Computerized Cognitive Retraining Programs for Patients Afflicted with Traumatic Brain Injury and Other Brain Disorders

2013 ◽  
pp. 11-32
Author(s):  
C.R. Mukundan
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Disorders ◽  
Cognitive Retraining

scholarly journals Endothelin ETB Receptor-Mediated Astrocytic Activation: Pathological Roles in Brain Disorders

2021 ◽  
Vol 22 (9) ◽  
pp. 4333
Author(s):  
Yutaka Koyama
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurotrophic Factors ◽  
Drug Target ◽  
Therapeutic Strategy ◽  
Reactive Astrocytes ◽  
Brain Disorders ◽  
Etb Receptor ◽  
Target Molecules ◽  
Endothelin B

In brain disorders, reactive astrocytes, which are characterized by hypertrophy of the cell body and proliferative properties, are commonly observed. As reactive astrocytes are involved in the pathogenesis of several brain disorders, the control of astrocytic function has been proposed as a therapeutic strategy, and target molecules to effectively control astrocytic functions have been investigated. The production of brain endothelin-1 (ET-1), which increases in brain disorders, is involved in the pathophysiological response of the nervous system. Endothelin B (ETB) receptors are highly expressed in reactive astrocytes and are upregulated by brain injury. Activation of astrocyte ETB receptors promotes the induction of reactive astrocytes. In addition, the production of various astrocyte-derived factors, including neurotrophic factors and vascular permeability regulators, is regulated by ETB receptors. In animal models of Alzheimer’s disease, brain ischemia, neuropathic pain, and traumatic brain injury, ETB-receptor-mediated regulation of astrocytic activation has been reported to improve brain disorders. Therefore, the astrocytic ETB receptor is expected to be a promising drug target to improve several brain disorders. This article reviews the roles of ETB receptors in astrocytic activation and discusses its possible applications in the treatment of brain disorders.

Profiles of Executive Function Across Children with Distinct Brain Disorders: Traumatic Brain Injury, Stroke, and Brain Tumor

2017 ◽  
Vol 23 (7) ◽  
pp. 529-538 ◽  
Author(s):  
Gabriel C. Araujo ◽  
Tanya N. Antonini ◽  
Vicki Anderson ◽  
Kathryn A. Vannatta ◽  
Christina G. Salley ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Tumor ◽  
Executive Function ◽  
Brain Injury ◽  
Executive Functions ◽  
Control Group ◽  
Medical Illness ◽  
Brain Disorders ◽  
Brain Disorder ◽  
Orthopedic Injury

AbstractObjectives:This study examined whether children with distinct brain disorders show different profiles of strengths and weaknesses in executive functions, and differ from children without brain disorder.Methods:Participants were children with traumatic brain injury (N=82; 8–13 years of age), arterial ischemic stroke (N=36; 6–16 years of age), and brain tumor (N=74; 9–18 years of age), each with a corresponding matched comparison group consisting of children with orthopedic injury (N=61), asthma (N=15), and classmates without medical illness (N=68), respectively. Shifting, inhibition, and working memory were assessed, respectively, using three Test of Everyday Attention: Children’s Version (TEA-Ch) subtests: Creature Counting, Walk-Don’t-Walk, and Code Transmission. Comparison groups did not differ in TEA-Ch performance and were merged into a single control group. Profile analysis was used to examine group differences in TEA-Ch subtest scaled scores after controlling for maternal education and age.Results:As a whole, children with brain disorder performed more poorly than controls on measures of executive function. Relative to controls, the three brain injury groups showed significantly different profiles of executive functions. Importantly, post hoc tests revealed that performance on TEA-Ch subtests differed among the brain disorder groups.Conclusions:Results suggest that different childhood brain disorders result in distinct patterns of executive function deficits that differ from children without brain disorder. Implications for clinical practice and future research are discussed. (JINS, 2017,23, 529–538)

scholarly journals Traumatic Brain Injury and Delayed Sequelae: A Review - Traumatic Brain Injury and Mild Traumatic Brain Injury (Concussion) are Precursors to Later-Onset Brain Disorders, Including Early-Onset Dementia

2007 ◽  
Vol 7 ◽  
pp. 1768-1776 ◽  
Author(s):  
Michael A. Kiraly ◽  
Stephen J. Kiraly
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Brain Injuries ◽  
Brain Disorders ◽  
Early Onset Dementia ◽  
Human Experiments ◽  
Delayed Consequences ◽  
Subsequent Onset

Brain injuries are too common. Most people are unaware of the incidence of and horrendous consequences of traumatic brain injury (TBI) and mild traumatic brain injury (MTBI). Research and the advent of sophisticated imaging have led to progression in the understanding of brain pathophysiology following TBI. Seminal evidence from animal and human experiments demonstrate links between TBI and the subsequent onset of premature, psychiatric syndromes and neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD). Objectives of this summary are, therefore, to instill appreciation regarding the importance of brain injury prevention, diagnosis, and treatment, and to increase awareness regarding the long-term delayed consequences following TBI.

scholarly journals Angiotensin II AT1 receptor blockers as treatments for inflammatory brain disorders

2012 ◽  
Vol 123 (10) ◽  
pp. 567-590 ◽  
Author(s):  
Juan M. Saavedra
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Angiotensin Ii ◽  
At1 Receptor ◽  
Brain Inflammation ◽  
Brain Disorders ◽  
Receptor Blockers ◽  
At1 Receptor Blockers

The effects of brain AngII (angiotensin II) depend on AT1 receptor (AngII type 1 receptor) stimulation and include regulation of cerebrovascular flow, autonomic and hormonal systems, stress, innate immune response and behaviour. Excessive brain AT1 receptor activity associates with hypertension and heart failure, brain ischaemia, abnormal stress responses, blood–brain barrier breakdown and inflammation. These are risk factors leading to neuronal injury, the incidence and progression of neurodegerative, mood and traumatic brain disorders, and cognitive decline. In rodents, ARBs (AT1 receptor blockers) ameliorate stress-induced disorders, anxiety and depression, protect cerebral blood flow during stroke, decrease brain inflammation and amyloid-β neurotoxicity and reduce traumatic brain injury. Direct anti-inflammatory protective effects, demonstrated in cultured microglia, cerebrovascular endothelial cells, neurons and human circulating monocytes, may result not only in AT1 receptor blockade, but also from PPARγ (peroxisome-proliferator-activated receptor γ) stimulation. Controlled clinical studies indicate that ARBs protect cognition after stroke and during aging, and cohort analyses reveal that these compounds significantly reduce the incidence and progression of Alzheimer's disease. ARBs are commonly used for the therapy of hypertension, diabetes and stroke, but have not been studied in the context of neurodegenerative, mood or traumatic brain disorders, conditions lacking effective therapy. These compounds are well-tolerated pleiotropic neuroprotective agents with additional beneficial cardiovascular and metabolic profiles, and their use in central nervous system disorders offers a novel therapeutic approach of immediate translational value. ARBs should be tested for the prevention and therapy of neurodegenerative disorders, in particular Alzheimer's disease, affective disorders, such as co-morbid cardiovascular disease and depression, and traumatic brain injury.

scholarly journals Photobiomodulation and the brain – has the light dawned?

2016 ◽  
Vol 38 (6) ◽  
pp. 24-28 ◽  
Author(s):  
Michael R. Hamblin
Keyword(s):  
Traumatic Brain Injury ◽  
Clinical Trials ◽  
Brain Injury ◽  
Near Infrared ◽  
Infrared Light ◽  
Great Promise ◽  
Brain Cells ◽  
Brain Disorders ◽  
Wide Range ◽  
The Brain

Evidence is mounting that photobiomodulation therapy (shining near-infrared light) can benefit a wide range of brain disorders. The photons can penetrate into the brain where they stimulate production of energy in brain cells, and trigger numerous signaling pathways. Acute ischaemic stroke was the first indication that progressed to human clinical trials. Acute and chronic stages of traumatic brain injury were then investigated. Currently, psychiatric disorders such as depression, and neurodegenerative diseases such as Alzheimer's and Parkinson's are under investigation. Although showing great promise, more trials are clearly needed before the therapy will be accepted.

Cognitive retraining after traumatic brain injury and its role in facilitating awareness

1989 ◽  
Vol 4 (3) ◽  
pp. 37-45 ◽  
Author(s):  
Pamela S. Klonoff ◽  
Kevin P. OʼBrien ◽  
George P. Prigatano ◽  
Dennis A. Chiapello ◽  
Marie Cunningham
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Retraining

scholarly journals Reversible Dysfunction of Receptors in Traumatic Brain Injury?

2010 ◽  
Vol 30 (10) ◽  
pp. 1671-1672 ◽  
Author(s):  
Wolf-Dieter Heiss
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Ligand Binding ◽  
Neuronal Damage ◽  
Benzodiazepine Receptor ◽  
Brain Disorders ◽  
Receptor Ligands ◽  
Irreversible Damage ◽  
Benzodiazepine Receptor Ligands ◽  
Central Benzodiazepine Receptor

In many brain disorders reduced binding of central benzodiazepine receptor ligands indicates irreversible neuronal damage. The data presented by Koizumi et al (2010) demonstrate that this is not the case in traumatic brain injury suggesting different pathogenetic mechanisms leading to tissue damage. The proof for this hypothesis requires further studies that should also consider thresholds of ligand binding as indicators of irreversible damage.

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