Chronic Cognitive Impairment Following Traumatic Brain Injury: A Closer Look

by Ioannis Mavroudis
65 minutes read

Introduction

Traumatic brain injuries (TBIs), particularly those classified as mild traumatic brain injuries (mTBIs) or concussions, stand at the forefront of public health concerns due to their high incidence and potential to inflict lasting cognitive and functional impairments. As our society becomes increasingly aware of the risks associated with recreational activities, sports, and occupational hazards, the issue of TBIs, especially mTBIs, has garnered significant attention from both the medical community and the general public. This increased awareness has spurred a surge in research aimed at unraveling the complexities of mTBI outcomes, challenging longstanding perceptions and driving a paradigm shift in our understanding of concussion aftermath. This article aims to delve into the nuanced landscape of cognitive impairment following TBI, highlighting the prevalence and characteristics of such impairments, exploring the underlying mechanisms and pathophysiology, and examining the critical role of psychology in both the manifestation and management of these conditions.

Historically, mTBIs were considered minor injuries with transient effects, warranting little medical intervention beyond rest and monitoring. This perspective was rooted in the initial absence of overt neurological deficits and the general expectation of a full recovery. However, as research delved deeper into the long-term consequences of mTBIs, a starkly different picture emerged. Studies began to document cases where individuals experienced persistent, sometimes debilitating, cognitive, emotional, and physical symptoms long after the initial injury, a condition now recognized as post-concussion syndrome (PCS).

The challenge in understanding and treating mTBIs lies not only in their diverse presentations but also in the variability of their outcomes. Cognitive impairments following mTBI can range from mild, short-lived difficulties with concentration and memory to severe, long-term deficits that significantly impact daily functioning and quality of life. The prevalence of such impairments has been historically underestimated, with recent evidence suggesting that a substantial proportion of individuals sustaining a single mTBI may experience cognitive difficulties at various stages post-injury. This revelation marks a crucial departure from the previously estimated figures, indicating a need to reevaluate our approaches to mTBI assessment and management.

The intricacies of cognitive impairment post-mTBI extend beyond mere prevalence. The mechanisms underlying these impairments involve complex pathophysiological processes initiated by the injury. Among these are diffuse axonal injury (DAI) and the neurometabolic cascade, which together disrupt the brain’s structural integrity and biochemical equilibrium. DAI affects the brain’s white matter tracts, leading to compromised neuronal communication and brain function. The neurometabolic cascade triggers a series of biochemical events that alter neurotransmitter activity and brain excitability, further complicating the brain’s ability to operate normally.

Adding another layer of complexity is the role of psychological factors in the development and management of cognitive impairments post-TBI. Psychological resilience, mental health disorders, and coping strategies significantly influence the manifestation of symptoms and the trajectory of recovery. Psychological interventions, such as cognitive-behavioral therapy, have shown promise in addressing the emotional and cognitive challenges faced by individuals post-injury. These interventions highlight the intertwined nature of the neurological and psychological aspects of mTBI, underscoring the necessity for a holistic approach to treatment that addresses both cognitive impairments and emotional well-being.

The evolving understanding of mTBI has profound implications for clinical practice, research, and public health policy. It challenges the adequacy of current diagnostic criteria and treatment protocols, which have traditionally focused on the physical aspects of injury. The recognition of the high incidence of cognitive impairment and the complex interplay of neurological and psychological factors calls for a reevaluation of how mTBIs are assessed, diagnosed, and managed. This reevaluation necessitates a shift towards more sensitive and comprehensive assessment tools that can detect subtle cognitive changes and a multidisciplinary approach to treatment that integrates neurological, psychological, and rehabilitative interventions.

As we continue to explore the long-term outcomes of mTBI, it is imperative that we translate these insights into practice. This involves not only improving diagnostic and treatment strategies but also enhancing education and prevention efforts to reduce the incidence of mTBI and mitigate its impact. By fostering a deeper understanding of the multifaceted nature of mTBI and its consequences, we can better support individuals affected by this injury, facilitating their recovery and improving their quality of life.

Prevalence and Characteristics

Cognitive impairment following traumatic brain injury (TBI), particularly mild traumatic brain injury (mTBI) or concussion, has emerged as a focal point of contemporary neurological research due to its significant impact on individuals’ lives and its broader societal implications. As the most common form of TBI, mTBI has traditionally been viewed through a lens that emphasized its transient nature, with expectations of full recovery. However, accumulating evidence challenges this perspective, revealing a nuanced and concerning picture of the long-term cognitive effects of even a single concussion. This section delves into the prevalence and characteristics of cognitive impairment after TBI, highlighting the critical need for a shift in both public perception and clinical approach.

Prevalence of Cognitive Impairment after TBI

Recent advancements in neuroimaging and neuropsychological assessment have illuminated the extent of cognitive impairments post-TBI, particularly following mTBIs. Contrary to earlier beliefs that pegged post-concussion syndrome (PCS)ā€”a constellation of symptoms including cognitive deficitsā€”at affecting about 15% of individuals, newer studies indicate that this number significantly underestimates the true prevalence. Research now suggests that upwards of 55% of individuals experiencing a single mTBI exhibit cognitive impairments at various stages post-injury. This stark discrepancy calls for an urgent reassessment of our understanding of mTBI outcomes, emphasizing the condition’s potential to cause long-lasting cognitive challenges.

The implications of these findings are profound, not only for those directly affected but also for healthcare systems and societal structures at large. The high prevalence of cognitive impairment following mTBI necessitates enhanced awareness, early detection, and comprehensive management strategies to address the needs of this substantial patient population.

Characteristics of Cognitive Impairment after TBI

Cognitive impairments following TBI can manifest across a broad spectrum, affecting various domains of cognitive function. These impairments often include difficulties with memory, attention and concentration, executive functions (such as planning, organizing, and problem-solving), processing speed, and language abilities. The manifestation of these impairments can vary significantly among individuals, influenced by factors such as the severity of the injury, the area of the brain affected, and individual patient characteristics, including pre-existing health conditions and resilience.

  1. Memory and Attention: Memory problems, especially difficulties with short-term memory, are among the most commonly reported cognitive impairments after TBI. Individuals may struggle to remember new information, follow conversations, or recall daily tasks. Attention deficits further complicate this picture, as individuals may find it challenging to focus, multitask, or maintain attention over extended periods.
  2. Executive Functioning: Executive functions are critical for independent, goal-directed behavior. Impairments in this area can result in difficulties with organizing tasks, making decisions, initiating actions, and regulating behavior. Such deficits can profoundly affect an individual’s ability to function in both personal and professional settings.
  3. Processing Speed and Language: Slowed processing speed is another hallmark of cognitive impairment post-TBI, with individuals often experiencing a noticeable lag in their ability to think, respond, and process information. Language impairments can range from finding the right words (aphasia) to understanding complex sentences, impacting communication and social interactions.

Variability and Individual Differences

The variability in cognitive impairment post-TBI underscores the complexity of the brain and the individualized nature of brain injury outcomes. Factors contributing to this variability include the injury’s location and severity, the individual’s age, gender, pre-injury cognitive and physical health status, and the presence of supportive environments or stressors. Moreover, the interplay between neurological damage and psychological factors, such as motivation, depression, and anxiety, can significantly influence the presentation and persistence of cognitive impairments.

The prevalence and characteristics of cognitive impairment following TBI, particularly mTBI, highlight a critical area of concern in both clinical practice and public health policy. The emerging understanding of these impairmentsā€”marked by their high prevalence, diverse manifestations, and significant impact on individuals’ daily livesā€”challenges previous perceptions and underscores the need for a comprehensive approach to diagnosis, treatment, and support. Recognizing the variability and individual differences in post-TBI cognitive impairment is crucial for developing personalized care plans that address the unique needs of each affected individual, ultimately improving outcomes and quality of life. As research continues to shed light on these issues, it is imperative that this knowledge informs clinical practices, public awareness campaigns, and policy decisions, ensuring that individuals affected by TBI receive the attention and resources they need to navigate the challenges of cognitive impairment.

Mechanisms and Pathophysiology

Understanding the mechanisms and pathophysiology underlying cognitive impairment after traumatic brain injury (TBI) is crucial for developing effective treatment strategies and improving patient outcomes. TBI, including its milder form, mild traumatic brain injury (mTBI) or concussion, triggers a complex cascade of biochemical, cellular, and physiological changes that can lead to lasting cognitive deficits. This section explores the intricate mechanisms and pathophysiological changes following TBI, shedding light on the intricate interplay between the brain’s structure and function that underpins cognitive impairment.

Primary and Secondary Injury Mechanisms

The pathophysiology of TBI can be categorized into primary and secondary injury mechanisms. Primary injury occurs at the moment of impact, resulting in immediate mechanical damage to the brain’s structure. This includes contusions, hemorrhages, and diffuse axonal injury (DAI), where the brain’s long connecting fibers are stretched or torn. While primary injuries are largely irreversible, understanding their nature and extent is vital for assessing the potential scope and trajectory of cognitive impairments.

Secondary injury mechanisms unfold in the minutes, hours, and days following the initial trauma. These involve a complex array of biochemical and physiological processes that exacerbate the damage initiated by the primary injury. Key elements of secondary injury include the neurometabolic cascade, inflammation, excitotoxicity, and disrupted cerebral blood flow, each contributing to the overall picture of cognitive impairment post-TBI.

The Neurometabolic Cascade

A hallmark of secondary injury is the neurometabolic cascade, a series of biochemical reactions triggered by the initial trauma. This cascade begins with a massive influx of ions across the neuronal membrane, leading to cellular depolarization and the excessive release of neurotransmitters. The brain’s attempt to restore ionic balance results in hyperglycolysis and increased metabolic demand, paradoxically coupled with reduced cerebral blood flow. This mismatch between supply and demand leads to energy crisis, cellular damage, and ultimately, cell death. The neurometabolic cascade is a critical factor in the development of cognitive impairments, as it affects the brain’s ability to process, encode, and retrieve information.

Diffuse Axonal Injury and White Matter Disruption

DAI is particularly relevant to cognitive impairment following TBI. It involves damage to the brain’s white matter tracts, the communication pathways that connect different brain regions. DAI disrupts these pathways, impairing the brain’s ability to integrate and process information across regions, leading to difficulties with attention, memory, and executive functions. Advanced imaging techniques, such as diffusion tensor imaging (DTI), have enhanced our ability to detect and quantify DAI, providing insights into the relationship between white matter damage and cognitive deficits.

Inflammation and Excitotoxicity

Inflammation plays a dual role following TBI. Initially, it is a protective response aimed at repairing damage and clearing debris. However, prolonged inflammation can exacerbate neuronal damage and contribute to cognitive impairment. Excitotoxicity, the pathological release of excitatory neurotransmitters like glutamate, further compounds this damage. High levels of glutamate overstimulate neurons, leading to calcium overload and activating a series of events that result in cell death. This neuronal loss and dysfunction are directly linked to the cognitive impairments observed after TBI.

Cerebral Blood Flow Dysregulation

Disrupted cerebral blood flow (CBF) following TBI further complicates the pathophysiological landscape. The initial trauma can lead to vascular injuries and blood-brain barrier disruption, resulting in altered perfusion and contributing to the secondary injury cascade. Changes in CBF can lead to ischemia in some regions while causing hyperperfusion in others, exacerbating cellular damage and contributing to cognitive decline.

The mechanisms and pathophysiology of cognitive impairment following TBI encompass a broad range of cellular, molecular, and physiological changes. From the initial mechanical damage to the complex secondary injury processes, each step in the cascade contributes to the cognitive deficits experienced by individuals post-TBI. Understanding these underlying mechanisms is crucial for developing targeted interventions and mitigating the long-term cognitive effects of TBI. As research advances, it is hoped that new insights into the pathophysiology of TBI will lead to more effective treatments and improved outcomes for those affected by this challenging condition.

The role of personality, psychological and social factors

The interplay of personality traits, psychological factors, and social factors plays a crucial role in the recovery and long-term outcomes of individuals with traumatic brain injury (TBI), including mild traumatic brain injuries (mTBIs). This complex interplay not only influences the manifestation and severity of cognitive impairments but also affects the overall recovery trajectory and quality of life post-injury. Understanding how these elements interact offers valuable insights into personalized care and rehabilitation strategies, highlighting the importance of a holistic approach to TBI recovery.

The Influence of Personality Traits

Personality traits can significantly impact how individuals cope with the aftermath of a TBI. Traits such as resilience, optimism, and conscientiousness have been linked to more positive outcomes, including better adjustment to changes in cognitive function and overall well-being. For instance, resilient individuals are more likely to employ adaptive coping strategies, facilitating their recovery and adaptation to new challenges posed by cognitive impairments. Conversely, traits like neuroticism may predispose individuals to negative emotional responses, such as anxiety and depression, which can complicate recovery and exacerbate cognitive deficits.

Personality traits also interact with cognitive impairments in nuanced ways. For example, an individual’s pre-injury personality may influence their awareness of cognitive deficits and motivation to engage in rehabilitation efforts. Those with a high degree of conscientiousness might be more diligent in following through with rehabilitation programs, thereby potentially enhancing their recovery outcomes.

Psychological Factors and Their Role in Recovery

Psychological factors, including mental health conditions such as depression and anxiety, significantly influence the recovery process and the experience of cognitive impairments following TBI. Depression is one of the most common psychological responses to TBI and can severely impact an individual’s motivation, energy levels, and engagement with rehabilitation, thereby influencing cognitive recovery. Anxiety, similarly, can exacerbate cognitive issues such as difficulties with concentration, memory, and executive function, creating a feedback loop that hinders recovery.

The psychological impact of TBI is not limited to these conditions. Factors such as self-efficacyā€”the belief in one’s ability to overcome challenges and achieve goalsā€”play a pivotal role in recovery. Higher levels of self-efficacy are associated with greater engagement in rehabilitation activities and better adjustment to post-injury life, highlighting the importance of psychological interventions that bolster self-efficacy and other adaptive psychological traits.

Social Factors and Support Systems

The role of social factors and support systems in the recovery from TBI cannot be overstated. Social support from family, friends, and professionals provides a buffer against the stress of injury and rehabilitation, offering emotional, informational, and practical assistance that is critical for recovery. Strong support networks are associated with better psychological well-being, reduced incidence of depression and anxiety, and improved cognitive outcomes.

The socio-economic status of the individual also plays a role in recovery, influencing access to healthcare, rehabilitation services, and support resources. Disparities in access can lead to differences in recovery trajectories and outcomes, underscoring the need for equitable healthcare policies and interventions that ensure all individuals with TBI have the support and resources necessary for optimal recovery.

The workplace and educational environments are additional social factors that significantly impact recovery and reintegration post-TBI. Accommodations and support in these settings can facilitate a smoother transition back to work or school, helping individuals regain a sense of normalcy and purpose. Conversely, environments that lack understanding or accommodations can exacerbate feelings of isolation and frustration, hindering recovery.

The Interplay of Personality, Psychological, and Social Factors

The recovery from TBI is a dynamic process influenced by the interplay of personality traits, psychological factors, and social support. This complex interaction underscores the importance of a holistic approach to TBI treatment and rehabilitation, one that considers the individual’s unique psychological makeup and social context. Tailoring interventions to address not only the physical and cognitive aspects of TBI but also the psychological and social dimensions can enhance recovery outcomes and quality of life for those affected.

Conclusion

In conclusion, personality traits, psychological factors, and social factors play integral roles in the recovery from traumatic brain injury, influencing the severity of cognitive impairments, the effectiveness of rehabilitation efforts, and the overall quality of life post-injury. Understanding and addressing these elements in a comprehensive and personalized manner is essential for optimizing recovery and supporting individuals in their journey back to health and well-being. As research in this area continues to evolve, it is hoped that greater insights into the interplay of these factors will lead to more effective, holistic treatment and rehabilitation strategies for TBI survivors.

Discussion

The multifaceted nature of traumatic brain injury (TBI), particularly mild traumatic brain injury (mTBI) or concussion, necessitates a comprehensive understanding of its outcomes, extending beyond the immediate physical and cognitive impairments to encompass the broader psychological and social domains. This discussion synthesizes insights from various sections, focusing on the prevalence and characteristics of cognitive impairment post-TBI, the underlying mechanisms and pathophysiology, and the significant role of personality traits, psychological factors, and social determinants in the recovery process. The goal is to highlight the interconnectedness of these elements and propose a holistic approach to treatment and rehabilitation that addresses the needs of individuals with TBI in their entirety.

Cognitive Impairment Post-TBI: A Prevalent and Complex Challenge

Cognitive impairments following TBI have been shown to be more prevalent and persistent than previously acknowledged, affecting a significant proportion of individuals. These impairments encompass a range of cognitive functions, including memory, attention, executive function, processing speed, and language abilities. The variability in the manifestation and severity of these impairments underscores the complexity of TBI outcomes and the necessity for individualized assessment and intervention strategies.

The high incidence of cognitive impairments post-TBI challenges the medical community to enhance diagnostic accuracy and develop more effective rehabilitation techniques. It also calls for a shift in societal perceptions, recognizing TBI not just as a transient physical injury but as a condition with potential long-term cognitive and psychological ramifications.

Unraveling the Mechanisms and Pathophysiology

The discussion on the mechanisms and pathophysiology of TBI reveals a cascade of biochemical, cellular, and physiological processes that contribute to cognitive impairment. This includes the immediate damage caused by the primary injury and the secondary injury mechanisms that unfold subsequently, such as the neurometabolic cascade, inflammation, excitotoxicity, and cerebral blood flow dysregulation. Understanding these processes is crucial for identifying therapeutic targets and developing interventions that can mitigate the secondary injury and promote neural recovery.

This knowledge also reinforces the need for continued research into innovative diagnostic tools, such as advanced neuroimaging techniques, which can provide deeper insights into the extent of brain injury and guide personalized rehabilitation plans. Furthermore, it highlights the importance of early intervention and ongoing monitoring to address the evolving nature of TBI pathophysiology.

The Role of Personality Traits, Psychological Factors, and Social Determinants

Personality traits, psychological factors, and social determinants play critical roles in the recovery and long-term outcomes of individuals with TBI. These elements influence the experience of cognitive impairments, the effectiveness of rehabilitation efforts, and the overall adjustment to post-injury life. For instance, traits such as resilience and optimism can facilitate recovery, while psychological conditions like depression and anxiety may hinder it. Similarly, strong social support systems can provide a buffer against the stress of recovery, while socio-economic disparities can limit access to care and resources, affecting outcomes.

The interplay between these factors underscores the necessity of a holistic approach to TBI care that encompasses not only medical and rehabilitative interventions but also psychological support and social reintegration programs. Tailoring treatment to the individual’s unique psychological profile and social context can enhance recovery and improve quality of life.

Implications for Treatment and Rehabilitation

Integrating the insights from cognitive impairments, mechanisms and pathophysiology, and the role of psychological and social factors leads to several implications for treatment and rehabilitation. Firstly, it emphasizes the need for a multidisciplinary approach to TBI care, involving neurologists, psychologists, rehabilitation therapists, and social workers, among others. This team can collaboratively address the physical, cognitive, emotional, and social aspects of TBI recovery.

Secondly, it calls for the development of personalized rehabilitation programs that consider the individual’s specific cognitive impairments, psychological state, and social environment. These programs should incorporate evidence-based interventions, including cognitive rehabilitation therapies, psychological counseling, and community reintegration activities.

Additionally, the discussion highlights the importance of patient and family education about TBI and its potential consequences. Educating patients, families, and the broader community can foster a supportive environment that recognizes the challenges faced by individuals with TBI and promotes empathy and understanding.

The Way Forward: Research and Policy Recommendations

Advancing the care and rehabilitation of individuals with TBI requires ongoing research focused on unraveling the complex interplay of factors influencing recovery. Future studies should aim to elucidate the mechanisms underlying cognitive impairments, develop more sensitive diagnostic tools, and evaluate the effectiveness of multidisciplinary rehabilitation approaches. Additionally, research into the psychological and social dimensions of TBI recovery can inform the development of interventions that address these critical aspects.

Policy recommendations include advocating for increased funding for TBI research, enhancing access to comprehensive rehabilitation services, and promoting policies that support the social reintegration of individuals with TBI. Furthermore, there is a need for public health initiatives that raise awareness about TBI prevention and the importance of early intervention.

Conclusion

The discussion of TBI and its aftermath highlights the condition’s complexity and the myriad factors influencing recovery. Cognitive impairments post-TBI are prevalent and multifaceted, underpinned by complex pathophysiological processes and significantly influenced by personality traits, psychological factors, and social determinants. Addressing the challenges posed by TBI requires a holistic approach to care that integrates medical, psychological, and social interventions, tailored to the individual’s unique needs. As research and clinical practice evolve, it is imperative to adopt strategies that enhance the recovery and well-being of individuals with TBI, ultimately leading to improved outcomes and quality of life.

Literature – further reading:

References

1. Shaw NA. The neurophysiology of concussion. Progress in Neurobiology. 2002;67(4):281ā€“344. [PubMed] [Google Scholar]

2. Cassidy JD, Carroll LJ, Peloso PM, Borg J, von Holst H, Holm L, et al. Incidence, risk factors and prevention of mild traumatic brain injury: results of the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. J Rehabil Med. 2004;43 Suppl:28ā€“60. [PubMed] [Google Scholar]

3. Definition of mild traumatic brain injury; Mild Traumatic Brain Injury Committee of the American Congress of Rehabilitation Medicine. Journal of Head Trauma Rehabilitation. 1993;8(3):86ā€“7. [Google Scholar]

4. Hall RCW, Hall RCW, Chapman MJ. Definition, diagnosis, and forensic implications of postconcussional syndrome. Psychosomatics. 2005;46(3):195ā€“202. 10.1176/appi.psy.46.3.195 [PubMed] [CrossRef] [Google Scholar]

5. Daneshvar DH, Riley DO, Nowinski CJ, McKee AC, Stern RA, Cantu RC. Long-term consequences: effects on normal development profile after concussion. Physical medicine and rehabilitation clinics of North America. 2011;22(4):683ā€“700. 10.1016/j.pmr.2011.08.009 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

6. Marshall S, Bayley M, McCullagh S, Velikonja D, Berrigan L. Clinical practice guidelines for mild traumatic brain injury and persistent symptoms. Canadian Family Physician. 2012;58(3):257ā€“67. [PMC free article] [PubMed] [Google Scholar]

7. Rutherford WH, Merrett JD, McDonald JR. Symptoms at one year following concussion from minor head injuries. Injury. 1979;10(3):225ā€“30. [PubMed] [Google Scholar]

8. Spinos P, Sakellaropoulos G, Georgiopoulos M, Stavridi K, Apostolopoulou K, Ellul J, et al. Postconcussion syndrome after mild traumatic brain injury in Western Greece. The Journal of trauma. 2010;69(4):789ā€“94. 10.1097/TA.0b013e3181edea67 [PubMed] [CrossRef] [Google Scholar]

9. Sterr A, Herron KA, Hayward C, Montaldi D. Are mild head injuries as mild as we think? Neurobehavioral concomitants of chronic post-concussion syndrome. BMC neurology. 2006;6:7-. 10.1186/1471-2377-6-7 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

10. Rabinowitz AR, Levin HS. Cognitive sequelae of traumatic brain injury. Psychiatr Clin North Am. 2014;37(1):1ā€“11. Epub 2014/02/18. 10.1016/j.psc.2013.11.004 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

11. Xiong K, Zhu Y, Zhang Y, Yin Z, Zhang J, Qiu M, et al. White matter integrity and cognition in mild traumatic brain injury following motor vehicle accident. Brain research. 2014;1591(1):86ā€“92. [PubMed] [Google Scholar]

12. Babikian T, McArthur D, Asarnow RF. Predictors of 1-month and 1-year neurocognitive functioning from the UCLA longitudinal mild, uncomplicated, pediatric traumatic brain injury study. Journal of the International Neuropsychological Society: JINS. 2013;19(2):145ā€“54. 10.1017/S135561771200104X [PubMed] [CrossRef] [Google Scholar]

13. Choe MC. The Pathophysiology of Concussion. Current pain and headache reports. 2016;20(6):42 10.1007/s11916-016-0573-9 [PubMed] [CrossRef] [Google Scholar]

14. Giza CC, Hovda DA. The New Neurometabolic Cascade of Concussion. Neurosurgery. 2014;75(0 4):S24ā€“S33. [PMC free article] [PubMed] [Google Scholar]

15. Inglese M, Makani S, Johnson G, Cohen BA, Silver JA, Gonen O, et al. Diffuse axonal injury in mild traumatic brain injury: a diffusion tensor imaging study. Journal of neurosurgery. 2005;103(2):298ā€“303. 10.3171/jns.2005.103.2.0298 [PubMed] [CrossRef] [Google Scholar]

16. Miles L, Grossman RI, Johnson G, Babb JS, Diller L, Inglese M. Short-term DTI predictors of cognitive dysfunction in mild traumatic brain injury. Brain injury. 2008;22(2):115ā€“22. 10.1080/02699050801888816 [PubMed] [CrossRef] [Google Scholar]

17. Mittl RL, Grossman RI, Hiehle JF, Hurst RW, Kauder DR, Gennarelli TA, et al. Prevalence of MR evidence of diffuse axonal injury in patients with mild head injury and normal head CT findings. AJNR American journal of neuroradiology. 1994;15(8):1583ā€“9. [PMC free article] [PubMed] [Google Scholar]

18. Topal NB, Hakyemez B, Erdogan C, Bulut M, Koksal O, Akkose S, et al. MR imaging in the detection of diffuse axonal injury with mild traumatic brain injury. Neurological research. 2008;30(9):974ā€“8. 10.1179/016164108X323799 [PubMed] [CrossRef] [Google Scholar]

19. Davenport EM, Whitlow CT, Urban JE, Espeland MA, Jung Y, Rosenbaum DA, et al. Abnormal white matter integrity related to head impact exposure in a season of high school varsity football. J Neurotrauma. 2014;31(19):1617ā€“24. 10.1089/neu.2013.3233 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

20. Colquhoun HL, Levac D, O’Brien KK, Straus S, Tricco AC, Perrier L, et al. Scoping reviews: time for clarity in definition, methods, and reporting. Journal of clinical epidemiology. 2014;67(12):1291ā€“4. 10.1016/j.jclinepi.2014.03.013 [PubMed] [CrossRef] [Google Scholar]

21. Grant MJ, Booth A. A typology of reviews: an analysis of 14 review types and associated methodologies. Health information and libraries journal. 2009;26(2):91ā€“108. 10.1111/j.1471-1842.2009.00848.x [PubMed] [CrossRef] [Google Scholar]

22. Arksey H, O’Malley O. Scoping studies; towards a methodological framework. International journal of social research methodology. 2005;8(1):19ā€“32. [Google Scholar]

23. Levac D, Colquhoun H, O’Brien KK. Scoping studies: advancing the methodology. Implementation science: IS. 2010;5:69 10.1186/1748-5908-5-69 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

24. McCrea M, Guskiewicz KM, Marshall SW, Barr W, Randolph C, Cantu RC, et al. Acute effects and recovery time following concussion in collegiate football players: the NCAA Concussion Study. JAMA. 2003;290(19):2556ā€“63. 10.1001/jama.290.19.2556 [PubMed] [CrossRef] [Google Scholar]

25. McCrea M, Guskiewicz K, Randolph C, Barr WB, Hammeke TA, Marshall SW, et al. Incidence, clinical course, and predictors of prolonged recovery time following sport-related concussion in high school and college athletes. Journal of the International Neuropsychological Society: JINS. 2013;19(1):22ā€“33. 10.1017/S1355617712000872 [PubMed] [CrossRef] [Google Scholar]

26. Rieger BP, Lewandowski LJ, Callahan JM, Spenceley L, Truckenmiller A, Gathje R, et al. A prospective study of symptoms and neurocognitive outcomes in youth with concussion vs orthopaedic injuries. Brain injury. 2013;27(2):169ā€“78. 10.3109/02699052.2012.729290 [PubMed] [CrossRef] [Google Scholar]

27. Phillipou A, Douglas J, Krieser D, Ayton L, Abel L. Changes in saccadic eye movement and memory function after mild closed head injury in children. Dev Med Child Neurol. 2014;56(4):337ā€“45. 10.1111/dmcn.12345 [PubMed] [CrossRef] [Google Scholar]

28. Tay SY, Ang BT, Lau XY, Meyyappan A, Collinson SL. Chronic impairment of prospective memory after mild traumatic brain injury. Journal of neurotrauma. 2010;27(1):77ā€“83. 10.1089/neu.2009.1074 [PubMed] [CrossRef] [Google Scholar]

29. Kwok FY, Lee TMC, Leung CHS, Poon WS. Changes of cognitive functioning following mild traumatic brain injury over a 3-month period. Brain injury. 2008;22(10):740ā€“51. 10.1080/02699050802336989 [PubMed] [CrossRef] [Google Scholar]

30. Su SH, Xu W, Li M, Zhang L, Wu YF, Yu F, et al. Elevated C-reactive protein levels may be a predictor of persistent unfavourable symptoms in patients with mild traumatic brain injury: a preliminary study. Brain, behavior, and immunity. 2014;38:111ā€“7. 10.1016/j.bbi.2014.01.009 [PubMed] [CrossRef] [Google Scholar]

31. Siman R, Giovannone N, Hanten G, Wilde EA, McCauley SR, Hunter JV, et al. Evidence that the blood biomarker SNTF predicts brain imaging changes and persistent cognitive dysfunction in mild TBI patients. Frontiers in Neurology. 2013;4 Nov(November):1ā€“8. [PMC free article] [PubMed] [Google Scholar]

32. Ponsford J, Cameron P, Fitzgerald M, Grant M, Mikocka-walus A. Long-term outcomes after uncomplicated mild traumatic brain injury: a comparison with trauma controls. Journal of neurotrauma. 2011;28(6):937ā€“46. 10.1089/neu.2010.1516 [PubMed] [CrossRef] [Google Scholar]

33. ParĆ© N, Rabin La, Fogel J, PĆ©pin M, Pare N, Rabin La, et al. Mild traumatic brain injury and its sequelae: characterisation of divided attention deficits. Neuropsychological rehabilitation. 2009;19(1):110ā€“37. 10.1080/09602010802106486 [PubMed] [CrossRef] [Google Scholar]

34. Kinsella GJ, Olver J, Ong B, Gruen R, Hammersley E. Mild traumatic brain injury in older adults: early cognitive outcome. Journal of the International Neuropsychological Society: JINS. 2014;20(6):663ā€“71. 10.1017/S1355617714000447 [PubMed] [CrossRef] [Google Scholar]

35. Marsh NV, Smith MD. Post-concussion syndrome and the coping hypothesis. Brain Injury. 1995;9(6):553ā€“62. [PubMed] [Google Scholar]

36. Xu L, Nguyen JV, Lehar M, Menon A, Rha E, Arena J, et al. Repetitive mild traumatic brain injury with impact acceleration in the mouse: Multifocal axonopathy, neuroinflammation, and neurodegeneration in the visual system. Experimental neurology. 2014. [PubMed] [Google Scholar]

37. Boussard CND, Lundin A, Karlstedt D, Edman G, Bartfai A. S100 and cognitive impairment after mild traumatic brain injury. J Rehabil Med. 2005;37(1):53ā€“7. 10.1080/16501970410015587 [PubMed] [CrossRef] [Google Scholar]

38. Hanten G, Li X, Ibarra A, Wilde Ea, Barnes A, McCauley SR, et al. Updating memory after mild traumatic brain injury and orthopedic injuries. Journal of neurotrauma. 2013;30(8):618ā€“24. 10.1089/neu.2012.2392 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

39. Heitger MH, Jones RD, Dalrymple-Alford JC, Frampton CM, Ardagh MW, Anderson TJ. Motor deficits and recovery during the first year following mild closed head injury. Brain injury. 2006;20(8):807ā€“24. 10.1080/02699050600676354 [PubMed] [CrossRef] [Google Scholar]

40. Bohnen N, Twijnstra A, Jolles J. Persistence of postconcussional symptoms in uncomplicated, mildly head-injured patients: A prospective cohort study. Neuropsychiatry, Neuropsychology and Behavioral Neurology. 1993;6(3):193ā€“200. [Google Scholar]

41. Rotarescu V, Ciurea AV. Quality of life in children after mild head injury. Journal of medicine and life. 2008;1(3):307ā€“22. [PMC free article] [PubMed] [Google Scholar]

42. Ponsford J, Willmott C, Rothwell A, Cameron P, Ayton G, Nelms R, et al. Cognitive and behavioral outcome following mild traumatic head injury in children. The Journal of head trauma rehabilitation. 1999;14(4):360ā€“72. [PubMed] [Google Scholar]

43. Ponsford J, Willmott C, Rothwell A, Cameron P, Kelly AM, Nelms R, et al. Factors influencing outcome following mild traumatic brain injury in adults. Journal of the International Neuropsychological Society: JINS. 2000;6(5):568ā€“79. [PubMed] [Google Scholar]

44. Maillard-Wermelinger A, Yeates KO, Gerry Taylor H, Rusin J, Bangert B, Dietrich A, et al. Mild traumatic brain injury and executive functions in school-aged children. Developmental neurorehabilitation. 2009;12(5):330ā€“41. 10.3109/17518420903087251 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

45. Levin HS, Fletcher JM, Kusnerik L, Kucera JA, Matthew A, Duffyl FF, et al. Semantic memory following pediatric head injury: relationship to age, severity of injury, and MRI. Cortex; a journal devoted to the study of the nervous system and behavior. 1996;32(3):461ā€“78. [PubMed] [Google Scholar]

46. Wong MN, Murdoch B, Whelan BM. Language disorders subsequent to mild traumatic brain injury (MTBI): Evidence from four cases. Aphasiology. 2010;24(10):1155ā€“69. [Google Scholar]

47. Muller K, Ingebrigtsen T, Wilsgaard T, Wikran G, Fagerheim T, Romner B, et al. Prediction of time trends in recovery of cognitive function after mild head injury. Neurosurgery. 2009;64(4):698ā€“704. 10.1227/01.NEU.0000340978.42892.78 [PubMed] [CrossRef] [Google Scholar]

48. Ellemberg D, Leclerc S, Couture S, Daigle C. Prolonged neuropsychological impairments following a first concussion in female university soccer athletes. Clinical Journal of Sport Medicine. 2007;17(5):369ā€“74. 10.1097/JSM.0b013e31814c3e3e [PubMed] [CrossRef] [Google Scholar]

49. Wrightson P, McGinn V, Gronwall D. Mild head injury in preschool children: evidence that it can be associated with a persisting cognitive defect. Journal of neurology, neurosurgery, and psychiatry. 1995;59(4):375ā€“80. [PMC free article] [PubMed] [Google Scholar]

50. Babikian T, Satz P, Zaucha K, Light R, Lewis RS, Asarnow RF. The UCLA longitudinal study of neurocognitive outcomes following mild pediatric traumatic brain injury. J Int Neuropsychol Soc. 2011;17(5):886ā€“95. 10.1017/S1355617711000907 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

51. Barrow I, Collins J, Md F, Britt L. The Influence of an Auditory Distraction on Rapid Naming After a Mild Traumatic Brain Injury: A Longitudinal Study. 2006. 5 [1142ā€“9]. Available from: http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=reference&D=ovfth&NEWS=N&AN=00005373-200611000-00017. [PubMed] [Google Scholar]

52. Catale C, Marique P, Closset A, Meulemans T. Attentional and executive functioning following mild traumatic brain injury in children using the Test for Attentional Performance (TAP) battery. Journal of clinical and experimental neuropsychology. 2009;31(3):331ā€“8. 10.1080/13803390802134616 [PubMed] [CrossRef] [Google Scholar]

53. Lee H, Wintermark M, Gean AD, Ghajar J, Manley GT, Mukherjee P. Focal lesions in acute mild traumatic brain injury and neurocognitive outcome: CT versus 3T MRI. Journal of neurotrauma. 2008;25(9):1049ā€“56. 10.1089/neu.2008.0566 [PubMed] [CrossRef] [Google Scholar]

54. Polissar NL, Fay GC, Jaffe KM, Liao S, Martin KM, Shurtleff HA, et al. Mild pediatric traumatic brain injury: Adjusting significance levels for multiple comparisons. Brain Injury. 1994;8(3):249ā€“63. [PubMed] [Google Scholar]

55. Kashluba S, Hanks RA, Casey JE, Millis SR. Neuropsychologic and functional outcome after complicated mild traumatic brain injury. Archives of physical medicine and rehabilitation. 2008;89(5):904ā€“11. 10.1016/j.apmr.2007.12.029 [PubMed] [CrossRef] [Google Scholar]

56. Romero K, Lobaugh NJ, Black SE, Ehrlich L, Feinstein A. Old wine in new bottles: Validating the clinical utility of SPECT in predicting cognitive performance in mild traumatic brain injury. Psychiatry Researchā€”Neuroimaging. 2015;231(1):15ā€“24. [PubMed] [Google Scholar]

57. Stalnacke B-M, Elgh E, Sojka P. One-year follow-up of mild traumatic brain injury: cognition, disability and life satisfaction of patients seeking consultation. Journal of Rehabilitation Medicine. 2007;39(5):405ā€“11. 10.2340/16501977-0057 [PubMed] [CrossRef] [Google Scholar]

58. Chadwick O, Rutter M, Brown G, Shaffer D, Traub MU. A prospective study of children with head injuries: II. Cognitive sequelae. Psychological medicine. 1981;11(1):49ā€“61. [PubMed] [Google Scholar]

59. Anderson V, Catroppa C, Morse S, Haritou F, Rosenfeld J. Outcome from mild head injury in young children: a prospective study. Journal of clinical and experimental neuropsychology: official journal of the International Neuropsychological Society. 2001;23(6):705ā€“17. [PubMed] [Google Scholar]

60. Waljas M, Iverson GL, Lange RT, Hakulinen U, Dastidar P, Huhtala H. et al. A prospective biopsychosocial study of the persistent post-concussion symptoms following mild traumatic brain injury. Journal of Neurotrauma. 2015;32(8):534ā€“47. 10.1089/neu.2014.3339 [PubMed] [CrossRef] [Google Scholar]

61. Dikmen S, Machamer J, Temkin N. Mild head injury: facts and artifacts. Journal of clinical and experimental neuropsychology. 2001;23(6):729ā€“38. 10.1076/jcen.23.6.729.1019 [PubMed] [CrossRef] [Google Scholar]

62. Zhou Y, Kierans A, Kenul D, Ge Y, Rath Reaume J, Grossman RI, et al. Mild traumatic brain injury: Longitudinal regional brain volume changes. Radiology. 2013;267(3):880ā€“90. 10.1148/radiol.13122542 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

63. Croall I, Cowie CJA, He J, Peel A, Wood J, Aribisala B, et al. White matter correlates of cognitive dysfunction after mild traumatic brain injury. Neurology. 2014;83(6):494ā€“501. 10.1212/WNL.0000000000000666 [PMC free article] [PubMed] [CrossRef] [Google Scholar]

64. Jaffe KM, Polissar NL, Fay GC, Liao S. Recovery trends over three years following pediatric traumatic brain injury. Archives of physical medicine and rehabilitation. 1995;76(1):17ā€“26. [PubMed] [Google Scholar]

65. Mangels JA, Craik FIM, Levine B, Schwartz ML, Stuss DT. Effects of divided attention on episodic memory in chronic traumatic brain injury: a function of severity and strategy. Neuropsychologia. 2002;40(13):2369ā€“85. [PubMed] [Google Scholar]

66. McCauley SR, Levin HS. Prospective Memory in Pediatric Traumatic Brain Injury: A Preliminary Study. Developmental Neuropsychology. 2004;25(1ā€“2):5ā€“20. 10.1080/87565641.2004.9651919 [PubMed] [CrossRef] [Google Scholar]

67. Geary EK, Kraus MF, Pliskin NH, Little DM. Verbal learning differences in chronic mild traumatic brain injury. Journal of the International Neuropsychological Society: JINS. 2010;16(3):506ā€“16. 10.1017/S135561771000010X [PubMed] [CrossRef] [Google Scholar]

68. Konrad C, Geburek A, Rist F, Blumenroth H, Fischer B, Husstedt I, et al. Long-term cognitive and emotional consequences of mild traumatic brain injury. Psychological medicine. 2011;41(6):1197ā€“211. 10.1017/S0033291710001728 [PubMed] [CrossRef] [Google Scholar]

69. Vanderploeg RD, Curtiss G, Belanger HG. Long-term neuropsychological outcomes following mild traumatic brain injury. J Int Neuropsychol Soc. 2005;11(3):228ā€“36. Epub 2005/05/17. 10.1017/S1355617705050289 [PubMed] [CrossRef] [Google Scholar]

70. Alexander M. Mild traumatic brain injury (C) 1996 American Academy of Neurology: Braintree, MA; 1996. [cited 46]. 5:[1489ā€“90]. http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=reference&D=yrovftb&NEWS=N&AN=00006114-199605000-00064. [Google Scholar]

71. Covassin T, Moran R, Wilhelm K. Concussion Symptoms and Neurocognitive Performance of High School and College Athletes Who Incur Multiple Concussions. The American journal of sports medicine. 2013;41(12):2885ā€“9. 10.1177/0363546513499230 [PubMed] [CrossRef] [Google Scholar]

72. Rutherford WH. Sequelae of concussion caused by minor head injuries. Lancet (London, England). 1977;1(8001):1ā€“4. [PubMed] [Google Scholar]

73. Larson MJ, Farrer TJ, Clayson PE. Cognitive control in mild traumatic brain injury: conflict monitoring and conflict adaptation. International journal of psychophysiology: official journal of the International Organization of Psychophysiology. 2011;82(1):69ā€“78. [PubMed] [Google Scholar]

74. Pontifex MB, O’Connor PM, Broglio SP, Hillman CH. The association between mild traumatic brain injury history and cognitive control. Neuropsychologia. 2009;47(14):3210ā€“6. 10.1016/j.neuropsychologia.2009.07.021 [PubMed] [CrossRef] [Google Scholar]

You may also like

Leave a Comment