Border zone infarcts in cerebrum and cerebellum .pptx

Border zone infarcts

1. Border zone infarcts: pathophysiology and imaging characteristics -Dr Rejo . P. John JR ( Radiodiagnosis)

2. Learning objectives: Border zone infarcts-concept Types Pathophysiology Imaging features Role of imaging in management

3. Concept Border zone or watershed infarcts are ischemic lesions that occur in characteristic locations at the junction between two main arterial territories. These lesions constitute approximately 10% of all brain infarcts

4. types Two types of border zone infarcts are recognized: external (cortical) and internal (subcortical). To select the most appropriate methods for managing these infarcts, it is important to understand the type and hence the underlying causal mechanisms.

5. The external or cortical border zones are located at the junctions of the anterior, middle, and posterior cerebral artery territories. The internal or subcortical border zones are located at the junctions of the anterior, middle, and posterior cerebral artery territories with the Heubner , lenticulostriate, and anterior choroidal artery territories.

6. pathophysiology Various theories have been proposed to explain their pathogenesis. It is believed that repeated episodes of severe systemic hypotension are the most frequent cause (3). Susceptibility of border zones to ischemia was proved in an autopsy study of patients with border zone infarcts (4). 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 (5,6). Internal border zone infarcts are caused mainly by hemodynamic compromise/hypoperfusion , whereas external border zone infarcts are believed to result from embolism but not always with associated hypoperfusion.

7. 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 internal 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

8. Exte rnal border zone infarcts The external, cortical border zones are located between the anterior, middle, and posterior cerebral arteries and are usually wedge-shaped or ovoid (Fig 2). Many studies have documented hemodynamic abnormalities in the anterior watershed or frontal cortical border zone. The cerebral or carotid vessels may appear entirely normal or show mild or moderate narrowing without hemodynamic compromise (Fig 2). 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 arteries 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.

9. Clinical course and outcome in external Border zone infarcts 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 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 better chance of developing a collateral supply through leptomeningeal or dural anastomoses .

10. Internal border zone infarcts Internal border zone infarcts appear in multiples, in a rosarylike pattern (Fig 3b). Internal border zone infarcts are classified on the basis of their radiologic appearance as either confluent or partial (8). Partial infarcts 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 partial infarct, and a longer period of compromise, to confluent infarcts (22).

11. In contrast to external border zone infarcts, internal border zone infarcts are caused mainly by arterial stenosis or occlusion, or hemodynamic compromise (Fig 3). As shown in Figure 3a, 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 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 deep 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. Internal border zone infarcts are associated with a poor prognosis and clinical deterioration (21,22). Patients may undergo prolonged hospitalization, and they have an increased likelihood of remaining in a disabled state during clinical follow-up.

12. Superficial perforator infarcts Internal border zone infarcts must be 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 (Fig 3), whereas internal border zone infarcts tend to localize in paraventricular regions (23). 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, they have sometimes been collectively described as subcortical white matter infarcts

13. Posterior border zone cortical infacrts 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 artery) may lead to posterior external border zone infarcts.

14. 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) (27) (Fig 4).

15. Vascular Border Zone Changes The lesions produced by neurotoxic effects of cyclosporine therapy have a distinct distribution in vascular anastomotic border zones but do not lead to infarction (28) (Fig 5). Reversible vasculopathy has been suggested as the mechanism for reversible posterior encephalopathy in patients with this condition

16. Hypereosinophilia and Border Zone Infarcts Multiple ischemic strokes have been reported as a rare complication of hypereosinophilia , which could be due to idiopathic hypereosinophilic syndrome or a parasitic infection ( eg , filariasis, trichinosis, or schistosomiasis) (29). 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 (Fig 6). The border zone infarcts could be 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.

17. Border Zone Infarcts in the Cerebellum Border 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 (Fig 7). The origin of these border 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 embolism). Often, these small border zone lesions coexist with large territorial lesions.

18. ROLE oF NEUROIMAGING IN BORDER ZONE INFARCTS The main goals of neuroimaging in patients with border zone infarcts are to determine whether hemodynamic impairment is present and to assess its severity. Two stages of hemodynamic impairment are differentiated according to the magnitude of the decrease in cerebral perfusion pressure (37) (Fig 8).

19. 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 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 Stage II Hemodynamic Impairment Further reduction in cerebral perfusion pressure causes inadequate autoregulatory vasodilation, and cerebral blood flow decreases. As blood flow decreases, the oxygen extraction fraction in the brain may increase. Such increases can be measured with PET. Measurement of the cerebral oxygen extraction fraction provides information about the hemodynamic status of patients with cerebrovascular disease

20. Diffusion and Perfusion Imaging Diffusion-weighted MR imaging not only has the advantage of enabling differentiation of acute stroke from chronic stroke in patients with border zone infarcts but also is more sensitive than standard MR imaging techniques and can better depict the location of border zone infarcts in relation to the vessels, which may be helpful for their classification as either internal or cortical. Perfusion MR or CT imaging also has been performed in patients with a border zone infarct detected at routine CT or MR imaging or diffusion-weighted MR imaging. The findings at perfusion imaging may vary, depending on the causal mechanism of border zone infarction

21. Normal Perfusion (Transient Perfusion Deficit) Normal perfusion may be seen in patients with a transient perfusion deficit due to hypotension, in the absence of large artery disease. A history of transient severe systemic arterial hypotension can usually be found in these patients’ medical records. Localized Perfusion Deficit Localized perfusion deficits matching the area of restricted diffusion are often found in patients with infarcts due to cardiac or embolic causes (Fig 10). Follow-up imaging in these patients may show reperfusion, a finding that supports the assumption that the causal mechanism is embolism. This perfusion pattern is predictive of a relatively good prognosis.

22. Extensive Perfusion Deficit Extensive perfusion deficits involving one or more vascular territories may be signaled by a mismatch between diffusion and perfusion imaging findings. Patients with an extensive perfusion deficit have severe stenosis or occlusion of large arteries, which predisposes them to hypoperfusion and resultant border zone infarction (Fig 11). This perfusion pattern implies a high risk of worsening clinical symptoms and a poor prognosis.

23. SPECT Evaluation SPECT evaluation of cerebral blood flow is performed by using one of two technetium (99mTc)- labeled compounds: 99mTc-hexametazime or 99mTc-ethylenecysteine dimer. Cerebral perfusion or hemodynamic status is measured at baseline and after vasodilation by using either acetazolamide administration or hypercapnia induction. Cerebrovascular reactivity measured after acetazolamide challenge has high sensitivity for the detection of regions of hemodynamic impairment.

24. PET Evaluation Oxygen extraction fraction and cerebral blood flow are two important parameters of hemodynamic impairment that can be measured with PET. Studies performed with PET have shown that patients who exhibited misery perfusion selectively in the border zone areas on PET images subsequently developed cerebral infarction in the same area (41). Multiple internal border zone infarcts that appear in a linear rosarylike pattern in the region of the centrum semiovale or corona radiata are strongly associated with an increased oxygen extraction fraction and, by implication, greater hemodynamic impairment (37,42) (Fig 12).

25. Doppler US Transcranial Doppler US with carbon dioxide reactivity measurements has shown increases in the volume of internal border zone infarcts at follow-up studies in patients with reduced carbon dioxide reactivity at baseline Doppler US. A hypothesized association between these findings and an embolic process in border zone areas is supported by the high prevalence of microembolic signals, which are believed to correspond to platelet and lipid deposits in distal small vessels, at transcranial Doppler US (43,44). Such findings are suggestive of the predisposition of hypoperfused regions to embolism.

26. Recent Advances in Regional Perfusion Imaging There is wide interindividual variability in perfusion territories and locations of border zones, mainly because of anatomic variations in the circle of Willis. Arterial spin labeling techniques have been devised for perfusion MR assessments of different vascular territories and identification of border zones. Perfusion measurements are obtained by spin labeling of blood flowing to the individual perfusion territories of major feeding vessels, one vessel at a time (45). An increase in arterial transit time may be helpful for identifying the border zones (Fig 13). Regional perfusion imaging techniques may also be useful for visualizing collateralized flow in patients with cerebrovascular stenosis or occlusion.

27. Conclusion: Internal (subcortical) border zone infarcts, which typically appear in a linear rosarylike pattern in the centrum semiovale , are caused mainly by hemodynamic compromise. External (cortical) border zone infarcts are believed to be caused by embolism, sometimes with associated hypoperfusion. External border zone infarcts usually follow a benign clinical course, whereas internal border zone infarcts are associated with higher morbidity and a higher risk for future stroke.

28. Different therapeutic approaches may be required to prevent early clinical deterioration in patients with different types of border zone infarcts. Advanced imaging techniques such as diffusion and perfusion MR imaging, PET, perfusion CT, and transcranial Doppler US can be helpful for understanding the pathophysiology of these infarcts, detecting associated hemodynamic compromise, and guiding disease management.

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