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A Clinical Approach to Abnormal Eye Movements
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Eye fixation can be disrupted by many abnormal eye movements. Broadly these abnormal movements are classified as ‘Nystagmus’ and the ‘Saccadic Intrusions’. Understanding the intricate network controlling the various eye movements and connecting them to various other structures like the vestibular system, the brainstem, the cerebellum and the cortex, may help in discerning the cause of abnormal eye movements in a given patient.
Vision and hearing
Published in Ajay Sharma, Helen Cockerill, Lucy Sanctuary, Mary Sheridan's From Birth to Five Years, 2021
Ajay Sharma, Helen Cockerill, Lucy Sanctuary
Poor visual behaviour or the presence of a squint or abnormal eye movements can be presenting features of rare but serious eye conditions or systemic disorders, such as cataracts, glaucoma and retinoblastoma, which are sight- or life-threatening and are treatable.
Neurology
Published in Kaji Sritharan, Jonathan Rohrer, Alexandra C Rankin, Sachi Sivananthan, Essential Notes for Medical and Surgical Finals, 2021
Kaji Sritharan, Jonathan Rohrer, Alexandra C Rankin, Sachi Sivananthan
When examining eye movements three questions will help establish the diagnosis: Does it fit a single nerve palsy?Third nerve palsy – eye is ‘down and out’ with the pupil dilated and ptosis (but can be partial +/- pupil-sparing, e.g. when associated with diabetes).Sixth nerve palsy – failure of abduction.Fourth nerve palsy – double vision on downward gaze.Is it an internuclear ophthalmoplegia? Difficulty in adduction with nystagmus in the contralateral eye (but normal convergence); can be bilateral, due to a lesion in the medial longitudinal fasciculus (which links ocular motor nuclei in the brainstem).Is it a ‘complex ophthalmoplegia’, i.e. does not fit a particular pattern? If it is not a combination of 3, 4 and/or 6th nerve palsies then think of myasthenia gravis, thyroid eye disease, ocular myopathy. Rarely there may be a supranuclear palsy (i.e. an UMN syndrome).
Saccadic Eye Movements in Patients with Mild Cognitive Impairment: A Longitudinal Study
Published in Journal of Motor Behavior, 2023
Müge Akkoyun, Koray Koçoğlu, Hatice Eraslan Boz, Pembe Keskinoğlu, Gülden Akdal
Mild cognitive impairment is not only the early stage of AD type dementia but also it may be a temporary or reversible state, which may be the precursor of other neurodegenerative diseases (Mitchell & Shiri‐Feshki, 2009; Pandya et al., 2016; Vos et al., 2015). Therefore, the follow-up to the clinical course of MCI is great importance in terms of early intervention for AD or other types of dementia (Limongi et al., 2017). It has been stated that changes in executive functions, attention control, and visuospatial abilities can be observed before memory in the preclinical stage of AD (Alichniewicz et al., 2013; Amieva et al., 2004; Pereira et al., 2014; Greenwood et al., 1997). Eye movements are a mechanism controlled by cognitive functions such as attention, working memory, and inhibition control (Crawford et al., 2011; Crawford & Higham, 2016). It has been suggested that changes in eye movements may indicate cognitive impairment before traditional neuropsychological assessments (Crawford & Higham, 2016). For this reason, studies have focused on the early diagnosis of MCI and evaluating the course of the disease with eye movements.
Two-muscle surgical treatment of a compensatory head tilt in an adult with acquired downbeat nystagmus
Published in Baylor University Medical Center Proceedings, 2023
Daniel Vinson, Jonathan Kopel, Caezaan Keshvani, James Lee, Kenn Freedman
Nystagmus in children and adults is an involuntary oscillatory eye movement disorder that can vary in intensity in different gaze positions. If there is a certain gaze position where the nystagmus is least active, this is known as a null point (or zone), and often the patients’ symptoms and vision improve when the eyes are deviated toward that null point/zone. Patients with an eccentric null point/zone will often assume a compensatory head tilt to set their eyes in that null zone and optimize their vision. This forms the basis of the Kestenbaum-Anderson–like operations, which have proven beneficial in treatment of compensatory head tilt in patients with infantile nystagmus. The Kestenbaum-Anderson procedures involve shifting the eyes in the direction of the abnormal head turn/tilt and away from the preferred direction of gaze. The Kestenbaum procedure involves bilateral recession of the yoke muscles opposite to the head turn, combined with bilateral resection of their antagonists. Anderson’s procedure only involves recession of the yoke muscles. However, the procedure’s use in acquired vertical nystagmus in adults with head tilt has rarely been reported.
Orbital inflammation in the setting of a nylon foil implant
Published in Orbit, 2022
Adrianna D. Jensen, Nickisa M. Hodgson, Rupin Parikh, Charles G. Eberhart, Amanda D. Henderson, Roxana Fu
The patient is a 61-year-old African American male with a past medical history of type II diabetes, hypertension, and hypercholesterolemia, who had previously been followed by ophthalmology for diabetic eye exams and monitoring of glaucoma suspect status, though he had never taken topical intraocular pressure lowering drops. In June 2019, the patient presented with left medial and inferior orbital wall fractures in the setting of an assault with an unknown object. During maxillofacial computerized tomography (CT) scan, the patient had fractures of the orbital medial wall and floor with herniation of fat and the medial rectus into the left-ethmoid air cells, and mild left proptosis with intraconal hemorrhage and air. Clinically, the patient presented with downgaze restriction and pain associated with eye movements, as well as diplopia on left and down gazes. We completed repairs at one week with implantation of a SupraFOIL® 0.35 mm orbital implant into the medial wall and orbital floor. The patient started a Medrol Dosepak on post-operative day one. However, at the post-operative week one visit, the patient still had intense edema and sharp pain in the left eye. We made the decision to repeat steroids at a higher dose, this time starting with 60 mg prednisone and tapering by 20 mg weekly, and the patient was improving clinically at his one-month post-operative visit.