Relationship of deep white matter hyperintensities and cerebral blood flow in severe carotid artery stenosis
T Patankar1, E Widjaja, H Chant
1Imaging Science and Biomedical Engineering, School of Medicine, University of Manchester, Manchester, UK. tufail.patankar@srht.nhs.uk
Insights
Leukoaraiosis (LA) is more severe in patients with carotid stenosis, but not due to reduced cerebral blood flow (CBF). Microvascular changes, not large vessel disease, appear to be the primary cause of LA.
Area of Science:
- Neurology
- Vascular Medicine
- Radiology
Background:
- Leukoaraiosis (LA) is linked to both large and small blood vessel issues.
- The exact cause of LA, especially in relation to cerebral blood flow (CBF) and large vessel disease, requires further clarification.
Purpose of the Study:
- To investigate the hypothesis that reduced global CBF due to occlusive extra-cranial arterial disease directly causes increased LA.
- To determine the relationship between severe carotid stenosis, CBF, and the severity of LA.
Main Methods:
- Magnetic Resonance (MR) imaging was used to assess LA severity and measure CBF via phase contrast MR angiography.
- 35 healthy subjects and 55 patients with >70% carotid stenosis were studied.
- Patients were categorized based on the presence or absence of MRI-confirmed infarction.
Main Results:
- LA was significantly more severe in patients with carotid stenosis compared to normal subjects (P<0.01).
- CBF was significantly lower in patients with carotid stenosis (with or without infarction) than in normal subjects.
- No correlation was found between LA severity and measured CBF in any group.
Conclusions:
- Increased LA severity in patients with severe carotid stenosis is not directly caused by reduced CBF.
- Microvascular abnormalities are likely the predominant pathogenic factor in LA, even when significant large vessel disease is present.
Abstract:
Leukoaraiosis (LA) has been associated with abnormalities of both large and small blood vessels. This study attempts to clarify the pathogenesis of LA by testing the hypothesis that increased frequency of LA with occlusive extra-cranial arterial disease results directly from global reduction in cerebral blood flow (CBF). Thirty-five normal subjects and 55 patients with carotid stenosis (>70%) were studied using MR. CBF was measured using phase contrast MR angiography and LA was scored using previously validated scoring system. Patients were divided into those with evidence of previous infarction on MRI and those without. LA was more severe in patients than in normal subjects (P<0.01) and correlated with age in normal subjects but not in patients. CBF in patients with (809+/-214 ml/min) and without infarction (mean 792+/-181 ml/min) was significantly lower than in normal subjects (mean 1073+/-194 ml/min). There was no correlation between the severity of LA and measured CBF in any group. The severity of LA is greater in patients with severe carotid stenosis but is not correlated to reductions in CBF. This suggests that microvascular abnormality is the dominant pathogenetic factor in LA even in the presence of severe stenotic/occlusive large vessel disease.
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