The correct combination
【Progress】
All patients were previously admitted to our hospital to take rehabilitation.
【Discussion】
There are three major arteries in the cerebrum: anterior cerebral artery (ACA), middle cerebral artery (MCA) and posterior cerebral artery (PCA). These arteries mainly supply cortex and white matter existing the surface of the cerebrum. The penetrating branches from the major cerebral artery communicate and possibly develop as collateral circulation at the surface of the cerebral cortex. Meanwhile, the deep components of the cerebrum are supplied by perforating arteries; Heubner’s artery from ACA, anterior choroidal artery, lateral lenticulo-striate artery from MCA. As a matter of course, there are several border zone areas between a major artery and a perforating artery, between major arteries and between perforating arteries. Border zone infarcts usually happen in the border zone between major arteries but rarely happen in the border zone between perforating arteries and between a major artery and a perforating artery probably because the perfusion of the perforating area is well retained compared to the perfusion of the peripheral area of the major arteries.
The border zone infarct (Watershed infarct) occurs approximately 10% of all brain infarcts (1-4). Previously, the border zone infarct was believed to only occur by hemodynamic hypoperfusion between the major cerebral arteries (2). Two types of the border zone infarcts are recognized: external (cortical) and internal (subcortical) (1). The commonly accepted hypothesis holds the external type results from peripheral embolism but not always with associated hypoperfusion (Case 1,3,4,5) (5-7). The emboli reached to the border zone area are difficult to washout because of hypoperfusion, leading to ischemic infarction. The frontal border zone infarcts occur in the border zone between territories between ACA and MCA, while the posterior zone infarct occur in the border zone among territories of ACA, MCA and PCA.
Meanwhile, the internal type is believed to result from hemodynamic hypoperfusion (Case 2,6)(1,5). The medullary penetrating arteries supplying corona radiata and centrum semiovale are most distal from the carotid artery and the lowest perfusion pressure (1, 5). Further, no anastomosis exists between deep perforating arteries and medullary penetrating arteries (1, 5). The stenosis or the occlusion of the major cerebral artery causes the internal type zone infarct as well as that of the internal carotid artery and common carotid artery does. Bilateral border zone damages also can occur in hyper-eosinophilia and cyclosporin toxic effects (1, 5). The combined type of external and internal inevitably exists and probably results from hypoperfusion and embolism (Case 7).
The border zone infarct is sometimes overlooked in CT and/or MRI diagnosis because of the less incidence and the less unfamiliar location. In this series, we present seven cases: 4 cortical type, 2 subcortical type and 1 combined with cortical and subcortical types.
【Summary】
We presented seven cases with border zone (watershed) infarction: external (cortical) type (4 cases), internal (subcortical, 2 cases) type and combined type (1 case). It is borne in mind that the border zone infarct occurs approximately 10% of all brain infarcts: the external type results from peripheral embolism but not always with associated hypoperfusion (Figs. 1,3,4,5). The emboli reached to the border zone area are difficult to washout because of hypoperfusion, leading to ischemic infarction. The internal type results from hemodynamic hypoperfusion (Figs. 2, 6). The medullary penetrating arteries supplying corona radiata and centrum semiovale are most distal from the carotid artery and the lowest perfusion pressure. No anastomosis exists between deep perforating arteries and medullary penetrating arteries. The stenosis or the occlusion of the major cerebral artery, the internal carotid artery and common carotid artery can cause the internal type. Bilateral border zone damages also can occur in hyper-eosinophilia and cyclosporin toxic effects.
【References】
1.Mangla, R et al. Border zone infarcts: pathophysiologic and imaging characteristics. RadioGraphics 2011; 31:1201–1214
2.Torvik A. The pathogenesis of watershed infarcts in the brain. Stroke 1984;15(2):221–223.
3.Romanul FC, Abramowicz A. Changes in brain and pial vessels in arterial border zones. Arch Neurol 1964;11:40–65.
4.Adams JH, et al. The effects of systemic hypotension upon the human brain: clinical and neuropathological observations in 11 cases. Brain 1966;89(2):235–268.
5.Brierley JB, et al. The pathogenesis of ischaemic neuronal damage along the cerebral arterial boundary zones in Papio anubis. Brain 1980;103(4):929–965.
6.Del Sette M, et al. Internal borderzone infarction: a marker for severe stenosis in patients with symptomatic internal carotid artery disease. For the North American Symptomatic Carotid Endarterectomy (NASCET) Group. Stroke 2000;31(3): 631–636.
7.Momjian-Mayor I, et al. The pathophysiology of watershed infarction in internal carotid artery disease: review of cerebral perfusion studies. Stroke 2005;36(3):567–577.
All patients were previously admitted to our hospital to take rehabilitation.
【Discussion】
There are three major arteries in the cerebrum: anterior cerebral artery (ACA), middle cerebral artery (MCA) and posterior cerebral artery (PCA). These arteries mainly supply cortex and white matter existing the surface of the cerebrum. The penetrating branches from the major cerebral artery communicate and possibly develop as collateral circulation at the surface of the cerebral cortex. Meanwhile, the deep components of the cerebrum are supplied by perforating arteries; Heubner’s artery from ACA, anterior choroidal artery, lateral lenticulo-striate artery from MCA. As a matter of course, there are several border zone areas between a major artery and a perforating artery, between major arteries and between perforating arteries. Border zone infarcts usually happen in the border zone between major arteries but rarely happen in the border zone between perforating arteries and between a major artery and a perforating artery probably because the perfusion of the perforating area is well retained compared to the perfusion of the peripheral area of the major arteries.
The border zone infarct (Watershed infarct) occurs approximately 10% of all brain infarcts (1-4). Previously, the border zone infarct was believed to only occur by hemodynamic hypoperfusion between the major cerebral arteries (2). Two types of the border zone infarcts are recognized: external (cortical) and internal (subcortical) (1). The commonly accepted hypothesis holds the external type results from peripheral embolism but not always with associated hypoperfusion (Case 1,3,4,5) (5-7). The emboli reached to the border zone area are difficult to washout because of hypoperfusion, leading to ischemic infarction. The frontal border zone infarcts occur in the border zone between territories between ACA and MCA, while the posterior zone infarct occur in the border zone among territories of ACA, MCA and PCA.
Meanwhile, the internal type is believed to result from hemodynamic hypoperfusion (Case 2,6)(1,5). The medullary penetrating arteries supplying corona radiata and centrum semiovale are most distal from the carotid artery and the lowest perfusion pressure (1, 5). Further, no anastomosis exists between deep perforating arteries and medullary penetrating arteries (1, 5). The stenosis or the occlusion of the major cerebral artery causes the internal type zone infarct as well as that of the internal carotid artery and common carotid artery does. Bilateral border zone damages also can occur in hyper-eosinophilia and cyclosporin toxic effects (1, 5). The combined type of external and internal inevitably exists and probably results from hypoperfusion and embolism (Case 7).
The border zone infarct is sometimes overlooked in CT and/or MRI diagnosis because of the less incidence and the less unfamiliar location. In this series, we present seven cases: 4 cortical type, 2 subcortical type and 1 combined with cortical and subcortical types.
【Summary】
We presented seven cases with border zone (watershed) infarction: external (cortical) type (4 cases), internal (subcortical, 2 cases) type and combined type (1 case). It is borne in mind that the border zone infarct occurs approximately 10% of all brain infarcts: the external type results from peripheral embolism but not always with associated hypoperfusion (Figs. 1,3,4,5). The emboli reached to the border zone area are difficult to washout because of hypoperfusion, leading to ischemic infarction. The internal type results from hemodynamic hypoperfusion (Figs. 2, 6). The medullary penetrating arteries supplying corona radiata and centrum semiovale are most distal from the carotid artery and the lowest perfusion pressure. No anastomosis exists between deep perforating arteries and medullary penetrating arteries. The stenosis or the occlusion of the major cerebral artery, the internal carotid artery and common carotid artery can cause the internal type. Bilateral border zone damages also can occur in hyper-eosinophilia and cyclosporin toxic effects.
【References】
1.Mangla, R et al. Border zone infarcts: pathophysiologic and imaging characteristics. RadioGraphics 2011; 31:1201–1214
2.Torvik A. The pathogenesis of watershed infarcts in the brain. Stroke 1984;15(2):221–223.
3.Romanul FC, Abramowicz A. Changes in brain and pial vessels in arterial border zones. Arch Neurol 1964;11:40–65.
4.Adams JH, et al. The effects of systemic hypotension upon the human brain: clinical and neuropathological observations in 11 cases. Brain 1966;89(2):235–268.
5.Brierley JB, et al. The pathogenesis of ischaemic neuronal damage along the cerebral arterial boundary zones in Papio anubis. Brain 1980;103(4):929–965.
6.Del Sette M, et al. Internal borderzone infarction: a marker for severe stenosis in patients with symptomatic internal carotid artery disease. For the North American Symptomatic Carotid Endarterectomy (NASCET) Group. Stroke 2000;31(3): 631–636.
7.Momjian-Mayor I, et al. The pathophysiology of watershed infarction in internal carotid artery disease: review of cerebral perfusion studies. Stroke 2005;36(3):567–577.
2019.5.22