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Research paper
A longitudinal MRI study of traumatic axonal injury in patients with moderate and severe traumatic brain injury
  1. Kent Gøran Moen1,2,
  2. Toril Skandsen1,3,
  3. Mari Folvik4,
  4. Veronika Brezova5,
  5. Kjell Arne Kvistad4,5,
  6. Jana Rydland4,
  7. Geoffrey T Manley6,
  8. Anne Vik1,2
  1. 1Department of Neuroscience, Norwegian University of Science and Technology (NTNU), Trondheim, Norway
  2. 2Department of Neurosurgery, St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway
  3. 3Department of Physical Medicine and Rehabilitation, St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway
  4. 4Department of Diagnostic Imaging, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway
  5. 5Department of Circulation and Diagnostic Imaging, Norwegian University of Science and Technology (NTNU), Trondheim, Norway
  6. 6Department of Neurosurgery, Brain and Spinal injury Center, University of California, San Francisco, USA
  1. Correspondence to Dr K G Moen, Department of Neuroscience, Norwegian University of Science and Technology (NTNU), Trondheim N-7489, Norway; kent.g.moen{at}ntnu.no

Abstract

Objective To study the evolution of traumatic axonal injury (TAI) detected by structural MRI in patients with moderate and severe traumatic brain injury (TBI) during the first year and relate findings to outcome.

Methods 58 patients with TBI (Glasgow Coma Scale score 3–13) were examined with MRI at a median of 7 days, 3 months and 12 months post injury. TAI lesions were evaluated blinded and categorised into three stages based on location: hemispheres, corpus callosum and brainstem. Lesions in T2* weighted gradient echo (GRE), fluid attenuated inversion recovery (FLAIR) and diffusion weighted imaging (DWI) were counted and FLAIR lesion volumes were estimated. Inter-rater reliability score was calculated. Outcome was assessed 12 months post injury using the Glasgow Outcome Scale Extended.

Results In the initial MRI, 31% had brainstem lesions compared with 17% at 3 months (p=0.008). In the FLAIR sequences, number and volumes of lesions were reduced from early to 3 months (p<0.001). In T2*GRE sequences, the number of lesions persisted at 3 months but was reduced at 12 months (p=0.007). The number of lesions in DWI and volume of FLAIR lesions on early MRI predicted worse clinical outcome in adjusted analyses (p<0.05).

Conclusion This is the first study to demonstrate and quantify attenuation of non-haemorrhagic TAI lesions on structural MRI during the first 3 months after TBI; most importantly, the disappearance of brainstem lesions. Haemorrhagic TAI lesions attenuate first after 3 months. Only early MRI findings predicted clinical outcome after adjustment for other prognostic factors. Hence valuable clinical information may be missed if MRI is performed too late after TBI.

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Footnotes

  • Funding KGM and TS have, during the study period, received a research grant from the liaison committee between the Central Norway Regional Health Authority (RHA) and the Norwegian University of Science and Technology (NTNU). VB has, during the study period, received a research grant from the National Resource Center for fMRI, Department of Diagnostic Imaging, St Olav University Hospital.

  • Competing interests None.

  • Ethics approval The local Regional Ethical Committee for Health Region Mid-Norway approved the study.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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