(Stroke. 1996;27:761-765.)
© 1996 American Heart Association, Inc.
Articles |
Ischemic Stroke and Incomplete Infarction
From the Department of Pathology, Henry Ford Hospital, Detroit, Mich, and Case Western Reserve University School of Medicine, Cleveland, Ohio (J.H.G.); the Clinical Physiology and Nuclear Medicine Department, Bispebjerg Hospital, Copenhagen, Denmark (N.A.L., B.S.); Neurologische Klinik der Friedrich-Schiller-Universität Jena, Germany (C.W.); and the Department of Neurosurgery, Nakamura Memorial Hospital, Sapporo, Japan (J.N.).
Correspondence to Julio H. Garcia, MD, Neuropathology, Henry Ford Hospital, K-6 (A-610), 2799 W Grand Blvd, Detroit, MI 48202-2689.
Background The concept of selective vulnerability or selective loss of 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.
Summary of Review 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 stages 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 
-aminobutyric acid–ergic
receptor sites at places where many neurons have been lethally injured.
Conclusions 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·100 g-1·min-1).
Key Words: cerebral blood flow • cerebral cortex • cerebral ischemia • cerebral ischemia, transient • putamen
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