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Brain white matter hyperintensities in Kawasaki disease: A case-control study
Dan Laukka1,2, Riitta Parkkola3, Jussi Hirvonen3
1Department of Neurosurgery, Neurocenter, Turku University Hospital, Turku, Finland.
Insights
Childhood Kawasaki disease (KD) is linked to increased white matter hyperintensities (WMH) in adulthood, indicating potential long-term cerebrovascular risks. This suggests KD may impact small vessel health later in life.
Area of Science:
- Neurology
- Pediatrics
- Cardiology
Background:
- Cerebrovascular complications of Kawasaki disease (KD) are understudied.
- White matter hyperintensities (WMH) are markers of cerebral small vessel disease and stroke risk.
Purpose of the Study:
- To determine if childhood KD is associated with adult WMH and other cerebrovascular findings.
- Investigate long-term neurological sequelae of KD.
Main Methods:
- Case-control study comparing KD patients (n=40) with migraine controls (n=160) using brain MRI.
- WMH burden assessed via modified Scheltens' scale and manual volume segmentation.
- Matched controls by age and sex; blinded neuroradiologist evaluation.
Main Results:
- KD patients showed significantly higher total WMH volume (0.26 vs 0.065 cm³), burden, and periventricular WMHs compared to controls.
- Increased odds of severe WMH scores (Scheltens' scale ≥2 or ≥3) in KD cases.
- Myocarditis during acute KD phase correlated with periventricular WMH; lacunes of presumed vascular origin were more frequent in KD cases.
Conclusions:
- Childhood KD history may be associated with increased adult WMH burden.
- Further research is needed to confirm these findings and elucidate the underlying mechanisms.
Background:
Cerebrovascular involvement of Kawasaki disease (KD) is poorly studied. White matter hyperintensities (WMH) indicate cerebral small vessel disease and increase the risk for stroke.
Purpose:
To investigate whether childhood KD is associated with WMHs and other cerebrovascular findings later in adulthood.
Materials And Methods:
In this case-control study, patients diagnosed with KD (cases) at our tertiary hospital between 1978 and 1995 were invited to brain magnetic resonance (MRI) between 2016 and 2017. Migraine patients (controls) with available brain MRI were matched with cases (ratio 4:1) by age (±2 years) and sex. Two blinded neuroradiologists evaluated independently cerebrovascular findings from the brain MRI scans. Modified Scheltens' visual rating scale was used to evaluate WMH burden and the total WMH volume was measured using manual segmentation.
Results:
Mean age [years, (SD)] at the time of brain MRI was 33.3 (3.8) and 32.8 (4.0) for cases (n = 40) and controls (n = 160), respectively (P = 0.53). Mean follow-up time for cases was 29.5 years (4.3). Total volume of WMHs (median) was 0.26 cm3 (IQR 0.34) for cases and 0.065 cm3 (IQR 0.075) for controls, P = 0.039. Cases had higher total WMH burden (P = 0.003), deep WMH burden (P = 0.003), and more periventricular WMHs (prevalence 7.5 vs. 0%, P = 0.008) than controls. Cases had greater risk of having total Scheltens' score ≥2 vs. < 2 (odds ratio, 6.88; 95% CI: 1.84-25.72, P = 0.0041) and ≥3 vs. < 3 (odds ratio, 22.71; 95% CI: 2.57-200.53, P = 0.0049). Diabetes type 1/type 2, hypertension, smoking status or hypercholesterolemia were not risk factors for WMH burden, p > 0.1. Myocarditis at the acute phase of KD increased the risk for periventricular WMHs (P < 0.05). Three cases (7.5%) and three controls (1.9%) had lacune of presumed vascular origin (P = 0.0096).
Conclusion:
History of KD could be associated with an increased WMH burden. More studies are needed to confirm our results.
