Neuroimaging Patterns Associated with Motor Control in Traumatic Brain Injury

Lotze, Martín; Grodd, Wolfgang; Rodden, Frank A.; Gut, E.; Schönle, P. W.; Kardatzki, Bernd; Cohen, Leonardo G.

doi:10.1177/1545968305282919

Cited by 27 publications

(13 citation statements)

References 24 publications

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“…As a result, it is not surprising that the majority of studies tracking neuroplastic responses to brain injury have focused on this critical postinjury time period. Yet, the functional recovery process can continue for 2 or more years after TBI (Lotze et al, 2006;Sbordone et al, 1995) or stroke (Mark et al, 2006), indicating that long-term studies investigating the underlying neuroplastic responses of prolonged recovery are needed. Such information could assist in the development of long-term treatment strategies aimed to facilitate and enhance the recovery process in patients with brain injury.…”

Section: Nagamoto-combs Et Almentioning

confidence: 99%

Long-Term Gliosis and Molecular Changes in the Cervical Spinal Cord of the Rhesus Monkey after Traumatic Brain Injury

Nagamoto-Combs

Morecraft

Darling

et al. 2010

Journal of Neurotrauma

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Recovery of fine motor skills after traumatic brain injury (TBI) is variable, with some patients showing progressive improvements over time while others show poor recovery. We therefore studied possible cellular mechanisms accompanying the recovery process in a non-human primate model system, in which the lateral frontal motor cortex areas controlling the preferred upper limb were unilaterally lesioned, and the animals eventually regained fine hand motor function. Immunohistochemical staining of the cervical spinal cord, the site of compensatory sprouting and degeneration of corticospinal axons, showed profound increases in immunoreactivities for major histocompatibility complex class II molecule (MHC-II) and extracellular signalregulated kinases (ERK1=2) up to 12 months post lesion, particularly within the lateral corticospinal tract (LCST). Double immunostaining demonstrated that phosphorylated ERK1=2 colocalized within the MCH-II þ microglia, suggesting a trophic role of long-term microglia activation after TBI at the site of compensatory sprouting. Active sprouting was observed in the LCST as well as in the spinal gray matter of the lesioned animals, as illustrated by increases in growth associated protein 43. Upregulation of Nogo receptor and glutamate transporter expression was also observed in this region after TBI, suggesting possible mechanisms for controlling aberrant sprouting and=or synaptic formation en route and interstitial glutamate concentration changes at the site of axon degeneration, respectively. Taken together, these changes in the non-human primate spinal cord support a long-term trophic=tropic role for reactive microglia, in particular, during functional and structural recovery after TBI.

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Section: Nagamoto-combs Et Almentioning

confidence: 99%

Long-Term Gliosis and Molecular Changes in the Cervical Spinal Cord of the Rhesus Monkey after Traumatic Brain Injury

Nagamoto-Combs

Morecraft

Darling

et al. 2010

Journal of Neurotrauma

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show abstract

“…Functional magnetic resonance imaging, positron emission tomography, diffusion tensor imaging of axons, evoked potentials, optical intrinsic signal imaging, and other methods could be used in parallel in animal and human trials to explore residual connectivity, the best site for a repair intervention, monitor remyelination, determine whether the motor network is engaged by task-specific rehabilitation, and monitor the dose of therapy needed to maximize cerebral reorganization after a biologic therapy Dobkin, 2005a;Carey et al, 2006;Lotze et al, 2006). Several studies of rehabilitation interventions for the upper extremity and for walking monitored by repeated fMRI or transcranial magnetic stimulation studies at regular intervals during therapy suggest that this approach may give insight into gradually adapting brain-behavior and dose-response relationships (Koski et al, 2004;Dobkin, 2005b;Dong et al, 2006).…”

Section: Outcome Measuresmentioning

confidence: 99%

Curiosity and cure: Translational research strategies for neural repair‐mediated rehabilitation

Dobkin

2007

Developmental Neurobiology

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Clinicians who seek interventions for neural repair in patients with paralysis and other impairments may extrapolate the results of cell culture and rodent experiments into the framework of a preclinical study. These experiments, however, must be interpreted within the context of the model and the highly constrained hypothesis and manipulation being tested. Rodent models of repair for stroke and spinal cord injury offer examples of potential pitfalls in the interpretation of results from developmental gene activation, transgenic mice, endogeneous neurogenesis, cellular transplantation, axon regeneration and remyelination, dendritic proliferation, activity-dependent adaptations, skills learning, and behavioral testing. Preclinical experiments that inform the design of human trials ideally include a lesion of etiology, volume and location that reflects the human disease; examine changes induced by injury and by repair procedures both near and remote from the lesion; distinguish between reactive molecular and histologic changes versus changes critical to repair cascades; employ explicit training paradigms for the reacquisition of testable skills; correlate morphologic and physiologic measures of repair with behavioral measures of task reacquisition; reproduce key results in more than one laboratory, in different strains or species of rodent, and in a larger mammal; and generalize the results across several disease models, such as axonal regeneration in a stroke and spinal cord injury platform. Collaborations between basic and clinical scientists in the development of translational animal models of injury and repair can propel experiments for ethical bench-to-bedside therapies to augment the rehabilitation of disabled patients.

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“…This observation is consistent with a previous study on hand movements in patients with TBI. 27 SMA is involved in the volitional aspect of motor planning in selfinitiated movement. 28 Therefore, the lack of significant SMA activation in patients may further suggest impaired planning of finger movement execution.…”

mentioning

confidence: 99%

Altered functional connectivity in the motor network after traumatic brain injury

Kasahara

Menon²,

Salmond³

et al. 2010

Neurology

100

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Background: A large proportion of survivors of traumatic brain injury (TBI) have persistent cognitive impairments, the profile of which does not always correspond to the size and location of injuries. One possible explanation could be that TBI-induced damage extends beyond obvious lesion sites to affect remote brain networks. We explored this hypothesis in the context of a simple and well-characterized network, the motor network. The aim of this cross-sectional study was to establish the residual integrity of the motor network as an important proof of principle of abnormal connectivity in TBI.Methods: fMRI data were obtained from 12 right-handed patients and 9 healthy controls while they performed the finger-thumb opposition task with the right hand. We used both conventional and psychophysiologic interaction (PPI) analyses to examine the integrity of functional connections from brain regions we found to be activated in the paradigm we used.Results: As expected, the analysis showed significant activations of the left primary motor cortex (M1), right cerebellum (Ce), and bilateral supplementary motor area (SMA) in controls. However, only the activation of M1 survived robust statistical thresholding in patients. In controls, the PPI analysis revealed that left M1, SMA, and right Ce positively interacted with the left frontal cortex and negatively interacted with the right supramarginal gyrus. In patients, we observed no negative interaction and reduced interhemispheric interactions from these seed regions.Conclusions: These observations suggest that patients display compromised activation and connectivity patterns during the finger-thumb opposition task, which may imply functional reorganization of motor networks following TBI.

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Neuroimaging Patterns Associated with Motor Control in Traumatic Brain Injury

Abstract: These observations raise the hypothesis that the magnitude of the fMRI-signal change in the cSM1 region could have prognostic value in the evaluation of patients with TBI.

Cited by 27 publications

References 24 publications

Long-Term Gliosis and Molecular Changes in the Cervical Spinal Cord of the Rhesus Monkey after Traumatic Brain Injury

Long-Term Gliosis and Molecular Changes in the Cervical Spinal Cord of the Rhesus Monkey after Traumatic Brain Injury

Curiosity and cure: Translational research strategies for neural repair‐mediated rehabilitation

Altered functional connectivity in the motor network after traumatic brain injury

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