Eye Movement Disorders

Eye movement

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Eye-tracking has become the tech trend du jour. Advertisers use data on where you look and when to better capture your attention. Designers employ it to improve products. Game and phone developers utilize it to offer the latest in hands-free interaction. But eye-tracking can do more than help sell products or give your finger a rest while playing Fruit Ninja. Years of research have found that our tiny, rapid eye movements called saccades serve as a window into the brain for psychologists just as for advertisers—but instead of giving clues about our preferred cookie brands pdf , they elucidate our inner mental functioning.

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For many researchers in this growing field, the outlook so far looks positive. Similarly distinct, abnormal eye-movement patterns occur in a number of mental disorders, scientists have found. Until recently, such insights have remained relegated to the lab setting, where researchers traditionally rely on special tools like mounted headgear and instructed tasks like following a moving target across a computer screen. The databases were last searched on 26 June No date or language restrictions were used in the electronic searches for trials.

We contacted researchers active in this field for information about further published or unpublished studies.

We included randomised controlled trials RCTs of any intervention for ocular alignment or motility deficits or both due to acquired brain injury. Two review authors independently selected studies and extracted data.

Shirley H. Wray

We used standard methods expected by Cochrane. We found five RCTs participants that were eligible for inclusion. These trials included conditions of acquired nystagmus , sixth cranial nerve palsy and traumatic brain injury-induced ocular motility defects. We did not identify any relevant studies of restitutive interventions. We identified one UK-based trial of a substitutive intervention , in which botulinum toxin was compared with observation in 47 people with acute sixth nerve palsy.

At four months after entry into the trial , people given botulinum toxin were more likely to make a full recovery reduction in angle of deviation within 10 prism dioptres , compared with observation risk ratio 1. These same participants also achieved binocular single vision. All adverse events recovered. We judged the certainty of evidence as low, downgrading for risk of bias and imprecision. It was not possible to mask investigators or participants to allocation, and the follow-up between groups varied.

We identified one USA-based cross-over trial of a compensatory intervention. Oculomotor rehabilitation was compared with sham training in 12 people with mild traumatic brain injury, at least one year after the injury. We judged the evidence from this study to be very low-certainty. The study was small, data for the sham training group were not fully reported, and it was unclear if a cross-over study design was appropriate as this is an intervention with potential to have a permanent effect.

We identified three cross-over studies of pharmacological interventions for acquired nystagmus , which took place in Germany and the USA. These studies investigated two classes of pharmacological interventions: GABAergic drugs gabapentin, baclofen and aminopyridines 4-aminopyridines AP , 3,4-diaminopyridine DAP. We judged the evidence from all three studies as very low-certainty because of small numbers of participants which led to imprecision and risk of bias they were cross-over studies which did not report data in a way that permitted estimation of effect size.

The follow-up period was two weeks. The dopaminergic nigrostriatal pathways and the superior cerebellar peduncle are reported to be involved in the pathological process resulting in prolonged latencies and mostly subtle cerebellar oculomotor signs, respectively [ 75 ]. Study of oculomotor dysfunctions both in PSP-RS and in PSP-P revealed a similar presentation comprising slowed vertical saccades, saccadic hypometria, prolonged latencies, and impaired pursuit eye movement [ 65 ]. In advanced stages, PSP patients are fairly disabled to generate large saccade amplitudes, preferentially vertical, as exemplified in Figure 4.

When vertical saccades become slowed, horizontal saccade velocity remains intact until the pathological process also involves horizontal burst neurons resulting in reduced horizontal peak eye velocities [ 3 , 76 ].

Eye Movement Abnormalities in Neurodegenerative Diseases

PSP patients also present with disrupted visual fixation when they attempt to fix their eyes upon stationary targets. The phenomenon of considerably higher prevalence of horizontal SWJ in combination with larger amplitudes may give a clue for PSP although microsaccades are observed preferentially in horizontal direction with increasing target size [ 24 ].

Two further explanations for the presence of abnormally large and frequent SWJ in PSP have been proposed: i since horizontal SWJ rate often increases during the release of vertical saccades, a SWJ coupling mechanism was suggested to enhance vertical saccade burst [ 13 ] and ii the decreased peak eye velocity and the resulting prolonged saccade duration may increase the probability that vision fades so that larger and more frequent SWJ could overcome visual fading in PSP [ 21 , 28 ].

The PSP patient reaches the target dashed line in a pathological multistep pattern, approximately 2. Abnormal horizontal square wave jerks SWJ manifest in the orthogonalized horizontal eye position gray line in the left panel , together with vertical saccades indicating a curved trajectory. In contrast, the horizontal eye position in the control subject gray line in the right panel exhibits no alteration.

The lower row shows the corresponding vertical eye velocity y -axis computed by use of sample-by-sample differences of the vertical eye position signal. The PSP patient left fails in generating larger saccades resulting in a reduced peak eye velocity PEV compared with the control subject.

Remarkably, SPEM remain intact even in severely impaired PSP patients as long as a target is continuously moving in a predictive manner with low peak velocity and acceleration. This could be demonstrated when patients were asked to track a sinusoidal oscillating spot with low frequency [ 24 ].

With increasing stimulus frequency, the ability to perform SPEM considerably declines due to the disability to perform catch-up saccades to refoveate the target [ 37 ]. In addition, vergence eye movements are reported to be affected early in the PSP course and may also be associated with horizontal diplopia in some cases [ 78 ]. In summary, pathologically slowed vertical saccades' peak velocities are the eponymous hallmark of PSP. The PSP-associated damage involves midbrain structures including the saccadic burst generator in the brainstem that is responsible for the impaired vertical eye muscles innervation.

Moreover, a hallmark of PSP is the early appearance of cognitive and behavioral deficits [ 79 ] that also manifest in oculomotor function by means of a considerable lack of inhibitory control of saccades e. Autosomal dominant Huntington's disease HD is a progressive neurodegenerative disease, clinically presenting with a hyperkinetic movement disorder chorea , cognitive decline, and behavioral symptoms [ 80 ].

The age of disease onset is predictable by the number of pathologically increased CAG repeats. Oculomotor deficits in patients with HD and presymptomatic gene carriers are reported to be one of the earliest signs [ 81 ]. They present as dysfunction of fixation ability [ 82 ], impaired initiation and inhibition of saccadic eye movements [ 83 ], impaired SPEM [ 2 , 84 ], and decreased inhibition control in the sense of erroneously responding to novel stimuli [ 85 — 87 ].

Moreover, slowed saccades become prominent in both vertical and horizontal directions, latencies have been reported to be increased, and saccadic hypometria can be observed in HD like in other movement disorders [ 3 ]. Slowing of saccades is likely caused by midbrain atrophy, in particular in the pontine nuclei critical for the saccadic burst; however, the pathophysiology in oculomotor-related midbrain areas is ill-defined, so far [ 88 ].

Eye Movement Disorders in Clinical Practice by Dr. Shirley H. Wray

Presymptomatic gene carriers show subtle cognitive and motor impairment due to striatal and cortical neuropathological changes that cause increased error rates during inhibition tests such as antisaccades [ 86 ] and likely reflect first clinical symptoms [ 7 ]. Reflexive saccades remain unaffected for a long time whereas both reflexive and voluntary-guided saccade performance decline with disease progression [ 89 ], since the structural connectivity between the frontal cortex and the caudate body seems to be particularly related to the control of voluntary-guided saccades [ 7 , 86 ].

Difficulties in voluntarily initiating saccades in the presence of excessive saccadic intrusions during attempted fixation and a lack of inhibition control in the sense of withholding gaze shifts to new stimuli are apparently contradicting findings; a comprehensive explanation for this phenomenon in HD remains to be identified.

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The latter one is apparently involved already in presymptomatic HD. Cerebellar signs manifest in many neurodegenerative movement disorders such as MSA and in the heterogeneous group of hereditary spinocerebellar ataxia. One prominent feature is cerebellar ataxia with impaired body posture; in addition, patients present with dysarthria, dysmetria, and dysdiadochokinesia [ 90 ]. Cerebellar dysfunctions in eye movement control frequently manifest in a variety of symptoms including the spectrum of pathological nystagmus, dysmetric saccades, abnormally large SWJ, postsaccadic drift as a consequence of pulse-step-mismatch, mildly slowed saccades, and a disturbed pursuit in the sense of corrective saccades interrupting SPEM [ 3 , 16 , 28 , 37 , 50 , 88 ].

These deficits become pronounced in advanced cases, while many patients present with less dominant oculomotor abnormalities in early stages. In order to detect these symptoms, VOG is helpful beyond pure visual inspection.

Oculomotor dysfunctions have been characterized by the genetically defined spinocerebellar ataxia subtypes [ 88 ]; for a comprehensive review, see [ 2 ]. Only a few studies investigated presymptomatic spinocerebellar ataxia gene carriers in contrast to HD. For spinocerebellar ataxia type 2 presymptomatic patients, a relation between CAG repeats, estimated time to disease onset, and decreased peak eye velocity has been reported [ 91 ]. Together, these VOG findings in cerebellar dysfunction mirror the cerebellar contribution to the oculomotor system, that is, refinement of saccade guidance, the adaptive strategy to perform perfect smooth pursuit, and the ability to hold the eye in a steady position.

To our knowledge, the role of the cerebellum in attentional oculomotor control remains incompletely defined yet and might be a promising issue for future investigations. In the absence of definitive biomarkers, VOG holds promise for a complementary noninvasive tool to characterize the oculomotor phenotype of distinct disease entities within the spectrum of neurodegenerative diseases. In the course of neurodegenerative disorders, disease-specific brain structures get systematically damaged. Hence, the resulting clinical condition might be considered as an investigational model for the contribution of functional components to eye movement control.

In vivo examination of the oculomotor system offers a valuable window into altered brain function in the pathological state of movement disorders. Thus, we can learn about the contribution of different functional systems that may interfere with the way we direct our attention in the visual scene. In addition, oculomotor control covers large portions of the whole brain that appear to be decomposable into two major subdivisions: i the oculomotor nuclei responsible for the innervation of the six extraocular eye muscles and ii the much more complex network of higher cognitive control that is strongly associated with visual attention.

The investigation of eye movements may become important to clinicians in the context of differential diagnostics of movement disorders such as in distinguishing between Parkinsonian syndromes or to uncover a possible cerebellar contribution to pathological processes. VOG provides a sensitive noninvasive in vivo method to detect alterations in oculomotion function in patients with neurodegenerative movement disorders. Malfunctioning oculomotor control appears to have some characteristic feature that can give clues to be attributed uniquely to the subtype of the movement disorder. More specifically, other neurodegenerative types of Parkinsonian syndromes can be differentiated from PD early in the course.

One should keep in mind that some of the Parkinsonian-associated hallmarks such as slowed eye velocities could also manifest in other neurodegenerative nonmovement disorders, resulting in the necessity for careful interpretation of VOG results in the light of the clinical presentation. Particular aspects such as SWJ or larger intruding eye movements may provide motivation for future investigations possibly together with functional brain imaging studies [ 9 , 92 ] to increase our understanding of the functional pathoanatomy of these neurodegenerative conditions.

Notably, attentional dysfunction in oculomotor control mostly presents early in the course of neurodegenerative movement disorders even while no obvious cognitive deficits exist. This finding prompts the notion that even a subtle pathology of cortical networks may cause a broad variety of oculomotor alterations.

To further investigate the complex nature of visual attention and the way we direct or withhold our gaze, it might be safe to assume that we can learn much from pathological conditions related to specific functional systems. This approach offers the possibility to refine our existing models of human oculomotor networks whose functional interaction may be considered an essential framework for higher functions such as visual attention.

The authors would gratefully acknowledge Professor Dr. Wolfgang Becker and Dr. The authors declare that there is no conflict of interests regarding the publication of this paper.

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