In search of the ‘self’: Holistic rehabilitation in restoring cognition and recovering the ‘self’ following traumatic brain injury: A case report

2021 ◽  
pp. 1-12
Author(s):  
Meenakshi Banerjee ◽  
Shantala Hegde ◽  
T Harish ◽  
Girish B. Kulkarni ◽  
Narasinga Rao
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Emotional Regulation ◽  
Anterograde Amnesia ◽  
Depression Score ◽  
The Self ◽  
Future Research ◽  
Post Injury ◽  
Moderate Traumatic Brain Injury

BACKGROUND: Following mild-moderate traumatic brain injury (TBI), an individual experiences a range of emotional changes. It is often difficult for the patient to reconcile with their post-injury persona, and the memory of pre-injury personhood is particularly painful. Insight into one’s cognitive deficits subsequent to injury can lead to an existential crisis and a sense of loss, including loss of self. OBJECTIVE: Restoration of cognitive functions and reconciliation with loss of pre-traumatic personhood employing a holistic method of neuropsychological rehabilitation in a patient suffering from TBI. METHODS: Ms. K.S, a 25-year-old girl, presented with emotional disturbances following TBI. She reported both retrograde and anterograde amnesia. A multidimensional holistic rehabilitation was planned. Treatment addressed cognitive deficits through the basic functions approach. Cognitive behavioural methods for emotional regulation like diary writing helped reduce irritability and anger outbursts. Use of social media created new modes of memory activation and interactions. Compensatory strategies were used to recover lost skills, music based attention training helped foster an individualised approach to the sense of one’s body and self. RESULTS: As a result of these differing strategies, changes were reflected in neuro-psychological tests, depression score and the patient’s self-evaluation. This helped generate a coherent self-narrative. CONCLUSION: Treatment challenges in such cases are increased due to patient’s actual deficits caused by neuronal/biochemical changes. Innovative and multi-pronged rehabilitation strategies which involve everyday activities provided an answer to some of these problems. This method of rehabilitation may provide an optimistic context for future research.

scholarly journals 3,6′-Dithiopomalidomide Ameliorates Hippocampal Neurodegeneration, Microgliosis and Astrogliosis and Improves Cognitive Behaviors in Rats with a Moderate Traumatic Brain Injury

2021 ◽  
Vol 22 (15) ◽  
pp. 8276
Author(s):  
Pen-Sen Huang ◽  
Ping-Yen Tsai ◽  
Ling-Yu Yang ◽  
Daniela Lecca ◽  
Weiming Luo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Short Term Memory ◽  
Post Injury ◽  
Behavioral Deficits ◽  
Cognitive Behaviors ◽  
Moderate Traumatic Brain Injury ◽  
Short And Long Term ◽  
Behavioral Impairments ◽  
Hippocampal Neurodegeneration

Traumatic brain injury (TBI) is a leading cause of disability and mortality worldwide. It can instigate immediate cell death, followed by a time-dependent secondary injury that results from disproportionate microglial and astrocyte activation, excessive inflammation and oxidative stress in brain tissue, culminating in both short- and long-term cognitive dysfunction and behavioral deficits. Within the brain, the hippocampus is particularly vulnerable to a TBI. We studied a new pomalidomide (Pom) analog, namely, 3,6′-dithioPom (DP), and Pom as immunomodulatory imide drugs (IMiD) for mitigating TBI-induced hippocampal neurodegeneration, microgliosis, astrogliosis and behavioral impairments in a controlled cortical impact (CCI) model of TBI in rats. Both agents were administered as a single intravenous dose (0.5 mg/kg) at 5 h post injury so that the efficacies could be compared. Pom and DP significantly reduced the contusion volume evaluated at 24 h and 7 days post injury. Both agents ameliorated short-term memory deficits and anxiety behavior at 7 days after a TBI. The number of degenerating neurons in the CA1 and dentate gyrus (DG) regions of the hippocampus after a TBI was reduced by Pom and DP. DP, but not Pom, significantly attenuated the TBI-induced microgliosis and DP was more efficacious than Pom at attenuating the TBI-induced astrogliosis in CA1 and DG at 7D after a TBI. In summary, a single intravenous injection of Pom or DP, given 5 h post TBI, significantly reduced hippocampal neurodegeneration and prevented cognitive deficits with a concomitant attenuation of the neuroinflammation in the hippocampus.

scholarly journals Disrupted Intrinsic Connectivity among Default, Dorsal Attention, and Frontoparietal Control Networks in Individuals with Chronic Traumatic Brain Injury

2016 ◽  
Vol 22 (2) ◽  
pp. 263-279 ◽  
Author(s):  
Kihwan Han ◽  
Sandra B. Chapman ◽  
Daniel C. Krawczyk
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Network Connectivity ◽  
Higher Order ◽  
Future Research ◽  
Resting State Functional Connectivity ◽  
Post Injury ◽  
Graph Theoretic ◽  
Multiple Networks ◽  
Network Disruptions

AbstractObjectives:Individuals with chronic traumatic brain injury (TBI) often show detrimental deficits in higher order cognitive functions requiring coordination of multiple brain networks. Although assessing TBI-related deficits in higher order cognition in the context of network dysfunction is promising, few studies have systematically investigated altered interactions among multiple networks in chronic TBI.Method:We characterized disrupted resting-state functional connectivity of the default mode network (DMN), dorsal attention network (DAN), and frontoparietal control network (FPCN) whose interactions are required for internally and externally focused goal-directed cognition in chronic TBI. Specifically, we compared the network interactions of 40 chronic TBI individuals (8 years post-injury on average) with those of 17 healthy individuals matched for gender, age, and years of education.Results:The network-based statistic (NBS) on DMN-DAN-FPCN connectivity of these groups revealed statistically significant (pNBS<.05; |Z|>2.58) reductions in within-DMN, within-FPCN, DMN-DAN, and DMN-FPCN connectivity of the TBI group over healthy controls. Importantly, such disruptions occurred prominently in between-network connectivity. Subsequent analyses further exhibited the disrupted connectivity patterns of the chronic TBI group occurring preferentially in long-range and inter-hemispheric connectivity of DMN-DAN-FPCN. Most importantly, graph-theoretic analysis demonstrated relative reductions in global, local and cost efficiency (p<.05) as a consequence of the network disruption patterns in the TBI group.Conclusion:Our findings suggest that assessing multiple networks-of-interest simultaneously will allow us to better understand deficits in goal-directed cognition and other higher order cognitive phenomena in chronic TBI. Future research will be needed to better understand the behavioral consequences related to these network disruptions. (JINS, 2016,22, 263–279)

Neuropsychiatric Predictors of Post-Injury Headache After Mild-Moderate Traumatic Brain Injury in Veterans

2016 ◽  
Vol 56 (4) ◽  
pp. 699-710 ◽  
Author(s):  
Jessica Bomyea ◽  
Ariel J. Lang ◽  
Lisa Delano-Wood ◽  
Amy Jak ◽  
Karen L. Hanson ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Post Injury ◽  
Moderate Traumatic Brain Injury

scholarly journals GERIATRIC TRAUMATIC BRAIN INJURY AND ALZHEIMER’S DISEASE SHARE SIMILAR PATTERNS OF WHITE MATTER DEGRADATION

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S96-S96
Author(s):  
Andrei Irimia ◽  
Kenneth Rostowsky ◽  
Nikhil Chaudhari ◽  
Maria Calvillo ◽  
Sean Lee
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Corpus Callosum ◽  
Diffusion Tensor ◽  
Future Research ◽  
Post Injury ◽  
Significant Difference

Abstract Although mild traumatic brain injury (mTBI) and Alzheimer’s disease (AD) are associated with white matter (WM) degradation, the nature of these alterations and the outcomes of their comparison have not been elucidated. Diffusion tensor imaging (DTI) has been utilized in both conditions, and has uncovered decreases in the fractional anisotropy (FA) of the corpus callosum and cingulum bundle, compared to healthy control (HC) volunteers [1, 2]. Despite mTBI being a potential risk factor for AD, no systematic quantitative comparison has been drawn between their WM degradation patterns. Here we investigated WM FA differences using DTI and tract-based spatial statistics (TBSS) between age- and sex-matched adults: 33 chronic mTBI patients, 67 AD patients and 81 HC participants. T1-weighted magnetic resonance imaging (MRI) and DTI were acquired at 3T. mTBI patients were scanned acutely and ~6 months post-injury. FSL software was used for artefact correction, FA computation and TBSS implementation. Statistical comparison of WM FA patterns between mTBI and AD patients was achieved by two one-sided t tests (TOSTs) of statistical equivalence, with equivalence bounds defined where Cohen’s d &lt; 0.3. A significant difference was found between the FA means of mTBI vs. HC groups, and the AD vs. HC groups (p &lt; 0.01, corrected). Mean FA differences between mTBI and AD were statistically equivalent in the corpus callosum and in the inferior longitudinal fasciculus (p &lt; 0.05, corrected). Future research should focus on clarifying the similarities between mTBI and AD, potentially leading to novel hypotheses and improved AD diagnosis.

Cognitive and neurobehavioral functioning after mild versus moderate traumatic brain injury in older adults

2001 ◽  
Vol 7 (3) ◽  
pp. 373-383 ◽  
Author(s):  
FELICIA C. GOLDSTEIN ◽  
HARVEY S. LEVIN ◽  
WILLIAM P. GOLDMAN ◽  
ALLISON N. CLARK ◽  
TRACY KENEHAN ALTONEN
Keyword(s):  
Older Adults ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Outcome ◽  
Cognitive Measures ◽  
Post Injury ◽  
Mild Tbi ◽  
Moderate Traumatic Brain Injury ◽  
Comparable Control ◽  
Neurobehavioral Outcomes

This study evaluated the early cognitive and neurobehavioral outcomes of older adults with mild versus moderate traumatic brain injury (TBI). Thirty-five patients who were age 50 years and older and sustained mild or moderate TBI were prospectively recruited from acute care hospitals. Patients were administered cognitive and neurobehavioral measures up to 2 months post-injury. Demographically comparable control participants received the same measures. Patients and controls did not have previous histories of substance abuse, neuropsychiatric disturbance, dementia, or neurologic illness. Moderate TBI patients performed significantly poorer than mild TBI patients and controls on most cognitive measures, whereas the mild patients performed comparably to controls. In contrast, both mild and moderate patients exhibited significantly greater depression and anxiety/somatic concern than controls. The results indicate that the classification of TBI as mild versus moderate is prognostically meaningful as applied to older adults. The findings extend previous investigations in young adults by demonstrating a relatively good cognitive outcome on objective measures, but subjective complaints after a single, uncomplicated mild TBI in older persons. (JINS, 2001, 7, 373–383.)

A-125 The Impact of Bilingualism on Symbol Digit Modalities Test Performance Following Traumatic Brain Injury

2021 ◽  
Vol 36 (6) ◽  
pp. 1175-1175
Author(s):  
Raelynn Munoz ◽  
Daniel W Lopez-Hernandez ◽  
Rachel A Rugh-Fraser ◽  
Jasman Sidhu ◽  
Pavel Y Litvin ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Test Performance ◽  
Oral Performance ◽  
Neurocognitive Performance ◽  
Post Injury ◽  
Cognitive Speed ◽  
The Impact ◽  
Larger Sample

Abstract Objective Traumatic brain injury (TBI) survivors exhibit cognitive deficits. Research suggests that multilingualism can influence neurocognitive performance. We examined the effects of TBI and bilingualism/monolingualism on a test of attention and cognitive speed (i.e., Symbol Digit Modalities Test; SDMT). Method The sample consisted of 55 healthy comparison (27 Spanish-English bilinguals; 28 English-monolinguals), 34 acute TBI (14 Spanish-English bilinguals; 23 English-monolinguals), and 27 chronic TBI (13 Spanish-English bilinguals; 12 English-monolinguals) participants. Acute TBI participants were tested 6 months post-injury; chronic TBI participants were tested 12 months or more post-injury. A series of 3X2 ANOVAs were conducted to determine the effect of TBI and language on SDMT written and oral performance. Results ANOVAs revealed the healthy comparison group outperformed both TBI groups on SDMT written, p = 0.000, ηp2 = 0.21. Also, the healthy comparison and chronic TBI groups outperformed the acute TBI group on SDMT oral, p = 0.000, ηp2 = 0.13. Interaction effects emerged between TBI and bilingualism/monolingualism. On SDMT written and oral, acute TBI English-monolinguals outperformed acute TBI Spanish-English bilinguals; meanwhile, chronic TBI Spanish-English bilinguals outperformed chronic TBI English-monolinguals, p &lt; 0.05, ηp2 = 0.09–0.10. Conclusion The acute TBI group performed worse than healthy comparison adults on both SDMT tasks. Furthermore, the chronic TBI group demonstrated better SDMT oral abilities compared to the acute TBI group. Relative to monolinguals with TBI, our findings suggest better cognitive recovery of attention and cognitive speed in bilingual TBI participants. Future studies with larger sample sizes should examine if learning English first or second impacts Spanish-English bilingual TBI survivors’ SDMT performance compared to English-monolingual TBI survivors.

Traumatic Brain Injury

2019 ◽  
pp. 503-525
Author(s):  
Irene Cristofori ◽  
Jordan Grafman
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Future Research ◽  
Important Health ◽  
Behavioral Treatments ◽  
Severe Tbi ◽  
External Forces

Traumatic brain injury (TBI) is an alteration in brain structure or function caused by external forces that result in vascular and axonal damage, edema, and neuronal cell death. This chapter examines the spectrum of TBI. TBI is a major cause of death and disability and, therefore, an important health and socioeconomic problem for societies. Individuals surviving a moderate to severe TBI frequently suffer from long-lasting cognitive deficits. Such deficits include different aspects of cognition, such as memory, attention, executive functions, social behavior, and awareness. Protective factors, well-detailed diagnostic criteria, and available pharmacological and behavioral treatments are described. Final considerations on current controversies, knowledge gaps, and future research targets are provided.

scholarly journals Meningeal lymphatic dysfunction exacerbates traumatic brain injury pathogenesis

2019 ◽  
Author(s):  
Ashley C. Bolte ◽  
Mariah E. Hurt ◽  
Igor Smirnov ◽  
Michael A. Kovacs ◽  
Celia A. McKee ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Lymphatic System ◽  
Lymphatic Drainage ◽  
Neurological Dysfunction ◽  
Increased Intracranial Pressure ◽  
Post Injury ◽  
Lymphatic Function ◽  
Increased Icp

ABSTRACTTraumatic brain injury (TBI) has emerged as a leading cause of death and disability. Despite being a growing medical issue, the biological factors that promote central nervous system (CNS) pathology and neurological dysfunction following TBI remain poorly characterized. Recently, the meningeal lymphatic system was identified as a critical mediator of drainage from the CNS. In comparison to other peripheral organs, our understanding of how defects in lymphatic drainage from the CNS contribute to disease is limited. It is still unknown how TBI impacts meningeal lymphatic function and whether disruptions in this drainage pathway are involved in driving TBI pathogenesis. Here we demonstrate that even mild forms of brain trauma cause severe deficits in meningeal lymphatic drainage that can last out to at least two weeks post-injury. To investigate a mechanism behind impaired lymphatic function in TBI, we examined how increased intracranial pressure (ICP) influences the meningeal lymphatics, as increased ICP commonly occurs in TBI. We demonstrate that increased ICP is capable of provoking meningeal lymphatic dysfunction. Moreover, we show that pre-existing lymphatic dysfunction mediated by targeted photoablation before TBI leads to increased neuroinflammation and cognitive deficits. These findings provide new insights into both the causes and consequences of meningeal lymphatic dysfunction in TBI and suggest that therapeutics targeting the meningeal lymphatic system may offer strategies to treat TBI.

scholarly journals Traumatic Brain Injury in Aged Mice Induces Chronic Microglia Activation, Synapse Loss, and Complement-Dependent Memory Deficits

2018 ◽  
Vol 19 (12) ◽  
pp. 3753 ◽  
Author(s):  
Karen Krukowski ◽  
Austin Chou ◽  
Xi Feng ◽  
Brice Tiret ◽  
Maria-Serena Paladini ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Brain Lesion ◽  
Clinical Intervention ◽  
Memory Deficits ◽  
Cell Number ◽  
Post Injury ◽  
Synapse Loss ◽  
Immune System Activation

Traumatic brain injury (TBI) is of particular concern for the aging community since there is both increased incidence of TBI and decreased functional recovery in this population. In addition, TBI is the strongest environmental risk factor for development of Alzheimer’s disease and other dementia-related neurodegenerative disorders. Critical changes that affect cognition take place over time following the initial insult. Our previous work identified immune system activation as a key contributor to cognitive deficits observed in aged animals. Using a focal contusion model in the current study, we demonstrate a brain lesion and cavitation formation, as well as prolonged blood–brain barrier breakdown. These changes were associated with a prolonged inflammatory response, characterized by increased microglial cell number and phagocytic activity 30 days post injury, corresponding to significant memory deficits. We next aimed to identify the injury-induced cellular and molecular changes that lead to chronic cognitive deficits in aged animals, and measured increases in complement initiation components C1q, C3, and CR3, which are known to regulate microglial–synapse interactions. Specifically, we found significant accumulation of C1q on synapses within the hippocampus, which was paralleled by synapse loss 30 days post injury. We used genetic and pharmacological approaches to determine the mechanistic role of complement initiation on cognitive loss in aging animals after TBI. Notably, both genetic and pharmacological blockade of the complement pathway prevented memory deficits in aged injured animals. Thus, therapeutically targeting early components of the complement cascade represents a significant avenue for possible clinical intervention following TBI in the aging population.

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