Long-term neuropsychological outcomes following mild traumatic brain injury

2005 ◽  
Vol 11 (3) ◽  
pp. 228-236 ◽  
Author(s):  
RODNEY D. VANDERPLOEG ◽  
GLENN CURTISS ◽  
HEATHER G. BELANGER
Keyword(s):  
Traumatic Brain Injury ◽  
Working Memory ◽  
Brain Injury ◽  
Head Injury ◽  
Mild Traumatic Brain Injury ◽  
Odds Ratio ◽  
Verbal Learning ◽  
Community Dwelling ◽  
Neuropsychological Outcomes

Mild traumatic brain injury (MTBI) is common, yet few studies have examined neuropsychological outcomes more than 1 year postinjury. Studies of nonreferred individuals with MTBI or studies with appropriate control groups are lacking, but necessary to draw conclusions regarding natural recovery from MTBI. We examined the long-term neuropsychological outcomes of a self-reported MTBI an average of 8 years postinjury in a nonreferred community-dwelling sample of male veterans. This was a cross-sectional cohort study derived from the Vietnam Experience Study. Three groups matched on premorbid cognitive ability were examined, those who (1) had not been injured in a MVA nor had a head injury (Normal Control;n= 3214), (2) had been injured in a motor vehicle accident (MVA) but did not have a head injury (MVA Control;n= 539), and (3) had a head injury with altered consciousness (MTBI;n= 254). A MANOVA found no group differences on a standard neuropsychological test battery of 15 measures. Across 15 measures, the average neuropsychological effect size of MTBI compared with either control group was −.03. Subtle aspects of attention and working memory also were examined by comparing groups on Paced Auditory Serial Addition Test (PASAT) continuation rate and California Verbal Learning Test (CVLT) proactive interference (PI). Compared with normal controls, the MTBI group evidenced attention problems in their lower rate of continuation to completion on the PASAT (odds ratio = 1.32,CI= 1.0–1.73) and in excessive PI (odds ratio = 1.66,CI= 1.11–2.47). Unique to the MTBI group, PASAT continuation problems were associated with left-sided visual imperceptions and excessive PI was associated with impaired tandem gait. These results show that MTBI can have adverse long-term neuropsychological outcomes on subtle aspects of complex attention and working memory. (JINS, 2005,11, 228–236.)

Concussion and sports-related head injury

2019 ◽  
pp. 531-536
Author(s):  
Mark Wilson
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Mild Traumatic Brain Injury ◽  
Return To Sport ◽  
Mild Head Injury ◽  
Long Term Effects ◽  
Dementia Pugilistica ◽  
Repeated Injury

Interest in concussion and sports-related injury has intensified in recent years for three main reasons: (1) it is a preventable form of brain injury; (2) there is increasing evidence that repeated injury can result in long-term neurocognitive loss; and (3) as a result there are potential medicolegal costs to organizations that, possibly inadvertently, allow this form of brain injury to occur within their sport. The long-term effects of boxing resulting in dementia pugilistica have been appreciated for some time, however the results of repeated mild head injury in other sports is now under focus. Concussion, increasingly termed mild traumatic brain injury, should be graded. Imaging, removal from, and return to sport are all discussed in this chapter.

Patterns of verbal learning and memory in traumatic brain injury

2001 ◽  
Vol 7 (5) ◽  
pp. 574-585 ◽  
Author(s):  
GLENN CURTISS ◽  
RODNEY D. VANDERPLOEG ◽  
JAN SPENCER ◽  
ANDRES M. SALAZAR
Keyword(s):  
Traumatic Brain Injury ◽  
Working Memory ◽  
Brain Injury ◽  
Memory Span ◽  
Verbal Learning ◽  
Central Executive ◽  
Long Term Memory ◽  
Term Memory ◽  
Memory Processes

CVLT and WMS–R Digit Span variables were used to calculate indexes of seven specific short- and long-term memory processes: working memory span and central executive functions, and long-term memory encoding, consolidation, retention, retrieval, control abilities. Scores on these indexes were then cluster-analyzed to determine whether subtypes of memory performance exist that correspond to deficits in these theoretical memory constructs. Parallel analyses were conducted with two large samples (N = 150 and N = 151) of individuals who had sustained a traumatic brain injury (TBI). Findings showed that TBI results in subgroups of memory disorders with specific deficits in consolidation, retention, and retrieval processes. Control problems (keeping track of list versus non-list items) only appeared in conjunction with retrieval deficits. Working memory span and central executive functioning (i.e., the ability to manipulate information in working memory) do not appear to be deficits characteristic of TBI as no such clusters emerged in the analyses. By using specific indexes of memory processes, and in contrast to previous studies, patterns of memory dysfunction were found that correspond to deficits in theoretically meaningful memory constructs. (JINS, 2001, 7, 574–585.)

scholarly journals GPR110 ligands reduce chronic optic tract gliosis and visual deficit following repetitive mild traumatic brain injury in mice

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Huazhen Chen ◽  
Karl Kevala ◽  
Elma Aflaki ◽  
Juan Marugan ◽  
Hee-Yong Kim
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Visual Evoked Potential ◽  
Evoked Potential ◽  
Optic Tract ◽  
Primary Microglia ◽  
Visual Dysfunction ◽  
The Brain

Abstract Background Repetitive mild traumatic brain injury (mTBI) can result in chronic visual dysfunction. G-protein receptor 110 (GPR110, ADGRF1) is the target receptor of N-docosahexaenoylethanolamine (synaptamide) mediating the anti-neuroinflammatory function of synaptamide. In this study, we evaluated the effect of an endogenous and a synthetic ligand of GPR110, synaptamide and (4Z,7Z,10Z,13Z,16Z,19Z)-N-(2-hydroxy-2-methylpropyl) docosa-4,7,10,13,16,19-hexaenamide (dimethylsynaptamide, A8), on the mTBI-induced long-term optic tract histopathology and visual dysfunction using Closed-Head Impact Model of Engineered Rotational Acceleration (CHIMERA), a clinically relevant model of mTBI. Methods The brain injury in wild-type (WT) and GPR110 knockout (KO) mice was induced by CHIMERA applied daily for 3 days, and GPR110 ligands were intraperitoneally injected immediately following each impact. The expression of GPR110 and proinflammatory mediator tumor necrosis factor (TNF) in the brain was measured by using real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) in an acute phase. Chronic inflammatory responses in the optic tract and visual dysfunction were assessed by immunostaining for Iba-1 and GFAP and visual evoked potential (VEP), respectively. The effect of GPR110 ligands in vitro was evaluated by the cyclic adenosine monophosphate (cAMP) production in primary microglia isolated from adult WT or KO mouse brains. Results CHIMERA injury acutely upregulated the GPR110 and TNF gene level in mouse brain. Repetitive CHIMERA (rCHIMERA) increased the GFAP and Iba-1 immunostaining of glia cells and silver staining of degenerating axons in the optic tract with significant reduction of N1 amplitude of visual evoked potential at up to 3.5 months after injury. Both GPR110 ligands dose- and GPR110-dependently increased cAMP in cultured primary microglia with A8, a ligand with improved stability, being more effective than synaptamide. Intraperitoneal injection of A8 at 1 mg/kg or synaptamide at 5 mg/kg significantly reduced the acute expression of TNF mRNA in the brain and ameliorated chronic optic tract microgliosis, astrogliosis, and axonal degeneration as well as visual deficit caused by injury in WT but not in GPR110 KO mice. Conclusion Our data demonstrate that ligand-induced activation of the GPR110/cAMP system upregulated after injury ameliorates the long-term optic tract histopathology and visual impairment caused by rCHIMERA. Based on the anti-inflammatory nature of GPR110 activation, we suggest that GPR110 ligands may have therapeutic potential for chronic visual dysfunction associated with mTBI.

Long-term outcomes after mild traumatic brain injury

2014 ◽  
Vol 219 (4) ◽  
pp. e144-e145
Author(s):  
Elizabeth Shinn ◽  
Amy Pate ◽  
Frederique Pinto ◽  
Akella Chendrasekhar
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Long Term Outcomes

Verbal Recall After Mild Traumatic Brain Injury: Sensitivity of the Rapid Screen of Concussion

2003 ◽  
Vol 4 (2) ◽  
pp. 155-167 ◽  
Author(s):  
Karleigh Jayne Kwapil ◽  
Gina Geffen ◽  
Ken McFarland ◽  
Veronica Eileen DeMonte
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Verbal Memory ◽  
Test Performance ◽  
Verbal Learning ◽  
Clinical Samples ◽  
Classification Rate ◽  
Delayed Recall ◽  
Learning Test

AbstractThe present study aimed to determine whether including a sensitive test of immediate and delayed recall would improve the diagnostic validity of the Rapid Screen of Concussion (RSC) in mild Traumatic Brain Injury (mTBI) versus orthopaedic clinical samples. Two studies were undertaken. In Study 1, the performance of 156 mTBI and 145 orthopaedic participants was analysed to identify the number of individuals who performed at ceiling on the verbal memory subtest of the RSC, as this test required immediate and delayed recall of only five words. A second aim was to determine the sensitivity and specificity levels of the RSC. Study 2 aimed to examine whether replacement of the verbal memory subtest with the 12-word Hopkins Verbal Learning Test (HVLT) could improve the sensitivity of the RSC in a new sample of 26 mTBI and 30 orthopaedic participants. Both studies showed that orthopaedic participants outperformed mTBI participants on each of the selected measures. Study 1 showed that 14% of mTBI participants performed at ceiling on the immediate and 21.2% on delayed recall test. Performance on the original battery yielded a sensitivity of 82%, specificity of 80% and overall correct classification of 81.5% participants. In Study 2, inclusion of the HVLT improved sensitivity to a level of 88.5%, decreased specificity to a level of 70% and resulted in an overall classification rate of 80%. It was concluded that although inclusion of the five-word subtest in the RSC can successfully distinguish concussed from non-concussed individuals, use of the HVLT in this protocol yields a more sensitive measure of subtle cognitive deficits following mTBI.

#3104 Is dipsogenic diabetes insipidus the same condition as psychogenic polydipsia?

2021 ◽  
Vol 92 (8) ◽  
pp. A11.2-A11
Author(s):  
Ewelina de Leon ◽  
Graeme Yorston
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Literature Review ◽  
Diabetes Insipidus ◽  
Endocrine Disruption ◽  
Psychiatric Disease ◽  
List Type ◽  
Psychogenic Polydipsia

Objectives/AimsTraumatic brain injury is a common cause of permanent or long-term disability,1 and up to 80% of people with moderate to severe brain injury have some degree of pituitary insufficiency. Endocrine disruption has been documented in medical literature since the 1940s,2-4 where central diabetes insipidus has been described as a common transient complication which causes polydipsia (insatiable thirst). However, polydipsia can be caused by other conditions. It is classified into dipsogenic, in a syndrome of disordered thirst-regulating mechanism in patients without psychiatric disease called dipsogenic diabetes insipidus, psychogenic, as a compulsive water drinking in patients with psychiatric conditions referred to as psychogenic polydipsia or psychogenic diabetes insipidus and iatrogenic where large quantities of water are consumed for health benefits. All of which are referred to as primary polydipsia if these conditions cannot be distinguished. Dipsogenic diabetes insipidus and psychogenic polydipsia can be easily mixed up, misdiagnosed or even unrecognised, mainly because their pathophysiology is still unclear. Are these conditions different, or is there anything that can relate them to each other? With this literature review, we are aiming to find the link between subsets of polydipsia after brain trauma, to compare proposed differential diagnosis and their functionality in clinical settings.MethodA literature review was conducted following a search of MEDLINE, CINAHL Plus, APA PsycArticles, APA PsycBooks, APA PsycInfo databases from 1858 onwards.ResultsWe will present our findings from the literature review.ConclusionPolydipsia is a common clinical problem and requires careful evaluation and management to prevent long term neurological sequelae, and there are no evidence-based treatment guidelines.References National Institute of Health and Care Excellence (NICE). (2019). Head Injury. CG176. Retrieved from: https://www.nice.org.uk/guidance/cg176 Escamilla RF, Lisser H. Simmonds disease: A clinical study with revie of the literature; Differentiation from anorexia nervosa by statistical analysis of 595 cases, 101 of which were provided pathologically. The Journal of Clinical Endocrinology & Metabolism 1942;2(2):6596. Porter RJ, Miller RA. Diabetes insipidus following closed head injury. Journal of Neurology, Neurosurgery, and Psychiatry 1946;11:528562. Webb NE, Little B, Loupee-Wilson S, Power EM. Traumatic brain injury and neuro-endocrine disruption: medical and psychosocial rehabilitation. NeuroRehabilitation (Reading, Mass.) 2014;34(4):625636.

scholarly journals Exosomal MicroRNA Differential Expression in Plasma of Young Adults with Chronic Mild Traumatic Brain Injury and Healthy Control

Biomedicines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 36
Author(s):  
Rany Vorn ◽  
Maiko Suarez ◽  
Jacob C. White ◽  
Carina A. Martin ◽  
Hyung-Suk Kim ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Young Adults ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Pathophysiological Mechanism ◽  
Post Injury ◽  
Persistent Symptoms ◽  
Healthy Control ◽  
Underlying Mechanisms

Chronic mild traumatic brain injury (mTBI) has long-term consequences, such as neurological disability, but its pathophysiological mechanism is unknown. Exosomal microRNAs (exomiRNAs) may be important mediators of molecular and cellular changes involved in persistent symptoms after mTBI. We profiled exosomal microRNAs (exomiRNAs) in plasma from young adults with or without a chronic mTBI to decipher the underlying mechanisms of its long-lasting symptoms after mTBI. We identified 25 significantly dysregulated exomiRNAs in the chronic mTBI group (n = 29, with 4.48 mean years since the last injury) compared to controls (n = 11). These miRNAs are associated with pathways of neurological disease, organismal injury and abnormalities, and psychological disease. Dysregulation of these plasma exomiRNAs in chronic mTBI may indicate that neuronal inflammation can last long after the injury and result in enduring and persistent post-injury symptoms. These findings are useful for diagnosing and treating chronic mTBIs.

scholarly journals Correction to: Long-term psychosocial outcome following mild traumatic brain injury and minor stroke: a direct longitudinal comparison

2021 ◽  
Vol 268 (11) ◽  
pp. 4404-4405
Author(s):  
Daan P. J. Verberne ◽  
Rudolf W. H. M. Ponds ◽  
Mariëlle E. A. L. Kroese ◽  
Melloney L. M. Wijenberg ◽  
Dennis G. Barten ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Minor Stroke ◽  
Psychosocial Outcome ◽  
Longitudinal Comparison
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