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Infection-Associated Ocular Cranial Nerve Palsies
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Hardeep Singh Malhotra, Imran Rizvi, Neeraj Kumar, Kiran Preet Malhotra, Gaurav Kumar, Manoj K. Goyal, Manish Modi, Ravindra Kumar Garg, Vivek Lal
Around 20–30% patients develop varied cranial nerve palsies. Involvement of cranial nerves occur due to ischemia (secondary to vascular compression/strangulation), nerve entrapment in the basal exudates, or as a false localizing sign due to increased ICP in 17–40% of cases. Cranial nerves commonly involved are the second, third, fourth, sixth, and seventh cranial nerves. Sixth cranial nerve is the most commonly involved cranial nerve, frequently occurring as a result of an increased ICP or brainstem involvement. Bilateral sixth nerve involvement is also common. Third nerve is next commonly involved ocular cranial nerve. Isolated trochlear nerve involvement has also been reported in literature. Encasement secondary to basal arachnoiditis or direct involvement of brainstem due to tuberculomas, infarction, or edema are the commonly implicated hypothesis. Formation of tuberculomas at other strategic sites too might lead to ophthalmoparesis. Kapadia et al. reported tuberculomas in cavernous sinus in a 48-year-old woman presenting with ophthalmoparesis (17). Other ocular signs like internuclear ophthalmoplegia have also been noted in isolated case reports. Tubercular abscess may also cause ophthalmoplegia due to direct compression or increased ICP.
Neuromuscular Junction Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Diana Mnatsakanova, Qin Li Jiang
Cranial neuropathy: MG never involves the pupil, distinguishing it from Horner's syndrome or a third nerve palsy.MG may mimic sixth nerve palsy with isolated lateral rectus weakness, but may be distinguished by fatigability and lack of pain.MG may produce a pseudointernuclear ophthalmoplegia with isolated medial rectus weakness. Patients with true internuclear ophthalmoplegia usually have spared convergence.
Ophthalmology
Published in Shibley Rahman, Avinash Sharma, A Complete MRCP(UK) Parts 1 and 2 Written Examination Revision Guide, 2018
Shibley Rahman, Avinash Sharma
Internuclear ophthalmoplegia: Internuclear tracts connect the ocular motor nuclei within the brainstem and coordinate eye movements. When affected by multiple sclerosis, there is limitation or slowing of adduction associated with abducting nystagmus in the fellow eye. A wall-eyed bilateral internuclear ophthalmoplegia (WEBINO) is also possible. This is a failure to adduct both eyes, but preservation of up and down gaze suggests a demyelinating process, and failure of ocular adduction in such cases should prompt the diagnosis of internuclear ophthalmoplegia.
The Spectrum of Ocular Manifestations in Patients with Waldenström’s Macroglobulinemia
Published in Ocular Immunology and Inflammation, 2022
Rosanna Dammacco, Walter Lisch, Tero T. Kivelä, Evangelos Terpos, Efstathios Kastritis, Dario Sisto, Alberto Mavilio, Roberto Ria, Giovanni Alessio, Angelo Vacca, Franco Dammacco
A striking and rare ophthalmological picture was observed in patient #15 (Table 1). She had been seen by three different neurologists because of a 5-year history of slowly progressive weakness in the lower extremities, paresthesia, ataxic gait, and a slight palpebral ptosis of the left eye. After routine laboratory tests revealed a conspicuous monoclonal component in the serum electrophoretic pattern, the patient was seen at the Department of Internal Medicine of our hospital, where a full clinical, hematological and immunological workup led to an unequivocal diagnosis of WM. A subsequent ophthalmological examination revealed left internuclear ophthalmoplegia, nystagmus, and paresis of the oculomotor nerve with restricted adduction and elevation movements of the eyeball. While anti-myelin-associated glycoprotein antibodies were absent, she tested positive for cold agglutinins and IgM antibodies against GD1b and GQ1b disialosyl epitopes, resulting in a final diagnosis of CANOMAD (chronic ataxic neuropathy, ophthalmoplegia, IgM monoclonal gammopathy, cold agglutinins, and disialosyl antibodies) syndrome.22
The Management of Childhood Intracranial Tumours and the Role of the Ophthalmologist
Published in Neuro-Ophthalmology, 2019
G. Mole, R. Edminson, A Higham, C. Hopper, D. Hildebrand
Other neuro-ophthalmic manifestations are shown in Table 3 the most common of which was non-paralytic strabismus (n=33) followed by sixth nerve palsy (n=19) and seventh nerve palsy (n=12). Only one child presented with non-paralytic strabismus which was an exotropia in the context of poor vision in one eye secondary to an optic nerve glioma. One child had a long-standing esotropia and had previously undergone strabismus surgery. Of the remaining 31 cases of non-paralytic strabismus observed during the period of follow up, 21 cases were convergent and 10 cases were divergent. Tumours located in the posterior fossa were more likely to lead to palsies of cranial nerves III, IV & VI (n = 16, 30%) and seventh nerve palsy (n = 11, 20%), when compared to supratentorial tumours and palsies affecting cranial nerves III, IV & VI (n = 8, 11%) and seventh nerve palsy (n=0, 0%). There was one-seventh nerve palsy in a child with tumour locations in both the posterior fossa and supratentorial region. All 10 cases of internuclear ophthalmoplegia were in children with tumours located in the posterior fossa.
Double vision in adults
Published in Journal of Binocular Vision and Ocular Motility, 2018
Five of 125 subjects developed diplopia due to cerebrovascular disease. One subject developed a vertical skew deviation associated with labyrinthitis, and another subject developed a skew deviation with ET and nystagmus after excision of a midbrain tumor. Of the subjects with cerebrovascular disease, one developed an acute ET measuring 7 PD in the primary position both at distance and near with a mild increase on left gaze. The diplopia resolved 2 months after onset. Two subjects with multiple cerebrovascular accidents developed a small acute vertical deviation which resolved. A 91-year-old subject developed an acute internuclear ophthalmoplegia that was presumably ischemic in origin. This subject’s motility improved over several months.