The megadolichobasilar anomaly

108

Background and Purpose-Vertebrobasilar dolichoectasia (VBD) may produce symptoms by direct compression of cranial nerves or the brain stem, by obstructive hydrocephalus, or by ischemia in the vertebrobasilar arterial territory. This study was undertaken to examine and characterize clinical and imaging findings in patients with stroke associated with VBD and compare these data with those for patients with VBD who did not have a stroke. Methods-We studied 40 consecutive stroke patients with associated VBD. All were evaluated by CT scan (nϭ9), MRI (nϭ6), or both (nϭ25). The diameter of the basilar artery (BA), height of bifurcation, and transverse position were evaluated. Clinical and imaging findings were compared with those found in a group of 40 VBD patients without stroke. Results-More than half of the patients (24 of 40) had infratentorial infarcts, located mainly in the midpons. Sixteen patients had supratentorial lesions localized in the thalamus (nϭ8) or in the superficial arterial territory of the posterior cerebral artery (PCA; nϭ8). The diameter and height of the bifurcation of the BA were correlated with the location of the lesion (PCA territory versus BA territory), in that severe ectasia and vertical elongation of the BA were significantly more often observed in patients with infarcts in PCA territory than in patients with infarcts in territories supplied by branches of the BA. Comparison of VBD patients with and without stroke showed that the incidence of arterial hypertension and the degree of ectasia and lateral displacement of the BA were not significantly different in the two groups. Patients with stroke more often had atherosclerotic changes of the posterior circulation (Pϭ.0006) and a higher degree of vertical elongation of the BA (Pϭ.025). Conclusions-In patients with VBD, superimposed atheromatous changes of the posterior circulation may have an important role in precipitating ischemia. However, other factors related to the severity of the dolichoectasia also favor ischemia and in some cases are the only factors responsible. (Stroke. 1998;29:653-659.)

Section: Discussionmentioning

confidence: 80%

Posterior Circulation Infarcts in Patients With Vertebrobasilar Dolichoectasia

Passero¹,

Filosomi²

1998

108

“…However, severe arteriosclerotic changes in the basilar artery were noticed on angiography with associated hypertension in 74% of twenty-three patients in this series. 6 artery must be confirmed by angiography, but the anomaly has been identified by CT scan. 7 ' 9~" In seventeen (74%) of our cases this abnormality was visualized with CT scan.…”

Section: Discussionmentioning

confidence: 99%

Dolichoectatic basilar artery: a review of 23 cases.

Nishizaki¹,

Tamaki²,

Takeda³

et al. 1986

118

SUMMARY The dolichoectatic basilar artery was found in 23 cases during a 10-year period. The 19 males and 4 females ranged in age from 30 to 69 years (mean: 55 years). Hypertension was noted in 17 patients. In seventeen (74%) of the present cases this anomaly could be visualized with CT scan. Seven patients (30%) presented with pontine infarction, which was identified on CT scan in all cases. Vertebro-basilar insufficiency was found in four patients. One patient had transient ischemic attacks. There were facial spasms in four patients and impairment of the lower cranial nerves in one. One patient exhibited cerebellar hemorrhage. In two patients this anomaly was found incidentally. Associated intracranial aneurysms were identified in seven patients, including fusiform aneurysms in 4 and saccular aneurysms in 3. Three patients had an accompanying hydrocephalus. The dolichoectatic basilar artery is associated with various consequences especially in relation to the pathogenesis of brainstem infarction. When this anomaly is diagnosed by CT findings, even if it is clinically asymptomatic, it may be better to treat these patients with medical therapy used to prevent ischemic stroke.

“…8 Other authors deny that the lesion is a true aneurysm and suggest that it be called an anomaly. 1 Mitts used the noncommittal term "fusi form enlargement." 25 The disorder usually presents as a posterior fossa mass with diverse symptomatology, including brainstem compression, multiple cranial neuropathies, hemifacial spasm, trigeminal neuralgia, supranuclear ophthalmoplegia, or obstructive hydro cephalus (table 1).…”

Section: Discussionmentioning

confidence: 99%

Fusiform basilar aneurysm as a cause of embolic stroke.

Steel¹,

Thomas²,

Strollo³

1982

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...