A 72-year-old man sought medical evaluationafter he awoke and was unableto open his right eyelid (A). He deniedpain, recent trauma, and diplopia. Thispatient’s history included well-controlledhypertension and hypercholesterolemia,for which he was taking atorvastatin.He did not have diabetes.
A 72-year-old man sought medical evaluationafter he awoke and was unableto open his right eyelid (A). He deniedpain, recent trauma, and diplopia. Thispatient's history included well-controlledhypertension and hypercholesterolemia,for which he was taking atorvastatin.He did not have diabetes.
When his right eyelid was lifted(here the lid is retracted and held inplace with tape), the patient immediatelynoted diplopia, although thevisual acuity was normal (B). In thisprimary position, the right eye wasabducted, indicating unopposed actionof the lateral rectus muscle. Thepupils appeared to be uninvolved.
During upward gaze (C), righteye elevation was limited, which indicatedweakness of the superior rectusmuscle; limited right eye depressionin downward gaze indicated weaknessof the inferior rectus muscle(D). Because the lateral rectus musclewas intact, normal abduction wasnoted in right gaze (E), whereas inleft gaze, weakness of the medial rectusmuscle resulted in limited righteye adduction (F).
The oculomotor (third) cranialnerve innervates 5 extraocular muscles-the levator; the superior, inferior,and medial rectus; and the inferioroblique-and carries the parasympatheticoutflow to the ciliary ganglionthat controls pupillary constrictionand accommodation. Any mechanismthat disrupts this outflow causes apartial or complete third-nerve palsy.
Third-nerve palsy can occur withany underlying vasculopathic disease,such as atherosclerosis, hypertension,hyperlipidemia, and diabetes. Diabeticthird-nerve palsies often are associatedwith periorbital pain.
The pupil is not involved in 80%of vasculopathic third-nerve palsies,1because the microangiopathy associatedwith these vascular disease lesionsinvolves the vasa nervorum,which causes infarction of the maintrunk of the nerve, but spares theparasympathetic pupillary fibers thatrun on the nerve externally and derivetheir blood supply from the pialblood vessels.2This pathology is mostcommon in older patients.
If the pupil is involved, stronglysuspect an aneurysm at the junction ofthe posterior communicating arterywith the internal carotid artery; parasympatheticpalsy results in a dilatedpupil. Aneurysmal lesions cause asmany as 95% of painful, pupil-associatedthird-nerve palsies.1
Rule out temporal arteritis-bythe history, erythrocyte sedimentationrate, and C-reactive proteinlevel-in patients who have ischemicmononeuropathy without pupil involvement.Otherwise, observationalone is sufficient because this typeof ischemic palsy that does not involvethe pupils generally resolveswithin a few months. Consult an ophthalmologist;the patient needs to bereevaluated 1 week after diagnosis toexclude late-onset pupil involvement.Consider a follow-up neuroimagingevaluation if any of these occur:
REFERENCES:1. Skorin L. Neuro-ophthalmic disease. In: OnofreyBE, Skorin L, Holdeman NR, eds. Ocular TherapeuticHandbook: A Clinical Manual. Philadelphia: Lippincott-Raven; 1998:506-509.
2. Kanski JJ. Clinical Ophthalmology: A SystematicApproach. 4th ed. Oxford, England: Butterworth-Heinemann; 1999:619-622.