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The mechanism of crossed cerebellar diaschisis (CCD) is considered to be secondary hypoperfusion due to neural deactivation. To elucidate the hemodynamics during neural deactivation, the hemodynamics of CCD was investigated. The cerebral blood flow (CBF), cerebral blood volume (CBV), cerebral oxygen extraction fraction (OEF), cerebral metabolic rate of oxygen (CMRO2), and vascular responses to hypercapnia and acetazolamide stress for CCD were measured in 20 patients with cerebrovascular disease by positron emission tomography with H2(15O), C15O, and 15O2. Vascular responses to hypercapnia and acetazolamide stress were almost the same between CCD side and unaffected side of the cerebellum, a finding that supports the idea that the mechanism of CCD is secondary hypoperfusion due to neural deactivation. The degree of decrease in CBF on the CCD side was almost the same as that in CBV, indicating that vascular blood velocity does not change during neural deactivation. The relation between CBF and CBV of the CCD and unaffected sides was CBV = 0.29 CBF0.56. On the CCD side, the degree of deerease in CMRO2 was less than that in CBF, resulting in a significantly increased OEF. The increased OEF along with the decreased CBV on the CCD side might indicate that neural deactivation primarily causes vasoconstriction rather than a reduction of oxygen metabolism.

The results of our study suggest that not all atherosclerotic plaques show high FDG accumulation. FDG-PET studies of plaques with the use of fused images can potentially provide detailed information about atherosclerosis.

The internal mammary artery contributes to the perfusion of lesions responsible for hemoptysis when the basic lesion involves the pulmonary parenchyma adjacent to the anterior pleural surface. Initial distal occlusion of the internal mammary artery may improve the efficacy of embolization of this artery for hemoptysis.

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