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The most common causes of acquired third nerve palsy were: Presumed microvascular (42 percent) Trauma (12 percent) Compression from neoplasm (11 percent) Post-neurosurgery (10 percent) Compression from aneurysm (6 percent) Pupil involvement.
Third cranial nerve palsy occurs when CN III loses function. This results in symptoms such as misaligned eyes, double vision, drooping eyelid or enlarged pupil. It can be present at birth or be the result of an injury, disease or infection.
Third nerve palsy has a variety of etiologies and can be a harbinger of serious pathology. This activity reviews the etiology, presentation, evaluation, and management of CN III palsy and reviews the role of the interprofessional team in evaluating, diagnosing, and managing the condition. Objectives:
The rare congenital 3 rd nerve palsy usually involves ptosis, an ophthalmoplegia of some degree, and pupillary mydriasis. It is often an isolated finding but may be associated with aberrant regeneration, other cranial nerve palsies, other central nervous system anomalies, or developmental delay.
The diagnosis and management of third nerve palsy varies according to the age of the patient, the characteristics of the third nerve palsy, and the presence of associated signs and symptoms. The manifestations and diagnosis of third nerve palsy in adults will be reviewed here.
An acquired oculomotor nerve palsy (OMP) results from damage to the third cranial nerve. It can present in different ways causing somatic extraocular muscle dysfunction (superior, inferior, and medial recti; inferior oblique; and levator palpebrae superioris) and autonomic (pupillary sphincter and ciliary) muscles. [1]
Cranial nerve palsy occurs when one of the 12 pairs of nerves that lead from the brain to the face, head or torso loses function. A loss of function of the cranial nerves to the eyes and face can cause symptoms such as weakness, limited movement, double vision, droopy eyelid or a dilated pupil.