Neurosurgery · 2001
Pseudomyasthenia resulting from a posterior carotid artery wall aneurysm: a novel presentation: case report.
Клинический случайСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Tummala R P, Harrison A, Madison M T, Nussbaum E S
Аннотация
OBJECTIVE AND IMPORTANCE: Painful oculomotor palsy can result from enlargement or rupture of intracranial aneurysms. The IIIrd cranial nerve dysfunction in this setting, whether partial or complete, is usually fixed or progressive and is sometimes reversible with surgery. We report an unusual oculomotor manifestation of a posterior carotid artery wall aneurysm, which mimicked ocular myasthenia gravis.
CLINICAL PRESENTATION: A 47-year-old woman developed painless, intermittent, partial IIIrd cranial nerve palsy. She presented with isolated episodic left-sided ptosis, which initially suggested a metabolic or neuromuscular disorder. However, digital subtraction angiography revealed a left posterior carotid artery wall aneurysm, just proximal to the origin of the posterior communicating artery.
INTERVENTION: The aneurysm was successfully clipped via a pterional craniotomy. During surgery, the aneurysm was observed to be compressing the oculomotor nerve. The patient's symptoms resolved after the operation.
CONCLUSION: The variability of incomplete IIIrd cranial nerve deficits can present a diagnostic challenge, and the approach for patients with isolated IIIrd cranial nerve palsies remains controversial. Although intracranial aneurysms compressing the oculomotor nerve classically produce fixed or progressive IIIrd cranial nerve palsies with pupillary involvement, anatomic variations may result in atypical presentations. With the exception of patients who present with pupil-sparing but otherwise complete IIIrd cranial nerve palsy, clinicians should always consider an intracranial aneurysm when confronted with even subtle dysfunction of the oculomotor nerve.
CLINICAL PRESENTATION: A 47-year-old woman developed painless, intermittent, partial IIIrd cranial nerve palsy. She presented with isolated episodic left-sided ptosis, which initially suggested a metabolic or neuromuscular disorder. However, digital subtraction angiography revealed a left posterior carotid artery wall aneurysm, just proximal to the origin of the posterior communicating artery.
INTERVENTION: The aneurysm was successfully clipped via a pterional craniotomy. During surgery, the aneurysm was observed to be compressing the oculomotor nerve. The patient's symptoms resolved after the operation.
CONCLUSION: The variability of incomplete IIIrd cranial nerve deficits can present a diagnostic challenge, and the approach for patients with isolated IIIrd cranial nerve palsies remains controversial. Although intracranial aneurysms compressing the oculomotor nerve classically produce fixed or progressive IIIrd cranial nerve palsies with pupillary involvement, anatomic variations may result in atypical presentations. With the exception of patients who present with pupil-sparing but otherwise complete IIIrd cranial nerve palsy, clinicians should always consider an intracranial aneurysm when confronted with even subtle dysfunction of the oculomotor nerve.