Traumatic Brain Injury: Recovery, Prediction, and the Clinician

WHAT DOES ONE SAY to the family of a young person who has been in an accident and is just regaining consciousness? The joy and relief of survival are very quickly followed by questions about the future—about how soon a return to normal life will happen, about what sort of treatment or rehabilitation will be needed, and so on. The possibility of long-term disability—that the person may never regain completely the old roles, abilities, and attributes—may only occur to a minority of families at this stage. The possibility of further decline after the acute recovery phase is an even rarer thought in the minds of both families and professionals.

This collection of articles is outstanding in a number of ways—in giving the clinician a sense of what can be said to the worried family and what cannot, and in offering researchers important insights from imaging and neuropsychology into the possible mechanisms for the postacute recovery process. But they are important in a third, even more important way: in yielding some real pointers as to how the course of recovery may be influenced.

TBI is an invisible disability in many parts of the world. It is common for people to be discharged after treatment of their orthopedic and other injuries into a bewildering world, which looks and feels very different now that the walking and talking person has profoundly changed. The development of imaging and other methods for diagnosing these often invisible problems may be one of the most important ways of increasing the visibility of the disability.

Wei et al1 show how DTI can distinguish between spinal cord–injured persons with and without a TBI, the former showing white matter changes in the genu and splenium of the corpus callosum, among other areas. Given that standard MRI often fails to reveal pathologies in people who have had TBI and who are showing significant neuropsychological deficits, the possible use of DTI to increase the capacity for diagnosis, and hence the visibility, of TBI is exciting. Bradbury et al2 highlight how important the TBI diagnosis is in the overall pathology and functional status of people who have had spinal cord injury.

Greenberg et al3 report a study of the highest importance to TBI research, in which progressive deterioration in crucial frontal and temporal white matter was observed over a 5-month 2.5-year postacute period. The complementary study by Ng et al4 shows that in 10 out of 14 people over a comparable 2-year postacute period, quantitative MRI-measured atrophy in the hippocampi was observed, as well as an increased cerebrospinal fluid volume. Taken together with the neuropsychological study by Till et al5 showing that roughly a quarter of persons showed a decline in cognitive function from 1 to 2.5 years postinjury, this collection of studies give a very important—if not daunting—picture on which clinicians will partly base their predictions when talking to people and families affected by TBI.

The study by Green et al6 of return to productivity—achieved by roughly 30% of a sample of moderate to severe TBI 1 year postinjury—is of great interest also. The superior methodology of this study compared with previous ones, eliminating motor slowness in measuring cognitive speed, for instance, yields some important and clinically very useful findings. Memory (and only Logical Memory—a memory test with a strong executive function loading) and executive function emerge as significant predictors of this most crucial of outcomes: return to productivity. Timed tests have no particular predictive value, confirming that the role of speed of processing in mediating the deficits of TBI is highly dubious compared with the executive functions so easily disrupted by white matter damage. Assessments at 2 months postinjury did not significantly predict return to productivity, but the 5-month assessment did, quite strongly. In another article examining prediction of outcome, Green et al7 demonstrated that using mixed-effects modeling and multiple assessment points, we can look at how (and not just whether) certain moderators may influence the pattern of cognitive recovery (eg, an impact on early vs late recovery). Such a “recuperative” impact of moderators has implications for the mechanisms of impairment and recovery (speaking to cognitive reserve capacity, for example) and on how we might want to deliver therapies. These are studies packed full of clinically applicable information that will help clinicians talk to the family in practical, robust ways.

Till et al5 found that those declining neuropsychologically between 12 and 24 years had a significantly smaller amount of therapy at 4.5 months postinjury, and this relationship was not mediated by the severity of the injury. While alcohol and insurance issues may explain this relationship, it is also possible that there is a causal link between the therapy and the decline, although this can only be a hypothesis at this stage. But what of the postacute apoptotic brain changes in white and grey matter, which should be such a source of concern to clinicians and families? Are any of these changes experience-dependent? Are they at least partly modifiable by behavioral or pharmacologic interventions (or indeed a combination of the 2)?

This series of studies points to a new level of sophistication in rehabilitation of TBI. They point to a future in which the nature and timing of rehabilitation are grounded in excellent science, state-of-the-art imaging, and a strong evidence base of effectiveness.8 The opening article by Christensen et al9 provides the context for the above articles, describing the sound methodologies and powerful statistical approaches of this larger program of research. The study by Bradbury et al10 of cognitive behavior therapy for TBI is an excellent exemplar of the possibility of behavior change, and the challenge now is first to develop more such methods and second to integrate them into a theoretic understanding of the nature of the brain impairment and its psychologic downstream effects.

Or perhaps one should also consider the possibility of psychologic impairments, which have downstream brain effects. The effects of stress on hippocampal function in nonbrain-damaged people is an example of this,11 and it may be that the shockingly changed world that the brain-injured person faces results in psychologic stressors that exacerbate the brain impairments caused by the original injury. It is not surprising, then, that the meta-analysis by Ruttan et al12 confirmed chronic neuropsychological impairments at both 1 year and 4.5+ years postinjury.

This series of articles is of the highest importance and is likely to have far-reaching consequences for the lives of people with TBI and their families throughout the world.