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Hemodynamic changes during neural deactivation in human brain: A positron emission tomography study of crossed cerebellar diaschisis

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Abstract

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, and15O2. 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 decrease 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.

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References

  1. Lenzi GL, Frackowiak RS, Jones T. Cerebral oxygen metabolism and blood flow in human cerebral ischemic infarction.J Cereb Blood Flow Metab 1982; 2: 321–335.

    PubMed  CAS  Google Scholar 

  2. Martin WR, Raichle ME. Cerebellar blood flow and metabolism in cerebral hemisphere infarction.Ann Neurol 1983; 14: 168–176.

    Article  PubMed  CAS  Google Scholar 

  3. Pantano P, Baron JC, Samson Y, Bousser MG, Derouesne C, Comar D. Crossed cerebellar diaschisis. Further studies.Brain 1986; 109: 677–694.

    Article  PubMed  Google Scholar 

  4. Yamauchi H, Fukuyama H, Kimura J. Hemodynamic and metabolic changes in crossed cerebellar hypoperfusion.Stroke 1992; 23: 855–860.

    PubMed  CAS  Google Scholar 

  5. Bogsrud TV, Rootwelt K, Russell D, Nyberg-Hansen R. Acetazolamide effect on cerebellar blood flow in crossed cerebral-cerebellar diaschisis.Stroke 1990; 21: 52–55.

    PubMed  CAS  Google Scholar 

  6. Ishii K, Kanno I, Uemura K, Hatazawa J, Okudera T, Inugami A, et al. Comparison of carbon dioxide responsiveness of cerebellar blood flow between affected and unaffected sides with crossed cerebellar diaschisis.Stroke 1994; 25: 826–830.

    PubMed  CAS  Google Scholar 

  7. Ito H, Takahashi K, Hatazawa J, Kim SG, Kanno I. Changes in human regional cerebral blood flow and cerebral blood volume during visual stimulation measured by positron emission tomography.J Cereb Blood Flow Metab 2001; 21: 608–612.

    Article  PubMed  CAS  Google Scholar 

  8. Iida H, Miura S, Kanno I, Ogawa T, Uemura K. A new PET camera for noninvasive quantitation of physiological functional parametric images: Headtome-V-dual. InQuantification of Brain Function Using PET, Myers R, Cunningham V, Bailey D, Jones T (eds). San Diego: Academic Press, 1996, 57–61.

    Google Scholar 

  9. Martin WR, Powers WJ, Raichle ME. Cerebral blood volume measured with inhaled C15O and positron emission tomography.J Cereb Blood Flow Metab 1987; 7: 421–426.

    PubMed  CAS  Google Scholar 

  10. Mintun MA, Raichle ME, Martin WR, Herscovitch P. Brain oxygen utilization measured with O-15 radiotracers and positron emission tomography.J Nucl Med 1984; 25: 177–187.

    PubMed  CAS  Google Scholar 

  11. Herscovitch P, Mintun MA, Raichle ME. Brain oxygen utilization measured with oxygen-15 radiotracers and positron emission tomography: Generation of metabolic images.J Nucl Med 1985; 26: 416–417.

    PubMed  CAS  Google Scholar 

  12. Iida H, Jones T, Miura S. Modeling approach to eliminate the need to separate arterial plasma in oxygen-15 inhalation positron emission tomography.J Nucl Med 1993; 34: 1333–1340.

    PubMed  CAS  Google Scholar 

  13. Lammertsma AA, Jones T. Correction for the presence of intravascular oxygen-15 in the steady-state technique for measuring regional oxygen extraction ratio in the brain: 1. Description of the method.J Cereb Blood Flow Metab 1983; 3: 416–424.

    PubMed  CAS  Google Scholar 

  14. Iida H, Kanno I, Miura S, Murukami M, Takahashi K, Uemura K. Error analysis of a quantitative cerebral blood flow measurement using H2 15O autoradiography and positron emission tomography, with respect to the dispersion of the input function.J Cereb Blood Flow Metab 1986; 6: 536–545.

    PubMed  CAS  Google Scholar 

  15. Iida H, Higano S, Tomura N, Shishido F, Kanno I, Miura S, et al. Evaluation of regional differences of tracer appearance time in cerebral tissues using [15O] water and dynamic positron emission tomography.J Cereb Blood Flow Metab 1988; 8: 285–288.

    PubMed  CAS  Google Scholar 

  16. Raichle ME, Martin WR, Herscovitch P, Mintun MA, Markham J. Brain blood flow measured with intravenous H2 15O. II. Implementation and validation.J Nucl Med 1983; 24: 790–798.

    PubMed  CAS  Google Scholar 

  17. Kanno I, Iida H, Miura S, Murakami M, Takahashi K, Sasaki H, et al. A system for cerebral blood flow measurement using an H2 15O autoradiographic method and positron emission tomography.J Cereb Blood Flow Metab 1987; 7: 143–153.

    PubMed  CAS  Google Scholar 

  18. Kanno I, Uemura K, Higano S, Murakami M, Iida H, Miura S, et al. Oxygen extraction fraction at maximally vasodilated tissue in the ischemic brain estimated from the regional CO2 responsiveness measured by positron emission tomography.J Cereb Blood Flow Metab 1988; 8: 227–235.

    PubMed  CAS  Google Scholar 

  19. Powers WJ, Grubb RL Jr, Raichle ME. Physiological responses to focal cerebral ischemia in humans.Ann Neurol 1984; 16: 546–552.

    Article  PubMed  CAS  Google Scholar 

  20. Grubb RL Jr, Raichle ME, Eichling JO, Ter-Pogossian MM. The effects of changes in PaCO2 on cerebral blood volume, blood flow, and vascular mean transit time.Stroke 1974; 5: 630–639.

    PubMed  Google Scholar 

  21. Shimosegawa E, Kanno I, Hatazawa J, Fujita H, Iida H, Miura S, et al. Photic stimulation study of changing the arterial partial pressure level of carbon dioxide.J Cereb Blood Flow Metab 1995; 15: 111–114.

    PubMed  CAS  Google Scholar 

  22. Inao S, Tadokoro M, Nishino M, Mizutani N, Terada K, Bundo M, et al. Neural activation of the brain with hemodynamic insufficiency.J Cereb Blood Flow Metab 1998; 18: 960–967.

    Article  PubMed  CAS  Google Scholar 

  23. Kuwabara Y, Ichiya Y, Sasaki M, Yoshida T, Fukumura T, Masuda K, et al. PET evaluation of cerebral hemodynamics in occlusive cerebrovascular disease pre- and postsurgery.J Nucl Med 1998; 39: 760–765.

    PubMed  CAS  Google Scholar 

  24. Raichle ME. Behind the scenes of functional brain imaging: A historical and physiological perspective.Proc Natl Acad Sci USA 1998; 95: 765–772.

    Article  PubMed  CAS  Google Scholar 

  25. Wenzel R, Wobst P, Heekeren HH, Kwong KK, Brandt SA, Kohl M, et al. Saccadic suppression induces focal hypooxygenation in the occipital cortex.J Cereb Blood Flow Metab 2000; 20: 1103–1110.

    Article  PubMed  CAS  Google Scholar 

  26. Fox PT, Raichle ME. Focal physiological uncoupling of cerebral blood flow and oxidative metabolism during somatosensory stimulation in human subjects.Proc Natl Acad Sci USA 1986; 83: 1140–1144.

    Article  PubMed  CAS  Google Scholar 

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Authors and Affiliations

  1. Department of Radiology and Nuclear Medicine, Akita Research Institute of Brain and Blood Vessels, 6-10 Senshu-kubota-machi, 010-0874, Akita, Japan

    Hiroshi Ito, Iwao Kanno, Eku Shimosegawa, Hajime Tamura, Kumiko Okane & Jun Hatazawa

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  1. Hiroshi Ito
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  2. Iwao Kanno
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  3. Eku Shimosegawa
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  4. Hajime Tamura
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  5. Kumiko Okane
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  6. Jun Hatazawa
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Correspondence to Hiroshi Ito.

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Ito, H., Kanno, I., Shimosegawa, E. et al. Hemodynamic changes during neural deactivation in human brain: A positron emission tomography study of crossed cerebellar diaschisis. Ann Nucl Med 16, 249–254 (2002). https://doi.org/10.1007/BF03000103

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  • DOI: https://doi.org/10.1007/BF03000103

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