Ischemic Stroke in Young Tunisian Adults.

INTRODUCTION: Ischemic Stroke in young adults is a real public health problem; it's a major cause of disability, alters quality of life and has a great socio-economic impact. AIM: determine risk factors and specify the etiology of arterial ischemic stroke in young Tunisian adults. METHODS: In this 5 years retrospective study (2015-2020), we included all young adults (18-50 years) admitted for arterial ischemic stroke (AIS). Risk factors were registered and analyzed. All patients were investigated using a standard protocol: biological tests, brain imaging, carotid ultrasound and cardiac assessment. Additional investigations were carried out at the discretion of the treating physician. The cause of ischemic stroke was classified according to the TOAST criteria. RESULTS: We collected 200 patients with AIS. The mean age was 41.37 years ± 6.99. Traditional vascular risk factors were observed in more than 1/4 patients. A definite cause of stroke was identified in 120 patients. Cardio-embolic causes were the most common among our patients (19%) followed by atherosclerosis of the large arteries (11.5%). Other determined etiologies were found in 27.5% of patients. The etiology remained unclear in 40% of cases: undetermined despite complete investigation in 17.5%, undetermined and incompletely investigated 14.5 % and more than one potential pathomechanisms in 8%. CONCLUSION: Through this study, we demonstrated the diversity of etiology of stroke in young Tunisian adults. Changes of lifestyle are responsible for the occurrence of the traditional risk factors at an early age. Rheumatic heart diseases remain a frequent cause of AIS in our area.

Acquired pial arteriovenous fistula secondary to cerebral cortical vein thrombosis: A case report and review of the literature.

Pial arteriovenous fistulas (AVFs) are rare neurovascular malformations. They differ from arteriovenous malformations (AVMs) in that they involve single or multiple feeding arteries, draining directly into a dilated cortical vein with no intervening nidus. Pial and dural AVFs differ in blood supply, as the first originate from pial or cortical arteries and the latter from outside the dural leaflets. Unlike dural AVFs, most of the pial AVFs are supratentorial. The vast majority are congenital, manifesting during infancy. Acquired pial AVFs are significantly rarer and occur after vasculopathy, head trauma, brain surgery, or cerebral vein thrombosis. We describe a unique case of an acquired pial AVF in a 50-year-old man secondary to a cortical vein thrombosis manifesting as a focal-onset seizure with secondary generalization. A cerebral digital subtraction angiography revealed a low-flow pial AVF fed by a postcentral branch of the left middle cerebral artery draining to the superior sagittal sinus via a cortical vein. It also showed a collateral venous circulation adjacent to the previously thrombosed left parietal vein. There was no evidence of an associated dural AVF or venous varix. Endovascular treatment was scheduled three months later, but the angiogram preceding the embolization showed spontaneous and complete closure of the malformation. To our knowledge, this is the first case illustrating acquired pure pial AVF unaccompanied by a dural component following cortical vein thrombosis, eventually resulting in an unprompted closure.

Traditional risk factors and combined genetic markers of recurrent ischemic stroke in adults.

BACKGROUND: The involvement of traditional risk factors and combined genetic markers of recurrent arterial ischemic stroke (AIS) in adults remains unclear. OBJECTIVE: This study aims to determine significant clinical and genetic factors of AIS recurrence, and to investigate the combined effect of genotypes on the occurrence of a second cerebral ischemic attack. METHODS: We investigated a cohort study of AIS patients (18-50 years old) followed in the neurology department over 5 years. Traditional and genetic risk factors were carried through a multivariable logistic regression model. We used a Cox proportional hazard model for identifying predictors of recurrence. RESULTS: Two hundred and seventy patients were enrolled in our study. The risk of AIS recurrence was 36.2% within 5 years. The potential risk of recurrence of AIS increased with traditional and genetic risk factors such as hypertension, diabetes mellitus, heart failure, and family history of cerebrovascular diseases. This risk increased with increasing number of genetic factors. The hazard ratio (HR) was 0.66 (95% confidence interval [CI] 0.97-2.67) for the subject with one genetic factor, 1.61 (95% CI 0.97-2.25) for combined methylenetetrahydrofolate reductase (MTHFR) polymorphisms, and 2.57 (95% CI 1.32-4.99) for combined factor V Leiden (FVL) and MTHFR polymorphisms (677 or 1298). The HR for the three polymorphisms combined was 6.04 (95% CI 2.40-15.16). CONCLUSIONS: Our findings suggest that cumulative effect of both traditional and common genetic risk factors was associated with recurrence of ischemic stroke. We demonstrated for the first time that a combined genotype FVL/MTHFR profile increase the risk of a second cerebral ischemic attack.

MTHFR (C677T, A1298C), FV Leiden polymorphisms, and the prothrombin G20210A mutation in arterial ischemic stroke among young tunisian adults.

Arterial ischemic stroke (AIS) in young adults is less common in older adults, but the underlying pathogenesis and risk factors are more multi-faceted. The role of inherited thrombophilia such as 5, 10-methylenetetrahydrofolate reductase (MTHFR) gene polymorphism, (C677T and A1298C), factor V of Leiden (FVL) polymorphism, and the prothrombin G20210A mutations remains unclear. This study aims to evaluate the role of prothrombin genetic factor in AIS among young adults in Tunisia and to assess the synergistic effect between thrombogenic mutations in the pathogenesis of AIS. In this case-control study, blood samples were collected from patients and healthy controls, all matched for age and gender. The difference between them is evaluated by using the chi-square test. The odds ratio (OR) was carried out to evaluate the associations between each polymorphism and AIS risk using a binary logistic regression model. Values were considered statistically significant when p < 0.05. Patients carrying simultaneously the MTHFR polymorphisms (677T and 1298C) have a higher risk to develop AIS compared to controls. The heterozygous variants FVL increased the risk of AIS only when it is associated with MTHFR C677T or MTHFR A1298C polymorphisms. In conclusion, our study confirmed the involvement of MTHFR polymorphisms as AIS's important risk factors. The existence of FVL polymorphism or prothrombin G20210A mutation alone doesn't correlate with the occurrence of stroke. We assume that the presence of both MTHFR and FVL polymorphisms has a synergistic effect and increased the risk of the AIS.