(Stroke. 1997;28:124-132.)
© 1997 American Heart Association, Inc.
Articles |
Incomplete Brain Infarction of Reperfused Cortex May Be Quantitated With Iomazenil
the Department of Neurosurgery and Nuclear Medicine, Nakamura Memorial Hospital, Sapporo, Japan (J.N.), and the Department of Clinical Physiology/Nuclear Medicine, Bispebjerg Hospital, Copenhagen, Denmark (B.S., N.A.L.).
Correspondence to Jyoji Nakagawara, MD, Department of Neurosurgery and Nuclear Medicine, Nakamura Memorial Hospital, South-1, West-14, Chuo-ku, Sapporo, 060, Japan. E-mail george@med.nmh.or.jp.
Background and Purpose [123I]Iomazenil is a specific radioligand for the central benzodiazepine receptor that may be useful as an indicator of the intactness of cortical neurons after focal cerebral ischemia. We evaluated the binding of this receptor in reperfused cortex among patients with ischemic stroke to detect viable neurons in cortex that appeared structurally intact on conventional neuroimaging studies.
Methods Fourteen patients were selected by (1) angiography within 24 hours of onset showing embolic occlusion of an intracranial artery, (2) cerebral blood flow showing ischemia of moderate severity in 12 cases and spontaneous reflow in 2 cases, and (3) thrombolysis with reperfusion within 24 hours in most cases. Thirty reperfused cortical areas that remained structurally intact, 7 infarcted cortical areas, and 6 contralateral cerebellar areas with reduced blood flow were selected as regions of interest to estimate receptor binding 5 days to 23 months after the stroke. A two-compartment model was used to compute the distribution volume (Vd) of iomazenil in relative units, with Vd proportional to benzodiazepine receptor concentration. The side-to-side asymmetry ratio of Vd was calculated.
Results The mean asymmetry ratio was 0.89±0.11 (range, 0.64 to 1.05), 0.50±0.15 (range, 0.23 to 0.67), and 0.97±0.05 (range, 0.90 to 1.04) in reperfused cortex, infarcted cortex, and contralateral cerebellum, respectively. Compared with unity, both reperfused cortex and infarcted cortex showed significant decrease of Vd (P<.00l). Contralateral cerebellum showing diaschisis had no reduction of Vd. On MRI, obtained 3 or 6 months after the stroke, mild cortical atrophy was observed in two reperfused areas where the asymmetry ratio was moderately reduced (0.64 and 0.80).
Conclusions The reduction of benzodiazepine receptor concentration in reperfused cortex that remained structurally intact is likely to be the result of injury involving only a limited number of neurons (ie, incomplete infarction). Our data suggest that the degree of viability of ischemic cortex apparently salvaged by early reperfusion can be quantified by iomazenil.
Key Words: cerebral blood flow • cerebral ischemia • reperfusion • tomography, emission-computed
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