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Effect of extracranial carotid artery stenosis and other risk factors for stroke on periventricular hyperintensity
T Adachi1, M Takagi, H Hoshino
1Third Division of Internal Medicine, Shimane Medical University, Izumo, Japan. adachi3@shimane-med.ac.jp
Insights
Periventricular hyperintensity (PVH) is linked to aging, hypertension, and prior stroke, but not carotid artery stenosis. Findings suggest small-vessel disease contributes to PVH development.
Area of Science:
- Neurology
- Vascular Neurology
- Neuroimaging
Background:
- Periventricular hyperintensity (PVH) pathogenesis remains unclear.
- Investigating PVH in relation to cerebrovascular disease risk factors is crucial.
Purpose of the Study:
- To examine the association between PVH and cerebrovascular disease risk factors.
- Specifically, to determine the relationship between PVH and extracranial carotid artery stenosis (ECAS).
Main Methods:
- 323 subjects studied using 1.5-T MRI for PVH quantification and cerebral infarction evaluation.
- Duplex carotid sonography assessed ECAS severity (five grades).
- Clinical history evaluated cerebrovascular disease risk factors and atherosclerotic complications.
Main Results:
- PVH correlated significantly with age, hypertension, and history of cerebrovascular accident.
- No significant correlation was found between PVH severity and ECAS.
- PVH was more severe in subjects with lacunar infarction or deep border zone infarction.
Conclusions:
- PVH is associated with age, hypertension, and prior cerebrovascular disease.
- PVH is not associated with ECAS.
- Small-vessel disease is implicated in the pathogenesis of PVH.
Background And Purpose:
The pathogenesis of periventricular hyperintensity (PVH) is still uncertain. We investigated the relationship between PVH and risk factors for cerebrovascular diseases, especially extracranial carotid artery stenosis (ECAS).
Methods:
We studied PVH and ECAS in 323 subjects between 1991 and 1994. Using 1.5-T MRI scan images, we measured PVH quantitatively at eight points and evaluated cerebral infarction. Duplex carotid sonography was performed on the carotid arteries bilaterally and used to divide the severity of ECAS into five grades. Risk factors for cerebrovascular diseases and atherosclerotic complications were assessed from the clinical history.
Results:
Age was significantly correlated with the size of frontal and whole PVH (P < .01). Frontal PVH was significantly more severe in subjects with hypertension (P < .05). Frontal, occipital, and whole PVH were significantly more severe in subjects with a history of cerebrovascular accident (P < .01). Other risk factors and atherosclerotic complications were not correlated with PVH. There were no significant differences in the severity of PVH among the five groups of ECAS. The severity of PVH in each region was not related to ECAS. There was no significant difference in the age of patients in relation to the five grades of ECAS. However, PVH was significantly more severe in subjects with lacunar infarction or infarction of the deep border zone (P < .05). There was no relationship between PVH and cortical infarction or infarction of the cortical border zone.
Conclusions:
PVH correlated with age, hypertension, and past history of cerebrovascular disease but not with ECAS. PVH was significantly more severe in lacunar infarction and infarction of the deep border zone. These results suggest that small-vessel disease may underlie the pathogenesis and development of PVH.