scholarly journals Wavelet Ridges in EEG Diagnostic Features Extraction: Epilepsy Long-Time Monitoring and Rehabilitation after Traumatic Brain Injury

Sensors ◽  
2021 ◽  
Vol 21 (18) ◽  
pp. 5989
Author(s):  
Yury Vladimirovich Obukhov ◽  
Ivan Andreevich Kershner ◽  
Renata Alekseevna Tolmacheva ◽  
Mikhail Vladimirovich Sinkin ◽  
Ludmila Alekseevna Zhavoronkova
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Spectral Power ◽  
Total Duration ◽  
Spectral Power Density ◽  
Cognitive Test ◽  
Cognitive Tests ◽  
Threshold Method ◽  
Diagnostic Features ◽  
Moderate Traumatic Brain Injury

Interchannel EEG synchronization, as well as its violation, is an important diagnostic sign of a number of diseases. In particular, during an epileptic seizure, such synchronization occurs starting from some pairs of channels up to many pairs in a generalized seizure. Additionally, for example, after traumatic brain injury, the destruction of interneuronal connections occurs, which leads to a violation of interchannel synchronization when performing motor or cognitive tests. Within the framework of a unified approach to the analysis of interchannel EEG synchronization using the ridges of wavelet spectra, two problems were solved. First, the segmentation of the initial data of long-term monitoring of scalp EEG with various artifacts into fragments suspicious of epileptic seizures in order to reduce the total duration of the fragments analyzed by the doctor. Second, assessments of recovery after rehabilitation of cognitive functions in patients with moderate traumatic brain injury. In the first task, the initial EEG was segmented into fragments in which at least two channels were synchronized, and by the adaptive threshold method into fragments with a high value of the EEG power spectral density. Overlapping in time synchronized fragments with fragments of high spectral power density was determined. As a result, the total duration of the fragments for analysis by the doctor was reduced by more than 60 times. In the second task, the network of phase-related EEG channels was determined during the cognitive test before and after rehabilitation. Calculation-logical and spatial-pattern cognitive tests were used. The positive dynamics of rehabilitation was determined during the initialization of interhemispheric connections and connections in the frontal cortex of the brain.

scholarly journals 3,6′-Dithiopomalidomide Ameliorates Hippocampal Neurodegeneration, Microgliosis and Astrogliosis and Improves Cognitive Behaviors in Rats with a Moderate Traumatic Brain Injury

2021 ◽  
Vol 22 (15) ◽  
pp. 8276
Author(s):  
Pen-Sen Huang ◽  
Ping-Yen Tsai ◽  
Ling-Yu Yang ◽  
Daniela Lecca ◽  
Weiming Luo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Short Term Memory ◽  
Post Injury ◽  
Behavioral Deficits ◽  
Cognitive Behaviors ◽  
Moderate Traumatic Brain Injury ◽  
Short And Long Term ◽  
Behavioral Impairments ◽  
Hippocampal Neurodegeneration

Traumatic brain injury (TBI) is a leading cause of disability and mortality worldwide. It can instigate immediate cell death, followed by a time-dependent secondary injury that results from disproportionate microglial and astrocyte activation, excessive inflammation and oxidative stress in brain tissue, culminating in both short- and long-term cognitive dysfunction and behavioral deficits. Within the brain, the hippocampus is particularly vulnerable to a TBI. We studied a new pomalidomide (Pom) analog, namely, 3,6′-dithioPom (DP), and Pom as immunomodulatory imide drugs (IMiD) for mitigating TBI-induced hippocampal neurodegeneration, microgliosis, astrogliosis and behavioral impairments in a controlled cortical impact (CCI) model of TBI in rats. Both agents were administered as a single intravenous dose (0.5 mg/kg) at 5 h post injury so that the efficacies could be compared. Pom and DP significantly reduced the contusion volume evaluated at 24 h and 7 days post injury. Both agents ameliorated short-term memory deficits and anxiety behavior at 7 days after a TBI. The number of degenerating neurons in the CA1 and dentate gyrus (DG) regions of the hippocampus after a TBI was reduced by Pom and DP. DP, but not Pom, significantly attenuated the TBI-induced microgliosis and DP was more efficacious than Pom at attenuating the TBI-induced astrogliosis in CA1 and DG at 7D after a TBI. In summary, a single intravenous injection of Pom or DP, given 5 h post TBI, significantly reduced hippocampal neurodegeneration and prevented cognitive deficits with a concomitant attenuation of the neuroinflammation in the hippocampus.

Confirmatory factor structure of the Center for Epidemiologic Studies-Depression scale (CES-D) in mild-to-moderate traumatic brain injury

Brain Injury ◽  
2006 ◽  
Vol 20 (5) ◽  
pp. 519-527 ◽  
Author(s):  
Stephen R. McCauley ◽  
Claudia Pedroza ◽  
Sharon A. Brown ◽  
Corwin Boake ◽  
Harvey S. Levin ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Factor Structure ◽  
Depression Scale ◽  
Epidemiologic Studies ◽  
Moderate Traumatic Brain Injury ◽  
Confirmatory Factor

Predictors of deterioration indicating a requirement for surgery in mild to moderate traumatic brain injury

2014 ◽  
Vol 127 ◽  
pp. 97-100 ◽  
Author(s):  
Eiichi Suehiro ◽  
Hiroyasu Koizumi ◽  
Yuichi Fujiyama ◽  
Hiroshi Yoneda ◽  
Michiyasu Suzuki
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Moderate Traumatic Brain Injury

Critical Care Resource Utilization and Outcomes of Children With Moderate Traumatic Brain Injury

2017 ◽  
Vol 18 (12) ◽  
pp. 1166-1174 ◽  
Author(s):  
Theerada Chandee ◽  
Vivian H. Lyons ◽  
Monica S. Vavilala ◽  
Vijay Krishnamoorthy ◽  
Nophanan Chaikittisilpa ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Critical Care ◽  
Brain Injury ◽  
Resource Utilization ◽  
Moderate Traumatic Brain Injury ◽  
Critical Care Resource

scholarly journals Enhancement of Neurogenesis and Memory by a Neurotrophic Peptide in Mild to Moderate Traumatic Brain Injury

Neurosurgery ◽  
2014 ◽  
Vol 76 (2) ◽  
pp. 201-215 ◽  
Author(s):  
Muhammad Omar Chohan ◽  
Olga Bragina ◽  
Syed Faraz Kazim ◽  
Gloria Statom ◽  
Narjes Baazaoui ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Dentate Gyrus ◽  
Parietal Cortex ◽  
Saline Solution ◽  
Neuronal Loss ◽  
Synaptic Density ◽  
Moderate Traumatic Brain Injury ◽  
Long Term Treatment ◽  
Newborn Neurons

ABSTRACT BACKGROUND: Traumatic brain injury (TBI) is a risk factor for Alzheimer disease (AD), a neurocognitive disorder with similar cellular abnormalities. We recently discovered a small molecule (Peptide 6) corresponding to an active region of human ciliary neurotrophic factor, with neurogenic and neurotrophic properties in mouse models of AD and Down syndrome. OBJECTIVE: To describe hippocampal abnormalities in a mouse model of mild to moderate TBI and their reversal by Peptide 6. METHODS: TBI was induced in adult C57Bl6 mice using controlled cortical impact with 1.5 mm of cortical penetration. The animals were treated with 50 nmol/d of Peptide 6 or saline solution for 30 days. Dentate gyrus neurogenesis, dendritic and synaptic density, and AD biomarkers were quantitatively analyzed, and behavioral tests were performed. RESULTS: Ipsilateral neuronal loss in CA1 and the parietal cortex and increase in Alzheimer-type hyperphosphorylated tau and A-β were seen in TBI mice. Compared with saline solution, Peptide 6 treatment increased the number of newborn neurons, but not uncommitted progenitor cells, in dentate gyrus by 80%. Peptide 6 treatment also reversed TBI-induced dendritic and synaptic density loss while increasing activity in tri-synaptic hippocampal circuitry, ultimately leading to improvement in memory recall on behavioral testing. CONCLUSION: Long-term treatment with Peptide 6 enhances the pool of newborn neurons in the dentate gyrus, prevents neuronal loss in CA1 and parietal cortex, preserves the dendritic and synaptic architecture in the hippocampus, and improves performance on a hippocampus-dependent memory task in TBI mice. These findings necessitate further inquiry into the therapeutic potential of small molecules based on neurotrophic factors.

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