Facial Nerve Palsy from Cerebral Venous Sinus Thrombosis: An Effect of Increased ICP

Hussain, Mohammed; Siddiqui, Muzaffar

doi:10.1017/cjn.2016.446

Cited by 2 publications

(6 citation statements)

References 10 publications

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“…Facial weakness improved in a month among 5 of the 6 patients who had follow-up data reported. One patient had complete resolution of facial weakness, headache, and diplopia immediately after lumbar puncture 2. One patient had left hemiplegia that resolved in 2 weeks of treatment with anticoagulation and acetazolamide 3.…”

Section: Resultsmentioning

confidence: 98%

“…More than 1 mechanism may play a role in atypical cranial nerve palsies in CVST. In one study, lumbar puncture resulted in a quick resolution of headache, diplopia, and facial weakness suggesting the role of raised intracranial pressure 2…”

Section: Discussionmentioning

confidence: 99%

“…Seven patients aged 17 to 42 years, 100% of women, had lower motor neuron type facial palsy associated with CVST. [2][3][4][5][6][7][8] Facial weakness developed up to 2 weeks after the onset of the headache except for one case where headache occurred 10 days after facial weakness. 8 CVST was commonly noted in SS (n = 7) and TS (n = 6); SSS was also involved in 3 patients.…”

Section: Cvst With Peripheral VII Palsymentioning

confidence: 99%

“…One patient had complete resolution of facial weakness, headache, and diplopia immediately after lumbar puncture. 2 One patient had left hemiplegia that resolved in 2 weeks of treatment with anticoagulation and acetazolamide. 3 Partial recanalization was seen in 2 (one of these patients had resolved facial palsy 10 d after imaging) of the 3 patients who reported follow-up imaging and 1 patient had persistent thrombosis at 6 months despite improved facial weakness.…”

Section: Cvst With Peripheral VII Palsymentioning

confidence: 99%

“…3 Partial recanalization was seen in 2 (one of these patients had resolved facial palsy 10 d after imaging) of the 3 patients who reported follow-up imaging and 1 patient had persistent thrombosis at 6 months despite improved facial weakness. 2,4,7 CVST With Vestibulocochlear Involvement…”

Section: Cvst With Peripheral VII Palsymentioning

confidence: 99%

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Nonabducent Cranial Neuropathies in Cerebral Venous Sinus Thrombosis

Nagaraja

Sabu²

2021

The Neurologist

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Introduction: Cerebral venous sinus thrombosis (CVST) can rarely present with cranial neuropathies other than abducent nerve palsy. The authors report a case and review the literature for nonabducent cranial neuropathies in CVST. Case Report: A 22-year-old woman with a history of oral contraceptive use developed right-sided headache, blurred vision, and dizziness for 4 days. Magnetic resonance venogram showed complete thrombosis of the right transverse sinus, sigmoid sinus, and internal jugular vein, and partial thrombosis of the superior sagittal sinus, left transverse sinus, and superior part of the left internal jugular vein. Hypercoagulable workup revealed heterozygous factor V Leiden mutation. About 2 weeks after symptom onset, she developed right facial droop and left eye ptosis. Examination revealed bilateral papilledema, partial left ptosis, complete right abducent, and right peripheral facial palsies. Acetazolamide 250 mg 2 times per day was initiated for the treatment of headache. Three days after starting acetazolamide left ptosis, right facial and abducent palsies improved that continued to get better with only slight deficits at discharge 4 weeks from symptom onset. Follow-up computed tomography venogram on day 24 showed partial recanalization of CVST. Conclusion: A systematic review identified 26 patients from 21 articles with nonabducent cranial neuropathies. Seven patients had lower motor neuron facial palsy, 13 patients had hearing loss or vertigo with vestibulocochlear involvement, and 6 patients had other mixed cranial nerve palsies with CVST. They are usually associated with transverse sinus and/or sigmoid sinus thrombosis. They have a good prognosis with improvement and complete resolution of cranial neuropathies in most cases usually in 1 month.

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Section: Resultsmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Cvst With Peripheral VII Palsymentioning

confidence: 99%

Section: Cvst With Peripheral VII Palsymentioning

confidence: 99%

Section: Cvst With Peripheral VII Palsymentioning

confidence: 99%

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Nonabducent Cranial Neuropathies in Cerebral Venous Sinus Thrombosis

Nagaraja

Sabu²

2021

The Neurologist

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Changing the paradigm of intracranial hypertension in brain tumor patients: a study based on non-invasive ICP measurements

et al. 2020

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Background The ultrasound based non-invasive ICP measurement method has been recently validated. Correlation of symptoms and signs of intracranial hypertension with actual ICP measurements in patients with large intracranial tumors is controversial. The purpose of this study was to assess ICP in patients with brain tumors, presenting with neurological signs and symptoms of elevated ICP and to further evaluate the value and utility of non-invasive ICP monitoring. Methods Twenty patients underwent non-invasive ICP measurement using a two-depth transcranial Doppler ultrasound designed to simultaneously compare pulse dynamics in the proximal (intracranial), and the distal (extracranial) intraorbital segments of the ophthalmic artery through the closed eyelid. Results Forty-eight measurements were analyzed. Radiological characteristics included tumor volume (range = 5.45–220.27cm3, mean = 48.81 cm3), perilesional edema (range = 0–238.27cm3, mean = 74.40 cm3), and midline shift (mean = 3.99 mm). All ICP measurements were in the normal range of 7–16 mmHg (ICPmean: 9.19 mmHg). The correlation of demographics, clinical and radiological variables in a bivariate association, showed a statistically significant correlation with neurological deficits and ICPmax (p = 0.02) as well as ICPmean (p = 0.01). The correlation between ICP and neurological deficits, showed a negative value of the estimate. The ICP was not increased in all cases, whether ipsilateral nor contralateral to the tumor. The multivariate model analysis demonstrated that neurological deficits were associated with lower ICPmax values, whereas maximum tumor diameter was associated with larger ICPmax values. Conclusions This study demonstrated that ICP in patients with intracranial tumors and mass effect is not necessarily increased. Therefore, clinical signs of intracranial hypertension do not necessarily reflect increased ICP.

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Facial Nerve Palsy from Cerebral Venous Sinus Thrombosis: An Effect of Increased ICP

Cited by 2 publications

References 10 publications

Nonabducent Cranial Neuropathies in Cerebral Venous Sinus Thrombosis

Nonabducent Cranial Neuropathies in Cerebral Venous Sinus Thrombosis

Changing the paradigm of intracranial hypertension in brain tumor patients: a study based on non-invasive ICP measurements

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