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 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.

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.)

scholarly journals Pattern of Neuronal and Axonal Damage, Glial Response, and Synaptic Changes in Rat Cerebellum within the First Week following Traumatic Brain Injury

2020 ◽  
Vol 79 (11) ◽  
pp. 1163-1182
Author(s):  
Petra Dolenec ◽  
Kristina Pilipović ◽  
Tamara Janković ◽  
Gordana Župan
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Damage ◽  
Cell Loss ◽  
Axonal Damage ◽  
Post Injury ◽  
Rat Cerebellum ◽  
Fluid Percussion Injury ◽  
Fluoro Jade B ◽  
Moderate Traumatic Brain Injury

Abstract We examined damage and repair processes in the rat cerebellum within the first week following moderate traumatic brain injury (TBI) induced by lateral fluid percussion injury (LFPI) over the left parietal cortex. Rats were killed 1, 3, or 7 days after the injury or sham procedure. Fluoro-Jade B staining revealed 2 phases of neurodegenerative changes in the cell bodies and fibers: first, more focal, 1 day after the LFPI, and second, widespread, starting on post-injury day 3. Purkinje cell loss was detected in posterior lobule IX 1 day following LFPI. Apoptosis was observed in the cerebellar cortex, on days 1 and 7 following LFPI, and was not caspase- or apoptosis-inducing factor (AIF)-mediated. AIF immunostaining indicated axonal damage in the cerebellar white matter tracts 3- and 7-days post-injury. Significant astrocytosis and microgliosis were noticed on day 7 following LFPI at the sites of neuronal damage and loss. Immunohistochemical labeling with the presynaptic markers synaptophysin and growth-associated protein-43 revealed synaptic perturbations already on day 1 that were more pronounced at later time points following LFPI. These results provide new insights into pathophysiological alterations in the cerebellum and their mechanisms following cerebral TBI.

scholarly journals Intranasal insulin treatment of an experimental model of moderate traumatic brain injury

2017 ◽  
Vol 37 (9) ◽  
pp. 3203-3218 ◽  
Author(s):  
Fiona Brabazon ◽  
Colin M Wilson ◽  
Shalini Jaiswal ◽  
John Reed ◽  
William H Frey ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Glucose Uptake ◽  
Male Rats ◽  
Lesion Volume ◽  
Intranasal Insulin ◽  
Post Injury ◽  
Fdg Uptake ◽  
Moderate Traumatic Brain Injury ◽  
18F Fdg

Traumatic brain injury (TBI) results in learning and memory dysfunction. Cognitive deficits result from cellular and metabolic dysfunction after injury, including decreased cerebral glucose uptake and inflammation. This study assessed the ability of intranasal insulin to increase cerebral glucose uptake after injury, reduce lesion volume, improve memory and learning function and reduce inflammation. Adult male rats received a controlled cortical impact (CCI) injury followed by intranasal insulin or saline treatment daily for 14 days. PET imaging of [18F]-FDG uptake was performed at baseline and at 48 h and 10 days post-injury and MRI on days three and nine post injury. Motor function was tested with the beam walking test. Memory function was assessed with Morris water maze. Intranasal insulin after CCI significantly improved several outcomes compared to saline. Insulin-treated animals performed better on beam walk and demonstrated significantly improved memory. A significant increase in [18F]-FDG uptake was observed in the hippocampus. Intranasal insulin also resulted in a significant decrease in hippocampus lesion volume and significantly less microglial immunolabeling in the hippocampus. These data show that intranasal insulin improves memory, increases cerebral glucose uptake and decreases neuroinflammation and hippocampal lesion volume, and may therefore be a viable therapy for TBI.

Alcohol Consumption Does not Impede Recovery from Mild to Moderate Traumatic Brain Injury

2016 ◽  
Vol 22 (8) ◽  
pp. 816-827 ◽  
Author(s):  
Noah D. Silverberg ◽  
William Panenka ◽  
Grant L. Iverson ◽  
Jeffrey R. Brubacher ◽  
Jason R. Shewchuk ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Alcohol Consumption ◽  
Alcohol Use ◽  
Diffusion Tensor ◽  
Alcohol Intoxication ◽  
Post Injury ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Moderate Traumatic Brain Injury

AbstractObjectives: To examine the effect of pre-injury alcohol use, acute alcohol intoxication, and post-injury alcohol use on outcome from mild to moderate traumatic brain injury (TBI). Methods: Prospective inception cohort of patients who presented to the Emergency Department with mild to moderate TBI and had a blood alcohol level (BAL) taken for clinical purposes. Those who completed the 1-year outcome assessment were eligible for this study (N=91). Outcomes of interest were the count of post-concussion symptoms (British Columbia Post-Concussion Symptom Inventory), low neuropsychological test scores (Neuropsychological Assessment Battery), and abnormal regions of interest on diffusion tensor imaging (low fractional anisotropy). The main predictors were pre-injury alcohol consumption (Cognitive Lifetime Drinking History interview), BAL, and post-injury alcohol use. Results: The alcohol use variables were moderately to strongly inter-correlated. None of the alcohol use variables (whether continuous or categorical) were related to 1-year TBI outcomes in generalized linear modeling. Participants in this cohort generally had a good clinical outcome, regardless of their pre-, peri-, and post-injury alcohol use. Conclusions: Alcohol may not significantly alter long-term outcome from mild to moderate TBI. (JINS, 2016, 22, 816–827)

scholarly journals Recovery of Theta Frequency Oscillations in Rats Following Lateral Fluid Percussion Corresponds With a Mild Cognitive Phenotype

2020 ◽  
Vol 11 ◽  
Author(s):  
Katelynn Ondek ◽  
Aleksandr Pevzner ◽  
Kayleen Tercovich ◽  
Amber M. Schedlbauer ◽  
Ali Izadi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Spatial Learning ◽  
Anterior Cingulate ◽  
Theta Oscillations ◽  
Return To Play ◽  
Barnes Maze ◽  
Post Injury ◽  
Moderate Traumatic Brain Injury ◽  
Theta Frequency

Whether from a fall, sports concussion, or even combat injury, there is a critical need to identify when an individual is able to return to play or work following traumatic brain injury (TBI). Electroencephalogram (EEG) and local field potentials (LFP) represent potential tools to monitor circuit-level abnormalities related to learning and memory: specifically, theta oscillations can be readily observed and play a critical role in cognition. Following moderate traumatic brain injury in the rat, lasting changes in theta oscillations coincide with deficits in spatial learning. We hypothesized, therefore, that theta oscillations can be used as an objective biomarker of recovery, with a return of oscillatory activity corresponding with improved spatial learning. In the current study, LFP were recorded from dorsal hippocampus and anterior cingulate in awake, behaving adult Sprague Dawley rats in both a novel environment on post-injury days 3 and 7, and Barnes maze spatial navigation on post-injury days 8–11. Theta oscillations, as measured by power, theta-delta ratio, peak theta frequency, and phase coherence, were significantly altered on day 3, but had largely recovered by day 7 post-injury. Injured rats had a mild behavioral phenotype and were not different from shams on the Barnes maze, as measured by escape latency. Injured rats did use suboptimal search strategies. Combined with our previous findings that demonstrated a correlation between persistent alterations in theta oscillations and spatial learning deficits, these new data suggest that neural oscillations, and particularly theta oscillations, have potential as a biomarker to monitor recovery of brain function following TBI. Specifically, we now demonstrate that oscillations are depressed following injury, but as oscillations recover, so does behavior.

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 A-126 Clinical Utility of Risk Factors to Predict Self-reported Neurobehavioral Outcome Following Traumatic Brain Injury: PTSD, Sleep, Resilience, and Lifetime Blast Exposure

2020 ◽  
Vol 35 (6) ◽  
pp. 919-919
Author(s):  
Lange R ◽  
Lippa S ◽  
Hungerford L ◽  
Bailie J ◽  
French L ◽  
...  
Keyword(s):  
Risk Factors ◽  
Traumatic Brain Injury ◽  
Risk Factor ◽  
Brain Injury ◽  
Clinical Utility ◽  
Poor Sleep ◽  
Post Injury ◽  
Poor Outcome ◽  
Blast Exposure ◽  
Neurobehavioral Outcome

Abstract Objective To examine the clinical utility of PTSD, Sleep, Resilience, and Lifetime Blast Exposure as ‘Risk Factors’ for predicting poor neurobehavioral outcome following traumatic brain injury (TBI). Methods Participants were 993 service members/veterans evaluated following an uncomplicated mild TBI (MTBI), moderate–severe TBI (ModSevTBI), or injury without TBI (Injured Controls; IC); divided into three cohorts: (1) < 12 months post-injury, n = 237 [107 MTBI, 71 ModSevTBI, 59 IC]; (2) 3-years post-injury, n = 370 [162 MTBI, 80 ModSevTBI, 128 IC]; and (3) 10-years post-injury, n = 386 [182 MTBI, 85 ModSevTBI, 119 IC]. Participants completed a 2-hour neurobehavioral test battery. Odds Ratios (OR) were calculated to determine whether the ‘Risk Factors’ could predict ‘Poor Outcome’ in each cohort separately. Sixteen Risk Factors were examined using all possible combinations of the four risk factor variables. Poor Outcome was defined as three or more low scores (< 1SD) on five TBI-QOL scales (e.g., Fatigue, Depression). Results In all cohorts, the vast majority of risk factor combinations resulted in ORs that were ‘clinically meaningful’ (ORs > 3.00; range = 3.15 to 32.63, all p’s < .001). Risk factor combinations with the highest ORs in each cohort were PTSD (Cohort 1 & 2, ORs = 17.76 and 25.31), PTSD+Sleep (Cohort 1 & 2, ORs = 18.44 and 21.18), PTSD+Sleep+Resilience (Cohort 1, 2, & 3, ORs = 13.56, 14.04, and 20.08), Resilience (Cohort 3, OR = 32.63), and PTSD+Resilience (Cohort 3, OR = 24.74). Conclusions Singularly, or in combination, PTSD, Poor Sleep, and Low Resilience were strong predictors of poor outcome following TBI of all severities and injury without TBI. These variables may be valuable risk factors for targeted early interventions following injury.

scholarly journals The Challenge of Managing Patients Suffering from TBI: The Utility of Multiparametric MRI

CNS Spectrums ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 178-179
Author(s):  
John L. Sherman ◽  
Laurence J. Adams ◽  
Christen F. Kutz ◽  
Deborah York ◽  
Mitchell S. Szymczak
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Family History ◽  
Diffusion Tensor ◽  
Multiparametric Mri ◽  
Psychiatric History ◽  
Post Injury ◽  
Negative Family History ◽  
Imaging Result ◽  
The Brain

AbstractTraumatic brain injury (TBI) is a complex phenomenon affecting multiple areas of the brain in multiple ways. Both right and left hemispheres are affected as well as supratentorial and infratentorial compartments. These multifocal injuries are caused by many factors including acute mechanical injury, focal intracranial hemorrhage, blunt and rotational forces, epidural and subdural hematoma, hypoxemia, hypotension, edema, axonal damage, neuronal death, gliosis and blood brain barrier disruption. Clinicians and patients benefit by precise information about the neuroanatomical areas that are affected macroscopically, microscopically and biochemically in an individual patient.Standard imaging studies are frequently negative or grossly underestimate the severity of TBI and may exacerbate and prolong patient suffering with an imaging result of “no significant abnormality”. Specifically, sophisticated imaging tools have been developed which reveal significant damage to the brain structure including atrophy, MRI spectroscopy showing variations in neuronal metabolite N-acetyl-aspartate, elevations of membrane related Choline, and the glial metabolite myo-inositol is often observed to be increased post injury. In addition, susceptibility weighted imaging (SWI) has been shown to be more reliable for detecting microbleeds versus calcifications.We have selected two TBI patients with diffuse traumatic brain injury.The first patient is a 43-year-old male who suffered severe traumatic brain injury from a motorcycle accident in 2016. Following the accident, the patient was diagnosed with seizures, major depression, and intermittent explosive disorder. He has attempted suicide and has neurobehavioral disinhibition including severe anger, agitation and irritability. He denies psychiatric history prior to TBI and has negative family history. Following the TBI, he became physically aggressive and assaultive in public with minimal provocation. He denies symptoms of thought disorder and mania. He is negative for symptoms of  cognitive decline or encephalopathy.The second patient is a 49-year-old male who suffered at least 3 concussive blasts in the Army and a parachute injury. Following the last accident, the patient was diagnosed with major depressive disorder, panic disorder, PTSD and generalized anxiety disorder. He denies any psychiatric history prior to TBI including negative family history of psychiatric illness. In addition, he now suffers from nervousness, irritability, anger, emotional lability and concurrent concentration issues, problems completing tasks and alterations in memory.Both patients underwent 1.5T multiparametric MRI using standard T2, FLAIR, DWI and T1 sequences, and specialized sequences including susceptibility weighted (SWAN/SWI), 3D FLAIR, single voxel MRI spectroscopy (MRS), diffusion tensor imaging (DTI), arterial spin labeling perfusion (ASL) and volumetric MRI (NeuroQuant). Importantly, this exam can be performed in 30–45 minutes and requires no injections other than gadolinium in some patients. We will discuss the insights derived from the MRI which detail the injured areas, validate the severity of the brain damage, and provide insight into the psychological, motivational and physical disabilities that afflict these patients. It is our expectation that this kind of imaging study will grow in value as we link specific patterns of injury to specific symptoms and syndromes resulting in more targeted therapies in the future.

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