Ischemic stroke and incomplete infarction

• Published in: Stroke (1970) 1996-04, Vol.27 (4), p.761-765
• Main Authors: GARCIA, J. H, LASSEN, N. A, WEILLER, C, SPERLING, B, NAKAGAWARA, J
• Format: Article
• Language: English
• Subjects: Animals; Autopsy; Biological and medical sciences; Brain - pathology; Cerebral Infarction - diagnosis; Cerebral Infarction - pathology; Cerebral Infarction - physiopathology; Cerebrovascular Disorders - pathology; Cerebrovascular Disorders - physiopathology; Humans; Intracranial Embolism and Thrombosis - physiopathology; Magnetic Resonance Imaging; Medical sciences; Neurology; Neurons - pathology; Reperfusion; Tomography, X-Ray Computed; Vascular diseases and vascular malformations of the nervous system
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/01.str.27.4.761

The concept of selective vulnerability or selective loss o f individual neurons, with survival of glial and vascular elements as one of the consequences of a systemic ischemic-hypoxic insult (eg, transient cardiac arrest or severe hypotension), has been recognized for decades. In contrast, selective neuronal death as one of the lesions that may develop in the brain after occluding an intracranial artery is an idea not readily acknowledged in the current medical literature dealing with human stroke. A review of pertinent publications reveals that selective neuronal injury after middle cerebral artery occlusion was observed in autopsy specimens over 40 years ago, although its pathogenesis remains unclear. Recent observations in both humans and animals suggest that selective neuronal necrosis (rather than infarct) is the consequence of either a short-term arterial occlusion or permanent occlusion accompanied by ischemia of moderate severity. During the acute and subacute states of an ischemic stroke, the loss of a limited number of neurons (ie, incomplete infarction) does not result in structural changes discernible by either CT or conventional MRI. However, the loss of a selected number of neurons may be demonstrable in vivo by calculating the corresponding loss of benzodiazepine receptors. The use of specific radiotracers in combination with single-photon emission CT or positron emission tomography allows demonstration of a decrease in gamma-aminobutyric acid-ergic receptor sites at places where many neurons have been lethally injured. We aim to alert physicians to the potential development of incomplete brain infarctions in patients with intracranial arterial occlusions. Recognizing incomplete infarcts is particularly important in the context of stroke therapy with thrombolytic and neuroprotective agents. This brain lesion is likely to be the consequence of an arterial occlusion with a resultant ischemia of moderate severity (eg, regional blood flows in the range of 15 to 20 mL x 100 g-1 x min-1).