Article

The embryologic basis for the anatomy of the cerebral vasculature related to arteriovenous malformations

Australian School of Advanced Medicine, Macquarie University, 2 Technology Place, Sydney, New South Wales 2109, Australia.
Journal of Clinical Neuroscience (Impact Factor: 1.32). 02/2011; 18(4):464-9. DOI: 10.1016/j.jocn.2010.12.004
Source: PubMed

ABSTRACT A detailed understanding of vascular anatomy is essential to facilitate appropriate decision-making by clinicians responsible for treating arteriovenous malformations (AVM) of the brain and dura. This work reviews the embryologic development of the cerebral vasculature, including the dural venous sinuses, with a focus on the relevant angioarchitecture. There is little doubt that dural AVM are acquired lesions; however, conflicting evidence exists regarding the pathophysiology of brain AVM. Patients described in this review provide support for both of the proposed mechanisms for the development of brain AVM (post-natal development compared to embryologic origin). Further work is required to improve our understanding of the pathophysiology of these lesions.

1 Bookmark
 · 
75 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: A long-held dogma in neurosurgery is that parenchymal arteriovenous malformations (AVMs) are congenital. However, there is no strong evidence supporting this theory. An increasing number of documented cases of de novo formation of parenchymal AVMs cast doubt on their congenital nature and suggest that indeed the majority of these lesions may form after birth. Further evidence suggesting the postnatal development of parenchymal AVMs comes from the exceedingly rare diagnosis of these lesions in utero despite the widespread availability of high-resolution imaging modalities such as ultrasound and fetal MRI. The exact mechanism of AVM formation has yet to be elucidated, but most likely involves genetic susceptibility and environmental triggering factors. In this review, the authors report 2 cases of de novo AVM formation and analyze the evidence suggesting that they represent an acquired condition.
    Neurosurgical FOCUS 09/2014; 37(3):E2. DOI:10.3171/2014.6.FOCUS14234 · 2.14 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: It is known that the brain can compensate for deficits induced by acquired and developmental lesions through functional reorganization of the remaining parenchyma. Arteriovenous malformations (AVM) usually appear prenatally before a functional regional organization of the brain is fully established and patients generally do not present with motor deficits even when the AVM is located in the primary motor area indicating the redistribution of functions in cortical areas that are not pathologically altered. Here we present reorganization of the motor cortex in a patient with a large AVM involving most of the left parietal lobe and the paramedian part of the left precentral gyrus that is responsible for controlling the muscles of the lower limbs. Functional MRI showed that movements of both the right and left feet activated only the primary motor cortex in the right hemisphere, while there was no activation in the left motor cortex. This suggests that complete ipsilateral control over the movements of the right foot had been established in this patient. A reconstruction of the corticospinal tract using diffusion tensor imaging showed a near-complete absence of corticospinal fibers from the part of the left precentral gyrus affected by the AVM. From this clinical presentation it can be concluded that full compensation of motor deficits had occurred by redistributing function to the corresponding motor area of the contralateral hemisphere.
    06/2013; 4(2):269-272. DOI:10.2478/s13380-013-0122-5
  • [Show abstract] [Hide abstract]
    ABSTRACT: To test the hypothesis that lymphocyte infiltration in brain arteriovenous malformation (bAVM) is not associated with iron deposition (indicator of microhemorrhage). Sections of unruptured, previously untreated bAVM specimens (n=19) were stained immunohistochemically for T-lymphocytes (CD3(+)), B-lymphocytes (CD20(+)), plasma cells (CD138(+)) and macrophages (CD68(+)). Iron deposition was assessed by hematoxylin and eosin and Prussian blue stains. Superficial temporal arteries (STA) were used as control. Both T lymphocytes and macrophages were present in unruptured, previously untreated bAVM specimens, whereas few B cells and plasma cells were detected. Iron deposition was detected in 8 specimens (42%; 95% confidence interval =20-67%). The samples with iron deposition tended to have more macrophages than those without (666±313 vs 478±174 cells/mm(2); P=0.11). T-cells were clustered on the luminal side of the endothelial surface, on the vessel-wall, and in the perivascular regions. There was no correlation between T lymphocyte load and iron deposition (P=0.88). No macrophages and lymphocytes were detected in STA controls. T-lymphocytes were present in bAVM specimens. Unlike macrophages, the load and location of T-lymphocytes were not associated with iron deposition, suggesting the possibility of an independent cell-mediated immunological mechanism in bAVM pathogenesis.
    01/2014; 1(3):147-152. DOI:10.4103/2347-8659.143674

Full-text

Download
0 Downloads
Available from
Feb 11, 2015