Rationale: Ng et al. (2008) demonstrated that sub-acute hippocampal atrophy occurred between 4.5 and 24 months following moderate-to-severe traumatic brain injury (TBI); it remains to be determined if atrophy occurred before 24 months. Objectives: (1) to determine if sub-acute hippocampal atrophy occurs by the first year of injury; (2) to determine associated clinical and demographic variables. Methods: Ten moderate-to-severe TBI patients underwent MRI at 5 and 12 months post-injury. Glasgow Coma Scale (GCS) and demographic variables were correlated with change. Results: Significant hippocampal volume decreases were observed for right (P< 0.002, Cohen’s d= 0.34) and left (P< 0.036, Cohen’s d= 0.22) sides. GCS was significantly correlated with right (r= -0.663, P< 0.037), but not left percent hippocampal volume change (r= -0.327, P< 0.356). No significant correlations were observed for demographic variables. Conclusion: Sub-acute hippocampal atrophy occurs between 5 and 12 months post-injury and is associated with injury severity.

Rationale: Ng et al. (2008) demonstrated that sub-acute hippocampal atrophy occurred between 4.5 and 24 months following moderate-to-severe traumatic brain injury (TBI); it remains to be determined if atrophy occurred before 24 months. Objectives: (1) to determine if sub-acute hippocampal atrophy occurs by the first year of injury; (2) to determine associated clinical and demographic variables. Methods: Ten moderate-to-severe TBI patients underwent MRI at 5 and 12 months post-injury. Glasgow Coma Scale (GCS) and demographic variables were correlated with change. Results: Significant hippocampal volume decreases were observed for right (P< 0.002, Cohen’s d= 0.34) and left (P< 0.036, Cohen’s d= 0.22) sides. GCS was significantly correlated with right (r= -0.663, P< 0.037), but not left percent hippocampal volume change (r= -0.327, P< 0.356). No significant correlations were observed for demographic variables. Conclusion: Sub-acute hippocampal atrophy occurs between 5 and 12 months post-injury and is associated with injury severity.

Preliminary novel research findings indicate that a subset of individuals with moderate to severe traumatic brain injury show bilateral hippocampal atrophy progressing beyond the acute stage post-injury. The present study proposes a novel, integrated model of neuroprotection against subacute hippocampal atrophy (i.e., atrophy occurring beyond the initial 3 months post-injury) via environmental enrichment, drawing on theoretical models and research findings from the fields of environmental enrichment, brain and cognitive reserve, and neuroplastic models of functional recovery from brain injury. Objectives: (a) to examine the relationship between environmental enrichment factors and subacute hippocampal atrophy and (b) to examine the relationship between subacute hippocampal atrophy and return to productivity. Design: Retrospective observational within-subjects. Participants: Patients (N=21) with moderate to severe TBI. Measures: Primary predictors: Self-report ratings of environmental enrichment factors (i.e., hours of cognitive, physical, and social activities, meditation/prayer, and therapy). Primary outcome: hippocampal volume change between 5 months and 24+ months post-injury based on initial and follow-up MRI scans; Brain Injury Community Rehabilitation Outcome Scales-39 (BICRO-39). Results: Generalized environmental enrichment (i.e., an aggregate of cognitive, physical, and social activity) was significantly negatively correlated with subacute bilateral hippocampal atrophy (p<.05). Cognitive activity was the environmental enrichment element that accounted for the greatest degree of variance (32%) in subacute bilateral hippocampal atrophy (p<.01). Frequency of meditation/prayer was significantly negatively correlated with right hippocampal subacute atrophy (<.05) after controlling for socioeconomic status and generalized environmental enrichment. Level of education and pre-injury occupational attainment did not correlate with subacute hippocampal atrophy. Conclusion: Findings suggest that a fixed degree of neural reserve at the time of brain injury may not confer neuroprotection against structural pathology in the manner suggested by the present study’s proposed model of neuroprotection via environmental enrichment. Instead, findings suggest that in order for environmental enrichment to positively modulate susceptibility to subacute hippocampal atrophy post-TBI, environmental enrichment exposure must occur during the subacute phase post-injury rather than prior to injury.

Preliminary novel research findings indicate that a subset of individuals with moderate to severe traumatic brain injury show bilateral hippocampal atrophy progressing beyond the acute stage post-injury. The present study proposes a novel, integrated model of neuroprotection against subacute hippocampal atrophy (i.e., atrophy occurring beyond the initial 3 months post-injury) via environmental enrichment, drawing on theoretical models and research findings from the fields of environmental enrichment, brain and cognitive reserve, and neuroplastic models of functional recovery from brain injury. Objectives: (a) to examine the relationship between environmental enrichment factors and subacute hippocampal atrophy and (b) to examine the relationship between subacute hippocampal atrophy and return to productivity. Design: Retrospective observational within-subjects. Participants: Patients (N=21) with moderate to severe TBI. Measures: Primary predictors: Self-report ratings of environmental enrichment factors (i.e., hours of cognitive, physical, and social activities, meditation/prayer, and therapy). Primary outcome: hippocampal volume change between 5 months and 24+ months post-injury based on initial and follow-up MRI scans; Brain Injury Community Rehabilitation Outcome Scales-39 (BICRO-39). Results: Generalized environmental enrichment (i.e., an aggregate of cognitive, physical, and social activity) was significantly negatively correlated with subacute bilateral hippocampal atrophy (p<.05). Cognitive activity was the environmental enrichment element that accounted for the greatest degree of variance (32%) in subacute bilateral hippocampal atrophy (p<.01). Frequency of meditation/prayer was significantly negatively correlated with right hippocampal subacute atrophy (<.05) after controlling for socioeconomic status and generalized environmental enrichment. Level of education and pre-injury occupational attainment did not correlate with subacute hippocampal atrophy. Conclusion: Findings suggest that a fixed degree of neural reserve at the time of brain injury may not confer neuroprotection against structural pathology in the manner suggested by the present study’s proposed model of neuroprotection via environmental enrichment. Instead, findings suggest that in order for environmental enrichment to positively modulate susceptibility to subacute hippocampal atrophy post-TBI, environmental enrichment exposure must occur during the subacute phase post-injury rather than prior to injury.

Addressing issues with sensitivity and specificity in TBI assessment this study compared the performance on neuropsychological tests and results from qEEG assessment between a heterogeneous TBI (N=20) group and a matched normal control group (N=20). The TBI group was performed worse on all measures. Significant differences in performance were found in the domains of information processing speed and executive function. Effect sizes of these differences were large. This was also true for the amplitude of the qEEG parameter P3NoGo along with P3Go latency and theta power in the temporal and frontal lobes. Binary logistic regression revealed higher sensitivity and specificity when combining neuropsychological tests and qEEG parameters, suggesting qEEG parameters in  combination with neuropsychological tests to be good assets in TBI assessment.

Traumatic brain injury (TBI) is a leading cause of disability globally. Cognitive deficits represent the primary source of on-going disability in this population, yet the mechanisms of these deficits remain poorly understood. Here functional and diffusion-weighted imaging techniques were employed to characterize the mechanisms of neurofunctional change following TBI and their relationship to cognitive function. TBI subjects who had sustained moderate to severe brain injury, demonstrated good functional and neuropsychological recovery, and screened positive for diffuse axonal injury but negative for focal brain lesions were recruited for the project. TBI subjects and matched controls underwent structural, diffusion-weighted and functional MRI. The functional scanning paradigm consisted of a complex working memory task with both load and executive control manipulations. Study one demonstrated augmented functional engagement for TBI subjects relative to healthy controls associated with executive control processing but not maintenance operations within working memory. In study two, multivariate neuroimaging analyses demonstrated that activity within a network of bilateral prefrontal cortex (PFC) and posterior parietal regions was compensatory for task performance in the TBI sample. Functional connectivity analyses revealed that a common network of bilateral PFC regions was active in both groups during working memory performance, although this activity was behaviourally relevant at lower levels of task demand in TBI subjects relative to healthy controls. In study three, diffusion-imaging was used to characterize the impact of diffuse white matter pathology on these neurofunctional changes. Unexpectedly, decreased white matter integrity was not correlated with working memory performance following TBI. However, markers of white matter pathology did inversely correlate with the compensatory functional changes observed previously. These results implicate diffuse white matter pathology as a primary mechanism of functional brain change following TBI. Moreover, reactive neurofunctional changes appear to mediate the impact of diffuse injury following brain trauma, suggesting new avenues for neurorehabilitation in this population.

Traumatic brain injury (TBI) is a leading cause of disability globally. Cognitive deficits represent the primary source of on-going disability in this population, yet the mechanisms of these deficits remain poorly understood. Here functional and diffusion-weighted imaging techniques were employed to characterize the mechanisms of neurofunctional change following TBI and their relationship to cognitive function. TBI subjects who had sustained moderate to severe brain injury, demonstrated good functional and neuropsychological recovery, and screened positive for diffuse axonal injury but negative for focal brain lesions were recruited for the project. TBI subjects and matched controls underwent structural, diffusion-weighted and functional MRI. The functional scanning paradigm consisted of a complex working memory task with both load and executive control manipulations. Study one demonstrated augmented functional engagement for TBI subjects relative to healthy controls associated with executive control processing but not maintenance operations within working memory. In study two, multivariate neuroimaging analyses demonstrated that activity within a network of bilateral prefrontal cortex (PFC) and posterior parietal regions was compensatory for task performance in the TBI sample. Functional connectivity analyses revealed that a common network of bilateral PFC regions was active in both groups during working memory performance, although this activity was behaviourally relevant at lower levels of task demand in TBI subjects relative to healthy controls. In study three, diffusion-imaging was used to characterize the impact of diffuse white matter pathology on these neurofunctional changes. Unexpectedly, decreased white matter integrity was not correlated with working memory performance following TBI. However, markers of white matter pathology did inversely correlate with the compensatory functional changes observed previously. These results implicate diffuse white matter pathology as a primary mechanism of functional brain change following TBI. Moreover, reactive neurofunctional changes appear to mediate the impact of diffuse injury following brain trauma, suggesting new avenues for neurorehabilitation in this population.

AN ABSTRACT OF THE THESIS OF CATHRINE HOEKSTRA, for the Master of Arts Degree in English, presented on May 6, 2016 at Southern Illinois University Carbondale. TITLE: INVISIBLE WOUNDS: PROCESSING TRAUMA IN WAR NARRATIVES THROUGHOUT LITERATURE MAJOR PROFESSOR: Dr. Edward Brunner Many Veterans face “invisible wounds” of war. By examining various types of war narratives in literature we can understand how these veterans cope with their invisible wounds and what others can do to help them process their trauma. This project considers types of trauma theory in addition to several short stories by Tim O’Brien and Phil Klay. Veterans of Vietnam, Iraq, and Afghanistan often face these “invisible wounds,” and these stories help us see that trauma in its complexity. War itself is a traumatic experience, but for some veterans post-traumatic-stress occurs after the war is over. It is my hope through this project we can understand the invisible wounds of war such as post-traumatic-stress disorder and traumatic brain injury while also understanding combat stress and the struggles that veterans face in their civilian life. By examining two texts of short stories from two completely different wars, we can look at trauma from different points of view. During Vietnam some veterans were faced with isolation, often times tempted with alcohol, drugs and suicide. These members of the armed forces were not welcomed home in most cases, and Tim O’Brien’s short stories let us understand just how daunting it was to be at war, and how storytelling is key to comprehending the difficulties of this war. Drawing on another kind of wartime experience is Phil Klay, who brings about the bureaucracies of Iraq and the difficulty that some Marines face when they are home trying to integrate into civilian life. Sometimes the stories are difficult, raw, and hard to comprehend, but processing trauma also allows one to improve the quality of life. By listening to these stories we are making the storyteller valued, and we are also learning about historical and cultural contexts. In my time as a Graduate Teaching Assistant, I was fortunate to work with student-veterans returning to the university after deployments. These students, all from diverse backgrounds allowed me to understand what it truly means to listen to the story and be attentive to what these students wanted and needed. By introducing war narratives, short stories, and poems in the classroom we give student-veterans an opportunity to see that writing is not only an outlet for self-expression, but also a way to let the public know what military life and deployments are like.

Machine Learning for Analysis of Brain Signals / Event-Related Potential (ERP) measures derived from the electroencephalogram (EEG) have been widely used in outcome prediction of brain disorders. Recently, the ERPs that are transient (EEG) responses to auditory, visual, or tactile stimuli, have been introduced as useful predictors of a positive coma outcome (i.e. emergence from coma). In this study, machine learning techniques were applied for detecting the Mismatch Negativity (MMN) component, which is a transient EEG response to auditory stimuli, and its existence has a high correlation with coma awakening, through analyzing ERPs signals recorded from healthy control brain signals. To this end, two different dimensionality reduction methods, Localized Feature Selection (LFS) and minimum-redundancy maximum-relevance (mRMR) were employed, where a localized classifier and the support vector machine (SVM) with radial basis function (RBF) kernel are used as classifiers. We trained both LFS and mRMR algorithms using signals of healthy brains and evaluated their performance for MMN detection on both healthy subjects and coma patients. The evaluation on healthy subjects, using leave-one-subject-out cross-validation technique, shows the detection accuracy performance of 86.6% (using LFS) and 86.5% (using mRMR). In addition to analyzing brain signals for MMN detection, we also implemented a machine learning algorithm for discriminating healthy subjects from those who have experienced TBI. The EEG signals used in the TBI study were recorded using an ERP paradigm. However, we treated the recorded signals as resting state signals. To this end, we used the mRMR feature selection method and fed the selected features into the SVM classifier that outputs the estimated class labels. This method gives us a poor performance compared to the methods that directly used ERP components (without considering them as resting signals.). We conclude that our hypothesis of treating ERP data as resting data is not valid for TBI detection. / Thesis / Master of Applied Science (MASc)

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