The diagnostic value of saccades in movement disorder patients: a practical guide and review

Termsarasab, Pichet; Thammongkolchai, Thananan; Rucker, Janet C.; Frucht, Steven J.

doi:10.1186/s40734-015-0025-4

Cited by 86 publications

(65 citation statements)

References 88 publications

(79 reference statements)

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“…Eye movements, specifically saccades, form the basis for visual exploration as they rapidly shift the fovea of the eye between areas of interest within the environment (Stuart et al, 2014a, Otero-Millan et al, 2008. Saccadic measurement has become prominent in many research fields, as deficient saccadic function can be used to understand cognitive (Hutton, 2008) or visual (Ibbotson and Krekelberg, 2011) processes, and help with neurological examination/diagnosis (Termsarasab et al, 2015) or to understand functional deficits in everyday tasks (e.g. walking) (Stuart et al, 2017a, Stuart et al, 2018.…”

Section: Introductionmentioning

confidence: 99%

Eye-tracker algorithms to detect saccades during static and dynamic tasks: a structured review

et al. 2019

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Section: Introductionmentioning

confidence: 99%

Eye-tracker algorithms to detect saccades during static and dynamic tasks: a structured review

et al. 2019

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“…In the fields of psychology and psychiatry, eye-tracking technology has recently been confirmed to be useful in diagnosing various diseases, including Parkinson's disease (25), Huntington's (26), abnormal gaze (27), nervous system degenerative diseases (28) and early Alzheimer's disease (29). Home eye-tracking systems can be used to follow up patients with vertigo (30).…”

Section: Discussionmentioning

confidence: 99%

Preliminary study of abnormalities in saccade dynamics in patients with hyperthyroidism with no pre‑existing eye damage

Sun

Xie

et al. 2020

Exp Ther Med

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The present study investigated the relationship between hyper thyroidism a nd thyroid-associated ophthalmopathy by examining saccade dynamics to identify defects in eye tracking in patients with hyperthyroidism with no pre-existing eye damage and sensitive indicators that discriminated eye tracking ability in hyperthyroidism. A total of 33 outpatients with hyperthyroidism and 26 healthy controls participated in visually guided saccade (VGS) analysis. Patients with hyperthyroidism were divided into groups based on their medication status (medicated vs. unmedicated). Main sequence analysis was performed to identify differences in peak velocity and duration, and a general linear model (GLM) was used to identify differences in latency, peak acceleration and peak deceleration among the groups. The present study compared differences in the Spearman's correlation coefficient of the duration of saccades and the acceleration asymmetric index (R AD) among the groups. V max values (V max was the asymptotic value of the PV of saccades of large amplitude) were significantly different between the healthy control and unmedicated-hyperthyroidism groups. The results of the GLM-based analysis indicated no significant differences in saccade latency among the three groups. Peak acceleration was significantly different between the healthy control and unmedicated-hyperthyroidism groups (P<0.01). Peak deceleration was significantly different between the healthy control, unmedicated-and medicated-hyperthyroidism groups (P<0.01). R AD was significantly different between the healthy control and medicated-hyperthyroidism groups (P=0.004). The results of the present study suggested that patients with hyperthyroidism with no pre-existing eye damage exhibited significantly altered saccade dynamics during VGS. Therefore, R AD may be used as an indicator to monitor the level of eye movement coordination.

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“…These include early and marked saccadic slowing, initial hyperreflexia that is followed by hyporeflexia, Parkinson rigidity and myoclonus or fasciculation like movements [102,103]. With the slowing of saccadic jumps for horizontal gaze being the noticeable oculomotor abnormality (Table 1) [104][105][106]. This is attributed to the early, and sometimes rapid degeneration of the pontine brainstem.…”

Section: Clinical Featuresmentioning

confidence: 99%

Polyglutamine ataxias: From Clinical and Molecular Features to Current Therapeutic Strategies

McIntosh¹,

Htut²,

Fletcher³

et al. 2017

J Genet Syndr Gene Ther

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Spinocerebellar ataxias are a large group of heterogeneous diseases that all involve selective neuronal degeneration and accompanied cerebellar ataxia. These diseases can be further broken down into discrete groups according to their underlying molecular genetic cause. The most common are the polyglutamine ataxias, of which there are six; Spinocerebellar ataxia type 1, 2, 3, 6, 7 and 17. These diseases are characterised by a pathological expanded cytosine-adenine-guanine (CAG) repeat sequence, in the protein coding region of a given gene. Common clinical features include lack of coordination and gait ataxia, speech and swallowing difficulties, as well as impaired hand and motor functions. The polyglutamine spinocerebellar ataxias are typically late onset diseases that are progressive in nature and often lead to premature death, for which there is currently no known cure or effective treatment strategy. Although caused by the same molecular mechanism, the causative gene and associated protein differ for each disease. The exact mechanism by which disease pathogenesis is caused remains elusive. However, the variable (CAG) n repeats are codons that may be translated to an expanded glutamine tract, leading to conformational changes in the protein, giving it a toxic gain of function. Several pathogenic pathways have been implicated in polyglutamine spinocerebellar ataxia diseases, such as the hallmark feature of neuronal nuclear inclusions, protein misfolding and aggregation, as well as transcriptional dysregulation. These pathways are attractive avenues for potential therapeutic interventions, as the potential to treat more than one disease exists. Research is ongoing, and several promising therapies are currently underway in an attempt to provide relief for this devastating class of diseases.. However, mutations can arise de novo, through errors in DNA replication such that two genetically healthy parents can give rise to an affected child.There are currently six characterised polyQ SCAs (1, 2, 3, 6, 7 and 17) (Table 1), and together with three other diseases, namely Huntington's disease, spinal and bulbar muscular atrophy and dentatorubropallidoluysian atrophy (DRPLA), form a larger category of polyQ diseases [7][8][9][10]. Th ere is little relief for individuals suffering from polyQ SCA disorders, with symptomatic treatments the only available option. Long term pharmacological treatment, although admirable, tends to fall short in an effective management strategy, as unwanted complications and low drug efficacy still exist. In addition, none of these diseases have any treatments that slow the progression of the disease; leaving affected individuals with the daunting reality that time may be a severe limiting factor. Several experimental approaches are currently being assessed to overcome these difficulties. This review will focus on the clinical and molecular features of polyQ SCA diseases (which will be referred to as SCA diseases), as well as highlight several promising and emerging therapeutic strategies...

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The diagnostic value of saccades in movement disorder patients: a practical guide and review

Cited by 86 publications

References 88 publications

Eye-tracker algorithms to detect saccades during static and dynamic tasks: a structured review

Eye-tracker algorithms to detect saccades during static and dynamic tasks: a structured review

Preliminary study of abnormalities in saccade dynamics in patients with hyperthyroidism with no pre‑existing eye damage

Polyglutamine ataxias: From Clinical and Molecular Features to Current Therapeutic Strategies

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