Magnetic Resonance Studies in Human Brain Oedema Following Administration of Hyperosmotic Agents

Special References to Relaxation Times and Proton MRS
  • M. Niiro
  • T. Asakura
  • K. Yatsushiro
  • M. Sasahira
  • K. Terada
  • T. Fujimoto
Conference paper
Part of the Acta Neurochirurgica book series (NEUROCHIRURGICA, volume 51)


Changes of proton relaxation times (T1 and T2) and proton Magnetic Resonance Spectroscopy (MRS) were studied in patients with brain oedema following administration of hyperosmotic agents. Relaxation times of oedema tended to decrease following infusion of hyperosmotic agents. In most patients examined, changes of relaxation times tended to achieve their lowest value at 30–60 minutes after infusion. However, the changes of relaxation times were not uniform. In some patients, relaxation times continued to decrease for more than 2 hours, while in other patients relaxation times which had earlier decreased subsequently had increased at 2 hours. The peak of water components, obtained by SIDAC (Spectroscopic Imaging by Dephasing Amplitude Changing) method was observed to change as did relaxation times. Changes of relaxation times and the peak of water component may vary depending upon factors including the kinds of lesions causing oedema, phase of oedema (acute or chronic), etc. Proton relaxation times and the peak of water component obtained by proton MRS were useful in evaluating the changes of oedematous area.


Relaxation Time Brain Oedema Proton Magnetic Resonance Spectroscopy Spectroscopic Image Magnetic Resonance Study 


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  1. 1.
    Albright AL, Latchaw RE, Robinson AG (1984) Intracranial and systemic effects of osmotic and oncotic therapy in experimental cerebral oedema. J Neurosurg 60: 481–489PubMedCrossRefGoogle Scholar
  2. 2.
    Horikawa Y, Naruse S, Tanaka C et al (1986) Proton NMR relaxation times in ischaemic brain oedema. Stroke 17: 1149–1152PubMedCrossRefGoogle Scholar
  3. 3.
    Kamiura T (1987) Effects of mannitol on ischaemic brain oedema. Teikyo Med J 10: 11–18Google Scholar
  4. 4.
    Kamman RL, Go KG et al (1988) Nuclear magnetic resonance relaxation in experimental brain oedema. Magn Reson Med 6: 265–274PubMedCrossRefGoogle Scholar
  5. 5.
    Kato H, Kogure H, Otomo H et al (1986) Magnetic resonance imaging of experimental cerebral ischaemia. Brain Nerve 38: 295–302PubMedGoogle Scholar
  6. 6.
    Miyazaki T, Yamamoto T, Iriguchi N (1989) Spectroscopic imaging by dephasing amplitude changing (SIDAC). Radiat Med 7: 1–15PubMedGoogle Scholar
  7. 7.
    Muizelaar JP, Wei EP, Kontos HA et al (1983) Mannitol causes compensatory cerebral vasoconstriction and vasodilation in response to blood viscosity changes. J Neurosurg 59: 822–828PubMedCrossRefGoogle Scholar
  8. 8.
    Naruse S, Horikawa Y, Tanaka C et al (1982) Nuclear magnetic resonance studies of effects of glycerol on brain oedema. Brain Nerve 34: 805–809PubMedGoogle Scholar
  9. 9.
    Nath F, Galbraith S (1986) The effects of mannitol on cerebral white matter content. J Neurosurg 65: 42–43Google Scholar
  10. 10.
    Takagi H, Saito T, Kitahara T et al (1984) The mechanism of ICP reducing effect of mannitol. Brain Nerve 36: 1905–1102Google Scholar
  11. 11.
    Wilkinson HA, Rosenfeld S (1983) Furosemide and mannitol in the treatment of acute experimental intracranial hypertension. Neurosurgery 12: 405–410PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag 1990

Authors and Affiliations

  • M. Niiro
    • 4
  • T. Asakura
    • 1
  • K. Yatsushiro
    • 1
  • M. Sasahira
    • 2
  • K. Terada
    • 2
  • T. Fujimoto
    • 3
  1. 1.Departments of Neurosurgery, Faculty of MedicineKagoshima UniversityFujimoto HospitalJapan
  2. 2.Department of NeurosurgeryFujimoto HospitalJapan
  3. 3.Department of PsychiatryFujimoto HospitalJapan
  4. 4.Department of Neurosurgery, Faculty of MedicineUniversity of KagoshimaUsuki-cho, Kagoshima City 890Japan

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