Post-operative environmental enrichment improves spatial and motor deficits but may not ameliorate anxiety- or depression-like symptoms in rats following traumatic brain injury

IntroductionIndividuals with moderate-severe traumatic brain injury (m-sTBI) experience progressive brain and behavioural declines in the chronic stages of injury. Longitudinal studies found that a majority of patients with m-sTBI exhibit significant hippocampal atrophy from 5 to 12 months post-injury, associated with decreased cognitive environmental enrichment (EE). Encouragingly, engaging in EE has been shown to lead to neural improvements, suggesting it is a promising avenue for offsetting hippocampal neurodegeneration in m-sTBI. Allocentric spatial navigation (ie, flexible, bird’s eye view approach), is a good candidate for EE in m-sTBI because it is associated with hippocampal activation and reduced ageing-related volume loss. Efficacy of EE requires intensive daily training, prohibitive within most current health delivery systems. The present protocol is a novel, remotely delivered and self-administered intervention designed to harness principles from EE and allocentric spatial navigation to offset hippocampal atrophy and potentially improve hippocampal functions such as navigation and memory for patients with m-sTBI.Methods and analysisEighty-four participants with chronic m-sTBI are being recruited from an urban rehabilitation hospital and randomised into a 16-week intervention (5 hours/week; total: 80 hours) of either targeted spatial navigation or an active control group. The spatial navigation group engages in structured exploration of different cities using Google Street View that includes daily navigation challenges. The active control group watches and answers subjective questions about educational videos. Following a brief orientation, participants remotely self-administer the intervention on their home computer. In addition to feasibility and compliance measures, clinical and experimental cognitive measures as well as MRI scan data are collected pre-intervention and post-intervention to determine behavioural and neural efficacy.Ethics and disseminationEthics approval has been obtained from ethics boards at the University Health Network and University of Toronto. Findings will be presented at academic conferences and submitted to peer-reviewed journals.Trial registration numberVersion 3, ClinicalTrials.gov Registry (NCT04331392).

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Feasibility of a home-based environmental enrichment paradigm to enhance purposeful activities in adults with traumatic brain injury: a case series

Disability and Rehabilitation ◽

10.1080/09638288.2020.1868583 ◽

2021 ◽

pp. 1-7

Author(s):

Devina S. Kumar ◽

James C. Galloway

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Environmental Enrichment ◽

Case Series ◽

Home Based

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Environmental enrichment may protect against hippocampal atrophy in the chronic stages of traumatic brain injury

Frontiers in Human Neuroscience ◽

10.3389/fnhum.2013.00506 ◽

2013 ◽

Vol 7 ◽

Cited By ~ 17

Author(s):

Lesley S. Miller ◽

Brenda Colella ◽

David Mikulis ◽

Jerome Maller ◽

Robin E. A. Green

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Environmental Enrichment ◽

Hippocampal Atrophy

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N-methyl-D-aspartate preconditioning improves short-term motor deficits outcome after mild traumatic brain injury in mice

Journal of Neuroscience Research ◽

10.1002/jnr.22300 ◽

2009 ◽

pp. n/a-n/a ◽

Cited By ~ 3

Author(s):

Tayana Costa ◽

Leandra C. Constantino ◽

Bruna P. MendonÃ§a ◽

Josimar G. Pereira ◽

Bruno Herculano ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Mild Traumatic Brain Injury ◽

Motor Deficits ◽

Short Term

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Implementing environmental enrichment strategies to help children who have sustained a moderate or severe traumatic brain injury

Support for Learning ◽

10.1111/1467-9604.12310 ◽

2020 ◽

Vol 35 (3) ◽

pp. 276-297

Author(s):

Paul B. Jantz

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Severe Traumatic Brain Injury ◽

Environmental Enrichment

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Reversible monoparesis following decompressive hemicraniectomy for traumatic brain injury

Journal of Neurosurgery ◽

10.3171/jns/2008/109/8/0245 ◽

2008 ◽

Vol 109 (2) ◽

pp. 245-254 ◽

Cited By ~ 78

Author(s):

Shirley I. Stiver ◽

Max Wintermark ◽

Geoffrey T. Manley

Keyword(s):

Traumatic Brain Injury ◽

Cerebrospinal Fluid ◽

Brain Injury ◽

Motor Function ◽

Ct Perfusion ◽

Motor Deficits ◽

Decompressive Hemicraniectomy ◽

Number Of Patients ◽

Motor Strength

Object The “syndrome of the trephined” is an uncommon and poorly understood disorder of delayed neurological deficit following craniectomy. From the authors' extensive experience with decompressive hemicraniectomy for traumatic brain injury (TBI), they have encountered a number of patients who developed delayed motor deficits, also called “motor trephine syndrome,” and reversal of the weakness following cranioplasty repair. The authors set out to study motor function systematically in this patient population to define the incidence, contributing factors, and outcome of patients with motor trephine syndrome. Methods The authors evaluated patient demographics, injury characteristics, detailed motor examinations, and CT scans in 38 patients with long-term follow-up after decompressive hemicraniectomy for TBI. Results Ten patients (26%) experienced delayed contralateral upper-extremity weakness, beginning 4.9 ± 0.4 months (mean ± standard error) after decompressive hemicraniectomy. Motor deficits improved markedly within 72 hours of cranioplasty repair, and all patients recovered full motor function. The CT perfusion scans, performed in 2 patients, demonstrated improvements in cerebral blood flow commensurate with resolution of cerebrospinal fluid flow disturbances on CT scanning and return of motor strength. Comparisons between 10 patients with and 20 patients (53%) without delayed motor deficits identified 3 factors—ipsilateral contusions, abnormal cerebrospinal fluid circulation, and longer intervals to cranioplasty repair—to be strongly associated with delayed, reversible monoparesis following decompressive hemicraniectomy. Conclusions Delayed, reversible monoparesis, also called motor trephine syndrome, is common following decompressive hemicraniectomy for TBI. The results of this study suggest that close follow-up of motor strength with early cranioplasty repair may prevent delayed motor complications of decompressive hemicraniectomy.

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Neuroimaging Patterns Associated with Motor Control in Traumatic Brain Injury

Neurorehabilitation and Neural Repair ◽

10.1177/1545968305282919 ◽

2006 ◽

Vol 20 (1) ◽

pp. 14-23 ◽

Cited By ~ 20

Author(s):

M. Lotze ◽

W. Grodd ◽

F. A. Rodden ◽

E. Gut ◽

P. W. Schönle ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Premotor Cortex ◽

Blood Oxygenation ◽

Motor Deficits ◽

Healthy Controls ◽

Cross Sectional ◽

Fmri Signal ◽

Signal Change ◽

Motor Areas

Objective. To determine if patients with traumatic brain injury (TBI) and motor deficits show differences in functional activation maps during repetitive hand movements relative to healthy controls. Are there predictors for motor outcome in the functional maps of these patients? Methods. In an exploratory cross-sectional study, functional magnetic resonance imaging (fMRI) was used to study the blood-oxygenation-level-dependent (BOLD) response in cortical motor areas of 34 patients suffering from moderate motor deficits after TBI as they performed unilateral fist-clenching motions. Twelve of these patients with unilateral motor deficits were studied 3 months after TBI and a 2nd time approximately 4 months later. Results. Compared to age-matched, healthy controls performing the same task, TBI patients showed diminished fMRI-signal change in the primary sensorimotor cortex contralateral to the moving hand (cSM1), the contralateral dorsal premotor cortex, and bilaterally in the supplementary motor areas (SMAs). Clinical impairment and the magnitude of the fMRI-signal change in cSM1 and SMA were negatively correlated. Patients with poor and good motor recovery showed comparable motor impairment at baseline. Only patients who evolved to “poor clinical outcome” had decreased fMRI-signal change in the cSM1 during baseline. Conclusions. 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.

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Attenuation of Brain Nitrostative and Oxidative Damage by Brain Cooling during Experimental Traumatic Brain Injury

Journal of Biomedicine and Biotechnology ◽

10.1155/2011/145214 ◽

2011 ◽

Vol 2011 ◽

pp. 1-8 ◽

Cited By ~ 11

Author(s):

Jinn-Rung Kuo ◽

Chong-Jeh Lo ◽

Ching-Ping Chang ◽

Mao- Tsun Lin ◽

Chung-Ching Chio

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Oxidative Damage ◽

Jugular Vein ◽

External Jugular Vein ◽

Motor Deficits ◽

Sham Operation ◽

Brain Cooling ◽

Cerebral Contusion ◽

Oxide Synthase

The aim of the present study was to ascertain whether brain cooling causes attenuation of traumatic brain injury by reducing brain nitrostative and oxidative damage. Brain cooling was accomplished by infusion of 5 mL of 4°C saline over 5 minutes via the external jugular vein. Immediately after the onset of traumatic brain injury, rats were randomized into two groups and given 37°C or 4°C normal saline. Another group of rats were used as sham operated controls. Behavioral and biochemical assessments were conducted on 72 hours after brain injury or sham operation. As compared to those of the sham-operated controls, the 37°C saline-treated brain injured animals displayed motor deficits, higher cerebral contusion volume and incidence, higher oxidative damage (e.g., lower values of cerebral superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, but higher values of cerebral malondialdehyde), and higher nitrostative damage (e.g., higher values of neuronal nitric oxide synthase and 3-nitrotyrosine). All the motor deficits and brain nitrostative and oxidative damage were significantly reduced by retrograde perfusion of 4°C saline via the jugular vein. Our data suggest that brain cooling may improve the outcomes of traumatic brain injury in rats by reducing brain nitrostative and oxidative damage.

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