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Brain vascular lesions: a clinicopathologic, immunohistochemistry, and ultrastructural approach
Marisol Galván Navarrete1, Alma Dalia Hernández2, Miguel Angel Collado-Ortiz3
1General Hospital of Guadalajara Hospital civil antiguo de Guadalajara Jalisco, Guadalajara, Mexico.
Insights
This study investigated brain vascular malformations, analyzing clinicopathologic features and molecular markers like VEGF. Findings correlate specific markers and clinical outcomes, improving understanding of these lesions.
Area of Science:
- Neurology
- Pathology
- Vascular Biology
Background:
- Brain vascular malformations are common and can cause severe neurological deficits or death.
- Understanding the molecular mechanisms of brain arteriovenous malformations remains limited.
Purpose of the Study:
- To analyze clinicopathologic features and immunohistochemistry of brain vascular lesions.
- To investigate the expression of common antibodies and ultrastructure in endothelial cells and vessel walls.
Main Methods:
- Examined 50 cases of brain vascular lesions (arteriovenous malformations and cavernomas).
- Performed clinicopathologic analysis and immunohistochemistry for markers including CD31, VEGF, and VEGFR2.
- Assessed ultrastructure of endothelial cells and vessel walls.
Main Results:
- Significant correlations found between age, sex, lesion rupture, brain hemorrhage, necrosis, hemosiderin deposit, VEGF, VEGFR2, and CD31 expression.
- Lesion size was larger in parieto-occipital locations.
- Clinical symptoms like loss of consciousness and visual deficit were associated with specific findings.
Conclusions:
- Clinicopathologic and immunohistochemical analysis reveals significant correlations between molecular markers and clinical presentation of brain vascular malformations.
- Further research is needed to elucidate the molecular mechanisms underlying the formation and growth of brain arteriovenous malformations.
Abstract:
Brain vascular malformations are relatively common lesions that cause serious neurologic disability or death in a significant proportion of individuals bearing them. The purpose of this study was to analyze the clinicopathologic and immunohistochemistry these lesions, looking for common antibodies expressed such as CD31, CD34, CD15, factor VIII, nestin, vimentin, vascular endothelial grow factor (VEGF), vascular endothelial grow factor receptor-2 (VEGF-R2), glial fibrillar acidic protien (GFAP), and fibroblastic grow factor β (β-FGF) and ultrastructure in endothelial cells as well as in vessel walls. Fifty cases of vascular lesions were included in this study: 29 (58%) of them were arteriovenous malformations and 21 (52%) were brain cavernomas. Twenty-six (52%) patients were women and 24 (48%) men. The age range was from 13 to 68 years (mean age, 35.86 ± 15.19 years). The size of the lesions ranged between 1 and 8 cm (3 ± 1.65 cm), and parieto-occipital lesions had a bigger size. Evolution time varied from 1 month to 1 year (mean, 7.5 months). There was a significant statistical correlation between age and sex (P = -035), rupture of lesion (P = .015), brain hemorrhage (P = .033), necrosis (P = .011), hemosiderin deposit (P = .042), VEGF (P = .015), and VEGFR (P = .037), as well as localization of rupture (P = .017), loss of consciousness (P = .000), visual deficit (P = .026), hyaline vessels (P = .000), and CD31 (.009). Interactions between endothelial cells and mural cells (pericytes and vascular smooth muscle cells) in blood vessel walls have recently come into focus as central processes in the regulation of vascular formation, stabilization, remodeling, and function in brain vascular lesions. However, the molecular mechanisms that underlie the formation and growth of brain arteriovenous malformations are still poorly understood.
