular motor screening (VOMS) total scores.Study Design:Case series.Level of Evidence:Level 3.Methods:A total of 71 patient charts were retrospectively analyzed between October 1, 2016, and January 31, 2017. Included charts consisted of patients between the ages of 10 and 18 years with a diagnosis of concussion and who had completed K-D testing and VOMS assessment at the initial physician visit. Univariate correlation between K-D testing time and the 7 VOMS items was assessed using Pearson correlation coefficients.Results:K-D testing time strongly correlated with all 7 VOMS items (r(69) = 0.325-0.585, P < 0.01). In a linear regression model that accounted for each VOMS item, the convergence (near point) item and the visual motion sensitivity item significantly predicted K-D testing time (β = 0.387, t(63) = 2.81, P < 0.01 and β = 0.375, t(63) = 2.35, P = 0.02, respectively). Additionally, 37.5% of the 24 patients with worsening symptoms after K-D testing freely reported increased visual problems.Conclusion:Our study suggests that prolonged K-D testing times in adolescents with concussion may be related to subtypes of vestibular/ocular motor impairment that extend beyond saccadic abnormalities.Clinical Relevance:Poor K-D testing performance of adolescents with concussion may indicate a range of vestibular/ocular motor deficits that need to be further identified and addressed to maximize recovery.

Vertical nystagmus associated with glutamic acid decarboxylase antibodies responding to cyclophosphamide

Several neurological disorders have been described in patients with autoimmunity associated with GAD antibodies. Among these disorders, nystagmus and oculomotor dysfunction are increasingly recognized, although they have been rarely reported isolated or as the main manifestation of anti-GAD autoimmunity. Moreover, therapeutic approaches for such patients are unclear. Here we present a 44-year-old man with disabling oscillopsia secondary to downbeat nystagmus, abnormal saccades, ocular pursuit and optokinetic nystagmus, as well as mild gait ataxia and cerebellar atrophy associated with high serum GAD antibodies with intrathecal secretion of such antibodies. The patient did not have clinical benefit with plasma exchange, but had a robust symptomatic improvement with cyclophosphamide. We discuss the possible pathogenic role of GAD antibodies in nystagmus and the role of immunotherapy in these patients.

Chapter 16 - Essential tremor and the cerebellum

Essential tremor (ET) is a progressive and highly prevalent neurologic disease. Along with the tremors, mild to moderate gait ataxia and other signs of cerebellar dysfunction may occur (i.e., subtle saccadic eye movement abnormalities and abnormalities of motor timing) as well as cognitive features, some of which may be due to cerebellar dysfunction. Numerous neuroimaging studies indicate the presence of functional, metabolic, and structural abnormalities in the cerebellum of a patient with ET. In tandem with these clinical and imaging studies, which were gathering increasing support for the notion that the cerebellum and/or cerebellar systems seemed to be at the root of ET, a growing postmortem literature is for the first time beginning to identify microscopic abnormalities in the ET brain, most of which are centered on the Purkinje cells and connected neuronal populations, and are likely to be degenerative. In terms of treatment, most of these pharmacotherapeutic agents serve to enhance GABAergic neurotransmission, further bolstering the notion that ET may very well be a disorder with a primary Purkinje cell dysfunction resulting in reduced cerebellar cortical inhibition. Similarly, the interruption of presumably abnormal cerebellar outflow pathways to the thalamus is the mechanism of deep-brain stimulation surgery, which is highly effective in treating ET.

Differences in regional grey matter volumes in currently ill patients with anorexia nervosa.

Neurobiological findings in anorexia nervosa (AN) are inconsistent, including differences in regional grey matter volumes. Methodological limitations often contribute to the inconsistencies reported. The aim of this study was to improve on these methodologies by utilising voxel-based morphometry (VBM) analysis with the use of diffeomorphic anatomic registration through an exponentiated lie algebra algorithm (DARTEL), in a relatively large group of individuals with AN. Twenty-six individuals with AN and 27 healthy controls underwent a T1-weighted magnetic resonance imaging (MRI) scan. AN participants were found to have reduced grey matter volumes in a number of areas including regions of the basal ganglia (including the ventral striatum), and parietal and temporal cortices. Body mass index (BMI) and global scores on the Eating Disorder Examination Questionnaire (EDE-Q) were also found to correlate with grey matter volumes in a region of the brainstem (including the substantia nigra and ventral tegmental area) in AN, and predicted 56% of the variance in grey matter volumes in this area. The brain regions associated with grey matter reductions in AN are consistent with regions responsible for cognitive deficits associated with the illness including anhedonia, deficits in affect perception and saccadic eye movement abnormalities. Overall, the findings suggest reduced grey matter volumes in AN that are associated with eating disorder symptomatology.

Eye movement abnormalities in AQP4-IgG positive neuromyelitis optica spectrum disorder

Background and purposeNeuromyelitis optica spectrum disorder (NMOSD) has been recognized as a disease characterized by severe visual afferent impairment. Abnormal eye movements, as the other important neuro-ophthalmic manifestation of NMOSD, were commonly overlooked. The aim of our study was to describe the ocular motor manifestations of AQP4-IgG positive NMOSD patients, and explore the value of eye movement abnormalities in the evaluation of the disabled disease. MethodsSystemic clinical bedside ocular motor examinations and quantitative horizontal saccadic eye movement assessments were performed in 90 patients with AQP4-IgG positive NMOSD. General disability was evaluated by expanded disability status scale (EDSS). Vision-specific functional status was evaluated by the National Eye Institute-Visual Function Questionnaire (NEI-VFQ 25) and the 10-item neuro-ophthalmic supplement. Brain magnetic resonance imaging (MRI) was acquired in all patients. ResultsIn clinical examination, eye movement abnormalities were found in 38% of NMOSD patients. Abnormalities in the quantitative saccadic test were found in 67% of NMOSD patients, including 48% of patients with clinically normal eye movements. EDSS scores in patients with clinical eye movement abnormality were significantly higher (P<0.001) than those with a normal examination. The 10-item neuro-ophthalmic supplement score was significantly associated with quantitative saccadic eye movement abnormalities (P=0.031). ConclusionsEye movement abnormalities were common in AQP4-IgG positive NMOSD patients, and were associated with general disability and specific visual handicap. The systemic clinical eye movement examination combined with the quantitative saccade test was easy to perform, and could provide additional useful information in evaluating NMOSD.

Prevalence of Oculomotor Dysfunction in Healthy Athletes Preseason: Implications for Concussion in Sport

Background: Measures of oculomotor function are becoming more frequently employed as part of comprehensive concussion assessments. However, performances on many of these oculomotor measures have not been examined in a healthy athletic cohort. The purpose of this study was to characterize performance of university level athletes on a battery of oculomotor tests and identify any potential influence of gender and history of concussion. Methods: 259 healthy university level athletes (males, n = 150; females, n = 109) completed an oculomotor screening battery prior to the start of their competitive season. The battery assessed stereopsis, visual acuity, monocular amplitude of accommodation, near point of convergence, monocular and binocular accommodative facility, vergence facility, positive and negative fusional vergence, and saccades. Athletes also completed the Convergence Insufficiency Symptom Survey (CISS). Results: Three oculomotor tests (stereopsis, convergence, saccades) showed significant differences between male and female athletes at P&lt;0.05, uncorrected. A high percentage of athletes were identified as having oculomotor deficiencies including abnormal acuity (34.2%), vergence infacility (28.6%), abnormal horizontal saccades (21.7%) and accommodative infacility (18.7%). Convergence insufficiency differed by method of assessment, ranging from 11.0-15.7%. Conclusion: A significant proportion of healthy athletes displayed abnormal performance across a variety of oculomotor indices. A history of lifetime concussion (i.e., greater than 12 months prior to study) did not significantly influence oculomotor test performance. Clinicians should be aware of such differences and potential implications associated with postconcussion evaluations.

Developmental visual perception deficits with no indications of prosopagnosia in a child with abnormal eye movements

Visual categories are associated with eccentricity biases in high-order visual cortex: Faces and reading with foveally-biased regions, while common objects and space with mid- and peripherally-biased regions. As face perception and reading are among the most challenging human visual skills, and are often regarded as the peak achievements of a distributed neural network supporting common objects perception, it is unclear why objects, which also rely on foveal vision to be processed, are associated with mid-peripheral rather than with a foveal bias.Here, we studied BN, a 9 y.o. boy who has normal basic-level vision, abnormal (limited) oculomotor pursuit and saccades, and shows developmental object and contour integration deficits but with no indication of prosopagnosia. Although we cannot infer causation from the data presented here, we suggest that normal pursuit and saccades could be critical for the development of contour integration and object perception. While faces and perhaps reading, when fixated upon, take up a small portion of central visual field and require only small eye movements to be properly processed, common objects typically prevail in mid-peripheral visual field and rely on longer-distance voluntary eye movements as saccades to be brought to fixation. While retinal information feeds into early visual cortex in an eccentricity orderly manner, we hypothesize that propagation of non-foveal information to mid and high-order visual cortex critically relies on circuitry involving eye movements. Limited or atypical eye movements, as in the case of BN, may hinder normal information flow to mid-eccentricity biased high-order visual cortex, adversely affecting its development and consequently inducing visual perceptual deficits predominantly for categories associated with these regions.

Novel PNKP mutation in siblings with ataxia-oculomotor apraxia type 4

The phenotypic and genetic spectrum of ataxia with oculomotor apraxia (AOA) disorders is rapidly evolving and new technologies such as genetic mapping using whole exome sequencing reveal subtle distinctions among the various subtypes. We report a novel PNKP mutation in two siblings with progressive ataxia, abnormal saccades, sensorimotor neuropathy and dystonia consistent with the AOA type 4 phenotype. Laboratory evaluation revealed hypoalbuminemia, hypercholesterolemia with elevated LDL, elevated IgE levels and normal α fetoprotein levels. Eye movement examination demonstrated a marked saccade initiation defect with profound hypometric horizontal saccades. Vertical saccades were also affected but less so. Also present were conspicuous thrusting head movements when attempting to change gaze, but rather than an apraxia these were an adaptive strategy to take advantage of an intact vestibulo-ocular reflex to carry the eyes to a new target of interest. This is demonstrated in accompanying videos.

The role of dentate nuclei in human oculomotor control: insights from cerebrotendinous xanthomatosis.

A cerebellar dentate nuclei (DN) contribution to volitional oculomotor control has recently been hypothesized but not fully understood. Cerebrotendinous xanthomatosis (CTX) is a rare neurometabolic disease typically characterized by DN damage. In this study, we compared the ocular movement characteristics of two sets of CTX patients, with and without brain MRI evidence of DN involvement, with a set of healthy subjects. Our results suggest that DN participate in voluntary behaviour, such as the execution of antisaccades, and moreover are involved in controlling the precision of the ocular movement. The saccadic abnormalities related to DN involvement were independent of global and regional brain atrophy. Our study confirms the relevant role of DN in voluntary aspects of oculomotion and delineates specific saccadic abnormalities that could be used to detect the involvement of DN in other cerebellar disorders. It is well known that the medial cerebellum controls saccadic speed and accuracy. In contrast, the role of the lateral cerebellum (cerebellar hemispheres and dentate nuclei, DN) is less well understood. Cerebrotendinous xanthomatosis (CTX) is a lipid storage disorder due to mutations in CYP27A1, typically characterized by DN damage. CTX thus provides a unique opportunity to study DN in human oculomotor control. We analysed horizontal and vertical visually guided saccades and horizontal antisaccades of 19 CTX patients. Results were related to the presence/absence of DN involvement and compared with those of healthy subjects. To evaluate the contribution of other areas, abnormal saccadic parameters were compared with global and regional brain volumes. CTX patients executed normally accurate saccades with normal main sequence relationships, indicating that the brainstem and medial cerebellar structures were functionally spared. Patients with CTX executed more frequent multistep saccades and directional errors during the antisaccade task than controls. CTX patients with DN damage showed less precise saccades with longer latencies, and more frequent directional errors, usually not followed by corrections, than either controls or patients without DN involvement. These saccadic abnormalities related to DN involvement but were independent of global and regional brain atrophy. We hypothesize that two different cerebellar networks contribute to the metrics of a movement: the medial cerebellar structures determine accuracy, whereas the lateral cerebellar structures control precision. The lateral cerebellum (hemispheres and DN) also participates in modulating goal directed gaze behaviour, by prioritizing volitional over reflexive movements.

Emulation of Physician Tasks in Eye-Tracked Virtual Reality for Remote Diagnosis of Neurodegenerative Disease.

For neurodegenerative conditions like Parkinson's disease, early and accurate diagnosis is still a difficult task. Evaluations can be time consuming, patients must often travel to metropolitan areas or different cities to see experts, and misdiagnosis can result in improper treatment. To date, only a handful of assistive or remote methods exist to help physicians evaluate patients with suspected neurological disease in a convenient and consistent way. In this paper, we present a low-cost VR interface designed to support evaluation and diagnosis of neurodegenerative disease and test its use in a clinical setting. Using a commercially available VR display with an infrared camera integrated into the lens, we have constructed a 3D virtual environment designed to emulate common tasks used to evaluate patients, such as fixating on a point, conducting smooth pursuit of an object, or executing saccades. These virtual tasks are designed to elicit eye movements commonly associated with neurodegenerative disease, such as abnormal saccades, square wave jerks, and ocular tremor. Next, we conducted experiments with 9 patients with a diagnosis of Parkinson's disease and 7 healthy controls to test the system's potential to emulate tasks for clinical diagnosis. We then applied eye tracking algorithms and image enhancement to the eye recordings taken during the experiment and conducted a short follow-up study with two physicians for evaluation. Results showed that our VR interface was able to elicit five common types of movements usable for evaluation, physicians were able to confirm three out of four abnormalities, and visualizations were rated as potentially useful for diagnosis.

What do eye movements tell us about patients with neurological disorders? - An introduction to saccade recording in the clinical setting.

Non-invasive and readily implemented in the clinical setting, eye movement studies have been conducted extensively not only in healthy human subjects but also in patients with neurological disorders. The purpose of saccade studies is to “read out” the pathophysiology underlying neurological disorders from the saccade records, referring to known primate physiology. In the current review, we provide an overview of studies in which we attempted to elucidate the patterns of saccade abnormalities in over 250 patients with neurological disorders, including cerebellar ataxia and brainstem pathology due to neurodegenerative disorders, and what they tell about the pathophysiology of patients with neurological disorders. We also discuss how interventions, such as deep brain stimulation, affect saccade performance and provide further insights into the workings of the oculomotor system in humans. Finally, we argue that it is important to understand the functional significance and behavioral correlate of saccade abnormalities in daily life, which could require eye tracking methodologies to be performed in settings similar to daily life.

Saccadic Eye Movement Abnormalities in Children with Epilepsy.

Childhood onset epilepsy is associated with disrupted developmental integration of sensorimotor and cognitive functions that contribute to persistent neurobehavioural comorbidities. The role of epilepsy and its treatment on the development of functional integration of motor and cognitive domains is unclear. Oculomotor tasks can probe neurophysiological and neurocognitive mechanisms vulnerable to developmental disruptions by epilepsy-related factors. The study involved 26 patients and 48 typically developing children aged 8–18 years old who performed a prosaccade and an antisaccade task. Analyses compared medicated chronic epilepsy patients and unmedicated controlled epilepsy patients to healthy control children on saccade latency, accuracy and dynamics, errors and correction rate, and express saccades. Patients with medicated chronic epilepsy had impaired and more variable processing speed, reduced accuracy, increased peak velocity and a greater number of inhibitory errors, younger unmedicated patients also showed deficits in error monitoring. Deficits were related to reported behavioural problems in patients. Epilepsy factors were significant predictors of oculomotor functions. An earlier age at onset predicted reduced latency of prosaccades and increased express saccades, and the typical relationship between express saccades and inhibitory errors was absent in chronic patients, indicating a persistent reduction in tonic cortical inhibition and aberrant cortical connectivity. In contrast, onset in later childhood predicted altered antisaccade dynamics indicating disrupted neurotransmission in frontoparietal and oculomotor networks with greater demand on inhibitory control. The observed saccadic abnormalities are consistent with a dysmaturation of subcortical-cortical functional connectivity and aberrant neurotransmission. Eye movements could be used to monitor the impact of epilepsy on neurocognitive development and help assess the risk for poor neurobehavioural outcomes.