Optometry - Journal of the American Optometric Association
Volume 81, Issue 9 , Pages 450-453, September 2010

Ophthalmic segment aneurysmal subarachnoid hemorrhage presenting with contralateral abducens nerve palsy: A false localizing sign

  • Sunil V. Furtado, M.S., M.Ch., D.N.B.

      Affiliations

    • Corresponding Author InformationCorresponding author: Sunil V. Furtado, M.S., M.Ch., D.N.B., Department of Neurosurgery, SSSIHMS, EPIP Area, Whitefield, Bangalore-560066, India.
    • ,
  • Dilip Mohan, M.S., M.Ch.
    • ,
  • Alangar S. Hegde, Ph.D., M.Ch.

Department of Neurosurgery, Sri Sathya Sai Institute of Higher Medical Sciences, EPIP Area, Whitefield, Bangalore, Karnataka State, India

published online 12 July 2010.

Article Outline

Abstract 

Background

Neuro-ophthalmic manifestations of aneurysmal subarachnoid hemorrhage are commonly linked to a palsy of the cranial nerve in close proximity to the aneurysm or to chronic intracranial hypertension.

Case Report

A patient with subarachnoid hemorrhage secondary to a rupture of an intracranial right ophthalmic segment internal carotid artery aneurysm presented with an acute-onset contralateral abducens nerve palsy. There were no clinical or radiologic features of chronic intracranial hypertension. Magnetic resonance imaging showed a co-existent ectatic basilar artery on the left side of the pons in close relation to the sixth nerve.

Conclusion

Abducens weakness in the above-50 age group is most commonly caused by a vascular etiology. The authors discuss the pathogenesis of this rare clinical entity and present pertinent literature review.

Keywords: Abducens nerve, Aneurysm, Basilar artery, Magnetic resonance imaging, Subarachnoid hemorrhage

 

The incidence of sixth nerve palsy is 11.3 in 100,000 and can be caused by a lesion anywhere along its course from its origin in the pons until its termination in the orbit.1

Two percent of abducens palsies have aneurysmal etiologies occurring in the basilar artery, anterior inferior cerebellar artery, or cavernous segment of the internal carotid artery (ICA).2, 3

An ectatic basilar artery can commonly irritate the fifth and seventh cranial nerves.4 The incidence of elongation and distension (dolicoectasia) of intracranial vessels ranges from 0.06% to 5.8%.3 The ophthalmic segment of the intracranial ICA extends from the distal dural ring covering the ICA at the anterior clinoid process to the origin of the posterior communicating artery. This report highlights the occurrence of abducens palsy in a patient with subarachnoid hemorrhage (SAH) contralateral to the site of ophthalmic segment ICA aneurysmal bleed. The unique presentation posed a clinical and diagnostic challenge.

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Case report 

A 59-year-old hypertensive man presented at a hospital with severe headache followed by loss of consciousness for about 5 minutes. On admission to our hospital a week later he complained of headache and horizontal binocular diplopia toward leftward gaze and was found to have left abduction deficit on examination (see Figure 1B). His sensorium was normal. Cover test found a left esotropia greater at distance than near. His blood pressure was 150/96 mmHg at admission. He had no papilledema to suggest raised intracranial pressure, or nystagmus, or internuclear ophthalmoplegia to suggest a brainstem lesion. His visual acuities were 20/30 in the right eye and 20/40 in the left eye, with normal pupil size and reactions to light. The rest of his neurologic examination was unremarkable. A computed tomography (CT) scan performed showed diffuse SAH (see Figure 1A). On further evaluation, a digital subtraction angiogram (DSA) found a right ophthalmic segment aneurysm (see Figure 2B). Magnetic resonance imaging (MRI), which was performed to elicit the source of the contralateral abduction deficit, showed that in addition to the ophthalmic segment aneurysm (see Figure 2A), there was an ectatic basilar artery on the left side of the midbrain and pons (see Figure 3). The patient underwent a right fronto-temporal craniotomy and clipping of the aneurysm. He had an uneventful postoperative period. His diplopia and abducens palsy recovered completely at 3 months follow-up.

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  • Figure 1 

    A, CT of the head shows Fisher grade 3 SAH. B, Left lateral rectus palsy in the patient demonstrable on left lateral gaze, C, Arrow in axial T2- and T1-weighted MRI pointing to a nonelevated optic disc.

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  • Figure 3 

    A, Axial SPGR (spoiled gradient recalled) and B, Coronal T2-weighted MRI demonstrating an ectatic basilar artery toward the left side in close relation to the VI nerve (arrow).

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Discussion 

Acquired sixth nerve palsies in children are commonly caused by tumors, trauma, and inflammation.5 In adults, especially those older than 50, it is associated with diabetes mellitus, hypertension, raised intracranial pressure, and atherosclerosis in addition to the causes mentioned in children.5 About 26% of sixth nerve palsies are considered idiopathic.6 The abducens nerve is the most frequently involved cranial nerve in intracranial pathologies, with a 10% incidence of bilateral paresis.3

The reported incidence for sixth nerve palsy caused by SAH is between 3.3 to 5.9%.3, 7 Because abducens palsy is usually apparent 3 to 14 days after SAH, it was speculated that vasospasm of the pontine branches of the basilar artery causing direct shock to the brainstem and decreased blood supply to the abducens nerve was the proximate cause.8 The stretching of the sixth nerve between the brainstem and skullbase by subarachnoid blood and local pressure changes in the cisterns by the blood clot and its decay products may, in addition, have affected the nutritional supply to the nerve.3

The sixth nerve is strained to a great extent between its pontine origin and the dural porus at the upper clivus and is fixed to its border by light connective tissue.9 The ectatic basilar artery in our case was on the left side of the pons, in close relation to the sixth nerve (see Figure 3). We postulate that either the subarachnoid blood clot in the prepontine cistern (see Figure 1A), or the sudden increase in intracranial pressure at the time of SAH, might have shifted this ectatic basilar artery so that it impinged upon the sixth nerve. This could have placed additional strain on the sixth nerve in its subarachnoid suspension. This mechanism provides a plausible explanation for our patient to have developed acute sixth nerve palsy immediately after the ictus, on the side contralateral to the offending aneurysm.

There was no evidence of third or fourth nerve palsy, which may have suggested cavernous sinus or superior orbital syndrome in our patient. Examination of the fifth, seventh, and eighth nerve complex and lower cranial nerves were normal. He did not have limb spasticity to suggest motor tract involvement in the brainstem and lacked cerebellar ataxia and dysdiadokinesia. Absence of these findings and a normal brainstem on the MRI ruled out an acute posterior circulation stroke syndrome.

Evaluation for aneurysm is not typically recommended in isolated abducens palsy.10 However, SAH causing raised intracranial pressure and papilledema can cause abducens palsy.10 Although the abduction deficit could be attributed to increased intracranial pressure or a vasculopathic etiology, the proximity of the ectatic basilar loop to the sixth nerve and the acute presentation in relation to the SAH event in our case suggests a neurocompressive syndrome of the abducens nerve. Moreover, our patient did not have papilledema, with spontaneous venous pulsations seen on ophthalmoscopic examination. Absence of papilledema was indirectly evidenced by the nonelevation of the optic disc into the globe on MRI (see Figure 1C). We feel that this represented a combination of SAH and ectatic basilar artery causing a reversible neurovascular compressive syndrome of the abducens nerve. Although we reviewed the patient 3 months after the bleeding, he had noticed subjective improvement in diplopia 2 months after the ictus. The compression on the nerve by the ectatic vessel would have been released once the cisternal blood was cleared. Sixth nerve palsy caused by SAH is known to recover spontaneously between 3 and 8 weeks after onset.3, 7 Previous reports of dolichoectatic cavernous carotid artery are associated with a single episode or multiple recurrent episodes of ipsilateral sixth nerve paresis.11, 12, 13 Because the abducens nerve innervates only one muscle, nerve remyelination over time may restore normal function.13 Based on previous reports of sixth nerve palsy of aneurysmal etiology11, 12, 13 and the acute presentation of contralateral abduction deficit in our patient, we believe that the dolicoectatic basilar artery closely related to the sixth nerve was the likely underlying cause in an acute setting of SAH, more so than a vasculopathic etiology. Microvascular decompression of the abducens nerve has been performed for ectatic basilar artery causing chronic, progressive neurovascular compression syndrome.14

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Conclusion 

This case is an example of a false localizing neurologic sign involving the abducens nerve. Dolicoectatic arteries of the posterior circulation, which are frequently noticed in the older population, can produce acute compression syndromes of adjacent cranial nerves by induced neurovascular contact. In our case, the volume of blood as a result of acute SAH caused a shift due to cisternal pressure changes, bringing the ectatic vessel in contact with the sixth nerve and producing reversible abducens palsy.

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References 

  1. Patel SV, Mutyala S, Leske DA, et al. Incidence, associations, and evaluation of sixth nerve palsy using a population-based method. Ophthalmology. 2004;111:369–375
  2. Brinar VV, Habek M, Ozretić D, et al. Isolated nontraumatic abducens nerve palsy. Acta Neurol Belg. 2007;107(4):126–130
  3. Munakata A, Ohkuma H, Nakano T, et al. Abducens nerve pareses associated with aneurysmal subarachnoid hemorrhage. Incidence and clinical features. Cerebrovasc Dis. 2007;24(6):516–519
  4. Titlic M, Tonkic A, Jukic I, et al. Clinical manifestations of vertebrobasilar dolichoectasia. Bratisl Lek Listy. 2008;109(11):528–530
  5. Hsu CS, Closmann JJ, Baus MR. Idiopathic unilateral cranial nerve VI palsy: a case report and review of the literature. J Oral Maxillofac Surg. 2008;66(6):1282–1286
  6. Richards BW, Jones FR, Younge BR. Causes and prognosis in 4,278 cases of paralysis of the oculomotor, trochlear, and abducens cranial nerves. Am J Ophthalmol. 1992;113(5):489–496
  7. Göksu E, Akyüz M, Gürkanlar D, et al. Bilateral abducens nerve palsy following ruptured anterior communicating artery aneurysm: report of 2 cases. Neurocirugia (Astur). 2007;18(5):420–422
  8. Suzuki J, Iwabuchi T. Ocular motor disturbances occurring as false localizing signs in ruptured intracranial aneurysms. Acta Neurochir (Wien). 1974;30(1-2):119–128
  9. Iaconetta G, Fusco M, Cavallo LM, et al. The abducens nerve: microanatomic and endoscopic study. Neurosurgery. 2007;61(3 Suppl):7–14
  10. Brazis PW. Isolated palsies of cranial nerves III, IV, and VI. Semin Neurol. 2009;29(1):14–28
  11. Foroozan R. Spontaneous resolution of sixth nerve palsy with ipsilateral cavernous carotid dolichoectasia. B J Ophthalmol. 2004;88:586–587
  12. Blumenthal EZ, Gomori JM, Dotan S. Recurrent abducens nerve palsy caused by dolichoectasia of the cavernous internal carotid artery. Am J Ophthalmol. 1997;124:255–257
  13. Nguyen DQ, Perera L, Kyle G. Recurrent isolated sixth nerve palsy secondary to an intracavernous carotid artery aneurysm. Eye (Lond). 2006;20(12):1416–1417
  14. De Ridder D, Menovsky T. Neurovascular compression of the abducent nerve causing abducent palsy treated by microvascular decompression. Case report. J Neurosurg. 2007;107(6):1231–1234

 Source of support: The authors have not received any support, in the form of grant, from any source for preparation of this article. Neither the authors nor the institute has any personal or institutional financial interest in drugs, materials, or devices described in their submissions.

PII: S1529-1839(10)00252-6

doi:10.1016/j.optm.2010.03.008

Optometry - Journal of the American Optometric Association
Volume 81, Issue 9 , Pages 450-453, September 2010

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