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Functional reorganisation of memory after traumatic brain injury: a study with H2150 positron emission tomography
  1. B Levine1,2,3,
  2. R Cabeza4,
  3. A R McIntosh1,2,
  4. S E Black1,3,
  5. C L Grady1,2,
  6. D T Stuss1,2,3
  1. 1Rotman Research Institute, Baycrest Centre for Geriatric Care, Toronto, Canada
  2. 2Department of Psychology, University of Toronto, Canada
  3. 3Department of Medicine (Neurology), University of Toronto
  4. 4Centre for Cognitive Neuroscience, Duke University, Durham, North Carolina, USA
  1. Correspondence to:
 Dr B Levine, Rotman Research Institute, Baycrest Centre for Geriatric Care, 3560 Bathurst Street, Toronto, Canada ON M6E 3A5;


Objective: To study the effects of moderate to severe traumatic brain injury (TBI) on the functional neuroanatomy supporting memory retrieval.

Methods: Subjects were six patients who had sustained a moderate to severe TBI about four years before scanning and had since made a good recovery. Eleven healthy young adults matched to the patients for age and education served as controls. An established H2150 positron emission tomography paradigm was used to elicit brain activations in response to memory retrieval. TBI patients' patterns of brain activation were compared statistically with those of control subjects. Both group and individual case data were analysed.

Results: Both TBI patients and controls engaged frontal, temporal, and parietal regions known to be involved in memory retrieval, yet the TBI patients showed relative increases in frontal, anterior cingulate, and occipital activity. The hemispheric asymmetry characteristic of controls was attenuated in patients with TBI. Reduced activation was noted in the right dorsomedial thalamus. Although local aspects of this pattern were affected by the presence of focal lesions and performance differences, the overall pattern was reliable across patients and comparable to functional neuroimaging results reported for normal aging, Alzheimer's disease, and other patients with TBI.

Conclusions: The TBI patients performed memory tasks using altered functional neuroanatomical networks. These changes are probably the result of diffuse axonal injury and may reflect either cortical disinhibition attributable to disconnection or compensation for inefficient mnemonic processes.

  • traumatic brain injury
  • memory
  • functional brain imaging
  • PET, positron emission tomography
  • TBI, traumatic brain injury
  • PASAT, paced auditory serial addition task
  • DAI, diffuse axonal injury

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  • Funding: this research was supported by the Canadian Institutes of Health Research, the Ontario Mental Health Foundation, and the Rotman Research Institute.

  • Competing interests: none declared.

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