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Clinical Examination in Neuro-Ophthalmology
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Selvakumar Ambika, Krishnakumar Padmalakshmi
Smooth pursuit stabilizes the image of an object on or near the fovea during slow movement of the object. To test smooth pursuit movement, the patient is asked to fixate at a target object which is moved across both in the horizontal and vertical directions. The target is moved at a speed of not more than 30 deg/second and not too laterally and the patient's eye movements are noted. Pursuits are affected in temporo-parieto-occipital cortex and ipsilateral deep parietal cortex lesions.
Remediating Brain Instabilities in a Neurology Practice
Published in Hanno W. Kirk, Restoring the Brain, 2020
The physical and neurological exam provide further clues on how to target the training. An elevated blood pressure and pressured speech indicate the need for parietal calming. Non-smooth pursuit in the eye exam, excessive involuntary motions, and seizures point to instabilities. Easy distractibility, left–right confusion, apraxias, and speech dysfluency, as well as overt focal deficits, all inform the neurofeedback clinician on how to prescribe the brain training protocol. Again, these findings are clearly listed in the initial assessment.
Motor Aspects of Lateralization: Evidence for Evaluation of the Hypotheses of Chapter 8
Published in Robert Miller, Axonal Conduction Time and Human Cerebral Laterality, 2019
Complementary results were reported by Bogousslavsky and Regli (1986) who studied smooth pursuit eye movement in brain-injured patients. Impairment was found for all lesions in the parieto-occipital lobes, but was severe only for lesions in the non-dominant hemisphere. The lateralized deficit was limited to contralateral pursuit. (Ipsilateral pursuit was similarly impaired by lesions in either hemisphere). The impairment with non-dominant hemisphere lesions was not due to neglect alone, because voluntary saccades were preserved. Since smooth pursuit eye tracking is a closed-loop form of movement, this result strengthens the evidence that the right (non-dominant) hemisphere can perform such movements better than the left.
The Effect of Target Velocity on the Fast Corrective Response during Reaching Movement
Published in Journal of Motor Behavior, 2022
Kosuke Numasawa, Tomohiro Kizuka, Seiji Ono
In our experiment, participants were required to track the target motion, unlike the MFR. When we look at a small moving object, smooth pursuit eye movements are used to hold the target image on the fovea (Krauzlis, 2004; Lisberger, 2010; Ono, 2015). Smooth pursuit eye movements are driven by retinal slip signals generated from the difference between actual target motion and eye velocity. In particular, retinal slip information carried in the MT/MST plays an important role in the initial part of smooth pursuit (Dursteler & Wurtz, 1988; Newsome et al., 1985). As mentioned above, since arm movements responding to visual motion are associated with neuronal activity in the MT/MST, we speculate that the fast corrective response shares the same visual motion processing as smooth pursuit eye movements. Indeed, our results indicate that the initial amplitude (first 50 ms) of the corrective response increases according to the target velocity. However, a previous study has reported that the initial part of smooth pursuit (open-loop period) is not dependent on target velocity (Lisberger & Westbrook, 1985). Thus, one possible explanation is that the initiation of arm movement is generated differently from the eye movement, even though they both share a common retinal slip signal. Indeed, Saijo et al. (2005) have suggested that the MFR and the eye movements elicited by the large-field visual motion are separated even they are processed by the same visual information in parallel (Saijo et al., 2005).
Eye Movement Abnormalities in Amyotrophic Lateral Sclerosis in a Tunisian Cohort
Published in Neuro-Ophthalmology, 2022
Arwa Rekik, Saloua Mrabet, Imen Kacem, Amina Nasri, Mouna Ben Djebara, Amina Gargouri, Riadh Gouider
Altered horizontal smooth pursuits were the most common eye movement abnormality among our patients. However, results do diverge when it comes to studying smooth pursuits in ALS patients. For example, Shaunak and collaborators found that smooth pursuits were normal in all of the 17 patients involved in their study.22 Gizzi and co-authors found them altered, but only in patients who had associated Parkinsonism.18 Recent studies conducted on the Korean population by Kang et al. found, similar to our study that altered horizontal pursuits were the main abnormality (64% of cases).19 Smooth pursuit eye movements are generated through the cerebro-ponto-cerebellar pathway. Cortical regions are considered as the generators of the pursuit movement with the pons being the final destination. The frontal lobe is implicated via the frontal eye fields (FEF), which encode and predict the pursuit trajectories.23,24 These anatomical data explain the established correlations of altered smooth pursuits with the presence of non-motor signs in general and specifically with bladder dysfunction and executive impairment. Such a combination may not be so surprising since both executive and bladder dysfunction are consistent with frontal lobe pathology.
Genetics of primary lateral sclerosis
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2020
Vincenzo Silani, Philippe Corcia, Matthew B. Harms, Guy Rouleau, Teepu Siddique, Nicola Ticozzi
A second gene associated to JPLS, ERLIN2, was identified in 2012 by performing autozygosisty mapping followed by DNA sequencing in a consanguineous family from Saudi Arabia with four affected siblings (59). The first symptoms appeared in all patients in the first months of life and progressed to complete loss of speech and articulation by the age of 2 and of ambulation by the age of 12. Cognition was apparently normal, but ocular movement abnormalities with disruption of smooth pursuit could be observed. Skeletal deformities were also part of the phenotype. The observed mutation causes the activation of a cryptic splice acceptor site in intron 7 of ERLIN2, and the inclusion of a sequence of intronic nucleotides containing a stop codon, leading in turn to loss of protein function through nonsense-mediated mRNA decay (59). Similarly to ALS2, mutations in ERLIN2 also display a degree of phenotypic heterogeneity spanning different motor neuron disorders, having also been observed in juvenile ALS (19), and a complicated form of hereditary spastic paraplegia with intellectual disability and skeletal abnormalities (SPG18) (60).