分水岭区梗死及影像学表现

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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 the

2、 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 matt

3、er 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 brain infarcts,are

4、 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 areas.The vascula

5、r 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 territories.These terri

6、tories 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 believed that repeated episodes of

7、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 regions and have advanced our understanding o

8、f 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.Misery perfusion(低灌注低灌注)represents a chron

9、ic 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 disease prognosis The external or cortical border

10、 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 middle cerebral arteries,and those in the parieto-

11、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 posterior cerebral artery territories with the Heubner,

12、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 anterior cho

13、roidalposterior 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 imaging and a

14、re 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 involve the junction of the distal fields of two nonanastomosing arterial sys

15、tems.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 areas in this setting confers an increased susceptibility to ischemia,which

16、 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（晕厥晕厥）,hypotension,and episodic fluctuating（情感波动情感波动）or progressive weakness of the hands are

17、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 noncompetent circle of Willis.Pathophysiology of Border Zone Infarcts In sharp contra

18、st 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 zone infarction in autopsy series.Preferential propagation of emboli in the border z

19、one 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,or decreased blood flow,is likely to impede the clearance(washout)of emboli.Because perfus

20、ion 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 embolization and decreased perfusion.Similarly,cardiac disease is often associated with microemb

21、olization 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 Appearance The external,cortical border zones are located between the anterior,middle,and posterior ce

22、rebral 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 sustained a border zone infarct on the basis of the location of the infarct in relation to the vessels on a CT or

23、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“territorial”infarct if it lies completely within the expected or possible maximum area of a vascular territory or

24、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 of cortical border zones can be complex,with marked variability due to individual differences in the territories suppli

25、ed 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 junctions of the anterior cerebral artery and middle cerebral artery territories(a)and the middle cerebral artery and posterior cere

26、bral 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 territories.Angiography of the right-sided common carotid and internal carotid arteries in the same patient showed normal vessels

27、with no occlusion or stenosis.Causal Mechanisms The mechanism of external border zone infarction has been widely debated.Many studies have documented hemodynamic abnormalities in the anterior watershed or frontal cortical border zone.However,in many recent studies,no evidence of such hemodynamic imp

28、airment was found.In other studies,substantially fewer severe stenoses or occlusions of major vessels than border zone infarcts were found.The cerebral or carotid vessels may appear entirely normal or show mild or moderate narrowing without hemodynamic compromise.Isolated cortical border zone infarc

29、ts may be embolic in nature and are less frequently associated with hemodynamic compromise.Microemboli from the heart or atherosclerotic plaques in major arteries may preferentially propagate to cortical border zones,which have lower perfusion than other areas of the vasculature,and,thus,a limited a

30、bility to wash out these emboli.Many patients with cortical border zone infarcts have concomitant smaller cortical infarcts.These findings support the hypothesis that an embolic mechanism plays a crucial role in the pathogenesis of external border zone infarctsClinical Course Patients with external

31、border zone infarcts have a more benign clinical course and a better prognosis than those with internal border zone infarcts,although the severity 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 be

32、tween the two patient groups.The external border zone is closer to the cortical surface,where penetrating arteries originate,and thus it has a better chance of developing a collateral supply through leptomeningeal or dural anastomoses.However,when external border zone infarcts occur in association w

33、ith internal border zone infarcts,there is a higher probability of hemodynamic impairment,and the prognosis may not be good.Internal Border Zone InfarctsImaging Appearance Internal border zone infarcts appear in multiples,in a rosarylike pattern.In one report,this pattern was described as a series o

34、f 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 centrum semiovale or corona radiata.Internal border zone infarcts are classified on the basis of their radiologic appearance as either confluent or partial Partial infar

35、cts are usually large,cigar shaped,and arranged in a pattern resembling the beads of a rosary,parallel and adjacent to the lateral 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 pa

36、rtial infarct,and a longer period of compromise,to confluent infarcts.Confluent internal border zone infarcts may be manifested 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 b

37、e differentiated from superficial perforator(medullary)infarcts,which may have a similar appearance on MR images.Superficial perforator infarcts,which are caused by the occlusion of medullary arteries from pial plexuses,are smaller,superficially located,and widely scattered,whereas internal border z

38、one infarcts tend to localize in paraventricular regions.Superficial perforator infarcts are associated with 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,the

39、y have sometimes been collectively described as subcortical white matter infarcts,but that term is diagnostically nonspecific.Causal MechanismsIn contrast to external border zone infarcts,internal border zone infarcts are caused mainly by arterial stenosis or occlusion,or hemodynamic compromise.The

40、greater vulnerability of internal border zones to hemodynamic compromise has been explained on the 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

41、by deep perforating lenticulostriate branches.The medullary penetrating arteries are the most distal 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 de

42、ep perforators and the white matter medullary arterioles.Therefore,the centrum semiovale and 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 clin

43、ical deterioration.Patients may undergo prolonged hospitalization,and they have an increased 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 str

44、oke during the first few days after infarction.Perfusion studies in patients with such 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 interna

45、l border zone infarcts represent the“tip of the iceberg”of decreased perfusion 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 su

46、ggestive of neuronal damage beyond the region of infarction seen on MR images.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 prog

47、ressive weakness and numbness for 6 months and a complete foot drop,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 a

48、rtery.Posterior External(Cortical)Border Zone Infarcts Anterior 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 ar

49、tery)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(vas

50、cular stenosis).Axial diffusion-weighted MR image and apparent diffusion coefficient map show bilateral posterior cortical border zone infarcts.Vascular Border Zone Changes The lesions produced by neurotoxic effects of cyclosporine therapy have a distinct distribution in vascular anastomotic border

51、zones but do not lead to infarction.Reversible vasculopathy has been suggested as the mechanism for reversible posterior encephalopathy in patients with this condition.Decreased cortical blood flow has been found in the border zones in these patients.Axial T2-weighted fluid-attenuated inversion reco

52、very MR images show abnormal regions of hyperintense signal in vascular watershed territories in a patient with toxic effects of cyclosporine therapy.Hypereosinophilia（红细胞增多症）and Border Zone InfarctsMultiple ischemic strokes have been reported as a rare complication of hypereosinophilia,which could

53、be due to idiopathic hypereosinophilic syndrome or a parasitic infection(eg,filariasis,trichinosis,or schistosomiasis).The resultant infarcts can be seen in the cortex as well as the border zone regions of the deep and superficial middle cerebral artery perforators.The border zone infarcts could be

54、due to either thromboembolism from endomyocardial fibrosis or to vascular endothelial toxic effects of eosinophilic cells;thromboemboli can occur in conjunction with cardiac involvement throughout the course of the disease.In a few cases,the infarcts have been attributed to local thrombus formation

55、instead of a thromboembolic cause.Axial diffusion-weighted MR images obtained in a 26-year-old man with a sudden onset of encephalopathy show multiple small abnormal regions with hyperintense signal distributed in vascular watershed territories.Idiopathic hypereosinophilic syndrome was subsequently

56、diagnosedBorder Zone Infarcts in the CerebellumBorder zone infarcts in the cerebellum are usually less than 2 cm in size and are seen at the borders of the anterior inferior cerebellar artery,superior cerebellar artery,posterior inferior cerebellar artery,and their branches.The origin of these borde

57、r zone infarcts is similar to that of territorial infarcts in the cerebellum:The infarction is due to stenosis or embolism of the vessels.The source of embolism could be atherosclerotic disease or dissection in a vertebrobasilar artery or a cardiac condition(eg,right heart thrombus in paradoxical em

58、bolism).Often,these small border zone lesions coexist with large territorial lesions.The management of border zone infarcts in the cerebellum is similar to that of territorial cerebellar infarcts In population-based studies of migraine patients,silent border zone infarcts were found in the posterior

59、 cerebellum.Schematic shows the border zones of the lateral(dark green)and medial(light green)superior cerebellar arteries,anterior inferior cerebellar artery(red),and lateral(dark blue)and medial(light blue)posterior inferior cerebellar arteries.Orange=anteromedial brainstem supply from anterior sp

60、inal,vertebral,and basilar arteries;yellow=lateral supply from basilar artery.Stage I Hemodynamic Impairment In stage I hemodynamic impairment,a decline in cerebral perfusion pressure leads to autoregulatory vasodilation of resistive vessels of the brain.This physiologic response to reduced cerebral

61、 perfusion pressure has been measured with various methods,including xenon-enhanced CT,Doppler ultrasonography(US),perfusion CT,perfusion MR imaging,single photon emission computed tomography(SPECT),and PET.Most of these modalities are useful for determining cerebral blood flow,cerebral blood volume

62、,and mean transit time,which are considered physiologic markers of hemodynamic impairment.Increased cerebral blood volume and increased mean transit time represent stage I hemodynamic compromise.Hemodynamic compromise may be further evaluated by measuring cerebrovascular reactivity in response to a

63、vasodilatory challenge(eg,induction of hypercapnia or administration of acetazolamide).To measure cerebrovascular reactivity,cerebral blood flow measurements are repeated after a vasodilatory challenge to the cerebral vessels.In a normal situation,an increase in cerebral blood flow is expected;howev

64、er,in a state of hemodynamic compromise,the cerebral blood flow is often not increased because autoregulation has already caused maximum vasodilation in response to decreased cerebral perfusion pressure.A decrease in cerebral blood flow after a vasodilatory challenge represents abnormal,decreased cerebrovascular reactivity.A reduced or exhausted vasodilatory capacity confers a higher risk for subsequent stroke.