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1、分水岭区梗死,Watershed Infarcts Watershed infarcts occur at the border zones between major cerebral arterial territories as a result of hypoperfusion. There are two patterns of border zone infarcts: Cortical border zone infarctionsInfarctions of the cortex and adjacent subcortical white matter located at
2、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 and the deep penetrating cortical branches of the MCA or at the border zone of deep white m
3、atter branches of the MCA and the ACA.,Cortica watershed strokes (CWS), or outer brain infarcts, are located between the cortical territories of the anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA). Internal watershed strokes (IWS), or subcortical bra
4、in 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 systems of the MCA and ACA.,Watersheds or border zones are areas that lie at the junction of two different drainage
5、 areas. The vascular supply of the cerebral parenchyma can be envisioned in a similar manner, with defined boundaries between different 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 te
6、rritories . These territories can be further classified in two broad categories as (a) external (cortical) or (b) internal (subcortical) border zones. Border zone infarcts constitute approximately 10% of all cerebral infarcts . Various theories have been proposed to explain their pathogenesis. It is
7、 believed that repeated episodes of severe systemic hypotension are the most frequent cause . Susceptibility of border zones to ischemia was proved in an autopsy study of patients with border zone infarcts . Various neuropathologic studies have shown neuronal necrosis from hypotension in these regio
8、ns and have advanced our understanding of the preferential distribution of border zone infarcts .,The appearances 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
9、. Misery perfusion(低灌注) represents a chronic failure of cerebral autoregulation associated with decreased 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 diseas
10、e prognosis,The external or cortical border zones are located at the junctions of 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 midd
11、le cerebral arteries, and those in the parieto-occipital areas (posterior external border zones) are found at the junction of the territories supplied by the middle and posterior cerebral arteries.,The internal or subcortical border zones are located at the junctions of the anterior, middle, and pos
12、terior cerebral artery territories with the Heubner, 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,
13、 anterior choroidalmiddle cerebral artery, and anterior 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 pialmidd
14、le cerebral artery, are the most commonly seen at imaging and are described in detail in this article .,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.,Border zone infarcts invol
15、ve 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 zone
16、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）, hypotensi
17、on, 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 noncomp
18、etent circle of Willis.,Pathophysiology of Border Zone Infarcts,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 been found within areas of border zon
19、e 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 and embolization . Hypoperfusion, o
20、r 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 internal carotid artery causes both e
21、mbolization 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 challenged on many accounts.,Imaging A
22、ppearance 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 sometimes difficult to determine whether a person has sustai
23、ned 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 defined. It is not uncommon to describe a cortical infarct as a “te
24、rritorial” 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 of the development of leptomeningeal collaterals . The anatomy
25、 of cortical border zones can be complex, with marked variability due to individual differences in the territories supplied by the major arteries of the brain.,(a, b) Coronal fluid-attenuated inversion recovery MR images show the distribution of external (cortical) border zone infarcts at the juncti
26、ons of the anterior cerebral artery and middle cerebral artery territories (a) and the middle cerebral artery and posterior cerebral artery territories (b). (c) Diffusion-weighted MR images show a cortical border zone infarct at the junction of the anterior cerebral artery and middle cerebral artery
27、 territories. Angiography of the right-sided common carotid and internal carotid arteries in the same patient showed normal vessels with no occlusion or stenosis.,Causal Mechanisms The mechanism of external border zone infarction has been widely debated. Many studies have documented hemodynamic abno
28、rmalities in the anterior watershed or frontal cortical border zone. However, in many recent studies, no evidence of such hemodynamic impairment was found . In other studies, substantially fewer severe stenoses or occlusions of major vessels than border zone infarcts were found . The cerebral or car
29、otid vessels may appear entirely normal or show mild or moderate narrowing without hemodynamic compromise . Isolated cortical border zone infarcts may be embolic in nature and are less frequently associated with hemodynamic compromise. Microemboli from the heart or atherosclerotic plaques in major a
30、rteries may preferentially propagate to cortical border zones, which have lower perfusion than other areas of the vasculature, and, thus, a limited ability to wash out these emboli. Many patients with cortical border zone infarcts have concomitant smaller cortical infarcts. These findings support th
31、e hypothesis that an embolic mechanism plays a crucial role in the pathogenesis of external border zone infarcts,Clinical Course Patients with external border zone infarcts have a more benign clinical course and a better prognosis than those with internal border zone infarcts, although the severity
32、of clinical signs and symptoms and the score on the National Institutes of Health Stroke Scale at the time of admission might not differ substantially between the two patient groups. The external border zone is closer to the cortical surface, where penetrating arteries originate, and thus it has a b
33、etter chance of developing a collateral supply through leptomeningeal or dural anastomoses. However, when external border zone infarcts occur in association with internal border zone infarcts, there is a higher probability of hemodynamic impairment, and the prognosis may not be good .,Internal Borde
34、r Zone Infarcts Imaging Appearance Internal border zone infarcts appear in multiples, in a rosarylike pattern . In one report, this pattern was described as a series of three or more lesions, each with a diameter of 3 mm or more, arranged in a linear fashion parallel to the lateral ventricle in the
35、centrum semiovale or corona radiata . Internal border zone infarcts are classified on the basis of their radiologic appearance as either confluent or partial Partial infarcts are usually large, cigar shaped, and arranged in a pattern resembling the beads of a rosary, parallel and adjacent to the lat
36、eral ventricle. The duration of hemodynamic compromise has been postulated as the cause of the varied radiologic appearances, with a brief episode of compromise leading to a partial infarct, and a longer period of compromise, to confluent infarcts . Confluent internal border zone infarcts may be man
37、ifested by a stepwise onset of contralateral hemiplegia. They also may be associated with a poorer recovery than is typical for partial infarcts,Internal border zone infarcts must be differentiated from superficial perforator (medullary) infarcts, which may have a similar appearance on MR images. Su
38、perficial perforator infarcts, which are caused by the occlusion of medullary arteries from pial plexuses, are smaller, superficially located, and widely scattered , whereas internal border zone infarcts tend to localize in paraventricular regions . Superficial perforator infarcts are associated wit
39、h less severe vascular stenoses and a better prognosis than internal border zone infarcts. Because of the difficulty of differentiating between the two types of infarcts on radiologic images, they have sometimes been collectively described as subcortical white matter infarcts, but that term is diagn
40、ostically nonspecific.,Causal Mechanisms In contrast to external border zone infarcts, internal border zone infarcts are caused mainly by arterial stenosis or occlusion, or hemodynamic compromise . The greater vulnerability of internal border zones to hemodynamic compromise has been explained on the
41、 basis of anatomic characteristics of the cerebral arterioles within these zones. the internal border zones are supplied by medullary penetrating vessels of the middle and anterior cerebral arteries and by deep perforating lenticulostriate branches. The medullary penetrating arteries are the most di
42、stal branches of the internal carotid artery and have the lowest perfusion pressure. The deep perforating lenticulostriate arteries have little collateral supply, and there are no anastomoses between the deep perforators and the white matter medullary arterioles. Therefore, the centrum semiovale and
43、 corona radiata are more susceptible than other regions to ischemic insults in the setting of hemodynamic compromise.,Clinical Course Internal border zone infarcts are associated with a poor prognosis and clinical deterioration . Patients may undergo prolonged hospitalization, and they have an incre
44、ased likelihood of remaining in a disabled state during clinical follow-up. The results of diffusion-weighted imaging studies suggest that patients with internal border zone infarcts have an increased risk for stroke during the first few days after infarction . Perfusion studies in patients with suc
45、h infarcts have shown a far greater area of misery perfusion than is reflected on diffusion-weighted images. Involvement of the adjacent cortex also has been found on perfusion images . Thus, the typically small internal border zone infarcts represent the “tip of the iceberg” of decreased perfusion
46、reserve and may be predictive of impending stroke. This hypothesis was tested further with quantitative carbon 11flumazenil positron emission tomography (PET), which showed a decrease in benzodiazepine receptors, a finding suggestive of neuronal damage beyond the region of infarction seen on MR imag
47、es .,a) Color overlay on a coronal MIP image from CT angiography in a healthy volunteer shows the probable location of the internal border zone (blue dots).,(b) Diffusion-weighted MR images, obtained in a 52-year-old woman with progressive weakness and numbness for 6 months and a complete foot drop,
48、 show multiple internal border zone infarcts in a rosarylike pattern along the left centrum semiovale. (c) Left internal carotid angiogram in the same patient demonstrates severe stenosis of the M1 segment of the left middle cerebral artery.,Posterior External (Cortical) Border Zone Infarcts Anterio
49、r external border zone infarcts are more common than posterior ones because of the high prevalence of internal carotid artery disease. Vertebrobasilar system disease with superimposed fetal circulation (ie, a fetal-type posterior cerebral artery) may lead to posterior external border zone infarcts. Unilateral posterior external border zone infarcts have been related to cerebral emboli either of cardiac origin or from the common carotid artery, whereas bilateral infarcts are more likely to be caused by underlying hemodynamic impairment (vascular stenosis) .,Axial diffusio