APIK Journal of Internal Medicine

: 2021  |  Volume : 9  |  Issue : 3  |  Page : 189--191

A case of bilateral lower motor neuron facial palsy in cerebral venous sinus thrombosis

Vaishal Shah, Vijay Sardana 
 Department of Neurology, Government Medical College, Kota, Rajasthan, India

Correspondence Address:
Prof. Vijay Sardana
Department of Neurology, MBS Hospital, Nayapura, Kota - 324 001, Rajasthan


Cerebral venous thrombosis commonly presents with headache, seizure, and motor weakness. Among cranial nerves, the abducens nerve is common to get involved. We report a patient who had cerebral venous sinus thrombosis involving superior sagittal sinus, right lateral sinus, and right internal jugular vein and presented with bilateral lower motor neuron (LMN) facial palsy besides bilateral abducens nerve palsy and bilateral optic nerve involvement in the form of papilledema. A few cases of cerebral venous thrombosis involving lateral sinus with ipsilateral LMN facial nerve palsy have been reported. Our case highlights the rare occurrence of bilateral LMN facial palsy with unilateral lateral sinus involvement.

How to cite this article:
Shah V, Sardana V. A case of bilateral lower motor neuron facial palsy in cerebral venous sinus thrombosis.APIK J Int Med 2021;9:189-191

How to cite this URL:
Shah V, Sardana V. A case of bilateral lower motor neuron facial palsy in cerebral venous sinus thrombosis. APIK J Int Med [serial online] 2021 [cited 2021 Sep 24 ];9:189-191
Available from: https://www.ajim.in/text.asp?2021/9/3/189/321656

Full Text


Presentation of cerebral vein thrombosis (CVT) is variable with a wide spectrum of neurological symptoms from headache to coma. Cranial nerve palsy in CVT is rare, with the most common being sixth nerve palsy and papilledema resulting from raised intracranial pressure (ICP). The rest of the cranial nerve involvement without other focal deficits is rare. In the early literature, facial nerve involvement ipsilateral to lateral sinus thrombosis has been reported.[1],[2] To our knowledge, bilateral facial nerve involvement has not been reported in CVT. We report a case of bilateral lower motor neuron (LMN) facial palsy in a patient with superior sagittal sinus, right lateral sinus, and right internal jugular vein (IJV) thrombosis.

 Case Report

A 16-year-old previously healthy male patient came with a history of new-onset severe and holocranial headache associated with nausea and vomiting for the last 12 days. On the 10th day of headache, he developed horizontal diplopia for far vision in both lateral gazes. On the very next day, he also noticed difficulty in closing both eyes. His examination showed bilateral papilledema, bilateral lateral rectus palsy, and bilateral LMN facial palsy with the involvement of taste sensation bilaterally. Other cranial nerves' examination was normal. His motor, sensory, and cerebellar examination was normal, with no signs of meningeal irritation.

Magnetic resonance imaging (MRI)/magnetic resonance venography showed superior sagittal sinus, right transverse and sigmoid sinus, right IJV thrombosis without the involvement of deep venous system, and no clear brainstem lesion to explain cranial neuropathy [Figure 1] and [Figure 2]. Initial workup for the venous hypercoagulable state including antinuclear antibody, lupus anticoagulant, anticardiolipin antibody, protein C, protein S, and antithrombin 3 was negative. Cerebrospinal fluid analysis, serum angiotensin-converting enzyme level, C-antineutrophil cytoplasmic antibody (ANCA), P-ANCA, glycosylated hemoglobin, human immunodeficiency virus, and serum venereal disease research laboratory tests were negative, which ruled out most infective/inflammatory cause for multiple cranial nerve palsies. Normal brainstem auditory evoked response and pure-tone audiometry ruled out subclinical eighth nerve involvement.{Figure 1}{Figure 2}

He was started on intravenous enoxaparin with acenocoumarol and short-term anti-edema measures in the form of mannitol. The patient improved symptomatically after 1 week of treatment. He was discharged on acetazolamide 500 mg/day and acenocoumarol 2 mg/day with a target INR between 2 and 2.5. On 15 days of follow-up, there was a partial recovery of cranial nerve palsies, which was complete by 45 days. Acetazolamide was tapered, and anticoagulation was continued.


CVT is an uncommon vascular disease that classically presents with headache, seizure, and focal neurological deficits which can progress to coma and death. The most common cranial nerves to get involved are abducens nerve and optic nerve. Our patient had additional bilateral LMN facial palsy, localized to the suprageniculate region. As facial nerve palsy is not commonly seen in CVT, we took enough efforts to rule out other causes, but workup came out to be negative. Few cases of unilateral facial nerve involvement with ipsilateral lateral sinus thrombosis have been reported.[1],[3] Facial nerve palsy can be attributed to the extension of thrombosis to venous channels leading to direct pressure from the clot, vascular congestion, and last, because of raised ICP.[2]

The first theory of extension of thrombosis in the deep venous system or direct clot pressure was unlikely in our case, as the MRI was not suggestive of the same. The theory of vascular congestion has been explained by Kuehnen et al.[1] and Straub et al.[2] Kuehnen et al. have reported five patients who had single/multiple cranial nerve palsies secondary to thrombosis of ipsilateral transverse and sigmoid sinus thrombosis. Lateral sinus drains blood from the cerebellum, brainstem and posterior portions of the cerebral hemispheres, veins from cranial nerves in the posterior fossa, the middle ear, and diploic veins. According to Kuehnen et al., thrombosis of lateral sinus can produce venous congestion and dilatation of cranial nerve veins with backpressure causing reversible compromised oxygen or glucose consumption within cranial nerve tissue.[1] Straub et al. described a 17-year-old female with right LMN facial palsy with ipsilateral transverse sinus thrombosis. They did transcranial magnetic stimulation and concluded that facial palsy was because of transient neurapraxia in the intracranial segment of the nerve. The explained mechanism was a leakage of fluids and ions into the endoneurial space of the nerve because of elevated venous pressure in the nerve's satellite vein, which ultimately drains to the ipsilateral transverse sinus. This causes impairment of saltatory current flow, with reversible slowing of conduction or even conduction block.[2] Both had found clinical improvement with radiological recanalization of venous sinuses, which reinforce their theories. This theory can explain facial nerve palsy only ipsilateral to lateral sinus thrombosis, while in our case, facial palsy was bilateral.

Contrary to cases reported,[1],[2],[3] our patient had additional involvement of superior sagittal sinus and right IJV besides right lateral sinus, which can lead to more pronounced ICP. This brings out the last theory of raised ICP causing facial nerve palsy. Although facial nerve is having short intracranial course and relative protection against the effects of pressure, it has been found to get involved with raised ICP secondary to idiopathic intracranial hypertension (IIH). Bilateral facial palsy has been reported in IIH with improvement also after pressure management.[4] In all reported cases of IIH, cranial nerve involvement was temporarily associated with increased ICP and subsequently improved with the management of underlying pressure.[4],[5] Further evidence for this hypothesis is found in case of a child with a ventriculoperitoneal shunt who presented with facial diplegia secondary to shunt malfunction and saw the complete resolution of their facial diplegia with correction of ICP.[6] We believe that facial palsy, bilateral in our case, can best be explained by raised ICP associated with CVT rather than venous congestion.


To our knowledge, this is the first reported case of simultaneous bilateral LMN facial palsy associated with the CVT. This case not only highlights the rare occurrence of bilateral facial nerve palsy in CVT but also brings the fact that facial nerve palsy can be the false localizing sign in case of raised ICP. We suggest that CVT should be included in the differential diagnosis of facial palsy in the presence of appropriate clinical scenarios.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


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