Basal ganglia calcifications were not significantly associated with stroke or small artery occlusion (OR 1.13; 95% CI 0.65-1.96), occurring in 10.1% of stroke patients and 11.9% of controls.
Case-Control (n=2,668)
Are basal ganglia calcifications associated with stroke, small artery occlusion, or white matter hyperintensities?
Basal ganglia calcifications are associated with white matter hyperintensities but do not appear to be independently associated with stroke or small artery occlusion.
Effect estimate: OR 1.13 (95% CI 0.65-1.96)
Absolute Event Rate: 10.1% vs 11.9%
p-value: p=0.136
Abstract Background and aims The clinical relevance of basal ganglia calcifications (BGCs) in stroke remains unclear despite reported links to white matter hyperintensities (WMH) and cerebral small vessel disease (SVD). We assessed BGCs prevalence in stroke patients and controls, and studied their association with WMH and SVD-related stroke, particularly small artery occlusion (SAO). Methods We included 1,430 patients with first-ever ischemic or hemorrhagic stroke from the Lund Stroke Register (2017-2023). Stroke etiology was classified using Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria for ischemic stroke, and medical record review for hemorrhagic stroke. BGCs were identified and graded on CT, while WMH were assessed on either MRI or CT. Similarly, CT scans of 1,238 individuals with no clinical or radiological evidence of stroke were reviewed for BGCs. Information about WMH were systematically extracted from radiology reports. Associations were analyzed using age and sex adjusted logistic regression. Results BGCs were identified in 10.1% of stroke patients and 11.9% of control subjects, with no significant between-groups differences (p = 0.136). Individuals with BGCs were older (median age 83 vs 78 years) than those without calcifications (p 0.001). BGCs were associated with WMH (p = 0.007). Adjusted analyses showed no association with stroke or SAO (OR 1.13, 95% CI 0.65–1.96). Conclusions Despite our prior reports of frequent cerebrovascular events in patients with BGCs, no association with stroke or SAO was found in this first ever stroke cohort. Our findings suggest that BGCs may serve as a marker of a specific cerebrovascular pathology rather than SAO-related stroke. Conflict of interest Maha Yektay Farahmand: nothing to disclose.
Farahmand et al. (Fri,) conducted a case-control in Stroke (n=2,668). Basal ganglia calcifications vs. Control subjects was evaluated on Association with stroke or small artery occlusion (OR 1.13, 95% CI 0.65-1.96, p=0.136). Basal ganglia calcifications were not significantly associated with stroke or small artery occlusion (OR 1.13; 95% CI 0.65-1.96), occurring in 10.1% of stroke patients and 11.9% of controls.