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Ocular Motor Cranial Neuropathies
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Zane Foster, Ashwini Kini, Bayan Al-Othman, Andrew G. Lee
The fourth cranial nerve arises from the trochlear nucleus in the midbrain. The trochlear nerve is unique in that not only does it exit dorsally from the brainstem but also it decussates and innervates the contralateral side. However, because it is a purely motor nerve and innervates only one muscle, it is impossible to localize a fourth nerve palsy to the nucleus or fascicle in the absence of any other brainstem signs without imaging studies. Despite this, neuroimaging generally has little clinical value in isolated cases. Many authors and textbooks recommended that clinically isolated fourth nerve palsy can be observed with imaging performed only in patients who do not improve after 3 months of evaluation, or in younger patients who have either a history of cancer or multiple neurological complaints.12 Neuroimaging in this setting, however, is a practice option.
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).
Binocular vision problems after refractive surgery
Published in Jan-Tjeerd de Faber, 28th European Strabismological Association Meeting, 2020
D.J.M. Godts, M.J. Tassignon, L. Gobin
The second patient was a 42-year-old man with complaints of intermittent diplopia after having had an uneventful LASIK for myopia of both eyes simultaneously. The patient underwent strabismus surgery on both eyes in 1990 for a congenital right fourth nerve palsy. Preoperative best-corrected visual acuity was 20/20 in both eyes. The refractive error before surgery was −5.25 in the right eye and −5.00 in the left eye. Postoperative uncorrected visual acuity was 20/40 in the right eye and 20/32 in the left eye. Postoperative best-corrected visual acuity at distance was 20/25 in the right eye and 20/20 in the left eye. The right eye needed an additional correction of −1.00 (−0.25 × 20°) and the left eye an additional correction of −0.50 (−0.25 × 170°). Uncorrected visual acuity at near was 20/40 in the right eye and 20/25 in the left eye. Orthoptic examination showed a right hyperphoria of 3 PD at near and 2 PD at distance, slightly increasing in down and left gaze. The right eye was dominant. Ocular motility evaluation showed a V pattern, an underaction of the right superior oblique muscle (Fig. 2) and a positive Bielschowsky head-tilt-test. Vertical fusion amplitude was increased to 6° on Synoptophore. Excyclotorsion of 1° was measured in both eyes. On fundus examination the left eye had an important torsion of the macula compared to the right eye. The diagnosis of a recurrent right fourth nerve palsy was made.
Evaluation and Management of Symptomatic Vertical Strabismus and Diplopia
Published in Journal of Binocular Vision and Ocular Motility, 2022
Joseph W. Fong, Laurie A. Hahn-Parrott, R. Michael Siatkowski
Vertical misalignment of the visual axes following damage to the supranuclear control areas for ocular movement is termed the Magendie-Hertwig syndrome or skew deviation.11 In skew deviation, damage may occur anywhere along the utriculo-ocular pathway, from the inner ear to the brainstem. The hypertropic eye is usually incyclotorted, but other patterns of skew deviation may occur depending on exactly where the lesion is.12 Of these, a skew deviation that mimics ipsilateral inferior rectus paresis is most common.13 Strabismus due to skew deviation may or may not get noticeably larger in contralateral gaze or ipsilateral head tilt and generally has incyclotorsion of the hypertropic eye. In comparison, a fourth nerve palsy should get noticeably larger in contralateral gaze and ipsilateral head tilt (unless there has been a spread of comitance) and generally produces excyclotorsion of the hypertropic eye. Skew deviation, however, can produce a comitant vertical strabismus with variable amounts of torsion.
Superior oblique palsy: A case report
Published in Cogent Medicine, 2020
Ngozika Esther Ezinne, Kingsley Kenechukwu Ekemiri, Aliyah Khan
The first step in treating cranial nerve palsies is to determine the etiology once the etiology is found, then treatment can begin (Mollan et al., 2009; Tamhankar et al., 2013). High satisfaction with prismatic correction has been reported in patients with decompensated SOP (Bagheri et al., 2010). Younger patients may use Fresnel’s prisms as a temporary option. However, excyclotorsion and incomitance of the deviation may leave some patients unsatisfied with prisms. If the fourth nerve palsy is due to previous trauma and has recently decompensated, the diplopia can be managed by the placement of vertical prisms in spectacles. When managing isolated CN IV palsy, it is advisable to delay prescribing permanent prisms for at least three months in order to allow for the palsy to recover. Otherwise, glasses with permanent prism correction can induce vertical diplopia should the palsy recover. Others, particularly those with ischemic palsies, in whom recovery is expected, can occlude the lower half of the lens over the affected eye (Prieto-Díaz et al., 2003). Opaque or black tape, for instance, can also be used to occlude the affected eye in the direction of action of the superior oblique muscle (Bagheri et al., 2010; Gunderson et al., 2001; Prieto-Díaz et al., 2003).
Neuro-Ophthalmic Literature Review
Published in Neuro-Ophthalmology, 2019
David Bellows, Noel Chan, John Chen, Hui-Chen Cheng, Peter MacIntosh, Jenny Nij Bijvank, Michael Vaphiades, Konrad Weber
Sixty-six patients aged 0–19 years old were included in this study. Neoplasia involving the central nervous system was the most common cause of third, fourth and sixth cranial nerve palsies both in children (20%) and adolescents (31%). Overall, apart from neoplasm (23%), the most common causes included idiopathic (14%), inflammation (11%) and non-aneurysmal vascular contact (11%). The most common cause of fourth cranial nerve palsy was late decompensation of congenital fourth nerve palsy (46%) with the evidence of absence or atrophy of fourth nerve and/or superior oblique muscle in the paretic eye. Only four patients presented with combined ocular motor nerve palsies of which 75% were attributable to Miller Fisher syndrome (MFS), while one patient was secondary to cavernous sinus thrombophlebitis. Of note, three patients with intracranial haemorrhage presented with isolated cranial nerve palsy without other additional neurological signs. Among six patients with MFS, two of them presented with bilateral sixth cranial nerve palsies and one presented with unilateral sixth cranial nerve palsy. The authors suggested to consider the possibility of MFS in cases of isolated third, fourth or sixth cranial nerve palsy as well.