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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
There are several additional anatomical considerations to consider with the sixth cranial nerve. First, the seventh cranial nerve wraps around the abducens nucleus, so lesions of the abducens nucleus often have seventh nerve involvement. Second, it has the longest course of the three ocular nerves, traveling vertically along the clivus, then turning a full 90 degrees to exit through Dorello's canal. This leaves it very susceptible to stretch and impingement against the rim of the clivus. Any lesion that causes downward displacement of the brainstem, or a change in intracranial pressure, either increase or decrease, can thus result in a sixth nerve palsy. For this reason, a sixth nerve palsy is typically described as “nonlocalizing.”18 In fact, upward of 30% of patients with pseudotumor cerebri may present with a sixth nerve lesion as the only feature of their condition.19
Neurology and neurosurgery
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
12.34, In the presence of raised intracranial pressure there may bebradycardia.bilateral sixth nerve palsy.arterial hypertension.somnolence.no papilledema in a newborn infant.
The useful of botulinum toxin Type-A in the treatment of chronic sixth ocular nerve palsy
Published in Jan-Tjeerd de Faber, 28th European Strabismological Association Meeting, 2020
L. Sabetti, L. D’Alessandri, K. Salvatori, E. Balestrazzi
Acquired sixth nerve palsy, is usually a consequence of vascular diseases, diabetes, head trauma or cerebral tumours (Jampolsky, 1976). Diagnosis and management of this neurogenic ocular palsy are often difficult and the poor or unknown clinical history of the patients is not able to help the ophthalmologist.
Inflammatory Sixth Nerve Palsy Post-COVID-19 Vaccination: Magnetic Resonance Imaging Findings
Published in Neuro-Ophthalmology, 2022
Emely Z. Karam, Patricia Ríos Macias, Gabriela Chahin, Jorge C Kattah
The laboratory tests (haematology, HbA1c, and complete chemistry) were normal. Sars-CoV-2 polymerase-chain reaction (PCR) test was negative. Orbital computer tomography scans were normal. Brain magnetic resonance imaging (MRI) obtained 10 days after symptom onset showed focal enlargement of the root exit zone and the cisternal portion of the left sixth nerve with post-gadolinium enhancement (Figure 2a,b). On follow–up, 2 weeks later, the sixth nerve palsy had begun to improve and it resolved within five weeks (Figure 1d–f). Parallel to the clinical improvement, further MRI 4 weeks after presentation showed decreased perineural contrast uptake (Figure 2c,d). Because of the steady, spontaneous improvement, we did not pursue additional investigation. Eight weeks later, the patient remained asymptomatic and contrast-enhance brain MRI showed residual minimal enhancement of the sixth nerve (Figure 2e,f).
Chameleons, red herrings, and false localizing signs in neurocritical care
Published in British Journal of Neurosurgery, 2022
Boyi Li, Tolga Sursal, Christian Bowers, Chad Cole, Chirag Gandhi, Meic Schmidt, Stephan Mayer, Fawaz Al-Mufti
Sixth nerve palsy is commonly encountered in ophthalmologic and neurological practices, and typically presents as an ipsilateral abduction deficit and esotropia, causing horizontal diplopia, which worsens at a distance and when looking in the direction of the affected nerve.5 True-localizing sixth nerve palsy is commonly caused by vascular disease such as intracavernous carotid aneurysm, and also has associations with hypertension, diabetes, and multiple sclerosis.5 Abducens nerve palsy is the extraocular nerve palsy with highest incidence (11.3 in 100,000).5,6 Abducens nerve palsies are also the most common FLS of elevated ICP, occurring in up to 1/3 of patients with IIH.3,7 The most cited series describes 101 patients with IIH where 14 patients had sixth nerve palsy (11 unilateral and 3 bilateral),8 whereas another study cites 2 out of 104 neurologically isolated cases.9 Several pathophysiologic mechanisms have been suggested; the most accepted being stretching of the nerve due to its long intracranial course.1 Another hypothesis involves compression of the nerve against the petrous ligament or ridge of the petrous temporal bone.1 Clinically, this FLS presents as sixty nerve palsy but with raised ICP that can be diagnosed on lumbar puncture, and as it is the most common FLS of elevated ICP, it should be considered in situations such as IIH. Neuroimaging can aid in identifying the etiology of sixth nerve palsy, even in those with evidence of possible vasculopathy.9
A modified vertical muscle transposition for the treatment of large-angle esotropia due to sixth nerve palsy
Published in Strabismus, 2018
Aliakbar Sabermoghadam, Mohammad Etezad Razavi, Mohammad Sharifi, Mohammad Yaser Kiarudi, Sadegh Ghafarian
The mean correction of esotropia in our study was approximately 49 PD. This is in agreement with the previous studies applied Nishida’s procedure. In Muraki and colleagues’ study,5 the mean correction in all nine patients was reported to be 46.3 ± 13.1 PD. In Murthy’s study, the correction obtained was 30–35 PD with transposition alone and with MR recession, it increased to 50 PD.7 Oh and Jang 12 reported one case of sixth nerve palsy treated with this method and found similar outcome. The correction effect of Nishida’s procedure is comparable with other VRT techniques. The conventional transposition of both vertical rectus muscles without MR recession or posterior fixation corrects 32 PD and with augmentation by botulinum toxin injection or posterior fixation sutures, it will be increased to about 50 PD.10 In our series, two patients showed small overcorrection at 1 month follow-up that disappeared in the final visit. We think that in this procedure, early small overcorrection is a favorable outcome and resolves during time.