Functional reorganisation of memory following traumatic brain injury: A study with H215O PET (editorial commentary)

Richardson, J. T. E.. (2002). Functional reorganisation of memory following traumatic brain injury: A study with H215O PET (editorial commentary). Journal of Neurology Neurosurgery and Psychiatry, 73(2) p. 111.



Traumatic brain injury (TBI) is a major cause of deaths following accidents and a major cause of disablement and morbidity among the survivors. The clinical problem of treating this vast number of patients is not going to be solved by a dramatic medical breakthrough. Rather, it must be tackled by seeking a better appreciation of the condition that these people present. The paper by Levine et al (this issue, pp 173–81)1 adds to the growing body of studies in which neuroimaging techniques have been used to study long term changes in survivors of moderate or severe TBI.

Levine et al carried out PET in six patients who had sustained TBI roughly four years previously and in 11 healthy controls. Separate scans were obtained during the encoding and retrieval phases of a simple cued recall task and attention was focused on the differences in activation between the two phases. The individual findings varied with focal lesions. However, as a group they had more widespread activation during the retrieval phase than the controls, with reduced activation in areas involved in normal memory retrieval. This was regarded as evidence for neural reorganisation due to diffuse axonal injury.

This study combined the application of neuroimaging technology with an understanding of the cognitive mechanisms involved in the relevant experimental task. Levine et al also paid due attention to both between group variation and within group variation. They considered but rejected the idea that these changes might just have been an artefact of impaired performance. Indeed, the same pattern was apparent in three patients whose retrieval was at a normal level, although some aspects were seen only in the three patients with poor performance.

Two issues need to be addressed in further research. Firstly, would similar changes be seen in patients with mild rather than severe TBI? The prevalence of mild TBI is many times greater than that of severe TBI, and many suspect that mild TBI may give rise to persistent yet subtle deficits even in patients who otherwise make a good functional recovery.2 Of course, such deficits may have predated the TBI and were not caused by it.3 This problem is inherent in any study that compares groups defined on the basis of their clinical history.

So a second issue raised by this study is this: are the apparent differences between patients with TBI causally related to their injuries? Ideally, one would like to have premorbid evidence from the people in question. Of course, the number of people who have undergone any specific PET procedure before sustaining a TBI is vanishingly small, but other evidence may be available. Bigler and Snyder4 compared computed tomography with magnetic resonance imaging carried out in four people before and after they sustained mild TBI. The authors failed to find any gross differences but more detailed analyses might have revealed clinically significant changes. With the increasingly widespread use of neuroimaging techniques, comparisons of this sort should be entirely feasible in the future.

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