Diffuse traumatic brain injury and the sensory brain

Alwis, Duwage Dasuni Sathsara; Johnstone, Victoria; Yan, Edwin BingBing; Rajan, Ramesh

doi:10.1111/1440-1681.12100

Cited by 26 publications

(35 citation statements)

References 139 publications

(219 reference statements)

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“…The effects of TBI may also be exerted through inflammatory processes: as we have noted previously (Alwis et al, 2013), activation of inflammatory cascades as part of the normal cellular response to injury can cause further injury to the already damaged brain (Menge et al, 2001; Morganti-Kossmann et al, 2002). The inflammatory response in TBI involves production of pro-inflammatory cytokines like interleukin-1 (IL-1), IL-6 and tumor necrosis factor (TNF-a), and anti-inflammatory cytokines such as IL-10 and IL-12, all of which are seen in the cerebrospinal fluid of TBI patients within a few hours of the primary injury.…”

Section: Mechanisms Promoting Improved Behavioral and Pathological Rementioning

confidence: 87%

“…There are two major forms of TBI—focal and diffuse. Focal brain injury is caused by direct, localized damage to the brain, while diffuse injury is most commonly caused by indirect forces, such as during rapid acceleration/deceleration of the head (Andriessen et al, 2010; Alwis et al, 2013). TBI affects approximately 2 million individuals every year in the US alone (Faul et al, 2010) and has been shown to result in a number of persistent sensory deficits, which are thought to underlie TBI-associated cognitive disabilities (Caeyenberghs et al, 2009; Davis and Dean, 2010; Lew et al, 2010; Folmer et al, 2011).…”

Section: Ee and The Damaged Brainmentioning

confidence: 99%

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Environmental enrichment and the sensory brain: the role of enrichment in remediating brain injury

Alwis

Rajan

2014

Front. Syst. Neurosci.

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108

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The brain's life-long capacity for experience-dependent plasticity allows adaptation to new environments or to changes in the environment, and to changes in internal brain states such as occurs in brain damage. Since the initial discovery by Hebb (1947) that environmental enrichment (EE) was able to confer improvements in cognitive behavior, EE has been investigated as a powerful form of experience-dependent plasticity. Animal studies have shown that exposure to EE results in a number of molecular and morphological alterations, which are thought to underpin changes in neuronal function and ultimately, behavior. These consequences of EE make it ideally suited for investigation into its use as a potential therapy after neurological disorders, such as traumatic brain injury (TBI). In this review, we aim to first briefly discuss the effects of EE on behavior and neuronal function, followed by a review of the underlying molecular and structural changes that account for EE-dependent plasticity in the normal (uninjured) adult brain. We then extend this review to specifically address the role of EE in the treatment of experimental TBI, where we will discuss the demonstrated sensorimotor and cognitive benefits associated with exposure to EE, and their possible mechanisms. Finally, we will explore the use of EE-based rehabilitation in the treatment of human TBI patients, highlighting the remaining questions regarding the effects of EE.

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Section: Mechanisms Promoting Improved Behavioral and Pathological Rementioning

confidence: 87%

Section: Ee and The Damaged Brainmentioning

confidence: 99%

Environmental enrichment and the sensory brain: the role of enrichment in remediating brain injury

Alwis

Rajan

2014

Front. Syst. Neurosci.

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108

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“…CR acts as a Ca 2+ buffer (Schwaller et al, ), regulating dendritic Ca 2+ transients (Edmonds et al, ) and affecting pre‐ and postsynaptic Ca 2+ signaling to ensure synchronization and synaptic plasticity in neuronal networks. In TBI there is excessive extracellular glutamate, resulting in overstimulation of neurons and glia, causing increased Ca 2+ , Na + , and K + fluxes (Alwis et al, ). The Ca 2+ influx triggers a cascade of cellular events culminating in cell death (Cotman and Iversen, ).…”

Section: Discussionmentioning

confidence: 99%

Differential susceptibility of cortical and subcortical inhibitory neurons and astrocytes in the long term following diffuse traumatic brain injury

Carron

Yan

Alwis

et al. 2016

J of Comparative Neurology

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Long-term diffuse traumatic brain injury (dTBI) causes neuronal hyperexcitation in supragranular layers in sensory cortex, likely through reduced inhibition. Other forms of TBI affect inhibitory interneurons in subcortical areas but it is unknown if this occurs in cortex, or in any brain area in dTBI. We investigated dTBI effects on inhibitory neurons and astrocytes in somatosensory and motor cortex, and hippocampus, 8 weeks post-TBI. Brains were labeled with antibodies against calbindin (CB), parvalbumin (PV), calretinin (CR) and neuropeptide Y (NPY), and somatostatin (SOM) and glial fibrillary acidic protein (GFAP), a marker for astrogliosis during neurodegeneration. Despite persistent behavioral deficits in rotarod performance up to the time of brain extraction (TBI = 73.13 ± 5.23% mean ± SEM, Sham = 92.29 ± 5.56%, P < 0.01), motor cortex showed only a significant increase, in NPY neurons in supragranular layers (mean cells/mm ± SEM, Sham = 16 ± 0.971, TBI = 25 ± 1.51, P = 0.001). In somatosensory cortex, only CR neurons showed changes, being decreased in supragranular (TBI = 19 ± 1.18, Sham = 25 ± 1.10, P < 0.01) and increased in infragranular (TBI = 28 ± 1.35, Sham = 24 ± 1.07, P < 0.05) layers. Heterogeneous changes were seen in hippocampal staining: CB decreased in dentate gyrus (TBI = 2 ± 0.382, Sham = 4 ± 0.383, P < 0.01), PV increased in CA1 (TBI = 39 ± 1.26, Sham = 33 ± 1.69, P < 0.05) and CA2/3 (TBI = 26 ± 2.10, Sham = 20 ± 1.49, P < 0.05), and CR decreased in CA1 (TBI = 10 ± 1.02, Sham = 14 ± 1.14, P < 0.05). Astrogliosis significantly increased in corpus callosum (TBI = 6.7 ± 0.69, Sham = 2.5 ± 0.38; P = 0.007). While dTBI effects on inhibitory neurons appear region- and type-specific, a common feature in all cases of decrease was that changes occurred in dendrite targeting interneurons involved in neuronal integration. J. Comp. Neurol. 524:3530-3560, 2016. © 2016 Wiley Periodicals, Inc.

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“…6 The processes leading to injury can be classified as primary and secondary injury mechanisms. [7][8][9][10][11] Primary mechanisms are attributed to mechanical events during impact with the brain and include brain contusion, hematomas, hemorrhage, and axonal disruption. [11][12][13] These events are followed by secondary injury processes that manifest over hours to days 14 and involve dynamic cascades that induce ionic imbalances, excitotoxicity, oxidative stress, hypoxia-ischemia, inflammation, and cerebral edema.…”

Section: Introductionmentioning

confidence: 99%

“…[11][12][13] These events are followed by secondary injury processes that manifest over hours to days 14 and involve dynamic cascades that induce ionic imbalances, excitotoxicity, oxidative stress, hypoxia-ischemia, inflammation, and cerebral edema. 8,9,11,15 For patients who survive the primary insults, mortality and functional outcomes are compounded by the secondary injury processes and the extent of their progression. 10 Very little is known about how the primary and secondary injury processes (and their interactions) affect the neuronal responses that underlie behavior.…”

Section: Introductionmentioning

confidence: 99%

The Acute Phase of Mild Traumatic Brain Injury Is Characterized by a Distance-Dependent Neuronal Hypoactivity

Johnstone

Shultz

Yan

et al. 2014

Journal of Neurotrauma

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The consequences of mild traumatic brain injury (TBI) on neuronal functionality are only now being elucidated. We have now examined the changes in sensory encoding in the whisker-recipient barrel cortex and the brain tissue damage in the acute phase (24 h) after induction of TBI (n = 9), with sham controls receiving surgery only (n = 5). Injury was induced using the lateral fluid percussion injury method, which causes a mixture of focal and diffuse brain injury. Both population and single cell neuronal responses evoked by both simple and complex whisker stimuli revealed a suppression of activity that decreased with distance from the locus of injury both within a hemisphere and across hemispheres, with a greater extent of hypoactivity in ipsilateral barrel cortex compared with contralateral cortex. This was coupled with an increase in spontaneous output in Layer 5a, but only ipsilateral to the injury site. There was also disruption of axonal integrity in various regions in the ipsilateral but not contralateral hemisphere. These results complement our previous findings after mild diffuse-only TBI induced by the weight-drop impact acceleration method where, in the same acute post-injury phase, we found a similar depth-dependent hypoactivity in sensory cortex. This suggests a common sequelae of events in both diffuse TBI and mixed focal/diffuse TBI in the immediate post-injury period that then evolve over time to produce different long-term functional outcomes.

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Diffuse traumatic brain injury and the sensory brain

Cited by 26 publications

References 139 publications

Environmental enrichment and the sensory brain: the role of enrichment in remediating brain injury

Environmental enrichment and the sensory brain: the role of enrichment in remediating brain injury

Differential susceptibility of cortical and subcortical inhibitory neurons and astrocytes in the long term following diffuse traumatic brain injury

The Acute Phase of Mild Traumatic Brain Injury Is Characterized by a Distance-Dependent Neuronal Hypoactivity

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