Cephalalgia : an international journal of headache · 2026
Cortical microstructure in persistent post-traumatic headache, migraine and healthy controls: A quantitative magnetic resonance imaging study.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Christensen Rune Häckert, Al-Khazali Haidar Muhsen, Ashina Messoud, Ashina Håkan
Аннотация
AimTo compare cortical microstructural features in people with persistent post-traumatic headache (PPTH), migraine and healthy controls (HCs) using quantitative magnetic resonance imaging (qMRI).MethodsThis cross-sectional study included 103 participants with PPTH, 296 with migraine and 155 HCs. All underwent 3.0 Tesla qMRI using standardized sequences to generate quantitative T2 (qT2), quantitative T1 (qT1) and apparent diffusion coefficient (ADC) maps. Intracortical voxel values were projected onto the cortical surface for surface-based analysis. Group comparisons were adjusted for age and sex, with correction for multiple comparisons. Associations with clinical variables were explored in regions showing significant group differences.ResultsCompared with HCs, participants with PPTH showed elevated qT2 values in the left lateral occipital cortex (pcluster = 0.0002). Compared with migraine, those with PPTH exhibited lower ADC values in the left superior frontal cortex (pcluster = 0.0020). Relative to migraine with aura, additional reductions in qT1 and ADC values were found in the right middle and inferior temporal gyri (all pcluster < 0.01), and, relative to migraine without aura, lower ADC values were detected in the right middle temporal gyrus (pcluster = 0.0002).ConclusionsCortical microstructural alterations in PPTH suggest underlying neurobiological processes distinct from both migraine and healthy adults. The findings support a pathophysiological model involving chronic low-grade neuroinflammation.