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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.
Infectious Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Susanna J. Dunachie, Hanif Esmail, Ruth Corrigan, Maria Dudareva
Symptoms include low-grade fever, headache and neck stiffness. Confusion or a reduced Glasgow coma score is present in 30–60%. Cranial nerve palsies occur in 30–50%. Tuberculoma may present with focal neurology or seizures.
The nervous system and the eye
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
James A.R. Nicoll, William Stewart, Fiona Roberts
Tumour cells may spread through the subarachnoid space, sometimes without an associated deposit of solid tumour in the brain or spinal cord. Patients often present with cranial nerve palsies. Malignant cells may be identified in the CSF (Figure 12.53). The neoplastic cells may be secondary (e.g. carcinoma, melanoma) or primary (e.g. medulloblastoma, ependymoma, glioblastoma).
Treatment of low flow, indirect cavernous sinus dural arteriovenous fistulas with external manual carotid compression – the UK experience
Published in British Journal of Neurosurgery, 2020
Pratipal Kalsi, Rajeev Padmanabhan, Manjunath Prasad K. S., Nitin Mukerji
CS-DAVF usually occur in middle aged and elderly females but they can occur in any age group or sex. Clinical symptoms depend on whether the fistula drains anteriorly or posteriorly. Anteriorly draining CS-DAVF often present with visual symptoms, which include conjunctival injection, chemosis, extraocular nerve palsies leading to ohthalmoplegia, proptosis, retro-orbital pain and obtundation if an intracerebral hemorrhage occurs. Some patients may also have a bruit.4,5 Raised episcleral venous pressure may lead to an increase in intracocular pressure and visual loss. Visual loss is less common than in direct CS-DAVF but can occur in up to 30% of patients.6,7 CS-DAVF draining into the superior and inferior petrosal sinuses are usually asymptomatic. These patients don’t usually have ocular symptoms but can present with cranial nerve palsies.8–10 Infrequently posteriorly draining fistulas can cause brainstem congestion and neurological deficits.11 20-50% CS-DAVFs of will close spontaneously.12,13 Intracranial haemorrhage is an extremely rare complication.14
Cranial nerve palsies due to incidental durotomy in lumbar Spine surgery: a case report
Published in British Journal of Neurosurgery, 2020
Thea Overgaard Wichmann, Sanja Karabegovic, Mikkel Mylius Rasmussen
Cranial nerve palsies are well-recognised symptoms of spontaneous intracranial hypotension subsequent to spontaneous CSF leaks.8 In such cases the time of onset of the leak is generally not known and therefore the timing of symptoms onset cannot be related to it. In our case it can. In the seven case reports on abducens nerve palsy the causative cause was ID during spine surgery. According to these reports, cranial nerve palsies are expected to occur days to weeks after ID, and to resolve completely within months, regardless of the treatment approach. In our case, a conservative approach was chosen initially. Since an ID seemed most likely to cause the progression in symptoms the leak was repaired surgically. In the previously reported cases similar approaches have been used. In all cases complete resolution was obtained.3 Chronicity and recurrence of symptoms have not been reported.
Combined neurosurgical and orbital intervention for spheno-orbital meningiomas - the Manchester experience
Published in Orbit, 2020
J. Young, F. Mdanat, A. Dharmasena, P. Cannon, B. Leatherbarrow, C. Hammerbeck-Ward, S. Rutherford, S. Ataullah
Post-operative cranial nerve palsies were found in 10 patients. This included abducens nerve (CN VI) palsy in six patients. Only one of those patients had a persisting CN VI deficit at last follow-up. Two patients had an oculomotor nerve (CN III) palsy, which persisted in one patient but was noted to have improved at last follow-up. Two patients had injuries involving three cranial nerves. One of them had an oculomotor nerve (CNIII) injury, hypoaesthesia of the ophthalmic branch of the trigeminal nerve (V1), and an abducens nerve (CN VI) palsy. The other had an oculomotor nerve (CN III) injury, as well as trochlear nerve (CN IV) and abducens nerve (VI) palsies. Both of these patients had persisting cranial nerve deficit at last follow-up. These cranial nerve palsies were most likely due to intraoperative manipulation, particularly in those patients with a tumour encroaching on or involving the superior orbital fissure and cavernous sinus.