Posts Tagged Brain Injuries

[Abstract] A Framework for Tele-rehabilitation Gaming System

Abstract

Brain damage resulting from stroke and traumatic brain injury is the primary cause of complicated disability and one of the major causes of mortality in most countries, burdening healthcare systems owing to the growth in the number of brain injury victims. Rehabilitation is required to deal with the brain damage. With fewer therapists available, it is very challenging to manage patients and even motivate them to participate actively in their rehabilitation. Patients have frequently complained that many traditional rehabilitation systems are monotonous and uninteresting. The study’s objective is to propose a telerehabilitation gaming system framework that can serve as guidance for developing an affordable rehabilitation gaming system that can motivate and engage patients and increase rehabilitation effectiveness. The research methodology is based on synthesizing related research and currently available technologies. The proposed framework includes the therapist and patient attached with vital constructs: tailoring tools, instructional content, game characteristics, tailored games, and performance. It is an internet-based communication structure that connects the Rehabilitation Gaming System to the hospital and other care provider networks. The proposed framework is evaluated by a panel of five experts. The results reveal that all experts believe that the proposed framework can serve as a useful guide for creating gaming interventions that can boost the patient’s motivation and engagement and increase the effectiveness of rehabilitation.

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[Guidebook] In‐home cognitive stimulation guidebook: Activities to stimulate thinking skills of people with brain disorders

Abstract

This guidebook offers a variety of activities designed to stimulate thinking skills of people who are recovering from a brain disorder. Many activities can be done by the person with brain injury on a device, like a computer, tablet, smartphone, or game console. Some setup assistance by the facilitator may be needed. Each activity provides a group of tasks, listed by their level of difficulty, that aim to stimulate one or more of the cognitive skills that may be affected by a brain disorder: academics, attention/concentration, fine motor, language, memory, problem solving, and processing speed.

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[Factsheet] Stress management for caregivers of individuals with traumatic brain injury

Abstract 

This fact sheet describes strategies that caregivers of individuals with traumatic brain injury (TBI) can use to manage stress. It includes tips on practicing mindfulness; accepting thoughts and feelings; maintaining personal activities; rewarding oneself; creative thinking and problem-solving; seeking support from family and friends, other caregivers, and professional counselors; and tips for caregivers of service members and veterans. 

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[Guidebook] In‐home cognitive stimulation guidebook: Activities to stimulate thinking skills of people with brain disorders

Instructions

This guidebook offers a variety of stimulating activities for people who are recovering from a brain
disorder. Most activities are intended to be done in a 1‐on‐1 setting with two people.

  1. Person with a brain injury – This includes anyone who has experienced a brain disorder that
    impairs the person’s basic cognitive (thinking) skills, which might include paying attention,
    concentrating, and remembering new information and events.
  2. Facilitator – This includes anyone who leads the activities, which might include a family
    member, a therapist or others.
    Many activities can be done by the person with brain injury on a device, like a computer, tablet,
    smartphone, or game console. Some setup assistance by the facilitator may be needed.

[…]

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[Abstract] Return to Driving After Moderate-to-Severe Traumatic Brain Injury: A Traumatic Brain Injury Model System Study

Abstract

Objective: Describe who is able to return to driving (RTD) after moderate-to-severe traumatic brain injury (TBI), when this occurs, who maintains that activity, and the association with outcome.

Design: Cross-sectional descriptive study.

Setting: Eight follow-up sites of the TBI Model Systems (TBIMS) program. Participants: 618 participants enrolled in the TBIMS and 88 caregivers (N=706).

Interventions: Not applicable.

Main Outcome Measures: A survey was completed from 1-30 years postinjury focusing on RTD. Descriptors included demographic information, injury severity, and current employment status. Outcome was assessed at the time of the interview, including depression, quality of life, functional status, and community participation.

Results: Of 706 respondents, 78% (N = 552) RTD, but 14% (N = 77) of these did not maintain that activity. Of those who RTD, 43% (N = 192) did so within 6 months of the injury and 92% did so within 24 months postinjury. The percentage of people driving after TBI did not differ significantly based on age at time of injury or follow-up. There were significant differences between drivers and nondrivers with respect to severity of injury, seizures, race, education, employment, rural vs urban setting, marital status, and family income. We performed a multivariate logistic regression to examine the association between driving status and demographic variables, adjusting for other variables in the model. The strongest associations were with current employment, family income, race, seizures, and severity of injury. Driving was associated with greater community participation, better functional outcomes, fewer symptoms of depression, and greater life satisfaction.

Conclusions: Over a span of 30 years, three-quarters of people experiencing moderate-to-severe TBI return to driving a personal vehicle, although not everyone maintains this activity. Employment, race, family income, and seizures are strongly associated with RTD.

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[Abstract] Relations Among Suicidal Ideation, Depressive Symptoms, and Functional Independence During the 10 Years After Traumatic Brain Injury: A Model Systems Study

Abstract

Objective: To investigate relative causality in relations among suicidal ideation (SI), depressive symptoms, and functional independence over the first 10 years after traumatic brain injury (TBI).

Design: Prospective longitudinal design with data collected through the Traumatic Brain Injury Model Systems (TBIMS) network at acute rehabilitation hospitalization as well as 1, 2, 5, and 10 years after injury.

Setting: United States Level I/II trauma centers and inpatient rehabilitation centers with telephone follow-up.

Participants: Individuals enrolled into the TBIMS National Database (N=9539) with at least 1 SI score at any follow-up data collection (72.1% male; mean age, 39.39y).

Interventions: Not applicable.

Main outcome measures: Patient Health Questionnaire-9 and FIM at years 1, 2, 5, and 10 post injury.

Results: A cross-lagged panel structural equation model, which is meant to indirectly infer causality through longitudinal correlational data, suggested that SI, depressive symptoms, and functional independence each significantly predicted themselves over time. Within the model, bivariate correlations among variables were all significant within each time point. Between years 1 and 2 and between years 2 and 5, depressive symptoms had a larger effect on SI than SI had on depressive symptoms. Between years 5 and 10, there was reciprocal causality between the 2 variables. Functional independence more strongly predicted depressive symptoms than the reverse between years 1 and 2 as well as years 2 and 5, but its unique effects on SI over time were extremely marginal or absent after controlling for depressive symptoms.

Conclusions: A primary goal for rehabilitation and mental health providers should be to monitor and address elevated symptoms of depression as quickly as possible before they translate into SI, particularly for individuals with TBI who have reduced functional independence. Doing so may be a key to breaking the connection between low functional independence and SI.

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[ARTICLE] Traumatic brain injury pharmacological treatment: recommendations – Full Text

ABSTRACT

This article presents the recommendations on the pharmacological treatment employed in traumatic brain injury (TBI) at the outpatient clinic of the Cognitive Rehabilitation after TBI Service of the Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, Brazil. A systematic assessment of the consensus reached in other countries, and of articles on TBI available in the PUBMED and LILACS medical databases, was carried out. We offer recommendations of pharmacological treatments in patients after TBI with different symptoms.

Traumatic brain injury (TBI) is an insult to the brain due to an external mechanical force. There is a potential temporary or permanent occurrence of cognitive, physical and psychosocial deficits, associated with, or without, a decrease or alteration of the level of consciousness1. It is one of the most frequent causes of morbidity and mortality worldwide, with an important impact on quality of life2.

In Brazil, TBI is responsible for high mortality rates, the main cause of which is traffic accidents, and is more prevalent in young males2. In 1993, in the state of São Paulo, 57,000 deaths from TBI were reported3. Brazilian data indicate that around 700,000 to 1.1 million people are victims of TBI, of whom 20-30% have moderate to severe TBI.

Therefore, guidelines for management of the person who has had a TBI are of paramount importance to guide the health team at all stages of the care and rehabilitation process. In this article, the emphasis on the motor component of rehabilitation will not be addressed, as it has already been covered in another guideline4.

The aim of this article is to update the practice parameters regarding late TBI care for outpatients, focusing on the question: Is pharmacological treatment effective in treating the cognitive-behavioral symptoms of TBI patients?

This guideline’s target audiences are neurosurgeons, neurologists, physiatrists, psychiatrists, ophthalmologists, neuropsychologists, psychologists, speech therapists, occupational therapists and nurses, to guide and provide information on the treatment of adults with traumatic brain injury, with emphasis on outpatient care.

METHODS

We systematically reviewed the literature (MEDLINE database) from 1966 to December 2016 for pertinent evidence. We assessed the evidence for quality and synthesized this into conclusions using the Grading of Recommendations Assessment, Development and Evaluation process. For some topics, we accessed papers from 2004 to April 2014, using organized questions based on “Patients”; “Intervention”; “Controls” and “Outcome”. As key words we used: TBI, head trauma, treatment, pharmacological treatment. We have organized the presentation of this paper according to the most frequently-asked questions in this area.

Is pharmacological treatment effective in treating the cognitive-behavioral symptoms of TBI patients?

With these descriptors, cross-references across databases were made according to the theme proposed in each topic of the questions. After analysis of this material, the articles with the most available scientific information were selected, and the evidences that based the guidelines of this document were established. For available randomized and controlled studies, the classification of the strength of evidence was based on the Jadad scale. Work done on children (under 16 years of age) and those written in languages other than Portuguese, English, French and Spanish were excluded. The recommendations regarding the questions in this guideline were prepared by the experts in their respective areas of activity and reviewed by all members in a forum created for this purpose (consensus). The preparation of this document was based on the methodological strategies advocated by the Appraisal of Guidelines for Research & Evaluation (AGREE II).

All the authors contributed equally to this work. Approved by the Guideline Development Subcommittee on May 31, 2014, specialists and several health professionals met in São Paulo, SP, to define the consensus for outpatient treatment of TBI patients. Neurologists, neurosurgeons, psychiatrists, ophthalmologists, occupational therapists, neuropsychologists, speech therapists and nurses were present.

Degree of recommendation and strength of evidence:

  1. Experimental or observational studies of greater consistency.
  2. Experimental or observational studies of less consistency.
  3. Case reports (uncontrolled studies).
  4. Opinion that is not critically-based on consensus, physiological studies or animal models.

Perspectives of the target population

Research was conducted with open questions among patients suffering from TBI and their relatives, at a specific outpatient clinic of a tertiary hospital. The main concerns were collected and the domains of greatest interest were selected.

RESULTS AND DISCUSSION

Is pharmacological treatment effective in treating the cognitive-behavioral symptoms of TBI patients?

The drug-based approach is based on the functional anatomic knowledge of the encephalic region affected by TBI4. Therefore, it is necessary to know the pathophysiology of the different types of TBI, assessing lesion location and specific clinical findings4.

Methylphenidate

In a study of 40 patients with moderate-to-severe TBI in the rehabilitation phase, the primary goal of which was to assess care, the administration of methylphenidate (3 mg/kg, 2x daily) increased the speed of information processing in several neuropsychological tests, when compared to the use of placebo5 (B).

Agomelatine

The use of agomelatine (25 mg every night) leads to greater sleep efficiency, with a lasting effect6 (C).

Modafinil

Modafinil promotes an increase in alertness by the activation of noradrenergic and dopaminergic systems. Two controlled clinical studies, totaling 115 patients, evaluated the use of modafinil for excessive drowsiness and fatigue in patients with severe TBI for longer than a year7,8. A meta-analysis of these studies showed a therapeutic effect of modafinil on fatigue (evaluated by a fatigue severity scale), with a mean difference of -0.82 (95%CI -1.54– -0.11 p = 0.02, I2 = 0%)9 Regarding excessive daytime sleepiness, the meta-analysis revealed no significant difference between the modafinil group and the placebo group. To assess this outcome, the heterogeneity between the two studies was very high (I2 = 70%) (A).

Amantadine

Amantadine is a dopaminergic and serotonergic agonist, and acts by blocking NMDA receptors. In a controlled study of 76 patients over six months of their TBI, the use of amantadine (100 mg, 2x daily for 28 days) was shown to be safe and effective in reducing the frequency and severity of irritability symptoms (-4.3 points in the irritability domain of the neuropsychiatric inventory, in the amantadine group, P = .0085)10. In this study, aggression symptoms were also reduced when 18 patients who had minimal or no symptoms of aggression were excluded (-4.5 points in the aggression domain of the neuropsychiatric inventory in the amantadine group, P = .046) (A). In a study of 184 patients in a persistent vegetative state or minimal state of consciousness between four and 16 weeks after TBI, the use of amantadine (200-400 mg / day) accelerated the rate of functional recovery during the first four weeks of treatment, compared to placebo (p = 0.007)11 (A).

Venlafaxine

One study on venlafaxine use was included in our guideline. A case report demonstrated that the use of venlafaxine (75 mg twice daily) in a post-obsessive-compulsive disorder might improve obsessive behaviors, irritability and sadness symptoms12(C).

Valproate

Two studies on valproate use were included in our guideline. Valproate appears to have benign neuropsychological effects, and is a safe drug to control established seizures or stabilize mood. However, it should not be used as a prophylactic measure in post-traumatic seizures as it does not prevent these13 (B). Valproate therapy showed no difference when compared with phenytoin therapy. Valproate should not be used routinely to prevent post-traumatic seizures14 (B).

Antidepressants

Five studies on antidepressant use were included in our guideline. The use of citalopram was not indicated for the prevention of relapse of major depression (measured by the Hamilton Depression Rating Scale) after TBI15 (B). The use of sertraline did not seem to prevent the development of cognitive and compartmental problems after TBI16 (B). There was no evidence that early administration of sertraline decreased the expression of depressive symptoms after discontinuation of the drug17 (B). The use of fluoxetine for six months in patients with post-traumatic stress decreased relapse rates, as measured by the Clinical Global Impressions Scale18 (B). Methylphenidate and sertraline had similar effects on depressive symptoms (evaluated by the Beck Depression Inventory and the Hamilton Depression Rating Scale). However, methylphenidate appeared to have more improvements in cognitive functions and was also beneficial in keeping the patient alert during the day. In addition, methylphenidate showed better tolerability than sertraline19 (B).

Dopaminergic agonist

One study on dopaminergic agonist use was included in our guideline.

The use of bromocriptine (5 g, 2 x daily) in post-TBI subjects with attentional problems did not improve alertness skills and may have been associated with a number of adverse effects20 (B).

Rivastigmine

One study on rivastigmine use was included in our guideline.

The use of rivastigmine demonstrated safety and was well tolerated by patients with TBI. Rivastigmine appeared promising in the subgroup of patients with moderate/ severe memory impairment. The Cambridge Automated Neuropsychological Assessment Battery and Hopkins’ Verbal Learning Test were used as evaluation measures21 (B).

Galantamine

One study on galantamine use was included in our guideline.

Acetylcholinesterase inhibitors have great potential in the treatment of chronic phase TBI, improving fatigue, memory, attention and initiative. However, there were no significant differences between the drugs galantamine, rivastigmine and donepezil22 (B).

Donepezil

Two studies on donepezil use were included in our guideline.

The use of donepezil in chronic traumatic encephalopathy patients with cognitive impairment promoted clinical improvement (observed in the Mini-Mental Status Examination, Wechsler Memory Test, Boston Naming Test and Color Progressive Matrix Test) and improved metabolism in the frontal, parietal, occipital and temporal lobes23 (B). The drug improved neuropsychological test scores (measured by the Wechsler-III Memory Scale and the Serially Paced Auditory Test) related to short-term memory and sustained attention24 (B).

Recommendations

The use of amantadine to improve functionality between four and 16 weeks is recommended. Although several drugs are being tested to improve the chronic symptoms of TBI, there is a lack of high quality data to testify to the benefits of these drugs. Even so, as long as they are used in a specific way for the symptoms as reported above, the drugs methylphenidate to ameliorate cognitive impairment; agomelatine to improve sleep; modafinil for fatigue; fluoxetine to alleviate depressive symptoms; and rivastigmine and donepezil for memory impairment; may be used in an individualized approach.

REFERENCES

1. Jang SH. Review of motor recovery in patients with traumatic brain injury. NeuroRehabilitation. 2009;24(4):349-53. https://do.org/10.3233/NRE-2009-0489 [ Links ]

2. Hyder AA, Wunderlich CA, Puvanachandra P, Gururaj G, Kobusingye OC. The impact of traumatic brain injuries: a global perspective. NeuroRehabilitation. 2007;22(5):341-53. [ Links ]

3. Andrade AF, Manreza LA, Giudicissi M. Filho, Miura FK. Normas de atendimento ao paciente com traumatismo crânio-encefálico. Temas Atuais Neurocirur. 1996;2:1-22. [ Links ]

4. Plantier D, Luauté J. Drugs for behavior disorders after traumatic brain injury: systematic review and expert consensus leading to French recommendations for good practice. Ann Phys Rehabil Med. 2016 Feb;59(1):42-57. https://doi.org/10.1016/j.rehab.2015.10.003 [ Links ]

5. Willmott C, Ponsford J. Efficacy of methylphenidate in the rehabilitation of attention following traumatic brain injury: a randomised, crossover, double blind, placebo controlled inpatient trial. J Neurol Neurosurg Psychiatry. 2009 May;80(5):552-7. https://doi.org/10.1136/jnnp.2008.159632 [ Links ]

6. O’Neill B, Gardani M, Findlay G, Whyte T, Cullen T. Challenging behaviour and sleep cycle disorder following brain injury: a preliminary response to agomelatine treatment. Brain Inj. 2014;28(3):378-81. https://doi.org/10.3109/02699052.2013.865264 [ Links ]

7. Kaiser PR, Valko PO, Werth E, Thomann J, Meier J, Stocker R et al. Modafinil ameliorates excessive daytime sleepiness after traumatic brain injury. Neurology. 2010 Nov;75(20):1780-5. https://doi.org/10.1212/WNL.0b013e3181fd62a2 [ Links ]

8. Jha A, Weintraub A, Allshouse A, Morey C, Cusick C, Kittelson J et al. A randomized trial of modafinil for the treatment of fatigue and excessive daytime sleepiness in individuals with chronic traumatic brain injury. J Head Trauma Rehabil. 2008 Jan-Feb;23(1):52-63. https://doi.org/10.1097/01.HTR.0000308721.77911.ea [ Links ]

9. Sheng P, Hou L, Wang X, Wang X, Huang C, Yu M et al. Efficacy of modafinil on fatigue and excessive daytime sleepiness associated with neurological disorders: a systematic review and meta-analysis. PLoS One. 2013 Dec;8(12):e81802. https://doi.org/10.1371/journal.pone.0081802 [ Links ]

10. Hammond FM1. Bickett AK, Norton JH, Pershad R. Effectiveness of amantadine hydrochloride in the reduction of chronic traumatic brain injury irritability and aggression. J Head Trauma Rehabil. 2014 Sep-Oct;29(5):391-9. https://doiorg/10.1097/01.HTR.0000438116.56228.de [ Links ]

11. Giacino JT, Whyte J, Bagiella E, Kalmar K, Childs N, Khademi A et al. Placebo-controlled trial of amantadine for severe traumatic brain injury. N Engl J Med. 2012 Mar;366(9):819-26. https://doi.org/10.1056/NEJMoa1102609 [ Links ]

12. Khouzam HR, Donnelly NJ. Remission of traumatic brain injury-induced compulsions during venlafaxine treatment. Gen Hosp Psychiatry. 1998 Jan;20(1):62-3. https://doi.org/10.1016/S0163-8343(97)00097-2 [ Links ]

13. Dikmen SS, Machamer JE, Winn HR, Anderson GD, Temkin NR. Neuropsychological effects of valproate in traumatic brain injury: a randomized trial. Neurology. 2000 Feb;54(4):895-902. https://doi.org/10.1212/WNL.54.4.895 [ Links ]

14. Temkin NR, Dikmen SS, Anderson GD, Wilensky AJ, Holmes MD, Cohen W et al. Valproate therapy for prevention of posttraumatic seizures: a randomized trial. J Neurosurg. 1999 Oct;91(4):593-600. https://doi.org/10.3171/jns.1999.91.4.0593 [ Links ]

15. Rapoport MJ, Mitchell RA, McCullagh S, Herrmann N, Chan F, Kiss A et al. A randomized controlled trial of antidepressant continuation for major depression following traumatic brain injury. J Clin Psychiatry. 2010 Sep;71(9):1125-30. https://doi.org/10.4088/JCP.09m05086blu [ Links ]

16. Baños JH, Novack TA, Brunner R, Renfroe S, Lin HY, Meythaler J. Impact of early administration of sertraline on cognitive and behavioral recovery in the first year after moderate to severe traumatic brain injury. J Head Trauma Rehabil. 2010 Sep-Oct;25(5):357-61. https://doi.org/10.1097/HTR.0b013e3181d6c715 [ Links ]

17. Novack TA, Baños JH, Brunner R, Renfroe S, Meythaler JM. Impact of early administration of sertraline on depressive symptoms in the first year after traumatic brain injury. J Neurotrauma. 2009 Nov;26(11):1921-8. https://doi.org/10.1089/neu.2009.0895 [ Links ]

18. Davidson JR, Connor KM, Hertzberg MA, Weisler RH, Wilson WH, Payne VM. Maintenance therapy with fluoxetine in posttraumatic stress disorder: a placebo-controlled discontinuation study. J Clin Psychopharmacol. 2005 Apr;25(2):166-9. https://doi.org/10.1097/01.jcp.0000155817.21467.6c [ Links ]

19. Whyte J, Vaccaro M, Grieb-Neff P, Hart T, Polansky M, Coslett HB. The effects of bromocriptine on attention deficits after traumatic brain injury: a placebo-controlled pilot study. Am J Phys Med Rehabil. 2008 Feb;87(2):85-99. https://doi.org/10.1097/PHM.0b013e3181619609 [ Links ]

20. Lee H, Kim SW, Kim JM, Shin IS, Yang SJ, Yoon JS. Comparing effects of methylphenidate, sertraline and placebo on neuropsychiatric sequelae in patients with traumatic brain injury. Hum Psychopharmacol. 2005 Mar;20(2):97-104. https://doi.org/10.1002/hup.668 [ Links ]

21. Whyte J, Vaccaro M, Grieb-Neff P, Hart T, Polansky M, Coslett HB. The effects of bromocriptine on attention deficits after traumatic brain injury: a placebo-controlled pilot study. Am J Phys Med Rehabil. 2008 Feb;87(2):85-99. https://doi.org/10.1097/PHM.0b013e3181619609 [ Links ]

22. Silver JM, Koumaras B, Chen M, Mirski D, Potkin SG, Reyes P et al. Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology. 2006 Sep;67(5):748-55. https://doi.org/10.1212/01.wnl.0000234062.98062.e9 [ Links ]

23. Tenovuo O. Central acetylcholinesterase inhibitors in the treatment of chronic traumatic brain injury-clinical experience in 111 patients. Prog Neuropsychopharmacol Biol Psychiatry. 2005 Jan;29(1):61-7. https://doi.org/10.1016/j.pnpbp.2004.10.006 [ Links ]

24. Kim YW, Kim DY, Shin JC, Park CI, Lee JD. The changes of cortical metabolism associated with the clinical response to donepezil therapy in traumatic brain injury. Clin Neuropharmacol. 2009 Mar-Apr;32(2):63-8. https://doi.org/10.1097/WNF.0b013e31816f1bc1 [ Links ]

25. Zhang L, Plotkin RC, Wang G, Sandel ME, Lee S. Cholinergic augmentation with donepezil enhances recovery in short-term memory and sustained attention after traumatic brain injury. Arch Phys Med Rehabil. 2004 Jul;85(7):1050-5. https://doi.org/10.1016/j.apmr.2003.10.014 [ Links ]

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[Abstract] Functional Change from Five to Fifteen Years after Traumatic Brain Injury

Abstract

Few studies have assessed the long-term functional outcomes of traumatic brain injury (TBI) in large, well-characterized samples. Using the Traumatic Brain Injury Model Systems cohort, this study assessed the maintenance of independence between years 5 and 15 post-injury and risk factors for decline. The study sample included 1381 persons with TBI who received inpatient rehabilitation, survived to 15 years post-injury, and were available for data collection at 5 or 10 years and 15 years post-injury. The Functional Independence Measure (FIM) and Disability Rating Scale (DRS) were used to measure functional outcomes. The majority of participants had no changes during the 10-year time frame. For FIM, only 4.4% showed decline in Self-Care, 4.9% declined in Mobility, and 5.9% declined in Cognition. Overall, 10.4% showed decline in one or more FIM subscales. Decline was detected by DRS Level of Function (24% with >1-point change) and Employability (6% with >1-point change). Predictors of decline factors across all measures were age >25 years and, across most measures, having less than or equal to a high school education. Additional predictors of FIM decline included male sex (FIM Mobility and Self-Care) and longer rehabilitation length of stay (FIM Mobility and Cognition). In contrast to studies reporting change in the first 5 years post-TBI inpatient rehabilitation, a majority of those who survive to 15 years do not experience functional decline. Aging and cognitive reserve appear to be more important drivers of loss of function than original severity of the injury. Interventions to identify those at risk for decline may be needed to maintain or enhance functional status as persons age with a TBI.

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[Abstract] The Brain Injury Functional Outcome Measure (BI-FOM): A single instrument capturing the range of recovery in moderate-severe traumatic brain injury

Abstract

Objective

To develop a measure of global functioning after moderate-severe TBI with similar measurement precision but a longer measurement range than the FIM.

Design

Phase 1: Retrospective analysis of 5 data sets containing FIM, DRS, and other assessment items, to identify candidate items for extending the measurement range of the FIM; Phase 2. Prospective administration of 49 candidate items from phase 1, with Rasch analysis to identify a unidimensional scale with an extended range.

Setting

Six TBI Model System rehabilitation hospitals.

Participants

184 individuals with moderate-severe injury recruited during inpatient rehabilitation or at 1-year telephone follow up.

Interventions

Participants were administered the 49 assessment items in person or via telephone.

Main Outcome Measure(s)

IRT parameters: item monotonicity, infit/outfit statistics, and Factor 1 variance.

Results

After collapsing misordered rating categories and removing misfitting items, we derived the Brain Injury Functional Outcome Measure (BI-FOM), a 31-item assessment instrument with high reliability, greatly extended measurement range, and improved unidimensionality in comparison to the FIM.

Conclusions

The BI-FOM improves global measurement of function after moderate-severe brain injury. Its high precision, relative lack of floor and ceiling effects, and feasibility for telephone follow up, if replicated in an independent sample, are substantial advantages.

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[Abstract] Understanding the multidimensional nature of sexuality after traumatic brain injury

Abstract

Objective

To investigate the association of sexuality with sociodemographic (age, sex, education), medical (injury severity, time since injury), physical (fatigue, pain, independence), neuropsychological (memory, attention, executive function), psychological (depression, anxiety, self-esteem), and social participation factors after traumatic brain injury (TBI).

Design

Survey. Individuals with TBI completed measures at a mean average of 2.78 years post-injury (range = 1-10.3 years).

Setting

All participants were community based at the time of data collection.

Participants

Eighty-four individuals with TBI consecutively recruited after discharge from rehabilitation and 88 age-, sex- and education-matched controls recruited from the general community.

Interventions

Not applicable.

Main Outcome Measure

Brain Injury Questionnaire of Sexuality (BIQS).

Results

Individuals with TBI performed significantly worse on sexuality, mood and self-esteem measures compared to the healthy control group, supporting previous findings. Research findings highlighted a range of significant correlations between sociodemographic, physical, neuropsychological, psychological and social participation factors and sexuality outcomes after TBI. In the multiple regression model, older age, greater depression and lower self-esteem were significant predictors of poorer sexuality post-injury. Further analyses indicated that depression mediated the independent relationships between lower social participation and greater fatigue with a decline in sexuality after TBI.

Conclusions

These findings support sexuality changes after TBI as a multidimensional construct, highlighting depression as a key mechanism through which other factors may impact sexual functioning. Further research is needed to target assessment and intervention services for sexuality problems after TBI.

via Understanding the multidimensional nature of sexuality after traumatic brain injury – Archives of Physical Medicine and Rehabilitation

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