Normal Cerebral Arterial Development and Variations
Department of Radiology, Johns Hopkins Hospital, Baltimore, MD 21287, USA. Seminars in Ultrasound CT and MRI
(Impact Factor: 1.2).
06/2011; 32(3):242-51. DOI: 10.1053/j.sult.2011.02.002
The cerebral vascular architecture is both unique and heterogeneous in its structure, organization, and function. For many years, it was believed that brain vasculature was dominated by nonanastomosing terminal or "end-arteries." This was primarily based upon the observation of discrete distribution of brain infarcts after embolic occlusion of particular vessels. It was not until the detailed anatomy work of Pfeiffer in 1928 that the new concept of an almost-uninterrupted vascular network of brain vasculature was proposed. Since then, the cerebral vascular anatomy and embryology has been studied in great detail. Its full description is beyond the scope of this article, and our aim is to provide a brief overview of the development of cranial arterial anatomy, with special emphasis on commonly encountered anatomical variations that may have clinical implications. The failure to recognize these can lead to misdiagnosis as well as otherwise-preventable iatrogenic injuries and complications. We describe the proposed underlying embryologic processes, pathology and clinical implications of these variations, including aberrant internal carotid arteries, carotid agenesis and hypoplasia, azygous anterior cerebral arteries, arterial fenestrations, and persistent embryonic vessels.
Available from: Hugo Cuellar
- "Bilateral ACA territory stroke from the occlusion of one vessel is also possible when one vessel is feeding both hemispheres as in the case of an azygos ACA  . Despite the frequent association with ACA aneurysm occurring with azygos ACA , there has not been significant evidence of increased risk of ischemia or stroke associated with an azygos ACA . The bihemispheric PICA and the azygos ACA present in this patient could have a common phylogenic link. "
[Show abstract] [Hide abstract]
ABSTRACT: Variations in intracranial vasculature are well known. We report a rare anatomic variation in a patient who underwent cerebral angiography for suspected intracranial aneurysm. Digital subtraction angiography revealed a bihemispheric posterior inferior cerebellar artery (PICA) and an azygous anterior cerebral artery (ACA). There was no evidence of any aneurysm or vascular abnormality. To our knowledge, this is the first reported case of a patient with a common PICA supplying both the cerebellar hemispheres and a common ACA supplying ACA territory bilaterally. It is important for the physician to be aware of these anatomical variations in order to differentiate a normal variant from a pathological condition.
05/2014; 2014(3-4):541081. DOI:10.1155/2014/541081
Available from: Olivier Brina
- "The adventitia is the outer layer composed of connective tissue, nutrient vessels (vasa vasorum) and autonomic nerves. When the cerebral vessels enter the subarachnoid space their adventitia is made up of leptomeningeal cells . The muscular or middle layer is the thickest because it consists of smooth muscle cells and elastic tissue taking care of the local vasoregulation. "
[Show abstract] [Hide abstract]
ABSTRACT: Aneurysm vasculopathies represents a group of vascular disorders that share a common morphological diagnosis: a vascular dilation, the aneurysm. They can have a same etiology and a different clinical presentation or morphology, or have different etiology and very similar anatomical geometry. The biology of the aneurysm formation is a complex process that will be a result of an endogenous predisposition and epigenetic factors later on including the intracranial hemodynamics. We describe the biology of saccular aneurysms, its growth and rupture, as well as, current concepts of hemodynamics derived from application of computational flow dynamics on patient specific vascular models. Furthermore, we describe different aneurysm phenotypes and its extremely variability on morphological and etiological presentation.
European journal of radiology 01/2013; 82(10). DOI:10.1016/j.ejrad.2012.12.012 · 2.37 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: As compared to the adult, the developing fetus and newborn infant are at much greater risk for dysregulation of cerebral blood flow (CBF), with complications such as intraventricular and germinal matrix hemorrhage with resultant neurologic sequelae. To minimize this dysregulation and its consequences presents a major challenge. Although in many respects the fundamental signal transduction mechanisms that regulate relaxation and contraction pathways, and thus cerebrovascular tone and CBF in the immature organism are similar to those of the adult, the individual elements, pathways, and roles differ greatly. Here, we review aspects of these maturational changes of relaxation/contraction mechanisms in terms of both electro-mechanical and pharmaco-mechanical coupling, their biochemical pathways and signaling networks. In contrast to the adult cerebrovasculature, in addition to attenuated structure with differences in multiple cytoskeletal elements, developing cerebrovasculature of fetus and newborn differs in many respects, such as a strikingly increased sensitivity to [Ca(2+)]i and requirement for extracellular Ca(2+) for contraction. In essence, the immature cerebrovasculature demonstrates both "hyper-relaxation" and "hypo-contraction". A challenge is to unravel the manner in which these mechanisms are integrated, particularly in terms of both Ca(2+)-dependent and Ca(2+)-independent pathways to increase Ca(2+) sensitivity. Gaining an appreciation of these significant age-related differences in signal mechanisms also will be critical to understanding more completely the vulnerability of the developing cerebral vasculature to hypoxia and other stresses. Of vital importance, a more complete understanding of these mechanisms promises hope for improved strategies for therapeutic intervention and clinical management of intensive care of the premature newborn.
Current Vascular Pharmacology 09/2013; 11(5):655-711. DOI:10.2174/1570161111311050008 · 2.97 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.