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A Clinical Approach to Abnormal Eye Movements
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Nystagmus is generally of two types: jerk nystagmus and pendular nystagmus: Jerk nystagmus has a slow phase drift followed by a rapid corrective saccade in the opposite direction.Pendular nystagmus refers to a sinusoidal oscillation with slow phases in both directions and no corrective saccades.
Ophthalmology
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
See-saw nystagmus: pendular nystagmus in which one eye elevates and intorts while the other eye depresses and extorts and then the eyes reverse. The commonest cause is chiasmal or parasellar tumours but it may also be seen in albinism as a transient finding, head trauma and syringobulbia.
Evaluation of Balance
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
As mentioned under ‘Clinical examination of eye movements’ above, jerk nystagmus can be of peripheral or central origin. A jerk nystagmus of peripheral vestibular origin has a typically linear slow phase (Figure 62.4). Linear means that the velocity of the slow phase is constant and it is so because the magnitude of the velocity at rest is a direct measure of the vestibular tonus asymmetry. CNS lesions can also create a vestibular imbalance but they usually involve in addition central integrating mechanisms. This makes the slow phase of nystagmus to be non-linear, particularly during eccentric gaze, typically with an exponentially decreasing slow phase in velocity (Figure 62.5). A jerk nystagmus with a slow-phase velocity exponentially increasing (Figure 62.20), however, strongly suggests the diagnosis of congenital nystagmus, although some exceptions have been reported.43 The diagnosis of pendular nystagmus is usually easy by simple clinical inspection and confirmed with recordings but establishing whether it is acquired or congenital is not possible on simple oculographic criteria. Patients with acquired pendular nystagmus usually have clinically severe vascular or demyelinating brainstem disease whereas patients with congenital pendular nystagmus have congenital or infantile visual loss and defects.
Ocular Involvement in Muckle-Wells Syndrome
Published in Ocular Immunology and Inflammation, 2020
Sukru Cekic, Ozgur Yalcinbayir, Sara Sebnem Kilic
Mean BCVA was 0.48 ± 0.81 logMAR units in this study (range: 0.0 to 3.0). Examination of ocular motility and alignment of cases were completely normal except for the index patient who had bilateral acquired pendular nystagmus and quite low vision. Anterior segment biomicroscopy showed that band keratopathy was present in four eyes of the two patients; namely in the index patient and the patient who had cataract removal. Corneal leukoma due to corneal scarring was present in both eyes of another patient who was a 42-years-old female (patient H in Tables 1 and 2). In this patient, corneal topography demonstrated central flattening as well as surrounding steepening (Figure 2). Posterior stromal corneal opacification with edema and accompanying anterior iris snychecia was present in one eye of the index patient (Figure 3). Mild cataract was present in the other eye of the index patient that had received dexamethasone implant for uveitis. Clinical signs consistent with past uveitis (e.g. pigment on the anterior lens capsule, hyalinized keratic precipitates) were present in four eyes of three individuals. (Table 2).
A novel PAX6 mutation causes congenital aniridia with or without retinal detachment
Published in Ophthalmic Genetics, 2019
Mehraban Mirrahimi, Hamideh Sabbaghi, Hamid Ahmadieh, Mehdi Jahanmard, Kiana Hassanpour, Fatemeh Suri
A 28-year-old man underwent ophthalmic examination as a member of the family affected with aniridia. RRD had occurred in the left eye 14 years ago followed by RRD in the right eye one year later. He had no previous ocular surgery at the time of RRD and a dislocated, cataractous lens was noticed in both of his eyes. Each eye underwent lensectomy, pars plana vitrectomy (PPV) and silicone oil (SO) injection. Retinal redetachment occurred in the left eye due to proliferative vitreoretinopathy resulting in reoperation. At the current examination, a pendular nystagmus was apparent. Visual acuity was a light perception in the right eye and hand motion in the left eye. IOP was measured 35 and 50 mmHg in the right and left eyes, respectively. Slit lamp examination revealed superficial punctate keratopathy, central corneal scar, limbal stem cell deficiency, peripheral corneal vascularization and corneal stromal edema due to silicone oil touch in both eyes. Fundus detail was not visible due to severe corneal opacity, but cryopexy and laser scars were visible, and retina seemed to be attached.
The distinct optic disk and peripapillary appearance in Donnai–Barrow syndrome
Published in Ophthalmic Genetics, 2018
Subject 5: A 20-month-old girl with a history of uneventful normal pregnancy and delivery was examined. She had been previously diagnosed with high myopia and retinal dystrophy but was not wearing her prescribed glasses. There was a small amplitude rapid pendular nystagmus and an intermittent small angle esotropia. She would fix and follow with either eye. Slit-lamp examination showed smooth, cryptless irides. The crystalline lenses were clear and in place. Cycloplegic retinoscopy was −12.00–3.50 x 090 in either eye. Fundus exam revealed widespread severe chorioretinal atrophy with a circumscribed patch of further central macular atrophy (macular pseudocoloboma). This ocular phenotype is pathognomonic for Knobloch syndrome (5). When the parents were specifically questioned regarding the presence of an occipital defect, a classic feature of Knobloch syndrome, they confirmed the child had a circumscribed cutaneous occipital lesion with overlying lack of hair (Figure 5). Genetic testing confirmed homozygosity for a novel COL18A1 mutation (NM_130455.3: c.2978_2987del; p.Pro993Leufs*35). LRP2 sequencing showed heterozygosity for the familial mutation.