Kan man se saccades
All eleven remaining subjects aged 27—70 years; 5 males and 6 females met clinical and genetic criteria for HD with a mean of The rater was blind to the eye movement data. Moreover, the only previous study 4 we are aware of that established any correlation between eye movement parameters and the UHDRS did not take into account age. All these structures are affected in HD and it is, therefore, not surprising that multiple eye movement deficits exist in patients with HD 4 — As a result of recent research focusing on further discriminating types of saccadic eye movements, two parallel systems have been proposed that differentially govern reflexive and volitional saccades 23 — Frontal structures and the basal ganglia play a key role in both voluntary saccades and control tonic inhibition of reflexive saccades.
Target stimuli were 0.
Horizontal Saccades
Before the start of an eye movement recording session, the subject was calibrated by moving their eyes to nine positions on the screen indicated by 0. Federal government websites often end in. Specifically, for saccade initiation, eye velocity had to be above HD patients with greater clinical severity were significantly slower in the prosaccade task.
The earliest documented cell loss in HD patients occurs in the basal ganglia, particularly in the striatal medium spiny neurons and the external segment of the global pallidus 1 , 2. All these correlations remained significant even when age was taken into account. We sought to evaluate whether reflexive and voluntary orienting prove useful as biomarkers of disease severity in HD.
Using an infrared eye tracker, we also measured latency and error rates of horizontal and vertical saccades using prosaccade and antisaccade eye movement tasks. The spatial and temporal resolutions of the eye tracker were approximately 0.
One subject did not complete the behavioral tasks and one elderly subject was excluded due to incomplete data. The results of the present age-controlled study show for the first time that both reflexive and voluntary eye motor control in HD patients decrease with increase in disease severity suggesting declines in both motor and cognitive function.
Eventually, degeneration is widespread and includes the brainstem 1 , 3.
Age is known to affect reflexive and voluntary eye movements Establishment of simple, non-invasive and age-controlled biomarkers of motor and cognitive disease severity is important for monitoring progression, preclinical diagnosis, differentiating subtypes, and development and evaluation of treatments Eye movement deficits, themselves, are also associated with increased risk of developing HD 13 , All study participants gave informed consent at the start of each testing session.
Saccade initiation and termination were defined by areal and velocity criteria. Prosaccade latency correlated with total chorea score. Six of the HD subjects were not receiving medication for HD. Subjects were seated in front of a inch CRT monitor with their heads placed in a stable chin rest that was positioned 72 cm from the screen. Eye movements critically depend on the coordinated functioning of the brainstem, thalamus, basal ganglia, and cortex.
Vestibulär yrsel
For the eye movement tasks, a gray fixation point 0. HD patients with greater clinical severity as measured by either measure made significantly more errors in the antisaccade task. Huntington disease HD is a genetic, neurodegenerative disorder characterized by chorea, behavioral co-morbidities, cognitive deficits, and eye movement abnormalities. We calculated simple and age-controlled correlations between eye movement and clinical parameters.
Some studies have shown that even presymptomatic HD patients have voluntary saccade deficits 21 , 22 , 28 — The performance of reflexive saccades in HD patients is less consistent, with some studies finding slowing 4 , 5 , 7 , 11 — 15 and others reporting them as intact 20 — The saccadic slowing affecting both reflexive and voluntary saccades, is usually attributed to the development of brainstem dysfunction 12 , 16 , 17 , Despite numerous eye movement studies in HD, only a few have correlated eye movement parameters with HD severity as measured by the Unified Huntington Disease Rating Scale UHDRS motor subscale to determine their usefulness as a biomarker for disease severity and progression 4.
More importantly, specific changes in saccade performance will provide a basis to infer specific neuropathological changes in HD. Eye movement deficits, particularly in voluntary saccades 4 , 8 , 12 , 16 , 20 , 21 , 26 , 27 and in fixation maintenance 8 , 10 , 12 , have been well documented in HD patients, even in early stages.
Thus, relatively simple eye movement parameters latency and error rate obtained from simple tasks prosaccade and antisaccade may serve as quantitative biomarkers of sub-cortical and cortical disease severity in HD and could aid in predicting onset, distinguishing subtypes, or evaluating disease progression and novel therapies. The site is secure.
In addition, both systems share common motor brainstem output nuclei. Thus, specific lesions will differentially impair the two types of saccades.