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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 60  |  Issue : 1  |  Page : 60-62

Case report of unilateral abducens nerve paresis: A common sign with an uncommon etiology


1 Department of Ophthalmology, Goa Medical College, Bambolim, Goa, India
2 Department of Radiology, Goa Medical College, Bambolim, Goa, India

Date of Submission24-Apr-2021
Date of Decision15-Aug-2021
Date of Acceptance10-Nov-2021
Date of Web Publication22-Mar-2022

Correspondence Address:
Dr. Valerie Menezes
Siddarth Apartments, No. 2/S-2, P.O. Caranzalem, Panaji - 403 002, Goa
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/tjosr.tjosr_50_21

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  Abstract 


Sixth nerve paresis is a rare presentation of intracranial aneurysms. We report an uncommon case of unilateral sixth nerve paresis in a young adult as the main presenting feature of an intracavernous aneurysm. The patient presented with pain and double vision in the right eye for 1 month. Computerized Tomography scan brain done elsewhere was normal. Examination showed right sixth nerve paresis with sensory loss in the first and second divisions of the trigeminal nerve. We suspected a cavernous sinus lesion and conveyed the same to the radiologist who therefore did additional and appropriate imaging, which revealed an intracavernous carotid aneurysm. This case is unique as to the best of our knowledge, it is the first case of its kind reported from India.

Keywords: Abducens nerve paresis, intracavernous carotid aneurysm, intracranial aneurysms


How to cite this article:
Menezes V, Menezes R. Case report of unilateral abducens nerve paresis: A common sign with an uncommon etiology. TNOA J Ophthalmic Sci Res 2022;60:60-2

How to cite this URL:
Menezes V, Menezes R. Case report of unilateral abducens nerve paresis: A common sign with an uncommon etiology. TNOA J Ophthalmic Sci Res [serial online] 2022 [cited 2022 Jun 29];60:60-2. Available from: https://www.tnoajosr.com/text.asp?2022/60/1/60/340364




  Introduction Top


In adults, the most common etiology of an isolated sixth nerve palsy is ischemic mononeuropathy due to diabetes mellitus, arteriosclerosis, or hypertension. Only 3% of cases of sixth nerve palsy are associated with intracranial aneursyms.[1] A literature search revealed that, over the last two decades, only five such cases due to intracavernous carotid aneurysm have been reported.

We report an interesting case of unilateral sixth nerve paresis, as the chief presenting feature of an intracavernous carotid artery aneurysm. To the best of our knowledge, this is the first case of its kind reported from India.

The key message of this report is that unilateral, painful abducens nerve damage especially associated with loss of sensations in the ophthalmic and maxillary divsions of the trigeminal nerve, should raise the suspicion of an intracranial aneurysm and the radiologist should be alerted for appropriate imaging studies.


  Case Report Top


A 20-year-old male patient presented to the ophthalmology outpatient department with a history of double vision and throbbing pain in the right eye radiating to the right side of the head for the past 1 month. The patient had no complaints of decreased vision. There was no history of ocular trauma. He was previously healthy with no history of any systemic illness.

On examination, he had mild right periorbital fullness, right lateral rectus paresis, and loss of sensations in the distribution of the ophthalmic and maxillary divisions of the trigeminal nerve on the right side [Figure 1]. Other cranial nerves were normal, and there were no neurologic deficits. Pupillary examination of the right eye revealed a central, circular, 3mm pupil reacting briskly to light. There was no relative afferent pupillary defect. Left eye pupil examination was normal. Visual acuity was 6/6 in both eyes, and fundus examination was normal.
Figure 1: The ocular movements in various gaze positions. The red arrow shows the right lateral rectus palsy

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Preliminary blood investigations including blood routine, erythrocyte sedimentation rate , C-reactive protein and sugar profile (Fasting blood sugar level, postprandial blood sugar level and glycosylated haemoglobin) were normal.A plain computerised tomography (CT) scan of the brain had been done 1 month back, elsewhere. However, it was reported as unremarkable.

Based on the findings of an isolated painful sixth nerve palsy associated with a loss of sensations in the distribution of the first and second divisions of the trigeminal nerve, a cavernous sinus lesion was suspected.

We performed a repeat unenhanced CT brain, in which the only finding was a bulky right cavernous sinus with convexity of its lateral wall [Figure 2]. In view of the clinical suspicion, this was further evaluated up with contrast magnetic resonance imaging (MRI) and CT angiography. These scans clearly demonstrated a partially thrombosed saccular aneurysm 1.5 cm × 1.2 cm × 1.3 cm, arising from the cavernous portion of the right internal internal carotid artery (ICA) [Figure 3] and [Figure 4]. The patient was referred to a higher center for endovascular coiling of the aneurysm. However unfortunately the patient was lost to follow-up.
Figure 2: Axial image from the unenhanced computerised tomography brain showing a convex bulging of the lateral wall of the right cavernous sinus (outlined in red). The normal concavity of the lateral wall of the left cavernous sinus is outlined in blue

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Figure 3: Axial image computerised tomography angiography brain. The anterior part of the aneurysmal sac (solid triangle) is patent whereas the posterior part is thrombosed (star). The arrow marks the cavernous potion of the internal carotid artery which is displaced by the aneurysmal sac

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Figure 4: Coronal image from the post contrast magnetic resonance imaging brain. The arrow shows the aneurysm causing a bulge in the right cavernous sinus

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  Discussion Top


Intracavernous carotid artery aneurysms account for 2%–9% of all intracranial aneurysms. The etiology of carotid cavernous aneuryms (CCA) can be traumatic, infectious, or idiopathic.[2] Most CCA arise from the horizontal segment of the cavernous part of the ICA.[3]

Isolated sixth nerve palsy is rare in a patient with intracavernous carotid aneurysm. The known frequency of abducens nerve palsy associated with intracranial aneurysms is around 3%.[4] Our patient had a right sixth nerve paresis along with sensory loss in the distribution of the ophthalmic and maxillary divisions of the trigeminal nerve on the right side.

Most patients with CCA are asymptomatic and lesions are detected incidentally on intracranial imaging acquired during the workup for unrelated conditions such as headache, closed-head trauma, or other nonspecific cranial, ocular or facial complaints.[2] Progressive mass effect can be due to the pressure of the aneurysm dome on the cavernous sinus and its associated cranial nerves, acute thrombosis, or spontaneous rupture, which are thought to be responsible for a majority of the symptomatic cases.[5]

The most common symptoms of mass effect from an unruptured CCA at presentation are diplopia and pain. Diplopia can result from oculomotor or abducens nerve paresis independently or in combination, or the cavernous sinus syndrome, occurring in 20% of patients which involves the third, fourth, and sixth cranial nerve often leading to a near complete ophthalmoplegia. Pain has been reported to be of various forms including unilateral headache, retro-orbital pain, and/or facial pain. Other oculofacial manifestations of symptomatic CCA include ocular sympathetic paresis, compressive optic neuropathy, corneal hyperesthesia, and trigeminal dysesthesias.[6]

The timing of the patient's presentation normally reflects the etiology of CCA symptoms. More insidious presentations of diplopia and/or pain usually occur from enlarging CCAs, resulting in a progressive mass effect. More acute presentations of diplopia and/or pain are usually related to ruptured CCAs. When rupture of a CCA does occur, the formation of a carotid cavernous fistula or a subarachnoid hemorrhage can occur.[6]

Treatment of CCAs is necessary for symptomatic lesions to prevent potentially permanent cranial neuropathies or re-rupture. Endovascular therapy is the primary treatment modality for symptomatic CCAs due to the technical difficulties and morbidity associated with surgical approaches to the cavernous sinus. Aneurysm obliteration with ICA preservation is the preferred treatment modality and can be accomplished with coil embolization with or without stent assistance. Although recurrence and retreatment can occur, the thromboembolic risk of endovascular treatment is low.[7]


  Conclusion Top


In cases of isolated painful sixth nerve paresis especially associated with a loss of sensation in the distribution of the first and second divisions of the trigeminal nerve, cavernous sinus lesions have to be ruled out by appropriate radiological investigations.

This case report emphasizes that it is critical to highlight the clinical suspicion of a cavernous sinus lesion to the radiology team as these lesions can be overlooked on unenhanced CT and need to be evaluated by contrast-enhanced CT or MRI.

Thorough systematic evaluation in young patients with diplopia can reveal life threatening underlying pathology which can be treated to prevent major complications.

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 initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Azarmina M, Azarmina H. The six syndromes of the sixth cranial nerve. J Ophthalmic Vis Res 2013;8:160-71.  Back to cited text no. 1
  [Full text]  
2.
Stiebel-Kalish H, Kalish Y, Bar-On RH, Setton A, Niimi Y, Berenstein A, et al. Presentation, natural history, and management of carotid cavernous aneurysms. Neurosurgery 2005;57:850-7.  Back to cited text no. 2
    
3.
Vasconcellos LP, Flores JA, Veiga JC, Conti ML, Shiozawa P. Presentation and treatment of carotid cavernous aneurysms. Arq Neuropsiquiatr 2008;66:189-93.  Back to cited text no. 3
    
4.
Kim YJ, Park CW, Yoo CJ, Kim EY, Kim JM, Kim WK. Unilateral abducens nerve palsy associated with ruptured anterior communicating artery aneurysm. Korean J Neurotrauma 2012;8:146-8.  Back to cited text no. 4
    
5.
Goldenberg-Cohen N, Curry C, Miller NR, Tamargo RJ, Murphy KP. Long term visual and neurological prognosis in patients with treated and untreated cavernous sinus aneurysms. J Neurol Neurosurg Psychiatry 2004;75:863-7.  Back to cited text no. 5
    
6.
Eddleman CS, Hurley MC, Bendok BR, Batjer HH. Cavernous carotid aneurysms: To treat or not to treat? Neurosurg Focus 2009;26:E4.  Back to cited text no. 6
    
7.
Choulakian A, Drazin D, Alexander MJ. Endosaccular treatment of 113 cavernous carotid artery aneurysms. J Neurointerv Surg 2010;2:359-62.  Back to cited text no. 7
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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