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Abstract：
BACKGROUND: Pure fusiform aneurysms of the anterior communicating artery (AcomA) are rare. We report a unique case of a patient with an AComA fusiform aneurysm in the setting of several unusual cranial neurocristopathies, including a hypoplastic internal carotid artery (ICA), persistent craniopharyngeal canal, transsphenoidal encephalocele, and ectopic, duplicated pituitary gland. We also review the literature on cranial base neurocristopathies and AComA fusiform aneurysms.
METHODS: This 46-year-old patient had a history of short stature, osteoporosis, obesity, cleft lip, decreased libido, congenital left eye blindness, headaches, and chronic nasal congestion. Magnetic resonance imaging revealed a 25 × 25 × 33 mm heterogenous soft tissue mass with an ectopic pituitary gland extending transsphenoidally and a duplicated pituitary stalk. A hormone panel revealed undetectable insulin-like growth factor 1 and growth hormone, central hypogonadism, and elevated prolactin. Before presentation, computed tomography angiography (CTA) had revealed a congenitally hypoplastic right ICA and 4.7 × 10.7 mm fusiform aneurysm of the AComA. Digital subtraction angiography confirmed stable morphology after 9 years. Nonoperative management of aneurysm and cephalocele was elected, with repeat CTA in 1 year.
CONCLUSIONS: This case provides evidence that inherent arterial wall defects can contribute to fusiform aneurysm formation in the AComA. We propose that small AComA fusiform aneurysms without sclerotic or symptomatic features can be safely observed by describing the longest reported conservative management for this type of aneurysm. A high degree of suspicion for cerebrovascular anomalies should be maintained in patients who present with cranial neurocristopathy.
METHODS: This 46-year-old patient had a history of short stature, osteoporosis, obesity, cleft lip, decreased libido, congenital left eye blindness, headaches, and chronic nasal congestion. Magnetic resonance imaging revealed a 25 × 25 × 33 mm heterogenous soft tissue mass with an ectopic pituitary gland extending transsphenoidally and a duplicated pituitary stalk. A hormone panel revealed undetectable insulin-like growth factor 1 and growth hormone, central hypogonadism, and elevated prolactin. Before presentation, computed tomography angiography (CTA) had revealed a congenitally hypoplastic right ICA and 4.7 × 10.7 mm fusiform aneurysm of the AComA. Digital subtraction angiography confirmed stable morphology after 9 years. Nonoperative management of aneurysm and cephalocele was elected, with repeat CTA in 1 year.
CONCLUSIONS: This case provides evidence that inherent arterial wall defects can contribute to fusiform aneurysm formation in the AComA. We propose that small AComA fusiform aneurysms without sclerotic or symptomatic features can be safely observed by describing the longest reported conservative management for this type of aneurysm. A high degree of suspicion for cerebrovascular anomalies should be maintained in patients who present with cranial neurocristopathy.
摘要：
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