Clinical Features of Ischemia in Cerebral Arterial Border Zones After Periods of Reduced Cerebral Blood Flow

Howard, Robin S.; Trend, Patrick; Russell, Richard A.

doi:10.1001/archneur.1987.00520210036016

Cited by 91 publications

(40 citation statements)

References 19 publications

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“…The role of severe arterial hypotension causing borderzone strokes has been described 20,27 and confirmed by experimental studies with primates. 28 Adams et al 20 identified borderzone infarcts in brains of patients who died shortly after cardiac surgery and ascribed it to 1 or more episodes of abrupt arterial hypotension.…”

Section: Discussionmentioning

confidence: 80%

Diffusion- and Perfusion-Weighted MRI Patterns in Borderzone Infarcts

Chaves¹,

Silver²,

Schlaug³

et al. 2000

Stroke

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Background and Purpose-The pathophysiology of borderzone infarcts is not well understood. We investigated whether combined diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) could identify pathophysiologically meaningful categories of borderzone infarcts. Methods-Seventeen patients with borderzone infarcts were identified from the Beth Israel Deaconess Medical Center Stroke Database. All patients had DWI and PWI, the majority of them within the first 24 hours of symptom onset.

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Section: Discussionmentioning

confidence: 80%

Diffusion- and Perfusion-Weighted MRI Patterns in Borderzone Infarcts

Chaves¹,

Silver²,

Schlaug³

et al. 2000

Stroke

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“…However, the cortical distal field may not always correspond to the WS in situations in which a shift of the latter (as revealed angiographically by the pattern of leptomeningeal anastomoses) has occurred because of additional hypoplasia or stenosis of the proximal ACA, PCA, or MCA. The occasional occurrence of syncope at onset of WS stroke, 13,14 and the typical clinical presentation of episodic, fluctuating, or progressive weakness of the hand, occasionally associated with upper limb shaking, are consistent with, and classically considered as markers of, hemodynamic failure. 3,15,16 This interpretation is further supported by radiological studies showing that WS infarcts distal to ICA disease are more likely with a noncompetent circle of Willis.…”

mentioning

confidence: 85%

The Pathophysiology of Watershed Infarction in Internal Carotid Artery Disease

Momjian-Mayor

Baron

2005

Stroke

315

224

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Background and Purpose-In carotid disease, infarcts can occur in the cortical as well as internal watershed (WS), or both.Better understanding the pathophysiology of WS infarcts would guide treatment. Two distinct hypotheses, namely low-flow and micro-embolism, are equally supported by neuropathological and physiological studies. Here we review the evidence regarding the mechanisms for WS stroke in carotid disease and whether they differ between cortical and internal WS infarcts. Summary of Review-After a brief account of the anatomy of the WS and the cerebrovascular physiology in circumstances of low perfusion pressure, the literature concerning the mechanisms of WS infarction in carotid disease is reviewed and discussed with emphasis on imaging and ultrasound studies of the cerebral hemodynamics. Conclusion-The evidence strongly favors a hemodynamic mechanism for internal WS infarction, especially regarding the so-called rosary-like pattern in the centrum semiovale. However, the relationships between cortical WS infarction and hemodynamic compromise appear more complicated. Thus, although severe hemodynamic compromise appears to underlie combined cortical and internal WS infarction, artery-to-artery embolism may play an important role in isolated cortical WS infarcts. Based on the high prevalence of microembolic signals documented by ultrasound in symptomatic carotid disease, a recent hypothesis postulates that embolism and hypoperfusion play a synergetic role, according to which small embolic material prone to lodge in distal field arterioles would be more likely to result in cortical micro-infarcts when chronic hypoperfusion prevails. Future studies combining imaging of brain perfusion, diffusion-weighted imaging, and ultrasound detection of microembolic signals should help resolve these issues. (Stroke. 2005;36:567-577.)

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“…Correlative clinical-pathologic or clinical-CT studies support the hypothesis that the distal field 28 of a cerebral arterial territory is most susceptible to hypoxic-ischemic injury. 46 - 52 In patients with systemic hypotension, initial damage occurs in the border zones of all three major cerebral arteries and, with increasing severity, spreads asymmetrically into the border zones between the ACA and MCA. 29 Recent clinical reports of patients with hemodynamically significant occlusive disease document the occurrence of orthostatic or positional cerebral ischemia in the retinal, hemispheric, and vertebrobasilar circulations.…”

Section: Resultsmentioning

confidence: 99%