Abstract
BackgroundArteriovenous malformations of the brain (bAVM) may rupture from aneurysms or ectasias of the feeding, draining, or nidal vessels. Moreover, they may rupture from the immature, fragile nidal vessels that are characteristic to bAVMs. How the histopathological changes of the nidal vessels associate with clinical presentation and hemorrhage of the lesion is not well known.Materials and methodsWe investigated tissue samples from surgically treated bAVMs (n = 85) using standard histological and immunohistochemical stainings. Histological features were compared with the clinical presentation of the patient.ResultsMicrohemorrhages from nidal vessels were found both in bAVMs with a history of clinically evident rupture and in bAVMs considered unruptured. These microhemorrhages were associated with presence of immature, pathological nidal vessels (p = 0.010) and perivascular inflammation of these vessels (p = 0.001), especially with adhesion of neutrophils (p < 0.001). In multivariate analysis, perivascular inflammation (OR = 19, 95% CI 1.6 to 230), neutrophil infiltration of the vessel wall (OR = 13, 95% CI 1.9 to 94), and rupture status (OR = 0.13, 95% CI 0.017 to 0.92) were significantly associated with microhemorrhages.ConclusionsClinically silent microhemorrhages from nidal vessels seem to be very common in bAVMs, and associate with perivascular inflammation and neutrophil infiltration. Further studies on the role of perivascular inflammation in the clinical course of bAVMs are indicated.
Highlights
Arteriovenous malformations of the brain are highflow vascular malformations which allow direct connections between cerebral arteries and veins [11]
BAVMs are relatively rare with an incidence of approximately 1 per 100,000 person years [1], and they often remain undiagnosed until rupture and subsequent intracerebral hemorrhage (ICH)
We found no association between microhemorrhages and prior fulminant rupture (p = 0.150, Table 1) or hemosiderin and prior fulminant rupture (p = 0.722)
Summary
Arteriovenous malformations of the brain (bAVMs) are highflow vascular malformations which allow direct connections between cerebral arteries and veins [11]. Since blood vessels adapt to changes in flow through flow-induced vessel wall remodeling [3], this abnormally high flow often causes ectatic (expansive, enlarging) remodeling of the veins draining the bAVM or of the arteries feeding it which, in addition to causing enlargement of the vessel caliber, may lead to formation of venous ectasias, intranidal aneurysms, or aneurysms of the feeding arteries. Arteriovenous malformations of the brain (bAVM) may rupture from aneurysms or ectasias of the feeding, draining, or nidal vessels. They may rupture from the immature, fragile nidal vessels that are characteristic to bAVMs. How the histopathological changes of the nidal vessels associate with clinical presentation and hemorrhage of the lesion is not well known. Histological features were compared with the clinical presentation of the patient
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