| Background and Purpose Perivascular spaces (PVS) are potential spaces surrouding cerebral perforating vessels. Recent studies revealed that perivascular spaces in basal ganglia and white matter were commonly prevalent. Mechnisms of perivascular spaces in various brain regions might be different. Perivascular spaces were also thought to be MRI marker of cerebral small vascular disease (cSVD). Through assessing the severity of PVS in a community-based population, we investigated the prevalence and distribution of PVS in different regions. We also analyzed the risk factors and association with other cSVD MRI markers of perivascular disease in each region.Methods 1786 participants from 5 villages in Shunyi District, Beijing were enrolled. Demographical characteristics and major cardiovascular risk factor were recorded. Finally 701 participants with good quality of brain MRI image and without low cognitive function, brain tumors or stroke history were collected. By grading the degree of PVS in basal ganglia(upper 2/3, lower 1/3), white matter, mid brain(ponto-mesencepalic junction, mesencephalo-diencephalic junction) and hippocampus, we evaluated the severity of perivascular space in different regions. The number and location of large PVS(≥ 3mm) were also recorded. Finally, multivariate Logistic regression was applied to analyze the risk factor of PVSs in different regions and their associations with other MRI markers of cerebral small vascular disease.Results1) PVS are observed in basal ganglia and white matter in each individual. PVS in hippocampus were seen in 67.9% of subjects, ponto-mesencepalic junction 50.2%, mesencephalo-diencephalic junction 14.4%. The prevalence of large PVS is 21.8%, with prevalence in basal ganglia 15.4%, white matter 4.0%, midbrain 1% and hippocampus 3.3%.2) After adjusting for age and sex, severity of PVS in total basal gangalia was positively associated with age (OR 1.81,p<0.01) and negatively associated with hyperlipidemia (OR 0.55, p<0.01). The severity of PVS in upper 2/3 of basal ganglia was associated with age (OR 2.38, p<0.01) and anti-hypertension drug history (OR 2.26,p<0.01).While in lower 1/3 of basal ganglia, the severity of PVS was asoociated with age (OR 1.35,p<0.01), hyperlipidemia(OR 0.53,p=0.04) and anti-hypertension drug history(OR 0.43,p=0.03) acted as protective factors. The degree of PVS in white matter was also asoociated with age (OR 1.39,p<0.01) and antihypertension drug history (OR 1.65,p=0.03). Severity of PVS in ponto-mesencepalic junction was only associated with age (OR 1.34,p<0.01). Severity of PVS in hippocampus was associated with women (OR 1.53,p=0.04) and hypertension (OR 1.68,p=0.01).3) The severity in total basal ganglia was associated with white matter hypertensity (periventricular white matter hyperintensity:OR 1.87, p<0.01; deep white matter hyperintensity:OR 1.98,p<0.01). The severity of PVS in lower 1/3 of basal ganglia was negatively associated with brain parenchymal fraction (OR 0.88,p=0.05). The severity of PVS in white matter and ponto-mesencepalic junction had no correlation with other cerebral small vascular diseases. The severity of PVS in hippocampus correlated with deep white matter hyperintensity (OR=1.49,p=0.01) and lacune (OR=1.82,p=0.04).Conclusion1) In this community-based population, the prevalence of PVS in basal ganglia and white matter are 100%. The severity in basal ganglia and white matter is relatively milder and in hippocampus more severe.2) The severity of PVS was associated with age, white matter hyertensity hypertensity in both basal ganglia and white matter. Severity in white matter and in upper 2/3 of basal ganglia was also associated with antihypertension drug history. The severity of PVS in hippocampus was associated with female, hypertension and lacunes.3) The mechnisms underlying the formation of PVS differ in various regions. PVS in upper 2/3 part of basal ganglia may be related to the hypertensive angiopathy and caused by permeability changes of arterial wall. PVS in white matter may be associated with cerebral amyloid angiopathy and caused by blockage of interstitial fluid. PVS in the lower 1/3 part of basal ganglia may be a physiological phenomenon caused by cerebral atrophy in elder population and by the spiral coursing and extrusion of cerebral perforating artery to adjacent anterior perforated substance. Thus, the severity PVS in upper 2/3 should be strongly considered in the evaluating of cerebral small vascular disease. |
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