Transient oculomotor nerve palsy due to non-aneurysmal neurovascular compression

Joshi, Stuti; Tee, William Wei Han; Franconi, Catherine; Prentice, David

doi:10.1016/j.jocn.2017.07.006

Cited by 17 publications

(12 citation statements)

References 6 publications

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“…The development of high-resolution magnetic resonance imaging (MRI) has enabled us to detect pathologies not detected or diagnosed in the past [12,13]. Schwannoma of cranial nerves in its early stage and nonaneurysmal vascular contact [14,15] are such examples. The use of three-dimensional steady-state free precession sequences and modified fully refocused steady-state sequences such as constructive interference in steady-state (CISS)/fast imaging employing steady-state acquisition cycled phases (FIESTA-C)/balanced fast field echo (B-FFE) has provided augmented visualization of cranial nerves in vivo.…”

Section: Introductionmentioning

confidence: 99%

Acquired onset of third, fourth, and sixth cranial nerve palsies in children and adolescents

Park

Min

et al. 2019

Eye

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Purpose To describe the causes of third, fourth, and sixth cranial nerve palsies in children and adolescents. Methods In this retrospective case series, a total of 66 patients aged 0-19 years with third, fourth, and sixth cranial nerve palsies seen in strabismus and neuro-ophthalmic practice from 2010 to 2017 were included. Causes of palsies were determined based on clinical assessment, high-resolution magnetic resonance imaging (MRI), and laboratory work-up. Results Thirty-five patients had sixth cranial nerve palsy, 14 patients had third cranial nerve palsy (7 partial, 7 complete), 13 patients had fourth cranial nerve palsy, and 4 patients had combined cranial nerve palsies in this study. Neoplasia involving central nervous system was one of the most common causes of third, fourth, and sixth cranial nerve palsies both in children (age: 0-14 years) and adolescents (age: 15-19 years) (20% and 31%, respectively). Overall, neoplasia (23%) was the most common cause of acute third, fourth, and sixth cranial nerve palsies, followed by idiopathic cause (14%), inflammation (11%), and non-aneurysmal vascular contact (11%). Neoplasia was also the most common cause of sixth and third cranial nerve palsies (25% and 29%, respectively). The most common cause of fourth cranial nerve palsy was late decompensation in congenital fourth cranial nerve palsy (46%). Conclusions A substantial proportion of pediatric and juvenile patients had serious pathologies for third, fourth, and sixth cranial nerve palsies. If nerve palsies are indicated, prompt diagnosis of etiologies using high-resolution MRI with contrast and laboratory work-up are important for this disease population.

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Section: Introductionmentioning

confidence: 99%

Acquired onset of third, fourth, and sixth cranial nerve palsies in children and adolescents

Park

Min

et al. 2019

Eye

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“…However, some studies suggest that mechanical compression caused by abnormal structures, such as aneurysms and intracranial lesions, can result in axonal membrane instability and nerve ischemia, which would further induce segmental demyelination and ephaptic neural transmission hyperexcitability[ 4 ]. Additionally, an acute reaction of pulsations on the ON may clarify the acute presentation of ONP[ 5 ], whereas the ischemic effect of pulsations and the atherosclerotic deformation associated with aging may explain the chronic and persistent forms of this condition[ 6 , 7 ].…”

Section: Discussionmentioning

confidence: 99%

Microvascular decompression for a patient with oculomotor palsy caused by posterior cerebral artery compression: A case report and literature review

Zhang¹,

Wei²,

Wang³

et al. 2022

WJCC

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BACKGROUND Aneurysm compression, diabetes, and traumatic brain injury are well-known causative factors of oculomotor nerve palsy (ONP), while cases of ONP induced by neurovascular conflicts have rarely been reported in the medical community. Here, we report a typical case of ONP caused by right posterior cerebral artery (PCA) compression to increase neurosurgeons’ awareness of the disease and reduce misdiagnosis and recurrence. CASE SUMMARY A 54-year-old man without a known medical history presented with right ONP for the past 5 years. The patient presented to the hospital with right ptosis, diplopia, anisocoria (rt 5 mm, lt 2.5 mm), loss of duction in all directions, abduction, and light impaired pupillary reflexes. Magnetic resonance angiography and computed tomography venography examinations showed no phlebangioma, aneurysm, or intracranial lesion. After conducting oral glucose tolerance and prostigmin tests, diabetes and myasthenia gravis were excluded. Cranial nerve magnetic resonance imaging showed that the right PCA loop was in direct contact with the cisternal segment of the right oculomotor nerve (ON). Microvascular decompression (MVD) of the culprit vessel from the ON through a right subtemporal craniotomy was carried out, and the ONP symptoms were significantly relieved after 3 mo. CONCLUSION Vascular compression of the ON is a rare pathogeny of ONP that may be refractory to drug therapy and ophthalmic strabismus surgery. MVD is an effective treatment for ONP induced by neurovascular compression.

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“…Apart from the intraocular muscular involvement during OMNP, pupillary involvement is also higher suspicion of compression because the pupillomotor fibers and their vascular component originates from overlying pia course along the superficial as well as superomedial aspect of the oculomotor nerve. 14,16 Also, trauma, stroke, post-surgical inflammation, neoplasms as well as microvascular damage from chronic disease have been implicated as cause of OMNP. 14,17 Our patient condition was initially misdiagnosed as an acute cerebral infarction and treated with aspirin, clopidogrel, fluvastatin and mecobalamin with no improvement.…”

Section: Discussionmentioning

confidence: 99%

Contrast-enhanced encephalopathy and massive cerebral edema after endovascular coiling of cerebral aneurysm. A case report

Zhou

Richard

Yin-sheng

et al. 2021

Veins and Lymphatics

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Contrast-induced encephalopathy (CIEP) is a rare complication after endovascular therapy. The etiology of CIEP is still a matter of debate. We present a rare occurrence of CIEP in a known hypertensive and type 2 diabetic patient after endovascular coiling of cerebral aneurysm with oculomotor nerve palsy. A 68-year old female presented with seven days history of headache and left ptosis or blepharoptosis with mild mydriasis. The headaches were localized mainly at the left side of the nose, orbit, and upper forehead while the left ptosis was associated with blurred vision. Computed tomography angiography revealed an aneurysm in between the C4 segment of the left internal carotid artery (ICA) and the bifurcation of the left posterior communicating artery. Digital subtraction angiography further confirmed the aneurysm. We used the transarterial approach to assess the aneurysm and subsequent coiling. Iohexol (Omnipaque) contrast agent was used during the endovascular procedure. The patient’s condition deteriorated into acute confusion state with cardinal symptomology of CIEP immediately after the operation. Computed tomography scan revealed cortical contrast enhancement in the vascular territory of the ICA as well as edema. Her symptomatology resolved 48 hours after treated with anticonvulsants, intracranial pressure reduction and hydration. Chronic hypertension as well as type 2 diabetics may be critical predisposing factors to CIEP. CIEP should be suspected in patients presenting with acute confusion state after endovascular therapy. Massive edema with ischemic brain changes in white matter of the brain before endovascular procedure should rise suspicion of CIEP.

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Transient oculomotor nerve palsy due to non-aneurysmal neurovascular compression

Cited by 17 publications

References 6 publications

Acquired onset of third, fourth, and sixth cranial nerve palsies in children and adolescents

Acquired onset of third, fourth, and sixth cranial nerve palsies in children and adolescents

Microvascular decompression for a patient with oculomotor palsy caused by posterior cerebral artery compression: A case report and literature review

Contrast-enhanced encephalopathy and massive cerebral edema after endovascular coiling of cerebral aneurysm. A case report

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