• Open Access

Clinical characteristics and pathophysiological mechanisms of focal and diffuse traumatic brain injury

Authors

  • Teuntje M. J. C. Andriessen,

    1. Department of Neurology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
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    • Both authors contributed equally to the paper.

  • Bram Jacobs,

    1. Department of Neurology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
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    • Both authors contributed equally to the paper.

  • Pieter E. Vos

    Corresponding author
    1. Department of Neurology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
      Correspondence to: Pieter E. VOS, M.D., Ph.D.,
      Department of Neurology (935),
      Radboud University Nijmegen Medical Centre,
      P.O. Box 9101, 6500 HB, Nijmegen, The Netherlands.
      Tel.: + 31 24 3613396
      Fax: + 31 24 3541122
      E-mail: P.Vos@neuro.umcn.nl
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Correspondence to: Pieter E. VOS, M.D., Ph.D.,
Department of Neurology (935),
Radboud University Nijmegen Medical Centre,
P.O. Box 9101, 6500 HB, Nijmegen, The Netherlands.
Tel.: + 31 24 3613396
Fax: + 31 24 3541122
E-mail: P.Vos@neuro.umcn.nl

Abstract

  • • Introduction
  • • Classifying TBI
    • - Clinical injury severity
    • - Focal injury or diffuse injury
  • • Clinical characteristics
    • - Coma, confusion and subacute impairments
    • - Imaging TBI
    • - Focal and diffuse TBI: separate entities?
  • • Pathophysiological mechanisms of focal injury
    • - The essentials: glutamate and Ca2+
  • • Pathophysiological mechanisms of diffuse injury
    • - A heterogeneous cascade of changes
    • - After axonal disconnection
  • • Conclusions

Traumatic brain injury (TBI) is a frequent and clinically highly heterogeneous neurological disorder with large socioeconomic consequences. TBI severity classification, based on the hospital admission Glasgow Coma Scale (GCS) score, ranges from mild (GCS 13–15) and moderate (GCS 9–12) to severe (GCS ≤ 8). The GCS reflects the risk of dying from TBI, which is low after mild (∼1%), intermediate after moderate (up to 15%) and high (up to 40%) after severe TBI. Intracranial damage can be focal, such as epidural and subdural haematomas and parenchymal contusions, or diffuse, for example traumatic axonal injury and diffuse cerebral oedema, although this distinction is somewhat arbitrary. Study of the cellular and molecular post-traumatic processes is essential for the understanding of TBI pathophysiology but even more to find therapeutic targets for the development of neuroprotective drugs to be eventually used in human beings. To date, studies in vitro and in vivo, mainly in animals but also in human beings, are unravelling the pathological TBI mechanisms at high pace. Nevertheless, TBI pathophysiology is all but completely elucidated. Neuroprotective treatment studies in human beings have been disappointing thus far and have not resulted in commonly accepted drugs. This review presents an overview on the clinical aspects and the pathophysiology of focal and diffuse TBI, and it highlights several acknowledged important events that occur on molecular and cellular level after TBI.

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