Introduction

Oculomotor nerve (ON) palsy following subarachnoid hemorrhage (SAH) is usually due to posterior communicating artery (pcom) aneurysm or uncommonly due to basilar artery - superior cerebral artery aneurysm. Rare aneurysms to cause ON palsy are, those arising from posterior inferior cerebral artery, distal anterior cerebral artery, anterior communicating artery, anterior choroidal artery and even rarer is middle cerebral artery (MCA). [₁, ₂,₃,₄,₅]. Subarachnoid hemorrhage due to any cause can lead to ON palsy in association with cerebral herniation [₅]. The involvement of ON can be partial or complete depending of various parameters like duration, severity and site of compression. [₆].

Case Report

A 58- year- old male presented with sudden onset of headache and vomiting. CT scan revealed presence of subarachnoid hemorrhage and there were clots seen in left crural, interpeduncular and left ambient cistern and there was no evidence of herniation. (Figure 1) .

Figure 1

Figure 1: CT scan showing presence of subarachnoid hemorrhage with clots in left crural and ambient cistern

The patient reported to us the next day and was having significant relief in headache and on examination he was in WFNS (world federation of neurological surgeons) grade I. His only neurological deficit was the presence of left oculomotor partial palsy. He had ptosis, pupillary dilatation not reacting to direct or consensual light and had paresis of adduction. The patient underwent digital subtraction angiogram which revealed presence of left middle cerebral artery aneurysm, a lobule of which was pointing medially (Figure 2)

Figure 2

Figure 2: Angiogram showing left middle cerebral artery aneurysm

Figure 3

The patient underwent endovascular coiling of the aneurysm. During the procedure, patient was administered intra-arterial nimodipine and he was started on hypervolemic therapy. He was receiving dexamethasone 16 mg for 24 hours along with nimodipine 60 mg 4 hourly. The blood pressure was maintained around 160 mm (Hg systolic). The next day ptosis reverted to normal followed by pupillary and ocular movements. The patient had complete normal nerve functions within 48 hours of intervention. CT scan done 48 hours after coiling showed complete resolution of perimesencephalic blood clots. (Figure3).

Figure 4

Figure 3: Post coiling CT scan showing resolution of perimesencephalic clots and coil is also seen

On the fifth day the patient deteriorated in sensorium and had dysphasia and left hemiparesis. Urgent angiogram was done which revealed presence of vasospasm. (Figure 4)

Figure 5

Figure 4: Presence of vasospasm on check angiogram , coil is also seen in the aneurysm

Intra-arterial nimodipine was administered and vasospasm got relieved. The weakness gradually improved and his dysphasia improved. After three weeks patient is able to walk independently and able to verbalize with mild difficulty.

Discussion

In absence of herniation syndrome, ON palsy can be caused by varied etiologies like ischemia of nerve due to disease like diabetes, direct trauma to nerve, neuritis, meningitis, intracranial aneurysms, midbrain hematoma or infarcts.[₇,₈,₉,₁₀,₁₁]. The clinical spectrum of ON involvement due to aneurysm is varied. The syndrome is very well described for the Pcom aneurysms due to their frequency. Orbital pain or headache usually proceeds the involvement of ON. The disturbance in ON function may be partial or complete. [₃,₆,₁₂] There may be only anisocoria, ptosis with or without pupil involvement or total opthalmoplegia depending on site, severity and duration of involvement of ON. Impairment of ON function in SAH can be because of any or multiple of following factors; direct compression of ON by aneurysm, irritation effect of blood and vasospasm leading to ischemia of nerve, or cerebral herniation.[₁₃,₁₄,₁₅] In our patient since aneurysm was arising from MCA away from the ON hence it is not the possible cause of involvement. In the absence of clinical or radiological features of raised ICP vasospasm and ischemia can be one of the possible explanations of ON palsy in our patient as he had clots seen in left crural, interpeduncular and left ambient cistern. Another possibility is that after aneurysm rupture jet of blood might have been directed medially as we had clots in left sided cisterns causing direct injury to ON.

Recovery of function after intervention: surgery or endovascular has been reported [₁₅,₁₆]. The recovery of function is first seen in ptosis followed by extra ocular muscle function and pupillary abnormalities [₁₃,₁₅,₁₆,₁₇]. In an important series on the subject, Laun A found regression of ON palsy in 39.2% of patients within 6months and in remaining deficits was permanent [₁₈]. In Sakurai, series regression was seen in 75% of the patient [₁₉].

Resolution of ON palsy following surgery is relatively easy to understand in case of compression of nerve by aneurysm. However, improvement in function following endovascular intervention is not easily understood. Birchall et al suggested decrease in pulsatility within aneurysmal sac following coiling could cause improvement. [₁₅] Some studies have reported decrease in cerebral edema adjoining aneurysms after endovascular coiling leading to improvement. [₁₅,₂₀,₂₁]. In our case both possibilities seen to be unlikely as the aneurysm was away from ON. The possible explanation can be use of intra arterial nimodipine during the procedure leading to decrease in spasm. The recovery could have been aided by good hydration aided by intravenous steroids given to the patient.

Conclusion

MCA aneurysms are rare cause of Oculomotor nerve palsy in absence of herniation syndromes. These probably result from transient vasospasm or direct injury due to jet of blood. Complete recovery may occur in such cases by conservative management without a need for surgical intervention.

Correspondence to

Dr. Abrar Ahad Wani Department of Neurosurgery Max Superspeciality hospital 1, Press Enclave Road, Saket, New Delhi India-110017 E mail: abrarwani@rediffmail.com