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A cranial nerve palsy of any of the three cranial nerves that supply the extraocular muscles can cause double vision.

In a complete third nerve palsy, there is ptosis with a divergent and slightly depressed eye (Figure 7–4). Extraocular movements are restricted in all directions except laterally (preserved lateral rectus function). Intact fourth nerve (superior oblique) function is detected by inward rotation on attempted depression of the eye. Pupillary involvement, manifesting as a relatively dilated pupil that does not constrict normally to light, usually means compression, which may be due to aneurysm of the posterior communicating artery or uncal herniation due to a supratentorial mass lesion. In acute painful isolated third nerve palsy with pupillary involvement, posterior communicating artery aneurysm must be excluded. Pituitary apoplexy is a rarer cause. Causes of isolated third nerve palsy without pupillary involvement include diabetes mellitus, hypertension, giant cell arteritis, and herpes zoster.

Fourth nerve palsy causes upward deviation of the eye with failure of depression on adduction. In acquired cases, there is vertical and torsional diplopia that is most apparent on looking down. Trauma is a major cause of acquired—particularly bilateral—fourth nerve palsy, but posterior fossa tumor and medical causes, such as in third nerve palsy, should also be considered. Similar clinical features are seen in congenital cases due to developmental anomaly of the nerve, muscle, or tendon.

Sixth nerve palsy causes convergent squint in the primary position with failure of abduction of the affected eye, producing horizontal diplopia that increases on gaze to the affected side and on looking into the distance (eFigure 7–68). It is an important sign of raised intracranial pressure and may also be due to trauma, neoplasms, brainstem lesions, petrous apex lesions, or medical causes (such as diabetes mellitus, hypertension, giant cell arteritis, and herpes zoster).

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