Thesis (doctoral)--Munich, 1934. / Includes bibliographical references (p. 19).

A small subset of individuals that have experienced mild traumatic brain injury (mTBI) may experience persistent cognitive deficits more than a year following the head injury. Neuroimaging studies reveal structural and functional changes in frontal areas of the brain, exacerbated when loss of consciousness is experienced, and indicate that these changes may be progressive in nature for some people. Social support and social participation have, however, been suggested to confer cognitive reserve - neurocognitive protection against cognitive decline. Analyses were run on Canadian Longitudinal Study on Aging (CLSA) neuropsychological data, consisting of individuals who experienced mTBI with loss of consciousness (n = 536 for less than 1 minute, and n = 435 for unconsciousness between 1 and 20 minutes) more than a year prior, and 13,163 no-head injury comparisons. These same individuals were re-assessed three years later. The results presented in this thesis suggest that at a year or more after a single mTBI with loss of consciousness, a small subset of individuals are more likely to be impaired on prospective memory and other executive functioning tasks, relative to comparisons. In addition, when examined at three-year follow-up, those who experienced mTBI with longer duration of unconsciousness were more likely to exhibit cognitive decline relative to those who experienced less unconsciousness or comparisons. Moreover, greater social participation over the past year, and more perceived social support were predictive of lessened cognitive deterioration in those individuals.

Patients presenting with an abrupt loss of postural control are commonly said to have had ‘collapse?cause’. This is a common presentation, accounting for up to 6% of emergency department cases, and 3% of hospital admissions. However, collapse?cause is a ‘catch-all’ term and there are many different causes which include falls, transient ischemic attacks, cerebrovascular accidents, road traffic accidents, metabolic abnormalities, intoxication, and transient loss of consciousness, (TLOC or ‘blackout’). A majority of patients fall into the latter category. Where TLOC has occurred, the causes are syncope, epilepsy and psychogenic blackouts. The clinical features of these three conditions can often be similar, albeit with subtle differences. A wide variation exists in the way such patients are assessed, investigated and managed, who manages them and where. There is an absence of simple clinical tools for assessment, poor risk stratification, inappropriate and overuse of investigations. Hospitalisation is often unnecessary and misdiagnoses are common. In this thesis, the problem of TLOC has been addressed in four projects. Section 1 (Chapter II): reports a simple new risk stratification scheme for patients presenting with TLOC, assessed in a specialist nurse lead, cardiologist supervised (SP), Rapid Access Blackouts Triage Clinic - RABTC. Frequently, after triage, a patient may be deemed to be at low risk, but blackouts continue, the cause remains unclear, and conventional tests, have been unhelpful. In Chapter III, we describe the option of investigating such patients by long term (up to 3 years) ECG monitoring using an implantable loop recorder (ILR). In order to address the specific question of misdiagnosis of epilepsy where convulsive syncope might be the true diagnosis, the REVISE Study- REVeal in the Investigation of Syncope and Epilepsy was undertaken, which is described in Chapter IV. Lastly, convulsive syncope is the likely explanation for a misdiagnosis in patients diagnosed with epilepsy, but the incidence of cardiac disease in patients with brain injury and epilepsy is unknown. Therefore a cohort of patients in a residential epilepsy centre was studied. In this setting, residents typically had a history of brain injury and suffered from recurrent epileptic seizures. The findings of cardiology assessment are presented in Section 4 (Chapter V).

Blast-related mild traumatic brain injury (mTBI) is a common injury among Operation Enduring Freedom/Operation Iraqi Freedom (OEF/OIF) veterans due to the frequent use of improvised explosive devices (IEDs). A significant minority of veterans with blast-related mTBI complain of postconcussion symptoms (PCS) and cognitive difficulties, even years after the injury. Studies have suggested that these behavioral sequelae are primarily linked to mental health disorders such as posttraumatic stress disorder (PTSD). However, mTBI is associated with neural changes and the impact of these changes on behavioral sequelae is unclear. As such, this dissertation had three goals. First, this dissertation assessed whether the severity of PCS in blast-exposed individuals is associated with the extent of mTBI-related neural injury. Results revealed that individuals with mTBI with loss of consciousness (LOC) had significantly more white matter abnormalities than no-TBI controls and that these white matter abnormalities were spatially variable across individuals. Importantly, the extent of white matter abnormality was associated with physical PCS severity and mediated the relationship between mTBI with LOC and physical PCS. Second, this dissertation examined whether these white matter abnormalities were also associated with overall cognitive impairment. In light of the observed variability in white matter injury, a measure of overall cognitive status that takes into account heterogeneity of cognitive impairment was used. Results showed that the extent of white matter abnormality was associated with cognitive status and mediated the relationship between mTBI with LOC and cognitive impairment. Third, this dissertation examined performance and brain function in the context of an experimental measure of cognitive control known to be sensitive to residual effects of mTBI. Results revealed that although behavioral performance was similar across groups, the mTBI group had enhanced functional connectivity between brain networks important for task performance, suggesting a potential compensatory mechanism in mTBI. Together, the findings of this dissertation suggest that mTBI is associated with structural and functional connectivity alterations years after the injury. Further, this dissertation suggests that whereas structural connectivity changes may have negative behavioral consequences, changes in functional connectivity may serve as a compensatory mechanism for successful performance.

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