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Literature Review Underpinning the Thesis
This chapter provides the context to this thesis by presenting definitions and research relating to TBI and disability. First, epidemiological data of TBI internationally and in New Zealand is examined and the relationship between TBI and its consequences is presented. Secondly, models of disability are presented to identify the relationship between TBI and impairment. Lastly, an overview of the literature regarding predictors of employment following injury is reviewed and the need for a systematic review of the predictors of employment after TBI is justified.
Traumatic Brain Injury
Traumatic Brain Injury has been defined as a nondegenerative, noncongenital insult to the brain by an external mechanical force, potentially leading to permanent or temporary impairments of cognitive, physical, and psychosocial functions, with an associated diminished or altered state of consciousness.(11) TBI is most commonly classified as mild, moderate, or severe using the Glasgow Coma Scale (GCS), duration of Post-Traumatic Amnesia (PTA), or duration of Loss of Consciousness (LOC). Although the GCS measures depth of impaired consciousness,(12) PTA the time between brain injury and return of continuous day-to-day memory,(13) and LOC the duration of the time that an individual remains unconscious following TBI, they can all be used to measure TBI severity (see Table 1). This can be problematic when severity is used to distinguish sub populations in TBI research as GCS, PTA, and, LOC quantify different aspects of physiological response to TBI at different timeframes. Additionally, because severity of injury does not differentiate between which areas of the brain are injured, TBI severities only give an indication of the likely type and levels of impairments and timeframe of recovery.
Incidence of Traumatic Brain Injury
Incidence rates of TBI in NZ are higher than most developed countries. For example, estimates of TBI incidence in North America range from 175-200 cases per 100,000 per annum (16) and 62.3 cases per 100,000 per annum in Canada.(17) In comparison, ACC reported 17,514 cases of concussion severe enough to warrant some form of funder intervention in NZ in 2003 (approximately 437 cases per 100,000 per annum),(18) with the cost of new and ongoing brain injury claims in NZ reported to be $45,930,000 in 2006.(19) New Zealand research also indicates that males sustain head injuries severe enough to warrant hospital intervention twice as often as females (315 and 142 cases per 100,000 per annum respectively) and that Maori incidences of TBI are twice that of non-Maori (463 and 204 cases per 100,000 per annum respectively).(20)
The high incidence rates of TBI in New Zealand may be explained by the high number of motor vehicle accidents in NZ and the influence of ACC‘s data collection methods. New Zealand has one of the highest rates of road traffic deaths and hospitalisations per fatality in OECD1 countries.(21, 22) High levels of vehicle accident are reflected in causation data from public hospital admissions in NZ that report that 36% of TBI‘s are caused by motor vehicle accidents, 29% by accidental falls, 14% by non-intentional accidents, 11% by assaults, and 10% by bicycle or animal rider crashes.(20) Additionally, statistics of TBI from countries other than NZ are generally compiled from reported hospital admissions. In comparison, ACC‘s reported incidence rates also include those who don‘t go to hospital but are still counted when they receive community based assessment or intervention for their TBI.
Biological Mechanisms of Traumatic Brain Injury
Damage to brain tissue can occur at the time of injury due to laceration, compression, tension, or shearing of neural tissue,(23) referred to as primary TBI, or as a consequence of a cascading sequence of interacting biological, chemical, and mechanical forces resulting in secondary TBI.(11) As a result, impairments following TBI can vary significantly depending on a number of factors including the area of brain injured and the level of damage to brain tissue. The following are widely accepted explanations of the biological processes of primary and secondary TBI.
Primary Brain Injury
Different patterns of brain injury can result from different types of trauma to the head and brain. Whilst focal injuries may result in localised primary brain damage, acceleration/deceleration forces (common in car accidents), can cause wide spread shearing of neural tissue of different densities and diffuse axonal injury.(24) Focal injury such as lacerations, contusions, and intracranial hematomas often result from collisions between the brain and the skull‘s internal bony ridges (coup injury) followed by collisions with the opposite side to the initial impact site of the skull (contrecoup injury) numerous times.(25) Tissue strain in the deepest brain structures of the midbrain and brain stem can also occur during primary injury causing damage to grey matter nuclei and axonal tracts.(26) Diffuse axonal injury occurs during primary TBI when rotational forces produce shearing of neural tissue of different densities,(27) resulting in micro-haemorrhages, tissue disruption, and eventual axonal degeneration.(25) While focal and diffuse patterns of damage have been presented as discrete patterns of brain injury in this section, they commonly occur together during accidents.
Primary injury may also cause damage at a cellular and molecular level where widespread changes in cell membrane functioning can result in neural cell death.(28, 29) Additionally, injured neural cells may release excitatory amino acids, cytokines, and other mediators of injury resulting in further damage to neighbouring cells.(26)
Secondary Traumatic Brain Injury
Secondary TBI can occur minutes, hours, and even days following primary TBI due to a combination of raised intracranial pressure, chemical reactions, and biological attempts by the brain to attain homeostasis. Because the skull is a closed system, increased intracranial pressure occurs when increased mass within the skull leads to decreased cerebral blood flow (and hence oxygen) being carried by blood to neural tissue.(30) The most common causes of mass increase within the skull following TBI are haematomas, oedema, and hydrocephalus (see Table 2). Brain shift may also occur during secondary TBI when brain tissue becomes compressed or herniated due to raised intracranial pressure.(26)
1 Introduction
1.1 Structure of Thesis
1.2 Context of research
1.3 Language
2 Literature Review Underpinning the Thesis
2.1 Traumatic Brain Injury
2.2 Biological Mechanisms of Traumatic Brain Injury
2.3 Impairment Following Traumatic Brain Injury
2.4 Definitions of Disability
2.5 Work Disability Following Traumatic Brain Injury
2.6 Prediction of Employment after Traumatic Brain Injury
3 Systematic Review of Predictors of Employment after Traumatic Brain Injury
3.1 Methodology for Systematic Review
3.2 Results of Systematic Review
3.3 Discussion
3.4 Conclusion
4 Influences of Employment after Traumatic Brain Injury from the Perspectives of Rehabilitation Stakeholders
4.1 Justification and Purpose of the Study
4.2 Methodology
4.3 Grounded Theory Informing Choice of Methods
4.4 Ethical Approval and Considerations
4.5 Methods
4.6 Vocational Rehabilitation Practitioner Focus Group Findings
4.7 Traumatic Brain Injury Participants Interview Findings
4.8 Other Professional Stakeholder Interview Findings
4.9 Discussion
4.10 Conclusion
5 Fatigue, Depression and Employment Following Traumatic Brain Injury: A Retrospective Cohort Study
5.1 Fatigue
5.2 Justification of Study
5.3 Methodology
5.4 Methods
5.5 Results
5.6 Fatigue Impact Scale and Modified Fatigue Impact Scale Principal Components Analysis
5.7 Discussion
6 Discussion
6.1 Summary of Research Findings in this Thesis
6.2 Applications of Work Disability as a Framework
6.3 Important Lessons Learnt Throughout Conduct of Research
6.4 Areas for Future Research
6.5 Conclusion
7 Appendices
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