A Qualitative Study on the Transition Support Needs of Indigenous Australians Following Traumatic Brain Injury

2019 ◽  
Vol 20 (2) ◽  
pp. 137-159 ◽  
Author(s):  
Michelle S. Fitts ◽  
Katrina Bird ◽  
John Gilroy ◽  
Jennifer Fleming ◽  
Alan R. Clough ◽  
...  

AbstractObjective:A growing body of qualitative literature globally describes post-hospital experiences during early recovery from a traumatic brain injury. For Indigenous Australians, however, little published information is available. This study aimed to understand the lived experiences of Indigenous Australians during the 6 months post-discharge, identify the help and supports accessed during transition and understand the gaps in service provision or difficulties experienced.Methods and Procedure:Semi-structured interviews were conducted at 6 months after hospital discharge to gain an understanding of the needs and lived experiences of 11 Aboriginal and Torres Strait Islander Australians who had suffered traumatic brain injury in Queensland and Northern Territory, Australia. Data were analysed using thematic analysis.Results:Five major themes were identified within the data. These were labelled ‘hospital experiences’, ‘engaging with medical and community-based supports’, ‘health and wellbeing impacts from the injury’, ‘everyday living’ and ‘family adjustments post-injury’.Conclusions:While some of the transition experiences for Indigenous Australians were similar to those found in other populations, the transition period for Indigenous Australians is influenced by additional factors in hospital and during their recovery process. Lack of meaningful interaction with treating clinicians in hospital, challenges managing direct contact with multiple service providers and the injury-related psychological impacts are some of the factors that could prevent Indigenous Australians from receiving the supports they require to achieve their best possible health outcomes in the long term. A holistic approach to care, with an individualised, coordinated transition support, may reduce the risks for re-admission with further head injuries.

2018 ◽  
Vol 19 (3) ◽  
pp. 246-257 ◽  
Author(s):  
India Bohanna ◽  
Michelle S. Fitts ◽  
Katrina Bird ◽  
Jennifer Fleming ◽  
John Gilroy ◽  
...  

Background: Traumatic brain injury (TBI) is a leading cause of disability in Australia. Evidence shows that multidisciplinary rehabilitation and support in the six months following TBI is important for successful independent living and social re-integration. Despite this, access to services and supports during this period is often limited by environmental, socio-economic, geographic and cultural factors. Australian studies on outcomes after brain injury have reported primarily on non-Indigenous people. This study will investigate key sentinel events during the transition from hospital to home after a TBI in the first longitudinal study with Indigenous Australians.Method: Indigenous Australians admitted to one of three major trauma hospitals in northern Australia with a TBI, and their care givers, will be recruited. Clinical and brain injury risk factor information, along with measures of cognitive function, transition events, mental health and community re-integration will be collected at three time points prior to hospital discharge, and at three and six months post-discharge. Qualitative interviews will also be conducted. Data will be analysed using regression methods for the quantitative component, and situational analysis for the qualitative component. Annual rates of brain injury will be calculated for patients admitted to tertiary hospital facilities in the study region with a diagnosis of TBI.Discussion: Understanding the experience and events which shape the transition period is critical to determining the services and supports that may enhance transition outcomes, and ensure that such services are culturally appropriate and endorsed by Indigenous families and communities.


2019 ◽  
Vol 20 (2) ◽  
pp. 160-170 ◽  
Author(s):  
India Bohanna ◽  
Michelle Fitts ◽  
Katrina Bird ◽  
Jennifer Fleming ◽  
John Gilroy ◽  
...  

AbstractBackground:Increasingly, narrative and creative arts approaches are being used to enhance recovery after traumatic brain injury (TBI). Narrative and arts-based approaches congruent with Indigenous storytelling may therefore provide benefit during the transition from hospital to home for some Indigenous TBI patients. This qualitative study explored the use and impact of this approach as part of a larger, longitudinal study of TBI transition with Indigenous Australians.Method:A combined narrative and arts-based approach was used with one Indigenous Australian artist to describe his transition experiences following TBI. Together with the researchers and filmmaking team, the artist was involved in aspects of the process. The artist contributed two paintings, detailing the story of his life and TBI. Based on the artworks, a film was co-created. Following the viewing of the film, impacts of the narrative and arts-based process were examined through semi-structured interviews with the artist, a service provider and a family member. Multiple sources of data were used in the final thematic analysis including transcripts of the interviews and filming, paintings (including storylines) and researcher notes.Results:Positive impacts from the process for the artist included positive challenge; healing and identity; understanding TBI and raising awareness.Discussion:This approach may enable the individual to take ownership over their transition story and to make sense of their life following TBI at a critical point in their recovery. A combined narrative and arts-based approach has potential as a culturally responsive rehabilitation tool for use with Indigenous Australians during the transition period following TBI.


2018 ◽  
Vol 10 (1) ◽  
pp. 81 ◽  
Author(s):  
Kelly M. Jones ◽  
Suzanne Barker-Collo ◽  
Priya Parmar ◽  
Nicola Starkey ◽  
Alice Theadom ◽  
...  

ABSTRACT INTRODUCTION There is growing consensus that adverse child outcomes may be evident in the early recovery phase following mild traumatic brain injury (TBI). However, controversy remains around the nature of children’s longer-term recovery. AIM To examine child cognitive, behavioural and quality-of-life outcomes over 12 months following mild injury, and to identify prognostic factors associated with outcomes. METHODS A prospective sample of 222 children (aged 2–15 years at injury) with mild TBI was assessed using a cognitive testing battery and parent-report questionnaires at ≤ 14 days, 1, 6 and/or 12-months post-injury. RESULTS Parents reported significant improvements in their child’s behavioural adjustment between baseline and 6 months (P = 0.003), with further improvements at 12 months following injury (P = 0.001). Cognitive recovery and quality-of-life improvements were more gradual with minimal changes in the first month (P > 0.05), but significant improvements by 12-months post-injury (P = 0.03, P = 0.02, respectively). Time since injury, male gender, living rurally and parent anxiety were associated with extent of recovery beyond the acute period. CONCLUSIONS Children’s recovery from mild TBI continues beyond the initial 6 months following injury. Health-care providers need to be vigilant about the varying trajectories in children’s recovery from TBI. On-going monitoring of children following injury will enable timely and proactive responses to persistent difficulties, with a view to minimising longer-term adverse consequences.


2018 ◽  
Vol 63 (4) ◽  
pp. 588-594
Author(s):  
Daniel W. Klyce ◽  
Kristin M. Graham ◽  
Russell W. Lacey ◽  
William E. Carter

2020 ◽  
Vol 35 (6) ◽  
pp. 919-919
Author(s):  
Lange R ◽  
Lippa S ◽  
Hungerford L ◽  
Bailie J ◽  
French L ◽  
...  

Abstract Objective To examine the clinical utility of PTSD, Sleep, Resilience, and Lifetime Blast Exposure as ‘Risk Factors’ for predicting poor neurobehavioral outcome following traumatic brain injury (TBI). Methods Participants were 993 service members/veterans evaluated following an uncomplicated mild TBI (MTBI), moderate–severe TBI (ModSevTBI), or injury without TBI (Injured Controls; IC); divided into three cohorts: (1) < 12 months post-injury, n = 237 [107 MTBI, 71 ModSevTBI, 59 IC]; (2) 3-years post-injury, n = 370 [162 MTBI, 80 ModSevTBI, 128 IC]; and (3) 10-years post-injury, n = 386 [182 MTBI, 85 ModSevTBI, 119 IC]. Participants completed a 2-hour neurobehavioral test battery. Odds Ratios (OR) were calculated to determine whether the ‘Risk Factors’ could predict ‘Poor Outcome’ in each cohort separately. Sixteen Risk Factors were examined using all possible combinations of the four risk factor variables. Poor Outcome was defined as three or more low scores (< 1SD) on five TBI-QOL scales (e.g., Fatigue, Depression). Results In all cohorts, the vast majority of risk factor combinations resulted in ORs that were ‘clinically meaningful’ (ORs > 3.00; range = 3.15 to 32.63, all p’s < .001). Risk factor combinations with the highest ORs in each cohort were PTSD (Cohort 1 & 2, ORs = 17.76 and 25.31), PTSD+Sleep (Cohort 1 & 2, ORs = 18.44 and 21.18), PTSD+Sleep+Resilience (Cohort 1, 2, & 3, ORs = 13.56, 14.04, and 20.08), Resilience (Cohort 3, OR = 32.63), and PTSD+Resilience (Cohort 3, OR = 24.74). Conclusions Singularly, or in combination, PTSD, Poor Sleep, and Low Resilience were strong predictors of poor outcome following TBI of all severities and injury without TBI. These variables may be valuable risk factors for targeted early interventions following injury.


CNS Spectrums ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 178-179
Author(s):  
John L. Sherman ◽  
Laurence J. Adams ◽  
Christen F. Kutz ◽  
Deborah York ◽  
Mitchell S. Szymczak

AbstractTraumatic brain injury (TBI) is a complex phenomenon affecting multiple areas of the brain in multiple ways. Both right and left hemispheres are affected as well as supratentorial and infratentorial compartments. These multifocal injuries are caused by many factors including acute mechanical injury, focal intracranial hemorrhage, blunt and rotational forces, epidural and subdural hematoma, hypoxemia, hypotension, edema, axonal damage, neuronal death, gliosis and blood brain barrier disruption. Clinicians and patients benefit by precise information about the neuroanatomical areas that are affected macroscopically, microscopically and biochemically in an individual patient.Standard imaging studies are frequently negative or grossly underestimate the severity of TBI and may exacerbate and prolong patient suffering with an imaging result of “no significant abnormality”. Specifically, sophisticated imaging tools have been developed which reveal significant damage to the brain structure including atrophy, MRI spectroscopy showing variations in neuronal metabolite N-acetyl-aspartate, elevations of membrane related Choline, and the glial metabolite myo-inositol is often observed to be increased post injury. In addition, susceptibility weighted imaging (SWI) has been shown to be more reliable for detecting microbleeds versus calcifications.We have selected two TBI patients with diffuse traumatic brain injury.The first patient is a 43-year-old male who suffered severe traumatic brain injury from a motorcycle accident in 2016. Following the accident, the patient was diagnosed with seizures, major depression, and intermittent explosive disorder. He has attempted suicide and has neurobehavioral disinhibition including severe anger, agitation and irritability. He denies psychiatric history prior to TBI and has negative family history. Following the TBI, he became physically aggressive and assaultive in public with minimal provocation. He denies symptoms of thought disorder and mania. He is negative for symptoms of  cognitive decline or encephalopathy.The second patient is a 49-year-old male who suffered at least 3 concussive blasts in the Army and a parachute injury. Following the last accident, the patient was diagnosed with major depressive disorder, panic disorder, PTSD and generalized anxiety disorder. He denies any psychiatric history prior to TBI including negative family history of psychiatric illness. In addition, he now suffers from nervousness, irritability, anger, emotional lability and concurrent concentration issues, problems completing tasks and alterations in memory.Both patients underwent 1.5T multiparametric MRI using standard T2, FLAIR, DWI and T1 sequences, and specialized sequences including susceptibility weighted (SWAN/SWI), 3D FLAIR, single voxel MRI spectroscopy (MRS), diffusion tensor imaging (DTI), arterial spin labeling perfusion (ASL) and volumetric MRI (NeuroQuant). Importantly, this exam can be performed in 30–45 minutes and requires no injections other than gadolinium in some patients. We will discuss the insights derived from the MRI which detail the injured areas, validate the severity of the brain damage, and provide insight into the psychological, motivational and physical disabilities that afflict these patients. It is our expectation that this kind of imaging study will grow in value as we link specific patterns of injury to specific symptoms and syndromes resulting in more targeted therapies in the future.


Author(s):  
Sara M. Lippa ◽  
Jessica Gill ◽  
Tracey A. Brickell ◽  
Louis M. French ◽  
Rael T. Lange

Abstract Objective: This study examines the relationship of serum total tau, neurofilament light (NFL), ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1), and glial fibrillary acidic protein (GFAP) with neurocognitive performance in service members and veterans with a history of traumatic brain injury (TBI). Method: Service members (n = 488) with a history of uncomplicated mild (n = 172), complicated mild, moderate, severe, or penetrating TBI (sTBI; n = 126), injured controls (n = 116), and non-injured controls (n = 74) prospectively enrolled from Military Treatment Facilities. Participants completed a blood draw and neuropsychological assessment a year or more post-injury. Six neuropsychological composite scores and presence/absence of mild neurocognitive disorder (MNCD) were evaluated. Within each group, stepwise hierarchical regression models were conducted. Results: Within the sTBI group, increased serum UCH-L1 was related to worse immediate memory and delayed memory (R2Δ = .065–.084, ps < .05) performance, while increased GFAP was related to worse perceptual reasoning (R2Δ = .030, p = .036). Unexpectedly, within injured controls, UCH-L1 and GFAP were inversely related to working memory (R2Δ = .052–.071, ps < .05), and NFL was related to executive functioning (R2Δ = .039, p = .021) and MNCD (Exp(B) = 1.119, p = .029). Conclusions: Results suggest GFAP and UCH-L1 could play a role in predicting poor cognitive outcome following complicated mild and more severe TBI. Further investigation of blood biomarkers and cognition is warranted.


2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Amer Toutonji ◽  
Mamatha Mandava ◽  
Silvia Guglietta ◽  
Stephen Tomlinson

AbstractActivation of the complement system propagates neuroinflammation and brain damage early and chronically after traumatic brain injury (TBI). The complement system is complex and comprises more than 50 components, many of which remain to be characterized in the normal and injured brain. Moreover, complement therapeutic studies have focused on a limited number of histopathological outcomes, which while informative, do not assess the effect of complement inhibition on neuroprotection and inflammation in a comprehensive manner. Using high throughput gene expression technology (NanoString), we simultaneously analyzed complement gene expression profiles with other neuroinflammatory pathway genes at different time points after TBI. We additionally assessed the effects of complement inhibition on neuropathological processes. Analyses of neuroinflammatory genes were performed at days 3, 7, and 28 post injury in male C57BL/6 mice following a controlled cortical impact injury. We also characterized the expression of 59 complement genes at similar time points, and also at 1- and 2-years post injury. Overall, TBI upregulated the expression of markers of astrogliosis, immune cell activation, and cellular stress, and downregulated the expression of neuronal and synaptic markers from day 3 through 28 post injury. Moreover, TBI upregulated gene expression across most complement activation and effector pathways, with an early emphasis on classical pathway genes and with continued upregulation of C2, C3 and C4 expression 2 years post injury. Treatment using the targeted complement inhibitor, CR2-Crry, significantly ameliorated TBI-induced transcriptomic changes at all time points. Nevertheless, some immune and synaptic genes remained dysregulated with CR2-Crry treatment, suggesting adjuvant anti-inflammatory and neurotropic therapy may confer additional neuroprotection. In addition to characterizing complement gene expression in the normal and aging brain, our results demonstrate broad and chronic dysregulation of the complement system after TBI, and strengthen the view that the complement system is an attractive target for TBI therapy.


2021 ◽  
Vol 22 (15) ◽  
pp. 8276
Author(s):  
Pen-Sen Huang ◽  
Ping-Yen Tsai ◽  
Ling-Yu Yang ◽  
Daniela Lecca ◽  
Weiming Luo ◽  
...  

Traumatic brain injury (TBI) is a leading cause of disability and mortality worldwide. It can instigate immediate cell death, followed by a time-dependent secondary injury that results from disproportionate microglial and astrocyte activation, excessive inflammation and oxidative stress in brain tissue, culminating in both short- and long-term cognitive dysfunction and behavioral deficits. Within the brain, the hippocampus is particularly vulnerable to a TBI. We studied a new pomalidomide (Pom) analog, namely, 3,6′-dithioPom (DP), and Pom as immunomodulatory imide drugs (IMiD) for mitigating TBI-induced hippocampal neurodegeneration, microgliosis, astrogliosis and behavioral impairments in a controlled cortical impact (CCI) model of TBI in rats. Both agents were administered as a single intravenous dose (0.5 mg/kg) at 5 h post injury so that the efficacies could be compared. Pom and DP significantly reduced the contusion volume evaluated at 24 h and 7 days post injury. Both agents ameliorated short-term memory deficits and anxiety behavior at 7 days after a TBI. The number of degenerating neurons in the CA1 and dentate gyrus (DG) regions of the hippocampus after a TBI was reduced by Pom and DP. DP, but not Pom, significantly attenuated the TBI-induced microgliosis and DP was more efficacious than Pom at attenuating the TBI-induced astrogliosis in CA1 and DG at 7D after a TBI. In summary, a single intravenous injection of Pom or DP, given 5 h post TBI, significantly reduced hippocampal neurodegeneration and prevented cognitive deficits with a concomitant attenuation of the neuroinflammation in the hippocampus.


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