Watershed cerebral infarctions (also known as border zone infarcts) occur at the border between cerebral vascular territories with no or little anastomosis.
It has been proposed that both, episodes of hypoperfusion and microembolisms, play a role in pathophysiology of this entity. Clearance of the microemboli are most likely to be impaired in watershed zones due to poorer perfusion. Episodes of systemic hypotension along with severe stenosis or occlusion of the feeding arteries, in particular intra- and extracranial carotid arteries can also contribute to the infarction. Watershed zone infarct in an isolated zone is more likely to be secondary to microembolism in the absence of significant systemic hypotension. Prolonged hypotension such as cardiac surgery or cardiac arrest commonly give a bilateral pattern 5 , on the other hand, severe carotid stenosis lesions are usually unilateral on the side of the stenosis.
WSI has been classified to:
- Cortical (external) border zones infarct: between ACA, MCA, and PCA territories and mostly due to microemboli
- Deep (internal) border zones infarct: between ACA, MCA, and PCA territories and perforating medullary, lenticulostriate, recurrent artery of Heubner and anterior choroidal arteries; mostly due to either severe hypotention or severe arterial stenosis
CT and MRI
Exact pattern depends on the bordering territories which is usually variable in different individuals. Imaging of WSI should also aim to determine presence and severity of arterial stenosis or occlusion.
Cortical (external) border zones infarct: usually wedge shape or gyriform
- ACA/MCA: in frontal cortex extending from anterior horn to the cortex
- MCA/PCA: in parietoloccipital region extending from posterior horn to the cortex
- parallel parafalcine stripes in subcortical white matter at the vertex- this type is seen when there was profound diffuse hypoperfusion
* triple watershed zone: most vulnerable region where ACA, MCA, and PCA converge posterior to lateral ventricles in parietoocciptal region
Deep (internal) border zones infarct:
- series of 3 or more lesions, each with 3 mm or more in diameter in a linear fashion parallel to the lateral ventricles in the centrum semi ovale or corona radiata which sometimes become more confluent and band-like 7 (case1)
- 1. Bladin CF, Chambers BR. Clinical features, pathogenesis, and computed tomographic characteristics of internal watershed infarction. Stroke. 1993;24 (12): 1925-32. Stroke (abstract) - Pubmed citation
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- 3. Momjian-mayor I, Baron JC. The pathophysiology of watershed infarction in internal carotid artery disease: review of cerebral perfusion studies. Stroke. 2005;36 (3): 567-77. doi:10.1161/01.STR.0000155727.82242.e1 - Pubmed citation
- 4. Moustafa RR, Izquierdo-garcia D, Jones PS et-al. Watershed infarcts in transient ischemic attack/minor stroke with > or = 50% carotid stenosis: hemodynamic or embolic? Stroke. 2010;41 (7): 1410-6. doi:10.1161/STROKEAHA.110.580415 - Pubmed citation
- 5. Gottesman RF, Sherman PM, Grega MA et-al. Watershed strokes after cardiac surgery: diagnosis, etiology, and outcome. Stroke. 2006;37 (9): 2306-11. doi:10.1161/01.STR.0000236024.68020.3a - Pubmed citation
- 6. Mangla R, Kolar B, Almast J et-al. Border zone infarcts: pathophysiologic and imaging characteristics. Radiographics. 2011;31 (5): 1201-14. Radiographics (full text) - doi:10.1148/rg.315105014 - Pubmed citation
- 7. Derdeyn CP, Khosla A, Videen TO et-al. Severe hemodynamic impairment and border zone-region infarction. Radiology. 2001;220 (1): 195-201. doi:10.1148/radiology.220.1.r01jl09195 - Pubmed citation
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