Estimation of the density of veins from susceptibility-weighted imaging by using Mamdani fuzzy-type rule-based system. Investigating the neurovascular coupling in migraine

BACKGROUND AND PURPOSE: An impaired neurovascular coupling has been described as a possible player in neurodegeneration and cognitive decline. Migraine is a recurrent and incapacitating disorder that starts early in life and has shown neurovascular coupling abnormalities. Despite its high prevalence, the physiology and underlying mechanisms are poorly understood. In this context, new biomarkers from magnetic resonance imaging (MRI) are needed to bring new knowledge into the field. The aim of this study was to determine the vein density from Susceptibility-Weighted Imaging (SWI) MRI, in subjects with migraine and healthy controls; and to assess whether it relates to Resting-State functional MRI (RS-fMRI). MATERIALS AND METHODS: The cohort included 30 healthy controls and 70 subjects with migraine (26 episodic, 44 chronic) who underwent a brain 3.0 T MRI. Clinical characteristics were also collected. Maps of density of veins were generated based on a Mamdani Fuzzy-Type Rule-Based System from the SWI MRI. Mean values of vein density were obtained in grey (GM) and white matter (WM) Freesurfer lobar parcellations. The Amplitude of Low-Frequency Fluctuations (ALFF) image was calculated for the RS-fMRI, and the mean values over the parcellated GM lobes were estimated. Differences between groups were assessed through and analysis of variance (age, sex, education and anxiety as covariates; p < 0.05), followed by post-hoc comparisons. Associations were run between clinical and MRI-derived variables. RESULTS: When comparing the density of veins in GM, no differences between groups were found, neither associations with clinical variables. The density of veins was significantly higher in the WM of the occipital lobe for subjects with chronic migraine compared to controls (30%, p < 0.05). WM vein density in either frontal, temporal or cingulate regions was associated with clinical variables such as headache days, disability scores, and cognitive impairment (r between 0.25 and 0.41; p < 0.05). Mean values of ALFF did not differ significantly between controls and subjects with migraine. Strong significant associations between vein density and ALFF measures were obtained in most GM lobes for healthy subjects (r between 0.50 and 0.67; p < 0.05), instead, vein density in WM was significantly associated with ALFF for subjects with migraine (r between 0.32 and 0.58; p < 0.05). CONCLUSIONS: Results point towards an increase in vein density in subjects with migraine, when compared to healthy controls. In addition, the association between GM vein density and ALFF found in healthy subjects was lost in migraine. Taken together, these results support the idea of abnormalities in the neurovascular coupling in migraine. Quantitative SWI MRI indicators in migraine might be an interesting target that may contribute to its comprehension.