scholarly journals Computer-based cognitive stimulation for posttraumatic cognitive impairment: a clinical case

2020 ◽  
Vol 12 (6) ◽  
pp. 131-136
Author(s):  
E. M. Zubritskaya ◽  
S. V. Prokopenko ◽  
E. Yu. Mozheyko ◽  
V. A. Gurevich
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Clinical Case ◽  
Positive Impact ◽  
Cognitive Stimulation ◽  
Moderate Cognitive Impairment ◽  
Computer Based ◽  
Post Traumatic

The paper describes a clinical case of applying a set of computer-based stimulation programs for cognitive impairment arising from severe open traumatic brain injury (TBI). It demonstrates the rehabilitation capabilities of a set of «Neurotechnology+» stimulation programs for correction of cognitive deficits in patients with dysregulated moderate cognitive impairment resulting from experienced severe open TBI. It is noted that the use of a set of the programs contributed to the improvement of impaired regulatory and neurodynamic functions, the expansion of phonemic and semantic speech activity, and the improvement of memory processes. The described case suggests that computer-based cognitive training has a positive impact on cognitive recovery after post-traumatic brain injury.

scholarly journals Addressing a continuum of recovery after acquired brain injury

1998 ◽  
Vol 4 (4) ◽  
pp. 409-409 ◽  
Author(s):  
THOMAS A. NOVACK ◽  
BRICK JOHNSTONE
Keyword(s):  
Cognitive Impairment ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Cognitive Rehabilitation ◽  
Spontaneous Recovery ◽  
Cognitive Disorders ◽  
Acquired Brain Injury ◽  
Cognitive Stimulation ◽  
Injured Brain ◽  
Opportune Time

In their dialogue published in JINS, Wilson (1997) and Prigatano (1997) have eloquently and concisely presented the challenges facing neuropsychology with respect to cognitive rehabilitation. However, both authors neglect two important issues that must be addressed if people with cognitive disorders are to be effectively treated. First, cognitive impairment must be treated during the acute stages of recovery; as to ignore cognitive deficits until patients are more fully recovered may bypass an opportune time for intervention. Evidence is mounting that the injured brain adapts to the losses sustained and that the adaptation will be enhanced by increasing interaction with the environment, as compared to more passive states (Johansson & Ohlsson, 1996; Stein et al., 1995). Given such information, it is difficult to justify withholding cognitive stimulation and remediation from people during acute stages of recovery and instead awaiting a point when spontaneous recovery (presumably) will be complete.

scholarly journals Traumatic Brain Injury by Weight-Drop Method Causes Transient Amyloid-β Deposition and Acute Cognitive Deficits in Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Hajime Shishido ◽  
Masaki Ueno ◽  
Kana Sato ◽  
Masahisa Matsumura ◽  
Yasunori Toyota ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Amyloid Β ◽  
Wild Type ◽  
Long Term Effects ◽  
Drop Method ◽  
Weight Drop

There has been growing awareness of the correlation between an episode of traumatic brain injury (TBI) and the development of Alzheimer’s disease (AD) later in life. It has been reported that TBI accelerated amyloid-β (Aβ) pathology and cognitive decline in the several lines of AD model mice. However, the short-term and long-term effects of TBI by the weight-drop method on amyloid-β pathology and cognitive performance are unclear in wild-type (WT) mice. Hence, we examined AD-related histopathological changes and cognitive impairment after TBI in wild-type C57BL6J mice. Five- to seven-month-old WT mice were subjected to either TBI by the weight-drop method or a sham treatment. Seven days after TBI, the WT mice exhibited significantly lower spatial learning than the sham-treated WT mice. However, 28 days after TBI, the cognitive impairment in the TBI-treated WT mice recovered. Correspondingly, while significant amyloid-β (Aβ) plaques and amyloid precursor protein (APP) accumulation were observed in the TBI-treated mouse hippocampus 7 days after TBI, the Aβ deposition was no longer apparent 28 days after TBI. Thus, TBI induced transient amyloid-β deposition and acute cognitive impairments in the WT mice. The present study suggests that the TBI could be a risk factor for acute cognitive impairment even when genetic and hereditary predispositions are not involved. The system might be useful for evaluating and developing a pharmacological treatment for the acute cognitive deficits.

Cognitive Deficits Post-Traumatic Brain Injury and Their Association with Injury Severity and Gray Matter Volumes

2017 ◽  
Vol 34 (7) ◽  
pp. 1466-1472 ◽  
Author(s):  
Abigail Livny ◽  
Anat Biegon ◽  
Tammar Kushnir ◽  
Sagi Harnof ◽  
Chen Hoffmann ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Gray Matter ◽  
Cognitive Deficits ◽  
Injury Severity ◽  
Post Traumatic ◽  
Gray Matter Volumes

scholarly journals Increased Behavioral Deficits and Inflammation in a Mouse Model of Co-Morbid Traumatic Brain Injury and Post-Traumatic Stress Disorder

ASN NEURO ◽  
2020 ◽  
Vol 12 ◽  
pp. 175909142097956
Author(s):  
Arman Fesharaki-Zadeh ◽  
Jeremy T. Miyauchi ◽  
Karrah St. Laurent-Arriot ◽  
Stella E. Tsirka ◽  
Peter J. Bergold
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Deficits ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Barnes Maze ◽  
Post Traumatic Stress ◽  
Place Avoidance ◽  
Post Traumatic

Comorbid post-traumatic stress disorder with traumatic brain injury (TBI) produce more severe affective and cognitive deficits than PTSD or TBI alone. Both PTSD and TBI produce long-lasting neuroinflammation, which may be a key underlying mechanism of the deficits observed in co-morbid TBI/PTSD. We developed a model of co-morbid TBI/PTSD by combining the closed head (CHI) model of TBI with the chronic variable stress (CVS) model of PTSD and examined multiple behavioral and neuroinflammatory outcomes. Male C57/Bl6 mice received sham treatment, CHI, CVS, CHI then CVS (CHI → CVS) or CVS then CHI (CVS → CHI). The CVS → CHI group had deficits in Barnes maze or active place avoidance not seen in the other groups. The CVS → CHI, CVS and CHI → CVS groups displayed increased basal anxiety level, based on performance on elevated plus maze. The CVS → CHI had impaired performance on Barnes Maze, and Active Place Avoidance. These performance deficits were strongly correlated with increased hippocampal Iba-1 level an indication of activated MP/MG. These data suggest that greater cognitive deficits in the CVS → CHI group were due to increased inflammation. The increased deficits and neuroinflammation in the CVS → CHI group suggest that the order by which a subject experiences TBI and PTSD is a major determinant of the outcome of brain injury in co-morbid TBI/PTSD.

scholarly journals Cognitive retraining in traumatic brain injury

2012 ◽  
Author(s):  
Diya Nangia ◽  
Keshav Kumar
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Functioning ◽  
Cognitive Deficits ◽  
Single Case ◽  
Cognitive Impairments ◽  
Cognitive Retraining ◽  
The Family ◽  
History Of ◽  
Post Traumatic

Traumatic brain injury (TBI) is often associated with cognitive impairments. The psychological sequelae of cognitive deficits and emotional problems contribute significantly to the disability in the patient and to the distress of the family. The study aimed to develop a cognitive retraining programme to enhance cognitive functioning in TBI. 25 years old male presenting with history of left temporal hemorrhagic contusion with cerebral edema underwent 2 months of a cognitive retaining programme, addressing executive functions impairment. A single case experimental design with pre- and postassessment was adopted to evaluate changes in the patient in response to the intervention. Improvements were found in cognitive functioning, and in symptom reduction and behaviour. The 2 months hospital based cognitive retraining programme was found to be efficacious in ameliorating symptoms and improving cognitive, social and occupational functioning post traumatic brain injury.

NEUROPSYCHOLOGICAL CHANGES IN PATIENTS WITH A CONSEQUENCE OF TRAUMATIC BRAIN INJURY

2020 ◽  
Vol 3 (1) ◽  
pp. 44-46
Author(s):  
Istatillo Shodjalilov ◽  
◽  
Saoda Igamova ◽  
Aziza Djurabekova
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Neuropsychological Testing ◽  
Anxiety And Depression ◽  
Psychopathological Symptoms ◽  
Neuropsychological Changes ◽  
The Relationship

The incidence of cognitive impairment in TBI is high, depending on the severity. At the same time, psychopathological symptoms in the form of asthenia, increased anxiety and depression are encountered among patients with TBI. The work studied the relationship between cognitive and psychopathological symptoms in patients with TBI using neuropsychological testing on scales.

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