DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY
COMMENTARIES
Would you rather have your brain injury at five or twenty-five? ROB FORSYTH Institute of Neuroscience, Newcastle University, Newcastle, UK. doi: 10.1111/dmcn.12397 This commentary is on the original article by Anderson et al. on pages 329–336 of this issue.
The age at injury debate is a long-running one in the field of paediatric acquired brain injury (ABI) research. In some respects, young brains appear remarkably robust to injury. Some studies of pre- and early postnatally acquired focal insults suggest milder cognitive deficits than would result from comparable insults in adults,1 and early functional hemispherectomy for treatment of intractable focal epilepsy can be well-tolerated. Such observations inevitably engender views that it is ‘better to be injured young’. In recent years, however, it has been recognized that this apparent resilience has a cost and does not hold for all forms of brain injury at all ages. Anderson et al.2 confirm previous findings of their group3 that early injuries (before the age of 2 or 3) are associated with particularly poor outcomes. The main challenge for empirical work of this nature is the difficulty of separating the age at injury effect itself from injury aetiology, anatomical extent, and the presence of comorbidities such as epilepsy, all of which are, to an extent, age-dependent and thus potential confounders.4 Contradictory messages in the literature about age at injury effects arise because different outcome domains are being considered in different clinical populations. The ‘young brains make remarkable accommodations after early injury’ position is particularly characteristic of literature on language outcomes after early focal injury. In contrast, poorer outcomes after young injury are an emphasis of the literature on cognitive outcome after (diffuse) traumatic brain injury.
At its heart this is a debate about the possible benefits of greater plasticity versus the challenge of having to complete the task of developmental maturation – ‘making a year’s progress every year’ – with an injured brain. This complex picture results from the interplay between age at injury and milestones in the development of the neural structures supporting the function(s) under consideration. After very early injury reconfiguration of cortical projections to and from distant targets can result in large-scale relocation of function to the uninjured cortex. One might hypothesize that such relocation is more possible for cortical functions that are more recent in evolutionary terms and supported by more pluripotent, less specialized cortex (e.g. language in contrast to vision). Once these projections are established however, the response to injury predominantly involves in situ reorganization of cortical maps and here an important idea proposed by that most prescient of neuroscientists, Donald Hebb, becomes relevant. On the basis of clinical observation of effects of pediatric frontal lobe injuries he hypothesized: ‘It appears that an early injury may prevent the development of some intellectual capacities that an equally extensive injury, at maturity, would not have destroyed. Some types of behavior that require a large amount of brain tissue for their first establishment can then persist when the amount of available tissue has been decreased. More fibers are necessary (for the first establishment of an assembly) than for its later function’.5 Naive views of plasticity of the immature brain have led to complacency in monitoring for, and under-recognition of, the late sequelae of ABI in young children. In this complex debate the paper by Anderson et al. provides an important reminder of the need to take ABI in very young children seriously and provide for long-term follow-up for possible emerging deficits.
REFERENCES 1. Stiles J, Reilly J, Paul B, Moses P. Cognitive develop-
3. Anderson V, Spencer-Smith M, Leventer R, et al.
5. Varier S, Kaiser M, Forsyth R. Establishing, versus
ment following early brain injury: evidence for neural
Childhood brain insult: can age at insult help us predict
maintaining, brain function: a neuro-computational
adaptation. Trends Cogn Sci 2005; 9: 136–43.
outcome? Brain 2009; 132: 45–56.
model of cortical reorganization after injury to the
2. Anderson VA, Spencer-Smith MM, Coleman L, et al.
4. Lidzba K, Wilke M, Staudt M, Krageloh-Mann I. Early
Predicting neurocognitive and behavioral outcome after
plasticity versus early vulnerability: the problem of het-
early brain insult. Dev Med Child Neurol 2014; 56: 329–
erogeneous lesion types. Brain 2009; 132: e128; author
36.
reply e129.
© 2014 Mac Keith Press
immature brain. J Int Neuropsychol Soc 2011; 17: 1030–8.
297
COMMENTARIES
Would you rather have your brain injury at five or twenty-five? ROB FORSYTH Institute of Neuroscience, Newcastle University, Newcastle, UK. doi: 10.1111/dmcn.12397 This commentary is on the original article by Anderson et al. on pages 329–336 of this issue.
The age at injury debate is a long-running one in the field of paediatric acquired brain injury (ABI) research. In some respects, young brains appear remarkably robust to injury. Some studies of pre- and early postnatally acquired focal insults suggest milder cognitive deficits than would result from comparable insults in adults,1 and early functional hemispherectomy for treatment of intractable focal epilepsy can be well-tolerated. Such observations inevitably engender views that it is ‘better to be injured young’. In recent years, however, it has been recognized that this apparent resilience has a cost and does not hold for all forms of brain injury at all ages. Anderson et al.2 confirm previous findings of their group3 that early injuries (before the age of 2 or 3) are associated with particularly poor outcomes. The main challenge for empirical work of this nature is the difficulty of separating the age at injury effect itself from injury aetiology, anatomical extent, and the presence of comorbidities such as epilepsy, all of which are, to an extent, age-dependent and thus potential confounders.4 Contradictory messages in the literature about age at injury effects arise because different outcome domains are being considered in different clinical populations. The ‘young brains make remarkable accommodations after early injury’ position is particularly characteristic of literature on language outcomes after early focal injury. In contrast, poorer outcomes after young injury are an emphasis of the literature on cognitive outcome after (diffuse) traumatic brain injury.
At its heart this is a debate about the possible benefits of greater plasticity versus the challenge of having to complete the task of developmental maturation – ‘making a year’s progress every year’ – with an injured brain. This complex picture results from the interplay between age at injury and milestones in the development of the neural structures supporting the function(s) under consideration. After very early injury reconfiguration of cortical projections to and from distant targets can result in large-scale relocation of function to the uninjured cortex. One might hypothesize that such relocation is more possible for cortical functions that are more recent in evolutionary terms and supported by more pluripotent, less specialized cortex (e.g. language in contrast to vision). Once these projections are established however, the response to injury predominantly involves in situ reorganization of cortical maps and here an important idea proposed by that most prescient of neuroscientists, Donald Hebb, becomes relevant. On the basis of clinical observation of effects of pediatric frontal lobe injuries he hypothesized: ‘It appears that an early injury may prevent the development of some intellectual capacities that an equally extensive injury, at maturity, would not have destroyed. Some types of behavior that require a large amount of brain tissue for their first establishment can then persist when the amount of available tissue has been decreased. More fibers are necessary (for the first establishment of an assembly) than for its later function’.5 Naive views of plasticity of the immature brain have led to complacency in monitoring for, and under-recognition of, the late sequelae of ABI in young children. In this complex debate the paper by Anderson et al. provides an important reminder of the need to take ABI in very young children seriously and provide for long-term follow-up for possible emerging deficits.
REFERENCES 1. Stiles J, Reilly J, Paul B, Moses P. Cognitive develop-
3. Anderson V, Spencer-Smith M, Leventer R, et al.
5. Varier S, Kaiser M, Forsyth R. Establishing, versus
ment following early brain injury: evidence for neural
Childhood brain insult: can age at insult help us predict
maintaining, brain function: a neuro-computational
adaptation. Trends Cogn Sci 2005; 9: 136–43.
outcome? Brain 2009; 132: 45–56.
model of cortical reorganization after injury to the
2. Anderson VA, Spencer-Smith MM, Coleman L, et al.
4. Lidzba K, Wilke M, Staudt M, Krageloh-Mann I. Early
Predicting neurocognitive and behavioral outcome after
plasticity versus early vulnerability: the problem of het-
early brain insult. Dev Med Child Neurol 2014; 56: 329–
erogeneous lesion types. Brain 2009; 132: e128; author
36.
reply e129.
© 2014 Mac Keith Press
immature brain. J Int Neuropsychol Soc 2011; 17: 1030–8.
297
