Vascular Surgery

1967

DOI: 10.1177/153857446700100305

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Fusiform Arteriosclerotic Aneurysm of the Basilar Artery

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Cited by 52 publications

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“…In two autopsy series comprising 20,500 cases, only 7 fusi form basilar aneurysms were found. 9 - 24 Dandy called it the " S " aneurysm. 8 Other authors deny that the lesion is a true aneurysm and suggest that it be called an anomaly.…”

Section: Discussionmentioning

confidence: 99%

“…They concluded that the cause of the tionably of arteriosclerotic origin." 8 The five cases dolicho-ectatic anomaly was a primary dysplasia of the reported by Hayes et al 9 all had extensive atheroscle muscularis with secondary changes in the elastic tissue rosis. Nijensohn et al 10 reviewed the clinical and gross pathological features of 27 saccular and 23 fusiform basilar aneurysms.…”

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confidence: 89%

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Fusiform basilar aneurysm as a cause of embolic stroke.

1982

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SUMMARY Giant fusiform basilar aneurysms (dolicho-ectatic basilar anomalies) are rare and have not previously been reported to cause embolic infarction in territory distal to the aneurysm. They most commonly present as posterior fossa mass lesions with brainstem compression and cranial neuropathies. Originally considered atherosclerotic in etiology, recent authors feel that they may represent a unique arteriopathy characterized by loss of elastin in the vessel wall. We report a case which presented solely as an occipital lobe infarction. To our knowledge, this is the first case in which a fusiform basilar aneurysm presented with an embolic infarction as its only manifestation. Stroke, Vol 13, No 5, 1982 GIANT FUSIFORM BASILAR ANEURYSMS (doli cho-ectatic basilar anomalies') are aneurysmal dilations of the basilar artery and usually present clinically as posterior fossa mass lesions ( 5 Emboli arising from in tracerebral aneurysms are unusual 22 -23 and to our knowledge have not been reported originating from a fusiform basilar aneurysm. We report a case which presented solely as an embolic occipital lobe in farction.Case Report A 59-year-old man with mild hypertension and Type IV hyperlipidemia experienced abrupt onset of right periorbital headache accompanied by loss of vision in the left visual field. He had no previous history of transient ischemic attacks (TIAs) or stroke. Several weeks prior to the event, he noted frequent right peri orbital headachees lasting 45-60 minutes without neurologic symptoms. Nine years previously he under went surgery for repair of an abdominal aortic aneu rysm. His risk factors included a 20 year history of mild hypertension (highest recorded pressure 140/100 mg Hg), smoking, hypertriglyceridemia, and moder ate obesity. His general physical examination was normal ex cept for early retinal vessel sclerosis. Blood pressure was 130/84 mm Hg. There were no carotid bruits. Neurologic examination demonstrated a left superior _, quadrantanopsia, but was otherwise unremarkable.The following studies were normal: serum electro lytes, complete blood count, syphilis serology, urinal ysis, coagulation profile, echocardiogram, and lumbar puncture. Serum triglycerides were 261 mg/dl (nor mal, 30-150 mg/dl). The electrocardiogram demon strated borderline nonspecific ST-T wave changes and rare multifocal premature ventricular contractions.A computed tomographic (CT) scan of the head demonstrated a nonhemorrhagic right occipital lobe infarction ( fig. 1), and a large eccentrically positioned basilar artery, with calcification in its walls, extending well above the posterior clinoids ( fig. 2a). The contrast enhanced ( fig. 2b) and reformatted coronal ( fig. 3) images revealed the presence of incomplete thrombo sis in the aneurysm which measured up to 2 cm in diameter. Pancerebral angiography ( fig. 4) confirmed the diagnosis of a partially thrombosed giant fusiform basilar aneurysm and showed the lesion to be continu ous with an ectatic and elongated dominant right verte bral artery. In additio...

“…In two autopsy series comprising 20,500 cases, only 7 fusi form basilar aneurysms were found. 9 - 24 Dandy called it the " S " aneurysm. 8 Other authors deny that the lesion is a true aneurysm and suggest that it be called an anomaly.…”

Section: Discussionmentioning

confidence: 99%

“…They concluded that the cause of the tionably of arteriosclerotic origin." 8 The five cases dolicho-ectatic anomaly was a primary dysplasia of the reported by Hayes et al 9 all had extensive atheroscle muscularis with secondary changes in the elastic tissue rosis. Nijensohn et al 10 reviewed the clinical and gross pathological features of 27 saccular and 23 fusiform basilar aneurysms.…”

mentioning

confidence: 89%

Fusiform basilar aneurysm as a cause of embolic stroke.

1982

View full text Add to dashboard Cite

SUMMARY Giant fusiform basilar aneurysms (dolicho-ectatic basilar anomalies) are rare and have not previously been reported to cause embolic infarction in territory distal to the aneurysm. They most commonly present as posterior fossa mass lesions with brainstem compression and cranial neuropathies. Originally considered atherosclerotic in etiology, recent authors feel that they may represent a unique arteriopathy characterized by loss of elastin in the vessel wall. We report a case which presented solely as an occipital lobe infarction. To our knowledge, this is the first case in which a fusiform basilar aneurysm presented with an embolic infarction as its only manifestation. Stroke, Vol 13, No 5, 1982 GIANT FUSIFORM BASILAR ANEURYSMS (doli cho-ectatic basilar anomalies') are aneurysmal dilations of the basilar artery and usually present clinically as posterior fossa mass lesions ( 5 Emboli arising from in tracerebral aneurysms are unusual 22 -23 and to our knowledge have not been reported originating from a fusiform basilar aneurysm. We report a case which presented solely as an embolic occipital lobe in farction.Case Report A 59-year-old man with mild hypertension and Type IV hyperlipidemia experienced abrupt onset of right periorbital headache accompanied by loss of vision in the left visual field. He had no previous history of transient ischemic attacks (TIAs) or stroke. Several weeks prior to the event, he noted frequent right peri orbital headachees lasting 45-60 minutes without neurologic symptoms. Nine years previously he under went surgery for repair of an abdominal aortic aneu rysm. His risk factors included a 20 year history of mild hypertension (highest recorded pressure 140/100 mg Hg), smoking, hypertriglyceridemia, and moder ate obesity. His general physical examination was normal ex cept for early retinal vessel sclerosis. Blood pressure was 130/84 mm Hg. There were no carotid bruits. Neurologic examination demonstrated a left superior _, quadrantanopsia, but was otherwise unremarkable.The following studies were normal: serum electro lytes, complete blood count, syphilis serology, urinal ysis, coagulation profile, echocardiogram, and lumbar puncture. Serum triglycerides were 261 mg/dl (nor mal, 30-150 mg/dl). The electrocardiogram demon strated borderline nonspecific ST-T wave changes and rare multifocal premature ventricular contractions.A computed tomographic (CT) scan of the head demonstrated a nonhemorrhagic right occipital lobe infarction ( fig. 1), and a large eccentrically positioned basilar artery, with calcification in its walls, extending well above the posterior clinoids ( fig. 2a). The contrast enhanced ( fig. 2b) and reformatted coronal ( fig. 3) images revealed the presence of incomplete thrombo sis in the aneurysm which measured up to 2 cm in diameter. Pancerebral angiography ( fig. 4) confirmed the diagnosis of a partially thrombosed giant fusiform basilar aneurysm and showed the lesion to be continu ous with an ectatic and elongated dominant right verte bral artery. In additio...

“…SAH resulting from rupture of a dolichoectatic intracranial artery has rarely been reported [15,19,20]. In larger series of patients with vertebrobasilar dolichoectasia [1,13,14], SAH occurred only in the presence of other, separate causes, such as concomitant saccular aneurysm, carotid fusiform aneurysm, or uncontrolled hypertension.…”

Section: Discussionmentioning

confidence: 99%

Treatment Options in Vertebrobasilar Dolichoectasia – Case Report and Review of the Literature

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et al. 2003

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“…1 Such aneurysms may present with subarachnoid hemorrhage, 8 with brain stem or cranial nerve compression which simulates a tumor, 14 Occlusion of perforating pontine blood vessels leading to the infarction was caused by partial thrombosis of the fusiform aneurysm or by dissection of blood within the wall of the basilar artery obstructing the origins of the small brain stem vessels. Dissecting aneurysms of the intracranial vessels have been reported in young individuals in the postpartum period," following a tonsillectomy, 18 or associated with cystic medial necrosis of the basilar artery, homocystinuria, trauma, migraine, syphilitic arteritis, segmental arteriosclerotic changes, or congenital medial defects.…”

Section: Discussionmentioning

confidence: 99%

Fusiform basilar aneurysm simulating carotid transient ischemic attacks.

1979

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FUSIFORM ANEURYSMS of the basilar artery are rare. They are known to present with subarachnoid hemorrhage, with brain stem signs indicating compression of the hindbrain by a mass, with transient ischemic attacks, or with dementia and gait disturbance secondary to hydrocephalus. One case of a fusiform aneurysm of the basilar artery is reported which presented with a focal brain stem infarction after recurring carotid territory transient ischemic attacks. This case emphasizes the need to consider other diagnoses which can simulate transient ischemic attacks, especially when the attacks are recurrent after appropriate treatment.Case Report A 51-year-old male was admitted to the hospital Feb. 13, 1977, after 12 hours of headache, lethargy, dysarthria, nausea and vomiting, and the onset of right-sided weakness. During the 3 days prior to admission the patient reported his right side was gradually becoming weaker.Previously, (Aug. 6, 1974) the patient had been admitted with a complaint of transient right-sided weakness and slurred speech. No carotid bruits were heard and blood pressure was 120/80. Angiography revealed a very small left internal carotid ulcerated arteriosclerotic plaque. An endarterectomy was performed, and the patient had a smooth postoperative course. A brain scan, EEG, and computed tomography (CT) scan were normal. A 5-hour glucose tolerance test suggested early diabetes because of late hypoglycemia.The patient was then well until Sept. 17,1974, when he developed right-sided weakness and dysarthria. Examination revealed a right central 7th paresis and a mild right hemiparesis, both of which cleared within The patient was then well until Aug. 7, 1976 when he developed right-sided weakness and dysarthria. Blood pressure was 118/80 and serum glucose was 110. The patient quickly recovered from his neurologic deficit and was continued on anticoagulant therapy.For 3 days prior to this admission the patient had not been taking warfarin.The general physical exam was normal, except for a surgical scar along the left side of the neck. No carotid bruits were heard. There was no neck rigidity. Blood pressure was 150/100. The patient was lethargic but followed verbal commands. The neurologic examination revealed the pupils to be equal, round, and reactive to light. The fundi were normal. There was first degree nystagmus on right lateral gaze. The patient could not look to the left, and the eyes could not be made to cross the midline with cold caloric testing. On gaze to the right there was incomplete adduction of the left eye. A left peripheral facial nerve paresis was present. The corneal reflexes were equal and present. A severe right spastic hemiparesis was present as were bilateral Babinski signs. Occasional ocular bobbing was visible.An injected CT scan revealed a mass with the density of blood lying behind the clivus and extending up into the third ventricle ( figs. 1, 2). A right brachial arteriogram revealed the presence of a large ectatic fusiform basilar aneurysm ( figs. 3, 4). The irregular 598 by gue...

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