The neural pathways and brain regions involved in eye movements during ocular fixation and gaze control include the cerebrum (motor-, pre-motor cortex and visual cortex), brainstem and cerebellum, and abnormal eye movements can indicate the presence of a variety of neuronal disorders, especially neurodegenerative diseases (ND) such as Alzheimer`s disease (AD) and Parkinson`s disease (PD). Careful clinical examination of eye movements in patients with ND is an invaluable adjunct to neurological and cognitive assessments (Anderson et.al. 2013).
Clinical examination on one hand lacks objectivity, the precision and accuracy of exact eye movement measurements. The recording with standard lab technology (video-oculography, electro-oculography (EOG), electromagnetic search-coil, etc.) on the other hand is time-limited and requires unnatural conditions (e.g. head fixation, contact lens). New miniaturization developments have opened up the possibility for long-term EOG measurements under natural conditions which allow the acquisition of a larger amount of eye movement data in long-term recording and longitudinal comparison. It is possible that by careful analysis of this data we can get access to eye movement parameters that have been unavailable by examination or lab measurements so far and might be used as new biomarkers for ND diagnosis or monitoring of progression or regression. There are promising results about the influence of ND in different tasks on oculomotoric coordination as e.g. the reduction of amplitudes of saccades while reading sentences in Mild stages of AD (Fernandez et al., 2015) or increased latency and variability of saccades in Freezing of gait of PD patients (Nemanich et al., 2016).
As an example, in patients suffering from PD, a reduced saccade amplitude can be detected in the early disease course, presumably reflecting degeneration in the basal ganglia, given that higher-level eye move- ment related areas are yet to be affected, while increased saccade latency occurs later in the disease course (Terao et al. 2011) and is associated with cognitive impairment (MacAskill et al. (2012), Mosimann et al. (2005)).
Other eye movement parameters could be saccade maximum velocity, saccade frequency, fixation duration or nystagmus amplitude and frequency during body rotations (Trobe et al. 1991).
The results of our study may hopefully lead to an improvement of the earlier detection and therefore better treatment of ND.
Anderson, T. J. & MacAskill, M. R. (2013). “Eye movements in patients with neurodegenerative disorders.” Nat Rev Neurol. (2):74-85. doi: 10.1038/nrneurol.2012.273.
Nemanich S.T., Earhart G.M. (2016) “Freezing of gait is associated with increased saccade latency and variability in Parkinson’s disease.” Clin Neurophysiol. 2016 Jun;127(6):2394-401. doi: 10.1016/j.clinph.2016.03.017
Terao, Y. et al. (2011). “Initiation and inhibitory control of saccades with the progression of Parkinson’s disease—changes in three major drives converging on the superior colliculus.” Neuropsychologia 49, 1794–1806
MacAskill, M. R. et al. (2012). “The influence of motor and cognitive impairment upon visually-guided saccades in Parkinson’s disease.” Neuropsychologia 50, 3338–3347
Mosimann, U. P. e tal. (2005). “Saccadic eye movement changes in Parkinson’s disease dementia and dementia with Lewy bodies.” Brain 128, 1267–1276
Trobe J. D., Sharpe J. A., Hirsh D. K., Gebarski S. S. (1991). “Nystagmus of Pelizaeus-Merzbacher disease. A magnetic search-coil study.” Arch Neurol. 48(1):87-91.