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LETTER TO EDITOR
Year : 2010  |  Volume : 58  |  Issue : 5  |  Page : 810-812

Vertebrobasilar dolichoectasia and a tale of two brothers


1 Department of Neurology, Ludhiana Mediciti Hospital, Ludhiana, Punjab - 142 027, India
2 Department of Radiodiagnosis, Christian Medical College and Hospital, Ludhiana, Punjab - 141 008, India
3 Department of Neurology, Christian Medical College and Hospital, Ludhiana, Punjab - 141 008, India

Date of Acceptance30-Jul-2010
Date of Web Publication28-Oct-2010

Correspondence Address:
Deepak Gupta
Department of Neurology, Ludhiana Mediciti Hospital, Ludhiana, Punjab - 142 027
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.72199

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How to cite this article:
Gupta D, George UB, Pandian JD. Vertebrobasilar dolichoectasia and a tale of two brothers. Neurol India 2010;58:810-2

How to cite this URL:
Gupta D, George UB, Pandian JD. Vertebrobasilar dolichoectasia and a tale of two brothers. Neurol India [serial online] 2010 [cited 2019 Dec 6];58:810-2. Available from: http://www.neurologyindia.com/text.asp?2010/58/5/810/72199


Sir,

Vertebrobasilar dolichoectasia (VBD) is characterized by marked elongation, dilatation and tortuosity of the vertebral and the basilar arteries. The mean diameter of the normal basilar artery (BA) is 3.17 mm at the level of the pons, and the bifurcation is located in the interpeduncular cistern adjacent to the dorsum sellae or in the suprasellar cistern below the level of the floor of the third ventricle. [1] BA is considered dolichoectatic if at any point along its course it lies lateral to the margin of the clivus or dorsum sellae or bifurcates above the plane of the suprasellar cistern and if the diameter of the BA is greater than 4.5 mm. [2],[3] Although the clinical manifestations of VBD are well known, [2],[4] it is unclear whether genetic factors or atherosclerosis is the primary inciting event in its pathogenesis. [5],[6] We report occurrence of VBD in two siblings in an attempt to highlight the role of genetic factors in the development of VBD.

Patient 1, a 55-year-old male, diabetic, hypertensive and dyslipidemic, presented with acute onset of slurring of speech and dizziness. Examination revealed only mild dysarthria. Magnetic resonance imaging (MRI) brain with diffusion-weighted imaging (DWI) showed an acute paramedian and right ventral pontine infarct [Figure 1]. There was a chronic right putaminal infarct also. Time of flight magnetic resonance angiography (TOF MRA) of cranial vessels showed dolichoectasia of the left vertebral artery (VA) and the entire BA till its bifurcation [Figure 2]. The maximum diameter of BA was 12.7 mm; and of left VA, 11.4 mm. The BA bifurcated above the level of suprasellar cistern. After discharge, he was noncompliant with his antiplatelets and was readmitted six months later with right hemiparesis. DWI did not show any fresh infarcts.
Figure 1 :MRI brain of patient 1. (a) DWI; (b) axial T2W images showing acute paramedian and right ventral pontine infarct; (c) axial T1W section above the level of floor of third ventricle showing the dolichoectatic basilar artery (arrow) has not bifurcated. Also note a chronic infarct in right putamen (DWI: diffusion-weighted imaging)

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Figure 2 :TOF MRA images of (a) patient 1 and (b) patient 2 showing dolichoectatic basilar (arrowheads) and left vertebral arteries (arrows) (TOF MRA: time of flight magnetic resonance angiography)

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Patient 2, a 67-year-old male, dyslipidemic and elder sibling of patient 1, presented with left hemiparesis and slurring of speech of 3 hours' duration. MRI brain with DWI showed an acute right paramedian pontine infarct [Figure 3]. In addition, there were chronic infarcts in left paramedian pons, bilateral globus pallidus and centrum semiovale. TOF MRA of cranial vessels showed dolichoectasia of the entire BA and the left VA with normal flow voids [Figure 2]. The maximum diameter of the BA was 6.9 mm; and of the left VA, 6.4 mm. The BA bifurcated above the level of dorsum sellae. MRA of the anterior circulation, ECG and transthoracic echocardiography were normal in both cases. There was family history of ischemic heart disease in three other siblings, two of whom died due to acute coronary events [Figure 4].
Figure 3 :MRI brain of patient 2. (a) DWI showing an acute right paramedian pontine infarct; (b) axial T1W image showing a chronic left paramedian infarct; (c) axial T2W image showing the dolichoectatic basilar artery (arrowhead) lying lateral to the dorsum sellae (DWI: diffusion-weighted imaging)

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Figure 4 :Family tree of the patients depicting the family history of cerebrovascular and ischemic heart disease

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The occurrence of VBD in the siblings in this report lends support to the hypothesis for possible genetic predisposition in this condition. Dolichoectatic arteries have a thin arterial wall, with prominent degeneration of the internal elastic lamina [5] and thinning of the media. A genetic predisposition would thereby involve defects in arterial wall extracellular matrix components, as collagen, elastin, proteoglycans, laminin, etc., thus making these vessels susceptible to dilatation. [7] Co-occurrence of intracranial arterial dolichoectasia (IADE) with abdominal aortic aneurysm [8] and coronary artery ectesias (CAE) [6] is known and would indicate that there is a generalized (genetic) rather than a local (atherosclerosis) cause for the abnormal arterial dilatation. Fernando and colleagues did not find any association between IADE and markers of atherosclerosis. [5] Also, there are series where no atherosclerosis was noted in the dolichoectatic vessels. [9]

The occurrence of infarcts in relation to VBD [2],[3] can also be explained without atherosclerosis. The most common infarcts due to VBD, paramedian pontine infarcts, involve distortion of the branches of BA due to elongation and tortuosity of the BA and hemodynamic factors such as significant reduction of flow velocity in the BA. [4] Therefore, atherosclerosis found in the dolichoectatic vessels may be a consequence of disturbed laminar blood flow in the dolichoectatic arteries, rather than its cause. Although we do not know the status of coronary and basilar arteries of the siblings in this family with ischemic heart disease, the co-occurrence of CAE and VBD is well known. [5],[6] In both VBD and CAE, thrombotic events can result due to slow blood flow in the dilated arteries.

 
 » References Top

1.Smoker WR, Price MJ, Keyes WD, Corbett JJ, Gentry LR. High-resolution computed tomography of the normal basilar artery: 1. Normal size and position. AJNR Am J Neuroradiol 1986;7:55-60.  Back to cited text no. 1
[PUBMED]    
2.Passero SG, Rossi S. Natural history of vertebrobasilar dolichoectasia. Neurology 2008;70:66-72.  Back to cited text no. 2
[PUBMED]  [FULLTEXT]  
3.Passero S, Filosomi G. Posterior circulation infarcts in patients with vertebrobasilar dolichoectasia. Stroke 1998;29:653-9.  Back to cited text no. 3
[PUBMED]  [FULLTEXT]  
4.Nishizaki T, Tamaki N, Takeda N, Shirakuni T, Kondoh T, Matsumoto S. Dolichoectatic basilar artery: A review of 23 cases. Stroke 1986;17:1277-81.  Back to cited text no. 4
[PUBMED]  [FULLTEXT]  
5.Pico F, Labreuche J, Touboul PJ, Amarenco P. GENIC Investigators. Intracranial arterial dolichoectasia and its relation with atherosclerosis and stroke subtype. Neurology 2003;61:1736-42.  Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.Pico F, Biron Y, Bousser MG, Amarenco P. Concurrent dolichoectasia of basilar and coronary arteries. Neurology 2005;65:1503-4.  Back to cited text no. 6
[PUBMED]  [FULLTEXT]  
7.Lamblin N, Bauters C, Hermant X, Lablanche JM, Helbecque N, Amouyel P. Polymorphisms in the Promoter Regions of MMP-2, MMP-3, MMP-9 and MMP-12 Genes as Determinants of Aneurysmal Coronary Artery Disease. J Am Coll Cardiol 2002;40:43-8.  Back to cited text no. 7
[PUBMED]  [FULLTEXT]  
8.Gautier JC, Hauw JJ, Awada A, Loron P, Gray F, Juillard JB. Dolichoectatic intracranial arteries. Association with aneurysms of the abdominal aorta. Rev Neurol (Paris) 1988;144:437-46.  Back to cited text no. 8
    
9.Hulten-Gyllesten IL, Lofstedt S, Von Reis G. Observations on generalized arteriectasis. Acta Med Scand 1959;163:125-30.  Back to cited text no. 9
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

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