Case Report
A Rare Case of Oculomotor Nerve Palsy after Endovascular Treatment in a Patient with Internal Carotid Artery Dissection

https://doi.org/10.1016/j.jstrokecerebrovasdis.2020.105555Get rights and content

Background

The oculomotor nerve has two major fibers: the outer autonomic fiber innervates the ciliary muscles and sphincter pupillae involved in pupil constriction, and the inner somatic fiber innervates the levator palpebrae superioris in the eyelid and four extraocular muscles involved in oculomotor dysfunction. We present a rare case of oculomotor nerve palsy with internal carotid artery (ICA) dissection and discuss the vascular anatomical feature of interest to be considered during treatment.

Case report

A 56-year-old man presented with language impairment, right visual field loss, and right-sided facial sensory loss, weakness, and hypesthesia 30 hours after the last seen normal. CT perfusion imaging revealed a large left middle cerebral artery distribution and possible salvageable ischemic penumbra. Angiography showed occlusion of the communicating segment of the left ICA. We performed mechanical thrombectomy for left ICA occlusion that led to partial recanalization after several attempts. A control digital subtraction angiography showed dissection features in the communicating part of the left ICA. The recanalized ICA got blocked again within ten minutes. Angioplasty was performed and the flow improved. Five hours after thrombectomy, the patient developed complete left oculomotor palsy with ptosis, a fixed mydriatic pupil, and lateral and downwards eyeball deviation suggesting oculomotor nerve palsy. MRI on the 23rd day after symptom onset revealed enhancement of the left oculomotor nerve.

Conclusions

The clinical and imaging course described in this case shows an injury to the oculomotor nerve with compressive plus ischemic injury in a patient with ICA dissection who received endovascular treatment.

Introduction

Symptoms in patients with intracranial internal carotid artery (ICA) dissection can be related either to mass effect, ischemia, subarachnoid hemorrhage, or rarely a combination of different mechanisms. Cranial nerves may be affected in 6-12% of patients with carotid artery dissection, but isolated oculomotor nerve palsy is rare.1 One presumes the mechanism for oculomotor nerve palsy in ICA dissection is an occlusion of the arterial supply to the nerve, causing ischemic neuropathy. Mechanical compression and stretching of the oculomotor nerve are alternative mechanisms.

The oculomotor nerve is a mixed cranial nerve containing motor and parasympathetic fibers.2 Oculomotor nerve palsy can present in different ways, causing dysfunctions of the somatic extraocular muscle (superior, inferior, and medial recti; inferior oblique; and levator palpebrae superioris) and autonomic (pupillary sphincter and ciliary) muscles.3 Parasympathetic pupillary dysfunction suggests that compression of the oculomotor nerve could cause cranial neuropathy. On the other hand, intrinsic vascular lesions occluding the vasa-nervorum produce central ischemic infarction within the nerve trunk. This ischemic type of oculomotor nerve palsy usually spares the parasympathetic fibers, causing weakness of the extra-ocular muscles of the oculomotor nerve with pupillary sparing. The retention of pupilloconstrictor function probably had as its anatomical basis the sparing of nerve fibers in the peripheral or subepineurial part of the nerve.4

Intracranial ICA dissection after intra-arterial thrombectomy (IAT) has not been reported as a cause of oculomotor nerve palsy. In this case, the patient had features of both compressive and ischemic oculomotor nerve palsy after IAT. We discuss possible mechanisms involved in oculomotor nerve palsy and draw attention to the appropriate digital subtraction angiographic (DSA) and magnetic resonance imaging (MRI) findings.

Section snippets

Case report

A 56-year-old man with hypertension visited our hospital with a chief complaint of right hemiparesis within 32 h of last seen well. Neurological examination showed language impairment, loss of the right visual field, right hemiparesis, and right-sided hypesthesia. There were no neurological symptom or findings of Horner syndrome. He denied any trauma to his head or neck. At presentation, his vital signs were unremarkable, with the exception of a systolic blood pressure of 159 mmHg. The patient

Discussion

Intracranial artery dissection is relatively infrequent in adults of European ethnic origin.5 It is more common in children and in Asian populations and mostly involves the posterior circulation. Risk factors for intracranial artery dissection are not well defined. Some cases of intracranial artery dissection have been associated with cervicocerebral trauma, intracranial or systemic infections, genetic risk factors, and connective tissue disorders (Loeys-Dietz syndrome, Ehlers-Danlos syndrome,

Conclusion

The clinical and imaging findings in our patient with ICA dissection who underwent mechanical thrombectomy followed by balloon angioplasty demonstrate injury to the oculomotor nerve.

Declaration of Competing Interest

None.

Reference (10)

  • S Debette et al.

    Epidemiology, pathophysiology, diagnosis, and management of intracranial artery dissection

    Lancet Neurol

    (2015)
  • B Mokri et al.

    Cranial nerve palsy in spontaneous dissection of the extracranial internal carotid artery

    Neurology

    (1996)
  • C Joyce et al.

    Neuroanatomy, Cranial Nerve 3 (oculomotor)

    (2020)
  • NR Miller et al.

    The Essentials: Walsh & Hoyt's Clinical Neuro-Ophthalmology

    (1999)
  • PM Dreyfus et al.

    Diabetic ophthalmoplegia; report of case, with postmortem study and comments on vascular supply of human oculomotor nerve

    AMA Arch Neurol Psychiatry

    (1957)
There are more references available in the full text version of this article.

Cited by (0)

View full text