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(Stroke. 1998;29:653-659.)
© 1998 American Heart Association, Inc.

Original Contributions

Posterior Circulation Infarcts in Patients With Vertebrobasilar Dolichoectasia

Stefano Passero, MD; Giuseppe Filosomi, MD

From the Istituto di Clinica delle Malattie Nervose e Mentali (S.P.) and Istituto di Scienze Eidologiche e Radiologiche (G.F.), Università di Siena (Italy).

Correspondence to Stefano Passero, MD, Istituto di Clinica delle Malattie Nervose e Mentali, Università di Siena, Viale Bracci, I-53100 Siena, Italy.

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
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 (n=9), MRI (n=6), or both (n=25). 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 (n=8) or in the superficial arterial territory of the posterior cerebral artery (PCA; n=8). 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 (P=.0006) and a higher degree of vertical elongation of the BA (P=.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.

Key Words: stroke, ischemic • vertebrobasilar circulation • vertebrobasilar dolichoectasia

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Vertebrobasilar dolichoectasia is an uncommon but well-recognized vascular anomaly, the diagnosis of which has been simplified by CT and MRI. An ectatic, elongated BA may produce symptoms by direct compression of cranial nerves or the brain stem, by obstructive hydrocephalus, or by ischemia in vertebrobasilar arterial territory.^{1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16} Bleeding associated with VBD has also been reported.^{4 10 13 17 18 19 20 21} There are many reports of patients with VBD complicated by compression of neural structures, whereas studies of ischemic complications are few and no attempt has been made to characterize this aspect.^{4 9 11 13}

This study was undertaken to systematically examine and characterize clinical and imaging findings in patients with stroke associated with VBD and to compare this data with that of patients with VBD but no stroke.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
We studied 40 consecutive stroke patients with associated VBD. All were evaluated by CT scan (n=9), MRI (n=6), or both (n=25). Eighteen patients underwent additional angiographic examination performed by the Seldinger method, and 11 underwent MRA. Other investigations included standard blood tests, Doppler ultrasonography, ECG, and transthoracic echocardiography. MR was performed with a 0.5-T superconducting magnet unit with use of spin-echo, multi-echo, and FAST techniques. The images (T1- and T2-weighted and proton density) were obtained in the sagittal, axial, and coronal planes. Slice thickness was 5.0 mm, with a 2.0-mm interval between successive slices. According to Smoker et al,²² the BA was judged elongated if at any point along its course it lay lateral to the margin of the clivus or dorsum sellae or bifurcated above the plane of the suprasellar cistern. Ectasia was diagnosed if the diameter of the artery was greater than 4.5 mm.

The following risk factors for cerebrovascular disease were examined: history of hypertension (previous diagnosis of arterial hypertension, ie, systolic blood pressure >160 mm Hg or diastolic >90 mm Hg or both and/or past or present use of antihypertensive agents), diabetes mellitus (previous diagnosis of diabetes and/or past or present use of antidiabetic agents), current smoking, alcohol abuse (ingestion of >400 mL/wk pure ethanol), hyperlipidemia (cholesterol level of >250 mg/100 mL or triglyceride level of >180 mg/100 mL or both), previous coronary artery disease (or myocardial infarction), and potential cardiac source of embolism.

Ischemic lesions in the posterior circulation were classified according to the anatomic site and the presumed vascular territory involved using the templates proposed by Pullicino,²³ Tatu et al,²⁴ and Damasio.²⁵ The diameter of the BA, height of bifurcation, and lateral displacement were evaluated as suggested by Smoker et al.²² The height of the BA bifurcation was scored as 1 (within the suprasellar cistern), 2 (at level of third ventricle floor), or 3 (indenting and elevating the floor of the third ventricle); lateral displacement was scored as 1 (medial to lateral margin of clivus or dorsum sellae), 2 (lateral to lateral margin of clivus or dorsum sellae), or 3 (in cerebellopontine angle cistern). A global index of dolichoectasia was calculated by adding the single scores.

Some clinical and imaging findings (parameters of the BA, presence of hypertension, and presence of atherosclerotic changes of the posterior circulation) were compared with those found in a group of 40 patients (9 women and 31 men; mean age, 61.6±8.6 years; median age, 63.0 years; range, 45 to 82 years) with VBD but no history of cerebrovascular events. None of these patients showed evidence of ischemic lesions in the posterior circulation on CT (n=9) or MRI (n=31) examinations. Sixteen patients also underwent conventional angiographic examination.

The ² test was used in the statistical procedures.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
The 40 patients (9 women and 31 men) ranged in age from 47 to 83 years (mean, 62.8±8.9 years; median, 63.0 years). Of these patients, 25 had experienced no previous cerebrovascular events. Twelve patients had suffered one or more previous transient ischemic attacks, and 3 patients had previous cerebral hemorrhages (1 thalamic, 1 putaminal, and 1 lobar). At the time of stroke all patients without previous history of cerebrovascular events and the 3 patients with previous cerebral hemorrhage were not being treated with antithrombotic drugs. Among the 12 patients with previous transient ischemic attacks, 5 were treated with aspirin (325 to 500 mg/d) and 5 with dipyridamole, while 2 patients were not under treatment at the time of stroke.

Vascular Concomitants
The most common risk factor was arterial hypertension, which was present in 29 patients. Six patients had diabetes, 20 patients hyperlipidemia, 17 patients were current smokers, 8 patients were alcohol abusers, and 6 patients had a history of coronary artery disease (4 angina pectoris and 2 old myocardial infarct) (Table 1). None had arrhythmia at the time of the event, and echocardiography performed in 37 patients revealed the presence of possible emboligenic abnormalities in 2 patients (left ventricular hypokinetic segment). Only 1 patient was free of risk factors; 7 patients had one, and 32 had more than one risk factor.

View this table: [in this window] [in a new window]   Table 1. Demographic and Clinical Characteristics of 40 Patients With Stroke Associated With Vertebrobasilar Dolichoectasia

Infarcts in Posterior Circulation
More than half of the patients (24 of 40) had infratentorial infarcts localized in the midbrain (n=4), pons (n=14), medulla (n=1), and cerebellum (n=5). Pontine lesions were mainly located in the midpons (9 of 14). Sixteen patients had supratentorial lesions localized in the thalamus (n=8) or in the superficial arterial territory of the PCA (n=8) (Table 2).

View this table: [in this window] [in a new window]   Table 2. Posterior Circulation Infarcts in 40 Patients With Vertebrobasilar Dolichoectasia

In 22 patients the lesion was located in arterial territories supplied by branches of the BA or vertebral artery, specifically, the penetrating arteries (anteromedial and anterolateral perforators) in 12 patients and the short and long circumferential arteries (lateral pontine artery, superior cerebellar artery, anterior inferior cerebellar artery, and posterior inferior cerebellar artery) in 10 patients. In the other 18 patients, the arterial territory involved was supplied by deep branches of the PCA, such as the anteromedial and anterolateral midbrain arteries (n=2), inferolateral thalamic arteries (n=5), paramedian thalamic arteries (n=2), posterior choroidal arteries (n=1), or by the superficial branches of the PCA (n=8). The latter included patients with infarct involving the entire superficial territory of the PCA (n=1), the territory of the posterior division (n=6), and the territory of the anterior division (n=1).

Other Infarcts and Lesions
One patient had an old asymptomatic occipital infarct (case 38) and 3 had supratentorial scars due to previous cerebral hemorrhage. Thirty-two patients had white matter lesions, with areas of focal abnormalities in 26 and a multifocal diffuse pattern (leukoencephalopathy) in 5 (cases 12, 13, 20, 31, and 32). In 7 patients (cases 11, 17, 21, 23, 28, and 40) no other lesions were found.

Arterial Lesions
None of the 29 patients in whom angiography or MRA was performed had occlusion or stenosis of >50% of the vertebral, basilar, and posterior cerebral arteries; 4 had unilateral or bilateral stenosis of >50% of the carotid arteries (cases 33, 34, 35, and 39); and 7 had stenosis of <50% of the anterior circulation (n=4), posterior circulation (n=2), or both (n=1). Diffuse atherosclerotic changes were observed in 13 patients, and in 2 patients (cases 19 and 23) no arterial lesions other than VBD were found . Other findings were ectasia (cases 6, 14, and 30) and saccular aneurysm (case 1) of the anterior circulation. One patient (case 6) had ectasia of the abdominal aorta on MRA. Ten of the 11 patients who were not examined by angiographic study underwent MRI, which showed no abnormal vertebrobasilar artery flow void signal. Doppler sonography showed atherosclerotic changes in all 11 patients. One patient (case 24) underwent CT examination only; however, a contrast-enhanced scan showed no evidence of BA intraluminal thrombus.

The diameter of the BA ranged in size from 4.8 to 10.9 mm. In 20 patients, elongation of the BA was very pronounced, with the bifurcation of the artery indenting the floor of the third ventricle or the artery lying in the cerebellopontine angle cistern. The most frequent deformation of the BA was C shaped (n=24), other types were S- (n=13) and J-shaped (n=3) deformities.

An attempt was made to correlate some aspects of the BA (diameter of the artery, degree of the lateral displacement, and height of the bifurcation) with the location of the ischemic lesions (PCA territory versus BA territory). Among these variables, diameter and height of the bifurcation of the BA were correlated with the location of the lesion, in that severe ectasia and vertical elongation of the BA were observed significantly more often in patients with infarcts in the PCA territory than in patients with infarcts in territories supplied by branches of the BA (Table 3). The same was true even when the analysis was repeated with the exclusion of patients with possible causes of posterior circulation infarct other than VBD. Among the 19 patients with pontine or cerebellar lesions (superior cerebellar and anterior inferior cerebellar artery territories), the location of infarct was opposite to the side of lateral displacement of the BA in 11 patients, on the same side in 5 patients, and at the same level as the side-to-side transition of the BA in 3 patients with S-shaped BAs.

View this table: [in this window] [in a new window]   Table 3. Location of Lesions and Severity of Vertebrobasilar Dolichoectasia

Other Causes of Stroke
In 23 patients there was no potential cause of posterior circulation infarct other than VBD. In 17 patients another possible cause of stroke coexisted with VBD. These included arteriolar lipohyalinosis in 15 hypertensive patients with lacunar infarcts in the thalamus or brain stem and a potential cardiac source of embolism (left ventricular hypokinetic segment) in 2 patients with infarcts in the superficial territory of the PCA.

Clinical Aspects
Classic lacunar syndromes were observed in 14 patients: 3 had pure motor hemiparesis with contralateral pontine infarcts; 4 had pure sensory stroke, with contralateral thalamic infarcts in 3 and a contralateral pontine infarct in the other; and 7 had sensory motor stroke, with contralateral thalamic infarcts in 3 and contralateral pontine infarcts in 4. Acute unilateral pseudobulbar palsy was observed in 4 patients, with contralateral midbrain infarcts in 3 and a contralateral pontine infarct in the other. One patient had hemichorea with a contralateral thalamic infarct. Alternating syndromes, including Weber's and Raymond's syndromes, were observed in 5 patients (Table 2).

Thirty-eight patients survived the acute event, 32 with mild to moderate disability and 6 with severe deficit. Two patients (cases 13 and 24) died of the stroke within 6 days of onset.

Comparison of VBD Patients With and Without Stroke
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 (P=.0006) and a higher degree of vertical elongation of the BA (P=.025; Table 4).

View this table: [in this window] [in a new window]   Table 4. Clinical and Imaging Findings in VBD Patients With and Without Stroke

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
The relationship between cerebrovascular events and VBD has been described in occasional cases and in a few patient series. In those reports with sufficient clinical and imaging data,^{3 4 5 8 9 10 11 13 15 26 27 28 29 30 31 32} the most frequently described ischemic lesion was brain stem infarction, observed in 39 of 56 patients. Ten patients were reported to have cerebellar infarcts, 4 thalamic infarcts, and 3 infarcts in the superficial PCA territory (Table 5). Brain stem infarcts were most often located in the pons (29 of 39). Other authors have observed VBD in study series of patients with cerebellar,^{33 34} pontine,³⁵ medullary,^{36 37} and thalamic³⁸ infarcts or in patients with posterior circulation strokes.³⁹

View this table: [in this window] [in a new window]   Table 5. Location of Ischemic Lesion as Demonstrated by CT Scan, MRI, or Autopsy in 96 Patients With Stroke Associated With Vertebrobasilar Dolichoectasia1

Unlike those in other series,^{4 9 11 13} our patients showed a higher incidence of supratentorial infarcts, especially in the superficial PCA territory. This discrepancy may result from many factors, including different patient enrollment criteria and different imaging methods. MRI has certainly aided recognition of small infarcts not detectable by CT. Moreover, in patients with acute stroke, CT scan often cannot detect the simultaneous presence of VBD unless the BA has calcifications or a contrast medium is used.

The precise pathophysiology of cerebral ischemic events associated with VBD is not clear. In this condition, mechanisms commonly observed in patients with cerebrovascular disease, such as arteriolar lipohyalinosis, obstruction by atheroma or intraluminal thrombus, and artery-to-artery embolism, may be operant. 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. The first is the fact that the infarcts located in the PCA territory were significantly associated with more severe ectasia and vertical elongation of the BA than those located in territories supplied by branches of the basilar or vertebral arteries. This suggests the involvement of hemodynamic or thromboembolic mechanisms related to the reduced blood flow velocity in severe dolichoectasia (as demonstrated by angiographic study and transcranial Doppler examination)¹² and to the distortion of the PCAs and their small branches. 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 al⁸ 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.

Some authors^{21 41} have suggested that atherosclerotic degeneration of the vascular wall, either alone or associated with arterial hypertension, is the initial pathogenetic factor in the development of this condition. Other authors maintain that atherosclerosis does not play a substantial role in the pathogenesis of arterial ectasia and that VBD is a congenital anomaly. The second hypothesis is backed by histological studies that show defects in the internal elastic lamina, with thinning of the media secondary to smooth muscle atrophy^{20 32 42} ; by the frequent absence of atherosclerosis^{42 43} ; and by the occurrence of arterial ectasia in all age groups.^{13 44 45 46 47} Furthermore, VBD may be (1) a component of generalized ectasia of the cerebral vessels, as indicated in our and other series^{1 4 6 7 10 11 26 32 42 43 46 48} ; (2) associated with aneurysm of the abdominal aorta^{4 13 21 32 43 44 46} ; or (3) associated with ectasia of other vascular districts,^{43 46} which suggests a more diffuse arterial defect.

It seems likely that a defect in the development of the arterial wall is responsible for ectasia, which may also be favored by arterial hypertension, associated in some cases with an atheromatous process that further damages the elastic elements. Thus VBD may occur in the absence of atheroma or with superimposed atheromatous changes, as in the present series and others.^{1 21 42 43 44} Superimposed atheromatous changes may have an important role in precipitating ischemia, as suggested by our comparison of VBD patients with and without stroke, which showed that ischemic complications of VBD were significantly more often observed in patients who had superimposed atheromatous changes of the posterior circulation. However, the present study shows that other factors related to the severity of the dolichoectasia also favor ischemia and in some cases are the only factors responsible.

Although our series does not necessarily describe the entire spectrum of ischemic lesions associated with VBD, it nevertheless gives a sufficiently complete view of the possible ischemic complications associated with this pathology.

	Selected Abbreviations and Acronyms

 

BA = basilar artery MRA = magnetic resonance angiography PCA = posterior cerebral artery VBD = vertebrobasilar dolichoectasia

	Acknowledgments

 
Supported in part by research grants from the University of Siena (Contributi per la Ricerca Scientifica, fondi 60%).

Received November 3, 1997; revision received December 18, 1997; accepted January 6, 1998.

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