Fusiform basilar aneurysm as a cause of embolic stroke.

Abstract

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...

Posterior Circulation Infarcts in Patients With Vertebrobasilar Dolichoectasia

“…Another aspect suggesting a hemodynamic mechanism is the fact that half of the patients with infarcts in the superficial PCA territory had occlusion or severe stenosis of the anterior circulation. This feature was also observed by Steel et al 8 in a patient with an occipital infarct associated with VBD and a severe stenosis of the internal carotid artery. Among infratentorial infarcts, we observed that the majority of the lesions in the arterial territories supplied by branches of the BA were contralateral to the side of the lateral displacement of the BA, which suggests a relationship between ischemia and distortion and/or stretching of the branches of the BA.…”

“…However, in VBD other specific mechanisms, such as distortion of branches of the BA due to elongation and tortuosity of this vessel and hemodynamic factors related to the significant reduction of flow velocity in the BA, may contribute to ischemia. On the basis of the imaging and angiographic findings and exclusion of patients with other potential cause of stroke, two pathophysiological mechanisms of infarction can be identified in our series: (1) infarcts in distal territories (thalamus, superficial PCA territory, cerebellum) that may be associated with artery-to-artery embolism 8,28 and (2) brain stem and some cerebellar infarcts that may be associated with atherothrombotic occlusion at the origin of BA branches (branch atheromatous disease). 40 Our study reveals three interesting aspects.…”

Thrombus in Vertebrobasilar Dolichoectatic Artery Treated with Intravenous Urokinase

“…The elongated dilated arteries may compress and distort the brainstem and the cranial nerves and can occasionally cause obstruction of the ventricular system [2, 3, 4, 5, 6, 7, 8, 9, 10]. Brain ischemia is also known to occur and the presumptive mechanisms of stroke have been described [11, 12, 13, 14]. Flow within the dilated dolichoectatic arteries, studied by transcranial Doppler ultrasound, is often abnormal with to and fro antegrade and retrograde passage of segments of the blood column [14, 15, 16].…”

“…Flow within the dilated dolichoectatic arteries, studied by transcranial Doppler ultrasound, is often abnormal with to and fro antegrade and retrograde passage of segments of the blood column [14, 15, 16]. The abnormal flow patterns and regions of stagnation within the dilated arteries can cause hypoperfusion and also promote intraluminal thrombus formation [11, 12]. The orifices of penetrating and circumferential branches of the intracranial vertebral and basilar arteries can be distorted or blocked by aneurysmal deformities, atheromatous plaques and intraluminal thrombus [11, 17].…”

Intracranial Bleeding in Patients With Vertebrobasilar Dolichoectasia

“…[7][8][9][10][11][12][13] However, pathological changes in the arterial wall, consisting primarily in defects in the internal elastic lamina with thinning of the media secondary to smooth muscle atrophy, 14 -16 may predispose patients to intracranial bleeding of various kinds. Knowledge of hemorrhagic stroke as a clinical feature of VBD has come from case reports involving a small number of patients.…”