Brain artery widening may drive lacunar stroke more than artery narrowing

By Dr. Liji Thomas, MDReviewed by Lauren HardakerMay 11 2026

Researchers tracking patients with mild stroke found that abnormal widening and distortion of brain arteries, not traditional large-artery narrowing, was most strongly linked to progressive small-vessel brain damage and lacunar stroke. 

Study: Implications of Cranial Arterial Stenosis and Dolichoectasia for Cerebral Small-Vessel Disease Etiopathogenesis: Findings From a Prospective Mild Stroke Cohort. Image credit: Hamara/Shutterstock.com

A recent study published in the journal Circulation reports that dolichoectasia and intracranial arterial widening are independently associated with small vessel disease in the brain and lacunar stroke.

Brain artery narrowing and widening show distinct effects

Scientists consider stenosis (narrowing) and dolichoectasia (abnormal elongation, tortuosity, and widening) of the cranial arteries to be distinct entities affecting the large arteries of the brain. Large artery stenosis (LAS) results from atherosclerotic plaque deposition, which causes focal narrowing. Conversely, dolichoectasia apparently arises due to nonatherosclerotic mechanisms.

These conditions affect downstream small vessels differently and are associated with distinct stroke types. Lacunar stroke accounts for 20 %-30 % of ischemic stroke. Such strokes are thought to arise primarily from intrinsic cSVD, in particular, segmental arteriolar disorganization.

In addition, about 15 % of lacunar stroke patients have potential sources of emboli, including atheromas in large arteries. However, whether these directly contribute to lacunar stroke remains uncertain. In addition, the relative importance of LAS and dolichoectasia in the etiology of cSVD remains unclear.

Multimodal imaging study

The researchers recruited 229 patients with lacunar (131 patients) or mild nonlacunar stroke, and compared multimodal imaging at baseline and after one year. Magnetic resonance imaging (MRI) or computed tomography (CT) was used to assess brain tissue at baseline at the time when the stroke occurred.

Cerebrovascular imaging was performed to identify stenosis of the intracranial or cervical artery, dolichoectasia of the basilar artery, and the diameters of the intracranial carotid and middle cerebral artery.

LAS linked to nonlacunar but not lacunar stroke

They found that LAS occurred in 20.5 % of patients, while dolichoectasia was present in 15.7 %. LAS was associated with nonlacunar stroke and with a greater number of index infarcts at presentation.

Conversely, LAS was associated with approximately 50 % lower odds of lacunar stroke compared to non-lacunar stroke. There was no consistent association with cSVD. Cortical infarcts were more common with LAS, but subcortical infarcts were more common with dolichoectasia.

Subcortical infarcts in patients with LAS were more likely to involve the corona radiata, centrum semiovale, and internal border zone, whereas subcortical infarcts in patients without LAS more frequently affected the basal ganglia, thalamus, and brainstem.

Dolichoectasia associated with lacunar stroke

Basilar artery dolichoectasia was associated with 4.7-fold odds of lacunar stroke and 2.6-fold odds of cSVD, compared to patients without this finding. Incident infarcts were 2.3 times more likely, mostly in the subcortical region.

Incident infarcts were more frequently cortical when caused by embolism, but subcortical when associated with dolichoectasia. LAS was associated with downstream cortical infarcts, but this was not the case with subcortical infarcts. These subcortical infarcts occurred mostly in cerebral white matter. White matter hyperintensities showed greater progression over the year of follow-up.

Widening of the intracranial carotid and middle cerebral arteries was associated with similar changes to those seen in basilar artery dolichoectasia.

Neither LAS nor dolichoectasia was linked to impaired cognitive tests, mobility, or functional outcomes after adjustment for age, sex, baseline cSVD burden, and vascular risk factors. Further analyses confirmed the validity of these associations.

Putative mechanisms underlying these associations

According to the authors, suggested mechanisms for the association of dolichoectasia and cSVD, as well as lacunar stroke, include genetic susceptibility to weak basement membrane proteins; shared abnormalities of the vessel wall connective tissue; and remodeling of small vessel walls by mechanical stress due to dolichoectasia of the large arteries, resulting in microvascular injury.

These may contribute to diffuse cerebrovascular degeneration, altered vascular elasticity, and abnormal hemodynamic stress, accounting for the association with cSVD.

Systematic review supports these findings

The researchers also carried out a systematic review. Their findings confirmed that associations between LAS and lacunar stroke were inconsistent, whereas cross-sectional studies showed that cSVD and lacunar stroke were linked to dolichoectasia.

Factors counteracting the causal role of LAS in lacunar stroke include the location of the stroke, which is as likely to be contralateral as ipsilateral to the stenosed artery.

Strengths and limitations

The study is among the earliest to examine two different large-artery disease processes, LAS and dolichoectasia, within the same well-characterized prospective stroke cohort. Its strengths included its prospective design, standardized data acquisition on a comprehensive scale, and blinded evaluation.

Despite this, limitations include the use of arterial-phase dynamic contrast-enhanced MRI rather than dedicated angiography to assess intracranial atherosclerotic stenosis; the inability to detect plaque at the origin of perforating arteries, which are affected in lacunar stroke; and the inclusion of patients from only one center, limiting generalizability.

Conclusions

Taken together, these findings do not support a major causal role for LAS in the pathogenesis of lacunar stroke. Conversely, dolichoectasia and widening of intracranial arteries are independently associated with cSVD, particularly lacunar stroke. This argues for a primary contribution of intrinsic microvascular disease rather than embolic large-artery disease.

These findings support a nonatheromatous, intrinsic microvascular pathology, particularly segmental arteriolar disorganization, as the principal mechanism of lacunar stroke and cSVD.

In consequence, the authors suggest that, in addition to secondary prevention targeting atherosclerotic disease of the large cerebral arteries, microvascular function should also be improved to reduce the risk of progressive brain damage due to cSVD. However, because this was an observational study, the findings demonstrate associations rather than definitive proof of causation.

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