Neuroplasticity following non-penetrating traumatic brain injury

The primary objective of this review is to examine the methodology and evidence for neuroplasticity operating in recovery from traumatic brain injury (TBI), as compared with previous findings in patients sustaining perinatal and infantile focal vascular lesions. The evidence to date indicates that the traditional view of enhanced reorganization of function after early focal brain lesions might apply to early focal brain lesions, but does not conform with studies of early severe diffuse brain injury. In contrast to early focal vascular lesions, young age confers no advantage in the outcome of severe diffuse brain injury. Disruption of myelination could potentially alter connectivity, a suggestion which could be confirmed through diffusion tensor imaging (DTI). Initial reports of DTI in TBI patients support the possibility that this technique can demonstrate alterations in white matter connections which are not seen on conventional magnetic resonance imaging (MRI) and might change over time or with interventions. Preliminary functional MRI studies of TBI patients indicate alterations in the pattern of brain activation, suggesting recruitment of more extensive cortical regions to perform tasks which stress computational resources. Functional MRI, coupled with DTI and possibly other imaging modalities holds the promise of elucidating mechanisms of neuroplasticity and repair following TBI.

[1]  C. Price,et al.  Mechanisms of recovery from aphasia: evidence from positron emission tomography studies , 1999, Journal of neurology, neurosurgery, and psychiatry.

[2]  G. Deutsch,et al.  Evidence for right-hemisphere involvement in recovery from aphasia. , 1988, Archives of neurology.

[3]  J. Mazziotta,et al.  Positron emission tomography study of human brain functional development , 1987, Annals of neurology.

[4]  Janine E. Janosky,et al.  Language development after unilateral brain injury , 1992, Brain and Language.

[5]  M. Kennard Age and other factors in motor recovery from precentral lesions in monkeys. , 1936 .

[6]  G J Barker,et al.  Diffusion imaging shows abnormalities after blunt head trauma when conventional magnetic resonance imaging is normal , 2001, Journal of neurology, neurosurgery, and psychiatry.

[7]  B M Bly,et al.  Functional magnetic resonance imaging of working memory impairment after traumatic brain injury , 2001, Journal of neurology, neurosurgery, and psychiatry.

[8]  Andrew J. Saykin,et al.  Differential Working Memory Load Effects after Mild Traumatic Brain Injury , 2001, NeuroImage.

[9]  K. Boone,et al.  Handbook of normative data for neuropsychological assessment, 2nd ed. , 2005 .

[10]  M. Rosenzweig Effects of differential experience on brain and cognition throughout the life span. , 1999 .

[11]  M. Dennis,et al.  Comprehension of syntax in infantile hemiplegics after cerebral hemidecortication: Left-hemisphere superiority , 1975, Brain and Language.

[12]  G. Cioni,et al.  Plasticity and Reorganization During Language Development in Children with Early Brain Injury , 2000, Cortex.

[13]  R. Buxton,et al.  Alternative brain organization after prenatal cerebral injury: Convergent fMRI and cognitive data , 2003, Journal of the International Neuropsychological Society.

[14]  P. Kelly,et al.  Aphasic disorder in patients with closed head injury. , 1976, Journal of neurology, neurosurgery, and psychiatry.

[15]  K. Boone,et al.  Handbook of Normative Data for Neuropsychological Assessment , 1999 .

[16]  D. Trauner,et al.  Developmental Change in Spatial Grouping Activity among Children with Early Focal Brain Injury: Evidence from a Modeling Task , 1996, Brain and Cognition.

[17]  R. Woods,et al.  Recovery from wernicke's aphasia: A positron emission tomographic study , 1995, Annals of neurology.

[18]  G. Goldenberg,et al.  Cerebral correlates of disturbed executive function and memory in survivors of severe closed head injury: a SPECT study. , 1992, Journal of neurology, neurosurgery, and psychiatry.

[19]  A. Saykin,et al.  Brain activation during working memory 1 month after mild traumatic brain injury , 1999, Neurology.

[20]  M Corbetta,et al.  Preserved speech abilities and compensation following prefrontal damage. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[21]  S. Kiebel,et al.  Training-induced brain plasticity in aphasia. , 1999, Brain : a journal of neurology.

[22]  E. Lenneberg Biological Foundations of Language , 1967 .

[23]  Edward E. Smith,et al.  A Parametric Study of Prefrontal Cortex Involvement in Human Working Memory , 1996, NeuroImage.

[24]  Elizabeth Bates,et al.  From first words to grammar in children with focal brain injury , 1997 .

[25]  W D Obrist,et al.  Computerized tomography, magnetic resonance imaging, and positron emission tomography in the study of brain trauma. Preliminary observations. , 1986, Journal of neurosurgery.

[26]  H S Levin,et al.  Reduction of corpus callosum growth after severe traumatic brain injury in children , 2000, Neurology.

[27]  S. Chapman,et al.  Word fluency in relation to severity of closed head injury, associated frontal brain lesions, and age at injury in children , 2001, Neuropsychologia.

[28]  S. Carey,et al.  Language deficits after apparent clinical recovery from childhood aphasia , 1979, Annals of neurology.

[29]  B. Woods The restricted effects of right-hemisphere lesions after age one; Wechsler test data , 1980, Neuropsychologia.

[30]  S. F. Witelson Hand and sex differences in the isthmus and genu of the human corpus callosum. A postmortem morphological study. , 1989, Brain : a journal of neurology.

[31]  H S Levin,et al.  Dyscalculia and dyslexia after right hemisphere injury in infancy. , 1996, Archives of neurology.