Oculomotor nerve palsy: Aneurysmal compression vs. Diabetic infarction

기억할 것. 동공을 조절하는 신경은 CN 3인데, 이 신경의 바깥쪽에는 parasympathetic fibers이 있고, 동공 조절 담당.

 

PCOM aneuryms과 같이 mechanical하게 compression하는 경우 pupil 조절이 잘 안될 것이고,

Diabetic 이 원인인 경우에는 주로 central nerve fiber에 영향을 주고 superficial parasympathetic fibers들은 sparing.

CN3 Palsy의 eyeball movement에서 가장 큰 특징은 Down & Out !

 

따라서 당연히 pupil check는 응급일 수 있기 때문에 중요하다

 

https://blog.optoprep.com/pupil-involved-vs.-pupil-sparing-acquired-oculomotor-nerve-palsy

 

Oculomotor nerve palsy presents with a characteristic combination of ptosis, ophthalmoplegia, and occasionally pupillary involvement. The key clinical distinction lies in whether the pupil is involved or spared, which often reflects the underlying pathophysiology. Among the most critical differentials are aneurysmal compression and diabetic ischemic neuropathy.

1. Anatomical considerations

The oculomotor nerve consists of:

• Somatic efferent fibers: innervate the extraocular muscles (except LR and SO) and the levator palpebrae superioris
• Parasympathetic fibers: control pupillary constriction via the sphincter pupillae and accommodation via the ciliary muscle

Anatomically, the parasympathetic fibers are located peripherally in the nerve, whereas the somatic motor fibers are located centrally.

This topographical organization underpins the distinct clinical manifestations seen in compressive versus ischemic lesions.

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2. Aneurysmal compression

The most common vascular etiology is compression by a posterior communicating artery (PCOM) aneurysm. In this scenario, the lesion typically exerts external pressure on the oculomotor nerve, initially compromising the superficial parasympathetic fibers.

Clinical features:

• Complete ptosis
• Eye deviated "down and out" (due to unopposed LR and SO)
• Mydriasis (fixed and dilated pupil)
• Loss of light reflex

Because pupillary fibers are affected early, pupil-involving oculomotor palsy must be presumed aneurysmal until proven otherwise. Prompt neuroimaging with CTA or MRA is indicated.

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3. Diabetic oculomotor neuropathy

In contrast, diabetic third nerve palsy is caused by microvascular infarction involving the vasa nervorum. This leads to selective damage of the central somatic motor fibers, sparing the peripheral parasympathetic fibers.

Clinical features:

• Ptosis
• Eye deviated down and out
• Pupillary function preserved (reactive, normal-sized pupil)
• Often painful
• Typically improves over weeks

This pattern is referred to as pupil-sparing third nerve palsy, which is highly suggestive of a microvascular ischemic etiology, particularly in older patients with diabetes or hypertension.

 

https://www.emdocs.net/em3am-oculomotor-nerve-palsy/

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4. Diagnostic and clinical implications

The following table summarizes the key differences.

Feature	Aneurysmal compression	Diabetic infarction
Mechanism	External compression	Internal ischemia
Pupillary involvement	Frequent (early)	Rare
Ptosis and ophthalmoplegia	Complete	Complete
Pain	Variable	Often present
Laterality	Usually unilateral	Unilateral
Imaging	Urgent vascular imaging required	Often not needed initially
Prognosis	Potentially life-threatening	Spontaneous recovery within weeks

 

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5. Summary

When confronted with oculomotor nerve palsy, pupillary status is the critical triage point. Pupil-involving palsy warrants immediate investigation for a compressive lesion, particularly aneurysm. In contrast, pupil-sparing palsy in a diabetic patient with vascular risk factors often represents a benign, self-limiting ischemic neuropathy.

In clinical practice, assume compressive etiology unless pupil is clearly spared and the clinical setting strongly suggests microvascular disease.