The diagnostic value of white matter hyperintensities (WMH) in different types of migraineare unknown. To evaluate the WMH pattern of different subtypes in migraine patients with no vascular risk factors. 92 migraine patients (73 females, mean age 34.6 ± 8.9; 61 episodic migraine, 31 chronic migraine, 36 migraine with aura, 56 migraine without aura) without vascular risk factors underwent brain MRI (3 T). We also included a matched healthy control group with no migraine (n = 24). The prevalence of WMH in different types of migraine was similar and ranged from 38.7 to 44.4%; the control group showed no WMH at all. Lesions were located within frontal, parietal and temporal lobes (in order of decreasing incidence) in juxtacortical and/or deep white matter. WMH appeared as round or slightly elongated foci with a median size of 2.5 mm [1.5; 3]. Total number, size and prevalence of WMH by lobes and white matter regions were similar between groups, and no interaction with age or sex was found. The number of lesions within the frontal lobe juxtacortical white matter correlated with the age of patients (r = 0.331, p = 0.001) and the duration since migraine onset (r = 0.264, p = 0.012). Patients with different migraine subtypes and without vascular risk factors are characterized by a similar pattern of WMH in the absence of subclinical infarctions or microbleedings. Therefore, WMH have no relevant prognostic value regarding the course of migraine and vascular complications. WMH pattern may be used to differentiate migraine as a primary disorder and other disorders with migraine-like headache and WMH.

Introduction. Cervical artery dissection (CeAD) is the most frequent cause of ischemic stroke in young adults. Arterial wall dysplasia underlies its weakness and predisposes to dissection. Objective. To assess clinical signs of connective tissue dysplasia (CTD) in patients with CeAD using special criteria of CTD, and to evaluate predisposing factors for the CeAD development. Materials and methods. We examined 80 patients (mean age 38,513,5; 49 females) with CeAD, verified by MRI/MRA and20 healthy volunteers. We estimated 48 signs of CTD included in the Villefranche diagnostic criteria for the vascular type of EhlersDanlos syndrome, the Ghent criteria for Marfan syndrome, the Beighton criteria of joint hypermobility and some others, as well as history of headache. Each sign was counted as present or absent, yielding the individual and mean CTD group scores. Results. Clinical CTD signs were more frequently detected in patients with CeAD than in controls (mean score 7.9 3.6 vs. 4.6 2.5; p 0.0039). Significant signs (more than 8 points) were present in 53% of patients. Regression analysis was performed to determine diagnostic-prognostic value of CTD signs. The main diagnostic criteria included history of headache (p=0.022), arterial hypotension (р=0.012), extensive bruising (р=0.011), and widened atrophic scars (р=0.019). The additional diagnostic criteria included translucent skin (р=0.034), high palate (р=0.034), predisposition to constipation (р=0.050), nasal bleeding (р=0.043), and blue sclera (р=0.050). In the presence of the 4 main and 2 additional criteria, the predictive value of dissection according to regression model is 7577% (ROC analysis: AUC 0.90, 95% CI, 0.840.96). Most patients 97% had various predisposing factors of CeAD development, either isolated 47% or combined 50%. Conclusions. The presence of the 4 main and 2 additional diagnostic criteria of CTD has a high predictive value of CeAD and can be used as its diagnostic-prognostic criteria. Dissection of the arterial wall with signs of dysplasia is provoked by various additional factors.

Cervical artery dissection (CeAD) is the primary cause of ischemic stroke in young adults. Monogenic heritable connective tissue diseases account for fewer than 5% of cases of CeAD. The remaining sporadic cases have known risk factors. The clinical, radiological, and histological characteristics of systemic vasculopathy and undifferentiated connective tissue dysplasia are present in up to 70% of individuals with sporadic CeAD. Genome-wide association studies identified CeAD-associated genetic variants in the non-coding genomic regions that may impact the gene transcription and RNA processing. However, global gene expression profile analysis has not yet been carried out for CeAD patients. We conducted bulk RNA sequencing and differential gene expression analysis to investigate the expression profile of protein-coding genes in the peripheral blood of 19 CeAD patients and 18 healthy volunteers. This was followed by functional annotation, heatmap clustering, reports on gene–disease associations and protein–protein interactions, as well as gene set enrichment analysis. We found potential correlations between CeAD and the dysregulation of genes linked to nucleolar stress, senescence-associated secretory phenotype, mitochondrial malfunction, and epithelial–mesenchymal plasticity.

The worldwide trend towards headache (HA) chronization is an important medical and social problem due to frequent psychological and social maladaptation of patients. Chronic HAs reduce quality of life and patients ability to work. The trend towards headache chronization is largely associated with acceleration of the pace of life, constant social and informational tension, leading to emotional disturbances, such as depression, anxiety, and asthenia. Single medical interventions do not seem to have a lasting effect. Thus, such patients require long-term comprehensive rehabilitation with regard to the type and characteristic features of HA, as well as triggers and comorbid condition. Rehabilitation should include adequate long-term drug therapy aimed at preventing exacerbations of HA. Additional approaches may include botulinum neurotoxin injections, physiotherapy (biofeedback, transcranial magnetic stimulation, transcranial electrical stimulation), psychotherapy, comorbid conditions diagnosis and treatment, lifestyle intervention.