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Ординатура / Офтальмология / Английские материалы / Evaluation and Management of Blepharoptosis_Cohen, Weinberg_2010.pdf
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J.W. Kim

 

 

vulnerable to compression within the cavernous sinus, and an ipsilateral abduction deficit, however minor, can be very helpful in localizing a third nerve palsy. Coexisting fourth nerve palsy can be difficult to detect in the presence of a complete third nerve paresis, but intorsion can be assessed on attempted downgaze by observing an ocular landmark, such as the conjunctival vessels at the limbus. Lesions at the orbital apex typically cause orbital signs, such as proptosis, conjunctival chemosis, and an optic neuropathy.

Common Etiologies for Third Nerve Palsy

Diagnostic considerations for acquired third nerve palsy vary to a great extent on the anatomic location of the injury (see Table 12.1) [7]. Nuclear or brainstem causes for third nerve palsy include neoplasm (e.g., glioma), stroke (e.g., basilar artery occlusion), inflammation (e.g., abscess), infiltration, and extrinsic compression. The fascicular portion of the third nerve is most commonly affected by vascular processes causing midbrain infarction. Multiple sclerosis is a rare cause of third nerve palsy and when it occurs, the lesion must involve the white matter of the third nerve fascicle before it leaves the brainstem. The most common lesion to affect the third nerve in its subarachnoid segment is a posterior­ communicating artery aneurysm (Fig. 12.1d). In addition to the acute ocular findings, there may be signs of subarachnoid hemorrhage, including sudden severe headache, stiff neck, and photophobia. Other causes of

third nerve palsy in this location include basal infiltration­ by metastatic tumors, meningeal infection (bacterial, fungal, viral), and granulomatous inflammation, such as sarcoidosis or tuberculosis. Within the cavernous sinus, the third nerve is susceptible to compression from a variety of pathologic processes, including aneurysms, meningiomas, metastatic tumors, lymphomas, carotid-cavernous fistulas, and lateral extension of pituitary adenomas (e.g., apoplexy). Nonspecific, granulomatous inflammation within the cavernous sinus causing painful ophthalmoplegia has been termed Tolosa–Hunt syndrome; this is a rare condition that is considered a diagnosis of exclusion when all neoplastic and structural lesions have been ruled out. Ophthalmoplegic migraine is a nonstructural cause of episodic third nerve palsy starting in childhood, with recurring bouts of ipsilateral headache and third nerve palsy that can last several weeks per episode.

Treatment of Blepharoptosis

in Third Nerve Palsy

For patients diagnosed with oculomotor palsy, treatment of the blepharoptosis is aimed at the primary lesion causing the neurogenic injury. For example, aneurysms of the posterior communicating artery are treated with either interventional neuroradiology techniques or an open surgical approach, i.e., craniotomy. Surgical options include gluing, coiling, or wrapping of the berry aneurysm to relieve the pressure on the third nerve and prevent future bleeding episodes.

Table 12.1Common etiologies for third nerve palsy

Location

Midbrain

Subarachnoid

Cavernous sinus

Orbit

Ischemia/stroke

Aneurysm

Meningioma

Perineural invasion

Neoplasm (glioma)

Meningitis

Aneurysm

Lymphoma

Infiltration

Carcinomatosis

Metastatic tumor

Cavernous hemangioma

Abscess

Granulomatous

Carotid-cavernous fistula

Orbital pseudotumor (idiopathic

 

inflammation

 

orbital inflammation)

Multiple sclerosis

Schwannoma

Tolosa–Hunt syndrome