Benzodiazepine receptors in chronic cerebrovascular disease: Comparison with blood flow and metabolism

The brain benzodiazepine (BZD) receptor distribution in patients with chronic cerebrovascular disease was assessed with ¹²³I-iomazenil (IMZ) SPECT, and the findings were compared with the data for the cerebral blood flow (CBF) and cerebral metabolism. Methods: We examined nine patients with chronic cerebrovascular diseases, six patients with cerebral infarction and three with moyamoya disease. Iodine-123-IMZ SPECT images were obtained for 15 min, 3 hr after the administration of 167 or 222 MBq ¹²³I-IMZ. In seven patients, the CBF and oxygen metabolism were measured by the ¹⁵O steady- state method. In two patients, the CBF and glucose metabolism were measured by ^99mTc-HMPAO SPECT and ¹⁸F-fluoro-2-deoxy-D-glucose-PET, respectively. The brain was initially classified into 18 regions, and abnormalities in the BZD receptor distribution, CBF and cerebral metabolism were visually evaluated. The count ratio of lesion-to-contralateral normal region (L-to-C ratio) was then used for comparison. Results: In the core of the infarct, the ¹²³I-IMZ uptake decreased (L-to-C ratios of the blood flow 0.42 ± 0.26; metabolism 0.45 ± 0.24; and ¹²³I-IMZ uptake 0.46 ± 0.14). In the peri- infarct region, the ¹²³I-IMZ uptake slightly decreased (L-to-C ratios of 0.81, 0.82 and 0.89, respectively). In the region of misery perfusion, the ¹²³I-IMZ uptake was preserved (L-to-C ratios of 0.73, 1.07 and 1.02, respectively). In the remote deafferentated areas in the ipsilateral cerebrum, the ¹²³I-IMZ uptake was preserved (L-to-C ratios of 0.76 ± 0.10, 0.75 ± 0.04 and 0.98 ± 0.05, respectively). In the remote areas in the contralateral cerebellum, the ¹²³I-IMZ uptake was preserved (L-to-C ratios of 0.84 ± 0.08, 0.85 ± 0.04 and 0.94 ± 0.05, respectively). Conclusion: The BZD receptor distribution, as measured by ¹²¹³I-IMZ SPECT, is not considered to reflect neuronal function, but it may reflect neuronal cell viability. Iodine-123-IMZ SPECT may, therefore, hold premise as a potential probe for neuronal damage.