Diabetic Hypertensive Cranial Nerve Palsies

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Chronic diabetes and hypertension can eventually create vascular compromise to the vasa nervorum of any CN. Frequently the patient will present with new-onset diplopia and an isolated CN III or VI palsy will be found on physical examination. The CN palsy is often painful, but it can be painless. The pupil is spared in acute diabetic CN III palsy due to vascular compromise of the central nerve fibers (the efferent pupillomotor fibers run in the periphery of the nerveā€”see Fig.230-19). Extraocular muscle testing will reveal an inhibition of ipsilateral medial gaze, upward gaze, and downward gaze as well as ptosis in an acute CN III palsy. Lateral gaze (abduction) will be preserved, and diplopia will be worse when the patient attempts to look toward the contralateral side due to inability to adduct the eye (medial rectus dysfunction). In an acute CN VI palsy, lateral gaze will be diminished (abduction) on the ipsilateral side and diplopia will be worse when the patient is trying to look to the affected side (lateral rectus dysfunction). If no other associated neurologic symptoms or findings are present and the blood sugar and blood pressure are under control, the patient can be discharged with ophthalmology and/or neurology follow-up. Many of these palsies will resolve or improve over the following 3 months. Imaging is indicated if the history or physical suggests an intracranial lesion or if the palsy fails to improve over the next 6 to 12 weeks.

FIG. 230-19. PCA aneurysm compresses the peripherally located pupillomotor fibers of cranial nerve III, causing a nerve palsy and pupillary dilation. Diabetes and hypertension can cause microvascular compromise of the central nerve fibers causing a nerve palsy with pupil sparing.

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