Advertisement

Induction of Brain Hypothermia

  • Nariyuki Hayashi
  • Dalton W. Dietrich

Abstract

The state of neuronal damage after severe brain injury may progress with time. Similary, the target of management may also differ within the injury time window in severely brain-injured patients. In addressing this clinical issue, early management is much easier and simpler than delayed induction of hypothermia treatment. Accordingly, the main targets of treatment at early and late stages need to be defined. In some cases, control of brain edema and intracranial pressure (ICP) elevation have been the focus of initial treatment for neuroprotection in severely brain-injured patients [2,11,14]. However, this approach is not correct because brain edema and ICP elevation occur as a result of neuronal hypoxia, adequate metabolic supply to the injured neurons, cerebral blood flow (CBF) disturbances, unsuccessful management of cardiopulmonary dysfunction, and hemoglobin dysfunction [4]. For brain hypothermia management of severe brain injury, the starting time is important and the main target of management will change according to the time after insults and trauma [3,4].

Keywords

Brain Edema Severe Brain Injury Early Induction Injured Neuron Critical Head Injury 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Baker AJ, Zornow MH, Scheller MS, Yaksh TL, Skilling SR, Smullin DH, Larson AA, Kuczenski R (1991) Changes in extrascellular concentrations of glutamate, aspartate, glycine, dopamine, serotonin, and dopamine metabolites after transient global ischemia in the rat. J Neurochemistry 57:1370–1379CrossRefGoogle Scholar
  2. 2.
    Feng H, Huang G, Gao L, Tan H, Liao X (2000) Effect of intracranial pressure and cerebral perfusion pressure on outcome prediction of severe traumatic brain injury. Chin J Traumatol 3:226–230PubMedGoogle Scholar
  3. 3.
    Hayashi N (1995) Cerebral hypothermia treatment. In: Hayashi N (ed) Cerebral hypothermia treatment. Sogo Igaku, Tokyo, pp 1–105Google Scholar
  4. 4.
    Hayashi N (2000) Enhanced neuronal damage in severely brain injured patients by hypothalamus, pituitary, and adrenal axis neuro-hormonal changes. In: Hayashi N (ed) Brain hypothermia. Springer, Berlin Heidelberg New York Tokyo, pp 3–26CrossRefGoogle Scholar
  5. 5.
    Hayashi N (2000) The clinical issue and effectiveness of brain hypothermia treatment for severe brain injured patients. In: Hayashi N (ed) Brain hypothermia. Springer, Berlin Heidelberg New York Tokyo, pp 121–151CrossRefGoogle Scholar
  6. 6.
    Hayashi N, Hirayama T, Utagawa A (1994) The cerebral thermo-pooling and hypothermia treatment of critical head injury patients. In: Nagai H (ed) Intracranial pres sure IX. Springer, Berlin Heidelberg New York Tokyo, pp 589–599Google Scholar
  7. 7.
    Hayashi N, Utagawa A, Kinosita K, Izumi T (1999) Application of a novel technique for clinical evaluation of nitric oxide-induced free radical reactions in ICU patients. Cell Mol Neurobiol 19:3–17PubMedCrossRefGoogle Scholar
  8. 8.
    Kagawa M, Nagao S, Bemana I (1996) Arginine vasopressin receptor antagonists for treatment of vasogenic brain edema: an experimental study. J Neurotrauma 13: 273–279PubMedCrossRefGoogle Scholar
  9. 9.
    Kow LM, Pfaff DW (1986) Vasopressin excites ventromedial hypothalamus glucose-responsive neurons in vitro. Physiol Behav 37:153–158PubMedCrossRefGoogle Scholar
  10. 10.
    Lin TW, Kuo YS (1996) Acute pulmonary oedema following administration of vasopressin for control of massive GI tract haemorrhage in a major burn patient. Burns 22:73–75PubMedCrossRefGoogle Scholar
  11. 11.
    Macintosh TK (1994) Neurological sequele of traumatic brain injury: therapeutic implications. Cerebrovasc Brain Metab Rev 6:109–162Google Scholar
  12. 12.
    Okuda C, Saito A, Miyazaki M, Kuriyama K (1986) Alteration of the turnover of dopamine and 5-hydroxytryptamine in rat brain associated with hypothermia. Pharmacol Biochem Behav 25:79–83CrossRefGoogle Scholar
  13. 13.
    Silvka A, Coben G (1985) Hydroxyl radical attack on dopamine. J Biol Chem 260:15466–15472Google Scholar
  14. 14.
    Suarez JI (2001) Treatment of acute brain edema. Rev Neurol 32:275–281PubMedGoogle Scholar

Copyright information

© Springer Japan 2004

Authors and Affiliations

  • Nariyuki Hayashi
    • 1
    • 2
  • Dalton W. Dietrich
    • 3
    • 4
  1. 1.Nihon University Emergency Medical CenterTokyoJapan
  2. 2.Department of Emergency and Critical Care MedicineNihon University School of MedicineTokyoJapan
  3. 3.Department of Neurological Surgery, Neurology and Cell Biology and AnatomyUniversity of Miami School of MedicineMiamiUSA
  4. 4.The Miami Project to Cure ParalysisMiamiUSA

Personalised recommendations