scholarly journals Depression following traumatic brain injury: a comprehensive overview

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Marc Fakhoury ◽  
Zaynab Shakkour ◽  
Firas Kobeissy ◽  
Nada Lawand
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Health Concern ◽  
First Year ◽  
Comprehensive Overview ◽  
Symptoms Of Depression ◽  
Current State ◽  
Post Traumatic ◽  
Brain Changes

Abstract Traumatic brain injury (TBI) represents a major health concern affecting the neuropsychological health; TBI is accompanied by drastic long-term adverse complications that can influence many aspects of the life of affected individuals. A substantial number of studies have shown that mood disorders, particularly depression, are the most frequent complications encountered in individuals with TBI. Post-traumatic depression (P-TD) is present in approximately 30% of individuals with TBI, with the majority of individuals experiencing symptoms of depression during the first year following head injury. To date, the mechanisms of P-TD are far from being fully understood, and effective treatments that completely halt this condition are still lacking. The aim of this review is to outline the current state of knowledge on the prevalence and risk factors of P-TD, to discuss the accompanying brain changes at the anatomical, molecular and functional levels, and to discuss current approaches used for the treatment of P-TD.

Time Interval Between Traumatic Brain Injury And Post Traumatic Epilepsy

2013 ◽  
Vol 21 (2) ◽  
pp. 222-228
Author(s):  
Daniel Garbin Di Luca ◽  
Glenda Corrêa Borges de Lacerda
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
First Year ◽  
Time Interval ◽  
Partial Seizures ◽  
Complex Partial Seizures ◽  
Post Traumatic ◽  
Faster Development ◽  
Post Traumatic Epilepsy ◽  
Traumatic Epilepsy

Introduction. The estimated time interval in which an individual can develop Post Traumatic Epilepsy (PTE) after a traumatic brain injury (TBI) is not clear. Objective. To assess the possible influence of the clinical features in the time interval between TBI and PTE develop­ment. Method. We analyzed retrospectively 400 medical records from a tertiary Brazilian hospital. We selected and reevaluated 50 patients and data was confronted with the time between TBI and PTE devel­opment by a Kaplan-Meier survival analysis. A Cox-hazard regression was also conducted to define the characteristics that could be involved in the latent period of the PTE development. Results. Patients devel­oped PTE especially in the first year (56%). We found a tendency of a faster development of PTE in patients older than 24 years (P<0.0001) and in men (P=0.03). Complex partial seizures evolving to generalized seizures were predominant in patients after moderate (37.7%) and severe (48.8%) TBIs, and simple partial seizures evolving to general­ized seizures in mild TBIs (45.5%). Conclusions. Our data suggest that the first year after a TBI is the most critical period for PTE de­velopment and those males older than 24 years could have a faster development of PTE.

scholarly journals Repeated Mild Traumatic Brain Injury Results in Long-Term White-Matter Disruption

2014 ◽  
Vol 34 (4) ◽  
pp. 715-723 ◽  
Author(s):  
Virginia Donovan ◽  
Claudia Kim ◽  
Ariana K Anugerah ◽  
Jacqueline S Coats ◽  
Udochuwku Oyoyo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Mild Traumatic Brain Injury ◽  
Diffusion Tensor ◽  
Ex Vivo ◽  
Health Concern ◽  
Sprague Dawley ◽  
G Ratio

Mild traumatic brain injury (mTBI) is an increasing public health concern as repetitive injuries can exacerbate existing neuropathology and result in increased neurologic deficits. In contrast to other models of repeated mTBI (rmTBI), our study focused on long-term white-matter abnormalities after bilateral mTBIs induced 7 days apart. A controlled cortical impact (CCI) was used to induce an initial mTBI to the right cortex of Single and rmTBI Sprague Dawley rats, followed by a second injury to the left cortex of rmTBI animals. Shams received only a craniectomy. Ex vivo diffusion tensor imaging (DTI), transmission electron microscopy (TEM), and histology were performed on the anterior corpus callosum at 60 days after injury. The rmTBI animals showed a significant bilateral increase in radial diffusivity (myelin), while only modest changes in axial diffusivity (axonal) were seen between the groups. Further, the rmTBI group showed an increased g-ratio and axon caliber in addition to myelin sheath abnormalities using TEM. Our DTI results indicate ongoing myelin changes, while the TEM data show continuing axonal changes at 60 days after rmTBI. These data suggest that bilateral rmTBI induced 7 days apart leads to progressive alterations in white matter that are not observed after a single mTBI.

scholarly journals Dentate Gyrus Proliferative Responses After Traumatic Brain Injury and Binge Alcohol in Adult Rats

2020 ◽  
Vol 15 ◽  
pp. 263310552096890
Author(s):  
Son T Ton ◽  
Natalie S Adamczyk ◽  
Jack P Gerling ◽  
Ian C Vaagenes ◽  
Joanna Y Wu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Dentate Gyrus ◽  
Proliferative Response ◽  
Male Rats ◽  
Public Health Issue ◽  
Adult Rats ◽  
Double Labeling ◽  
Post Traumatic

Background: Traumatic brain injury is a significant public health issue that results in serious disability in survivors. Traumatic brain injury patients are often intoxicated with alcohol when admitted to the hospital; however, it is not clear how acute intoxication affects recovery from a traumatic brain injury. Our group has previously shown that binge alcohol prior to traumatic brain injury resulted in long-term impairment in a fine sensorimotor task that was correlated with a decreased proliferative and neuroblast response from the subventricular zone. However, whether binge alcohol prior to traumatic brain injury affects the proliferative response in the hippocampal dentate gyrus is not yet known. Methods: Male rats underwent binge alcohol (3 g/kg/day) by gastric gavage for 3 days prior to traumatic brain injury. Cell proliferation was labeled by BrdU injections following traumatic brain injury. Stereological quantification and immunofluorescence confocal analysis of BrdU+ cells in the hippocampal dorsal dentate gyrus was performed at 24 hours, 1 week and 6 weeks post traumatic brain injury. Results: We found that either traumatic brain injury alone or binge alcohol alone significantly increased dentate gyrus proliferation at 24 hours and 1 week. However, a combined binge alcohol and traumatic brain injury regimen resulted in decreased dentate gyrus proliferation at 24 hours post-traumatic brain injury. At the 6 week time point, binge alcohol overall reduced the number of BrdU+ cells. Furthermore, more BrdU+ cells were found in the dentate hilar region of alcohol traumatic brain injury compared to vehicle traumatic brain injury groups. The location and double-labeling of these mismigrated BrdU+ cells was consistent with hilar ectopic granule cells. Conclusion: The results from this study showed that pre-traumatic brain injury binge alcohol impacts the injury-induced proliferative response in the dentate gyrus in the short-term and may affect the distribution of newly generated cells in the dentate gyrus in the long-term.

Traumatic Brain Injury and Risk of Long-Term Brain Changes, Accumulation of Pathological Markers, and Developing Dementia: A Review

2019 ◽  
Vol 70 (3) ◽  
pp. 629-654 ◽  
Author(s):  
Christian LoBue ◽  
Catherine Munro ◽  
Jeffrey Schaffert ◽  
Nyaz Didehbani ◽  
John Hart, ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Changes

scholarly journals Neurorehabilitation of Traumatic Brain Injury (TBI): A Clinical Review

2019 ◽  
Vol 7 (3) ◽  
pp. 47 ◽  
Author(s):  
Michael Oberholzer ◽  
René M. Müri
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Recovery Of Function ◽  
Neuropsychological Rehabilitation ◽  
Paroxysmal Sympathetic Hyperactivity ◽  
Initial Sequence ◽  
Clinical Consequences ◽  
Severe Tbi ◽  
Post Traumatic

Traumatic brain injury (TBI) and its potential long-term consequences are of major concern for public health. Neurorehabilitation of affected individuals has some specific characteristics in contrast to neurorehabilitation of patients with acquired brain lesions of other aetiology. This review will deal with the clinical consequences of the distinct lesions of TBI. In severe TBI, clinical course often follows a typical initial sequence of coma; followed by disturbed consciousness; later, post-traumatic agitation and amnesia; and finally, recovery of function occurs. In the different phases of neurorehabilitation, physicians should be aware of typical medical complications such as paroxysmal sympathetic hyperactivity, posttraumatic hydrocephalus, and posttraumatic neuroendocrine dysfunctions. Furthermore, we address questions on timing and on existing evidence for different rehabilitation programmes and for holistic neuropsychological rehabilitation approaches.

Post-traumatic amnesia predicts long-term cerebral atrophy in traumatic brain injury

Brain Injury ◽  
2006 ◽  
Vol 20 (7) ◽  
pp. 695-699 ◽  
Author(s):  
Elisabeth A. Wilde ◽  
Erin D. Bigler ◽  
Claudia Pedroza ◽  
David K. Ryser
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Atrophy ◽  
Traumatic Amnesia ◽  
Post Traumatic

The scope of early traumatic brain injury as a long-term health concern in two nationwide samples: Prevalence and prognostic factors

Brain Injury ◽  
2011 ◽  
Vol 26 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Jonas G. Halldorsson ◽  
Kjell M. Flekkoy ◽  
Gudmundur B. Arnkelsson ◽  
Kristinn Tomasson ◽  
Hulda Bra Magnadottir ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Prognostic Factors ◽  
Brain Injury ◽  
Health Concern

Long-term structural brain changes 10 years after pediatric traumatic brain injury

NeuroImage ◽  
2009 ◽  
Vol 47 ◽  
pp. S46
Author(s):  
MH Beauchamp ◽  
VA Anderson ◽  
C Catroppa ◽  
JJ Maller ◽  
C Godfrey ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Pediatric Traumatic Brain Injury ◽  
Brain Changes ◽  
Structural Brain

scholarly journals Main mechanisms of post-traumatic brain’s epileptization (Literature review)

2020 ◽  
pp. 79-83
Author(s):  
Serhii Antonenko
Keyword(s):  
Risk Factors ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Epileptic Seizures ◽  
Increased Risk ◽  
Post Traumatic ◽  
Post Traumatic Epilepsy ◽  
Traumatic Epilepsy

The problem of traumatic brain injury, its consequences in the long term is relevant for neurologists and doctors of related specialties involved in the treatment, diagnosis and rehabilitation of such a contingent of patients. There are about a dozen syndromes; yaks are most common after an injury. However, one of the most frequent and formidable consequences of traumatic brain damage is post-traumatic epilepsy, which is the main identified cause of symptomatic epilepsy at a young age. The work highlights the “trigger” mechanisms of traumatic brain injury, in particular, oxidative stress, which is an essential component both in the early and long-term periods of CNS damage and leads to the disintegration of all its levels, contributes to the development of basic neuropathological syndromes and primarily post-traumatic epilepsy. The problems of interpreting terminology are considered, when the diagnosis is based only on the fact of the presence of a brain injury, differentiation of this kind of symptomatic convulsive syndrome from other epileptic seizures, the dependence of development on the severity of a head injury (severe injury gives an increased risk of seizures 29 times higher than mild), staging and major risk factors for this type of epileptogenesis, as well as disorganization and damage to the antiepileptic system. A spectrum of convulsive seizures is described, in particular partial, taking into account the localization characteristic of a traumatic brain injury with the predominance of its lesion forms. It is necessary to take into account the occurrence of delayed brain damage, in particular disorders of the immune system, the correlation of the course of post-traumatic epilepsy with the degree of development of hydrocephalus, hypoperfusion of brain areas, glial barrier insufficiency, will contribute to the formation of convulsive activity. It is necessary to take into account the family history. Keywords: post-traumatic epilepsy, epileptogenesis, risk factors

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