Picture quiz: Surgical or medical third nerve palsy?

A 76 year old woman presented to the eye department with a one week history of left eye pain and drooping eyelid. She had a history of hypertension and atrial fibrillation controlled with drugs. On examination visual acuity was normal at 6/9 in each eye. There was complete ptosis and ophthalmoplegia of four of the six extraocular muscles of the left eye. In primary position the left eye was depressed (that is, “down”) and abducted (that is, “out”). One week later she presented with increasing left eye pain and pupil involvement. Magnetic resonance imaging and angiography was normal. Subsequent cerebral angiography was also normal. Within three months all symptoms and signs had resolved with full recovery of ocular movements.

Questions

(1) From figs 1 to 4^{1 2 3 4} which eye movements are absent?

(2) From figs 1 to 4^{1 2 3 4} what position of gaze and which cranial nerve is intact?

(3) From figs 5 and 6^{5 6} what other ophthalmic abnormalities are noticeable?

(4) What do the findings signify and what is the immediate next step in management?

Answers

(1) The left eye fails to adduct (medial rotation; fig 1¹), elevate (fig 2²), or depress (fig 4⁴).

(2) Abduction (lateral rotation; fig 3³) of the left eye is intact due to sparing of the sixth cranial nerve.

(3) There is complete ptosis of the left upper eyelid (fig 5⁵) and a dilated left pupil, which is poorly reactive to light (fig 6⁶).

(4) This is a complete left third nerve palsy with pupillary involvement. Urgent magnetic resonance imaging and magnetic resonance angiography is warranted to rule out compression from a probable posterior communicating artery aneurysm.

Discussion

The third cranial nerve innervates four extraocular muscles (which control elevation, depression, and abduction of the eye), the levator palpebrae superioris (which controls eyelid elevation), and the pupillary sphincter (which controls pupillary constriction). The diagnostic challenge to the clinician is determining whether the underlying aetiology of an isolated third nerve palsy is due to ischaemia (“medical”) or compression (“surgical”). See table.

If the pupil is involved it is likely to be a compression problem. This is because pupil fibres of the third cranial nerve run superficially and are more likely to be damaged by compression from an expanding aneurysm or tumour.¹

The most common cause of a third nerve palsy is ischaemia in patients with vasculopathic risk factors such as diabetes or hypertension.^{1 2} The pupil should be checked in the first week of onset of a third nerve palsy, however, because pupillary involvement, indicating compression, may sometimes be delayed by five to seven days.^{1 3} An intracranial aneurysm (usually posterior communicating aneurysm) is a common cause of isolated third nerve palsy, involving up to 56% of cases.¹ Diagnosis is important as a ruptured cerebral aneurysm results in significant morbidity or mortality.¹

Although pupil involvement indicates a compressive lesion and pupil sparing indicates ischaemia,^{1 2} this did not apply in our case. Pupil involvement has previously been reported in ischaemic third nerve palsies and occurs in up to 38% of cases.^{1 2} As almost all aneurysmal third nerve palsies involve the pupil,¹ progressive pupil involvement requires urgent investigation with appropriate neuroimaging.

Pain around the forehead or the orbit often occurs in aneurysmal third nerve palsy due to involvement of the trigeminal fibres on the oculomotor nerve.¹ The presence or absence of pain is not a useful indicator, however,⁴ as the severity or quality of ischaemic pain may be indistinguishable from aneurysmal pain.

Although cerebral angiography is the gold standard for identifying intracranial aneurysms, patients aged more than 75 have a higher risk of developing a catheter angiogram related complication such as stroke. Hence, less invasive neuroimaging techniques, such as magnetic resonance angiography have evolved and have improved the investigation of intracranial aneurysms.⁵ The risk of angiography must be weighed against the risk of missing an aneurysm.

Despite the progressive development of pupil involvement, a medical cause was assigned for this case of third nerve palsy on the basis of the patient’s medical history, neuroimaging results, and clinical course. Hypertension was most likely responsible for microvascular ischaemia of the third nerve trunk. Although our patient was taking oral anticoagulation for atrial fibrillation, she was not at greater risk of an intracranial bleed from a possible aneurysm. A systematic review on atrial fibrillation management identified the following patient characteristics as risk factors for anticoagulation related bleeding complications: advanced age, uncontrolled hypertension, history of myocardial infarction or ischaemic heart disease, cerebrovascular disease, anaemia or a history of bleeding, and the concomitant use of other drugs such as antiplatelet agents. The presence of diabetes mellitus, controlled hypertension, and gender were not identified as significant risk factors.⁶

Competing interests: None declared.

Patient consent: Obtained.

Provenance and peer review: Not commissioned; externally peer reviewed.

1. Lee AG, Hayman LA, Brazis PW. The evaluation of isolated third nerve palsy revisited: an update on the evolving role of magnetic resonance, computed tomography, and catheter angiography. Surv Ophthalmol 2002;47:137-57.
2. Jacobson DM. Pupil involvement in patients with diabetes-associated oculomotor nerve palsy. Arch Ophthalmol 1998;16:723-7.
3. Yanovitch T, Buckley E. Diagnosis and management of third nerve palsy. Curr Opin Ophthalmol 2007;18:373-8.
4. Jacobson DM. Relative pupil-sparing third nerve palsy: etiology and clinical variables predictive of a mass. Neurology 2001;56:797-8.
5. Lee AG, Brazis PW. The emerging role of magnetic resonance angiography in the management of patients with third nerve palsy. Am J Ophthalmol 2000;129:115-6.
6. National Institute for Health and Clinical Excellence. Atrial fibrillation. National clinical guideline for management in primary and secondary care. 28 June 2006. http://www.nice.org.uk/nicemedia/pdf/cg036fullguideline.pdf.

   

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