scholarly journals MMP-9 Contributes to Dendritic Spine Remodeling Following Traumatic Brain Injury

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Barbara Pijet ◽  
Marzena Stefaniuk ◽  
Leszek Kaczmarek
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Dendritic Spine ◽  
Contralateral Side ◽  
Spine Density ◽  
Morphological Transformation ◽  
Physical Trauma ◽  
Spine Shape ◽  
Wide Range

Traumatic brain injury (TBI) occurs when a blow to the head causes brain damage. Apart from physical trauma, it causes a wide range of cognitive, behavioral, and emotional deficits including impairments in learning and memory. On neuronal level, TBI may lead to circuitry remodeling and in effect imbalance between excitatory and inhibitory neurotransmissions. Such change in brain homeostasis may often lead to brain disorders. The basic units of neuronal connectivity are dendritic spines that are tiny protrusions forming synapses between two cells in a network. Spines are dynamic structures that undergo morphological transformation throughout life. Their shape is strictly related to an on/off state of synapse and the strength of synaptic transmission. Matrix metalloproteinase-9 (MMP-9) is an extrasynaptically operating enzyme that plays a role in spine remodeling and has been reported to be activated upon TBI. The aim of the present study was to evaluate the influence of MMP-9 on dendritic spine density and morphology following controlled cortical impact (CCI) as animal model of TBI. We examined spine density and dendritic spine shape in the cerebral cortex and the hippocampus. CCI caused a marked decrease in spine density as well as spine shrinkage in the cerebral cortex ipsilateral to the injury, when compared to sham animals and contralateral side both 1 day and 1 week after the insult. Decreased spine density was also observed in the dentate gyrus of the hippocampus; however, in contrast to the cerebral cortex, spines in the DG became more filopodia-like. In mice lacking MMP-9, no effects of TBI on spine density and morphology were observed.

scholarly journals Advancing age and ischemia elevate the electric threshold to elicit spreading depolarization in the cerebral cortex of young adult rats

2016 ◽  
Vol 37 (5) ◽  
pp. 1763-1775 ◽  
Author(s):  
Péter Hertelendy ◽  
Ákos Menyhárt ◽  
Péter Makra ◽  
Zoltán Süle ◽  
Tamás Kiss ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Dendritic Spine ◽  
Age Groups ◽  
Young Patients ◽  
Spine Density ◽  
Adult Rats ◽  
Doppler Flowmetry ◽  
Spreading Depolarization ◽  
Cumulative Duration

Spreading depolarizations of long cumulative duration have been implicated in lesion development and progression in patients with stroke and traumatic brain injury. Spreading depolarizations evolve less likely in the aged brain, but it remains to be determined at what age the susceptibility to spreading depolarizations starts to decline, especially in ischemia. Spreading depolarizations were triggered by epidural electric stimulation prior and after ischemia induction in the cortex of 7–30 weeks old anesthetized rats ( n = 38). Cerebral ischemia was achieved by occlusion of both common carotid arteries. Spreading depolarization occurrence was confirmed by the acquisition of DC potential and electrocorticogram. Cerebral blood flow variations were recorded by laser-Doppler flowmetry. Dendritic spine density in the cortex was determined in Golgi-COX stained sections. Spreading depolarization initiation required increasingly greater electric charge with older age, a potential outcome of consolidation of cortical connections, indicated by altered dendritic spine distribution. The threshold of spreading depolarization elicitation increased with ischemia in all age groups, which may be caused by tissue acidosis and increased K+ conductance, among other factors. In conclusion, the brain appears to be the most susceptible to spreading depolarizations at adolescent age; therefore, spreading depolarizations may occur in young patients of ischemic or traumatic brain injury at the highest probability.

scholarly journals Traumatic Brain Injury: Effect of Litigation Status on Executive Functioning—A Pilot Study

2020 ◽  
Author(s):  
Simi Prakash K. ◽  
Rajakumari P. Reddy ◽  
Anna R. Mathulla ◽  
Jamuna Rajeswaran ◽  
Dhaval P. Shukla
Keyword(s):  
Traumatic Brain Injury ◽  
Working Memory ◽  
Depressive Symptoms ◽  
Brain Injury ◽  
Concept Formation ◽  
Verbal Working Memory ◽  
Self Report ◽  
Semantic Fluency ◽  
Set Shifting ◽  
Wide Range

AbstractTraumatic brain injury (TBI) is associated with a wide range of physiological, behavioral, emotional, and cognitive sequelae. Litigation status is one of the many factors that has an impact on recovery. The aim of this study was to compare executive functions, postconcussion, and depressive symptoms in TBI patients with and without litigation. A sample of 30 patients with TBI, 15 patients with litigation (medicolegal case [MLC]), and 15 without litigation (non-MLC) was assessed. The tools used were sociodemographic and clinical proforma, executive function tests, Rivermead Post-Concussion Symptom Questionnaire, and Beck Depression Inventory. Assessment revealed that more than 50% of patients showed deficits in category fluency, set shifting, and concept formation. The MLC group showed significant impairment on verbal working memory in comparison to the non-MLC group. The performance of both groups was comparable on tests of semantic fluency, visuospatial working memory, concept formation, set shifting, planning, and response inhibition. The MLC group showed more verbal working memory deficits in the absence of significant postconcussion and depressive symptoms on self-report measures.

scholarly journals Biomechanics of Traumatic Brain Injury: Influences of the Morphologic Heterogeneities of the Cerebral Cortex

2008 ◽  
Vol 36 (7) ◽  
pp. 1203-1215 ◽  
Author(s):  
R.J.H. Cloots ◽  
H.M.T. Gervaise ◽  
J.A.W. van Dommelen ◽  
M.G.D. Geers
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury

Prognostic Factors for Persistent Symptoms in Adults With Mild Traumatic Brain Injury: an Overview of Systematic Reviews

2021 ◽  
Author(s):  
Julien Déry ◽  
Béatrice Ouellet ◽  
Élaine de Guise ◽  
Ève-Line Bussières ◽  
Marie-Eve Lamontagne
Keyword(s):  
Traumatic Brain Injury ◽  
Prognostic Factors ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Systematic Reviews ◽  
Clinical Decision Making ◽  
Clinical Decision ◽  
Persistent Symptoms ◽  
Wide Range ◽  
Overview Of Systematic Reviews

Abstract Background: Mild traumatic brain injury (mTBI) is an increasing public health problem, because of its persistent symptoms and several functional consequences. Understanding the prognosis of a condition is an important component of clinical decision-making and can help to guide prevention of persistent symptoms following mTBI. Prognosis of mTBI has stimulated several empirical primary research papers and many systematic reviews leading to the identification of a wide range of factors. We aim to synthesize these factors to get a better understanding of their breadth and scope.Methods: We conducted an overview of systematic reviews. We searched in databases systematic reviews synthesizing evidence about prognosis of persistent symptoms after mTBI in the adult population. Two reviewers independently screened all references and selected eligible reviews based on eligibility criteria. They extracted relevant information using an extraction grid. They also rated independently the risk of bias using the ROBIS tool. We synthesized evidence into a comprehensive conceptual map to facilitate the understanding of prognostic factors that have an impact on persistent post-concussion symptoms.Results: From the 3857 references retrieved in database search, we included 25 systematic reviews integrating the results of 312 primary articles published between 1957 and 2019. We examined 35 prognostic factors from the systematics reviews. No single prognostic factor demonstrated convincing and conclusive results. However, age, sex and multiple concussions showed an affirmatory association with persistent post-concussion outcomes in systematic reviews.Conclusion: We highlighted the need of a comprehensive picture of prognostic factors related to persistent post-concussion symptoms. We believe that these prognostic factors would guide clinical decision and research related to prevention and intervention regarding persistent post-concussion symptoms.Systematic review registration: PROSPERO CRD42020176676

Development of a de novo arteriovenous malformation after severe traumatic brain injury

2014 ◽  
Vol 14 (4) ◽  
pp. 418-420 ◽  
Author(s):  
Brandon A. Miller ◽  
David I. Bass ◽  
Joshua J. Chern
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Arteriovenous Malformation ◽  
Severe Traumatic Brain Injury ◽  
Arteriovenous Malformations ◽  
De Novo ◽  
First Report ◽  
Congenital Lesions

Arteriovenous malformations (AVMs) are typically considered congenital lesions, although there is growing evidence for de novo formation of these lesions as well. The authors present the case of an AVM in the same cerebral cortex that had been affected by a severe traumatic brain injury (TBI) more than 6 years earlier. To the best of the authors' knowledge, this is the first report attributing the formation of an AVM directly to TBI.

Temporal Lobe Syndromes

2020 ◽  
pp. 122-135
Author(s):  
Arpit Parmar ◽  
G. S. Kaloiya ◽  
Harsimarpreet Kaur
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Middle Cerebral Artery ◽  
Temporal Lobe ◽  
Cerebral Artery ◽  
Left Temporal Lobe ◽  
Temporal Lobes ◽  
Functional Aspects ◽  
The Common

Temporal lobes are one of the four major lobes of the cerebral cortex and perform a complex array of interrelated functions. They play an important role in various day-to-day functioning. The common pathologies leading to isolated temporal lobe dysfunction are infarction (of the middle cerebral artery), hemorrhage, seizures, tumors, encephalitis, and traumatic brain injury. Temporal lobe syndromes include a wide array of various neurological (Kluver-Bucy syndrome, Geschwind Gastaut syndrome, etc.), elementary (e.g., vertiginous syndromes, hallucinations, etc.), neuropsychiatric (e.g., anxiety, agitation, aggression, etc.), and cognitive (e.g., Korsakoff amnesia, cortical deafness, etc.) disorders. The presentation depends on a multitude of factors including involvement of dominant or non-dominant lobe. Left temporal lobe involvement usually leads to various forms of aphasia while right side involvement leads to more covert and varied syndromes. In this chapter, the authors discuss the anatomy of the temporal lobe, its functional aspects, and various syndromes of temporal lobe dysfunction.

scholarly journals Comorbidity in adults with traumatic brain injury and all-cause mortality: a systematic review

BMJ Open ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. e029072 ◽  
Author(s):  
Chen Xiong ◽  
Sara Hanafy ◽  
Vincy Chan ◽  
Zheng Jing Hu ◽  
Mitchell Sutton ◽  
...  
Keyword(s):  
Systematic Review ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Self Report ◽  
Qualitative Description ◽  
Comorbid Condition ◽  
Comorbid Conditions ◽  
Eligibility Criteria ◽  
Wide Range ◽  
All Cause Mortality

ObjectivesComorbidity in traumatic brain injury (TBI) has been recognised to alter the clinical course of patients and influence short-term and long-term outcomes. We synthesised the evidence on the effects of different comorbid conditions on early and late mortality post-TBI in order to (1) examine the relationship between comorbid condition(s) and all-cause mortality in TBI and (2) determine the influence of sociodemographic and clinical characteristics of patients with a TBI at baseline on all-cause mortality.DesignSystematic review.Data sourcesMedline, Central, Embase, PsycINFO and bibliographies of identified articles were searched from May 1997 to January 2019.Eligibility criteria for selecting studiesIncluded studies met the following criteria: (1) focused on comorbidity as it related to our outcome of interest in adults (ie, ≥18 years of age) diagnosed with a TBI; (2) comorbidity was detected by any means excluding self-report; (3) reported the proportion of participants without comorbidity and (4) followed participants for any period of time.Data extraction and synthesisTwo independent reviewers extracted the data and assessed risk of bias using the Quality in Prognosis Studies tool. Data were synthesised through tabulation and qualitative description.ResultsA total of 27 cohort studies were included. Among the wide range of individual comorbid conditions studied, only low blood pressure was a consistent predictors of post-TBI mortality. Other consistent predictors were traditional sociodemographic risk factors. Higher comorbidity scale, scores and the number of comorbid conditions were not consistently associated with post-TBI mortality.ConclusionsGiven the high number of comorbid conditions that were examined by the single studies, research is required to further substantiate the evidence and address conflicting findings. Finally, an enhanced set of comorbidity measures that are suited for the TBI population will allow for better risk stratification to guide TBI management and treatment.PROSPERO registration numberCRD42017070033

Increased expression of ferritin in cerebral cortex after human traumatic brain injury

2012 ◽  
Vol 34 (7) ◽  
pp. 1173-1180 ◽  
Author(s):  
Huan-Dong Liu ◽  
Wei Li ◽  
Zhen-Rui Chen ◽  
Meng-Liang Zhou ◽  
Zong Zhuang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury

scholarly journals Multiple Sites of Vasopressin Synthesis in the Injured Brain

2010 ◽  
Vol 31 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Joanna Szmydynger-Chodobska ◽  
Brian J Zink ◽  
Adam Chodobski
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Impact Model ◽  
Proinflammatory Mediators ◽  
Injured Brain ◽  
Pathophysiological Role ◽  
Cerebrovascular Endothelium ◽  
Vasopressin Synthesis

Previous studies have indicated that the primary targets for vasopressin actions on the injured brain are the cerebrovascular endothelium and astrocytes, and that vasopressin amplifies the posttraumatic production of proinflammatory mediators. Here, the controlled cortical impact model of traumatic brain injury in rats was used to identify the sources of vasopressin in the injured brain. Injury increased vasopressin synthesis in the hypothalamus and cerebral cortex adjacent to the posttraumatic lesion. In the cortex, vasopressin was predominantly produced by activated microglia/macrophages, and, to a lesser extent, by the cerebrovascular endothelium. These data further support the pathophysiological role of vasopressin in brain injury.

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