分水岭区梗死及影像学表现课件.ppt
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1、分水岭区梗死及影像学表现,分水岭区梗死及影像学表现分水岭区梗死及影像学表现,分水岭区梗死及影像学表现分水岭区梗死及影像学表现分水岭区梗死,分水岭区梗死及影像学表现课件,分水岭区梗死及影像学表现课件,分水岭区梗死及影像学表现课件,Watershed Infarcts www.radiologyassistant.nl/images/48e9bb7f02d66Basis-waterscheiding2.png as a result of hypoperfusion. There are two patterns of border zone infarcts: Cortical border z
2、one infarctionsInfarctions of the cortex and adjacent subcortical white matter located at the border zone of ACA/MCA and MCA/PCA Internal border zone infarctions Infarctions of the deep white matter of the centrum semiovale and corona radiata at the border zone between lenticulostriate perforators a
3、nd the deep penetrating cortical branches of the MCA or at the border zone of deep white matter branches of the MCA and the ACA.,Watershed Infarcts,Cortica watershed strokes (CWS), or outer brain infarcts, are located between the cortical territories of the anterior cerebral artery (ACA), middle cer
4、ebral artery (MCA), and posterior cerebral artery (PCA). Internal watershed strokes (IWS), or subcortical brain infarcts, are located in the white matter,along and slightly above the lateral ventricle,between the deep and the superficial arterial systems of the MCA, or between the superficial system
5、s of the MCA and ACA.,Cortica watershed strokes (,分水岭区梗死及影像学表现课件,分水岭区梗死及影像学表现课件,Watersheds or border zones are areas that lie at the junction of two different drainage areas. The vascular supply of the cerebral parenchyma can be envisioned in a similar manner, with defined boundaries between differe
6、nt arterial systems. Cerebral infarcts in border zones were first discussed in 1883 and were defined as ischemic lesions in an area between two neighboring vascular territories . These territories can be further classified in two broad categories as (a) external (cortical) or (b) internal (subcortic
7、al) border zones. Border zone infarcts constitute approximately 10% of all cerebral infarcts . Various theories have been proposed to explain their pathogenesis. It is believed that repeated episodes of severe systemic hypotension are the most frequent cause . Susceptibility of border zones to ische
8、mia was proved in an autopsy study of patients with border zone infarcts . Various neuropathologic studies have shown neuronal necrosis from hypotension in these regions and have advanced our understanding of the preferential distribution of border zone infarcts .,Watersheds or border zones,The appe
9、arances of border zone infarcts depicted by standard imaging modalities are well described. Advanced imaging techniques can help identify areas of misery perfusion associated with these infarcts. Misery perfusion(低灌注) represents a chronic failure of cerebral autoregulation associated with decreased
10、cerebral perfusion pressures in the presence of extracranial and intracranial atheromatous disease. The important information derived from imaging can be useful for patient management and disease prognosis,The appearances of border,The external or cortical border zones are located at the junctions o
11、f the anterior, middle, and posterior cerebral artery territories. Infarcts in the anterior external border zones and paramedian white matter are found at the junction of the territories supplied by the anterior and middle cerebral arteries, and those in the parieto-occipital areas (posterior extern
12、al border zones) are found at the junction of the territories supplied by the middle and posterior cerebral arteries.,The external or cortical b,The internal or subcortical border zones are located at the junctions of the anterior, middle, and posterior cerebral artery territories with the Heubner,
13、lenticulostriate, and anterior choroidal artery territories. Internal border zone infarcts thus may be designated as infarcts of the lenticulostriatemiddle cerebral artery, lenticulostriateanterior cerebral artery, Heubneranterior cerebral artery, anterior choroidalmiddle cerebral artery, and anteri
14、or choroidalposterior cerebral artery territories . Infarcts of the lenticulostriatemiddle cerebral artery border zone, which is supplied by the end branches of deep perforating lenticulostriate arteries and medullary penetrators from the pialmiddle cerebral artery, are the most commonly seen at ima
15、ging and are described in detail in this article .,The internal or subcortical bo,Color overlays on axial T2-weighted magnetic resonance (MR) images of normal cerebrum show probable locations of external (blue) and internal (red) border zone infarcts.,Color overlays on axial T2-,Border zone infarcts
16、 involve the junction of the distal fields of two nonanastomosing arterial systems . The conventional theory implicates hemodynamic compromise produced by repeated episodes of hypotension in the presence of a severe arterial stenosis or occlusion. The lower perfusion pressure found within the border
17、 zone areas in this setting confers an increased susceptibility to ischemia, which can lead to infarction. This causal role of severe arterial hypotension has been well described and confirmed by the results of experimental studies in animals . The typical clinical manifestations of syncope(晕厥), hyp
18、otension, and episodic fluctuating(情感波动) or progressive weakness of the hands are also supportive of this theory of hemodynamic failure . Radiologic studies also support the hypothesis that border zone infarcts distal to internal carotid artery disease are more likely to occur in the presence of a n
19、oncompetent circle of Willis.,Pathophysiology of Border Zone Infarcts,Border zone infarcts involv,In sharp contrast with this widely prevalent interpretation, several pathologic investigations have emphasized an association between border zone infarction and microemboli, and embolic material has bee
20、n found within areas of border zone infarction in autopsy series . Preferential propagation of emboli in the border zone regions also has been found in experimental studies . Border zone infarction may be better explained by invoking a combination of two often interrelated processes: hypoperfusion a
21、nd embolization . Hypoperfusion, or decreased blood flow, is likely to impede the clearance (washout) of emboli. Because perfusion is most likely to be impaired in border zone regions, clearance of emboli will be most impaired in these regions of least blood flow. Severe occlusive disease of the int
22、ernal carotid artery causes both embolization and decreased perfusion. Similarly, cardiac disease is often associated with microembolization from the heart and aorta with periods of diminished systemic and brain perfusion. This theory, although it seems reasonable, remains unproved and has been chal
23、lenged on many accounts.,In sharp contrast with thi,Imaging Appearance The external, cortical border zones are located between the anterior, middle, and posterior cerebral arteries and are usually wedge-shaped or ovoid . However, their location may vary with differences in the arterial supply. It is
24、 sometimes difficult to determine whether a person has sustained a border zone infarct on the basis of the location of the infarct in relation to the vessels on a CT or MR imag. Because of this extensive anatomic variation, minimum and maximum distribution territories of each vessel have been define
25、d. It is not uncommon to describe a cortical infarct as a “territorial” infarct if it lies completely within the expected or possible maximum area of a vascular territory or as a “potential” infarct if it is outside these maxima . Furthermore, the location of cortical border zones may vary because o
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