Effects Of Traumatic Brain Injury Research Articles

Editors' Note: Exosomal Neurofilament Light: A Prognostic Biomarker for Remote Symptoms After Mild Traumatic Brain Injury?

In attempt to identify more sensitive biomarkers of neurologic injury and posttraumatic cognitive dysfunction, the Chronic Effects of Neurotrauma Consortium (CENC) investigators evaluated the relationship between traumatic brain injury (TBI) and exosomal and plasma neurofilament light chains. Levels of both biomarkers were elevated among patients with more frequent TBI events and strongly correlated with more significant neuropsychiatric disease—including symptoms of depression, posttraumatic stress disorder (PTSD), and cognitive impairment. Dr. Kawada comments that other biomarkers, such as exosomal tau, correlate strongly with a variety of neurocognitive consequences of TBI, whereas biomarkers such as IL-10 may better correlate with PTSD. The CENC investigators agree that a serial pattern of biomarkers may one day be an indicator of a particular neuropsychiatric condition, but larger validation studies are necessary in the meantime. In attempt to identify more sensitive biomarkers of neurologic injury and posttraumatic cognitive dysfunction, the Chronic Effects of Neurotrauma Consortium (CENC) investigators evaluated the relationship between traumatic brain injury (TBI) and exosomal and plasma neurofilament light chains. Levels of both biomarkers were elevated among patients with more frequent TBI events and strongly correlated with more significant neuropsychiatric disease—including symptoms of depression, posttraumatic stress disorder (PTSD), and cognitive impairment. Dr. Kawada comments that other biomarkers, such as exosomal tau, correlate strongly with a variety of neurocognitive consequences of TBI, whereas biomarkers such as IL-10 may better correlate with PTSD. The CENC investigators agree that a serial pattern of biomarkers may one day be an indicator of a particular neuropsychiatric condition, but larger validation studies are necessary in the meantime.

Pathogenetic mechanisms of mild traumatic brain injury in patients of different ages

This study was carried out to reveal the influence of mechanical energy, which triggers a whole cascade of pathological and compensatory processes of different depth and duration in the brain in traumatic brain injury (TBI). One of the most common consequences of TBI is impaired working memory – the ability to temporarily hold small pieces of information necessary for current mental activity. The aim of the work is to study the relationship between the TBI mechanism and the types of brain damage, as well as the consequences of trauma in patients of different ages. 95 case histories of patients with closed TBI were studied. All patients were treated in the Neurosurgical department of the Emergency hospital, Chernivtsi. Among them were 76 men and 19 women. The study found that TBI of patients in most cases was obtained as a result of traffic and others accidents. All patients had closed TBI. Contusion foci in all age groups were equally identified in the frontal, temporal and occipital lobes, less in the parietal lobe. The incidence of contusion increased slightly with increasing age of patients. In the presence of hemorrhages in patients, hemiparesis and liquor-hypertensive syndrome occurred. In men, TBI was more common than in women, and was expressed as moderate brain contusion, subacute and chronic compression of the brain. This TBI development was more common in young patients. It is promising to further study the nature of combined TBI in people of all ages and analyze the results of specialized neurosurgical care. Keywords: traumatic brain injury, neurosurgical care, liquor-hypertensive syndrome.

Global decrease in brain sodium concentration after mild traumatic brain injury.

The pathological cascade of tissue damage in mild traumatic brain injury is set forth by a perturbation in ionic homeostasis. However, whether this class of injury can be detected in vivo and serve as a surrogate marker of clinical outcome is unknown. We employ sodium MRI to test the hypotheses that regional and global total sodium concentrations: (i) are higher in patients than in controls and (ii) correlate with clinical presentation and neuropsychological function. Given the novelty of sodium imaging in traumatic brain injury, effect sizes from (i), and correlation types and strength from (ii), were compared to those obtained using standard diffusion imaging metrics. Twenty-seven patients (20 female, age 35.9 ± 12.2 years) within 2 months after injury and 19 controls were scanned with proton and sodium MRI at 3 Tesla. Total sodium concentration, fractional anisotropy and apparent diffusion coefficient were obtained with voxel averaging across 12 grey and white matter regions. Linear regression was used to obtain global grey and white matter total sodium concentrations. Patient outcome was assessed with global functioning, symptom profiles and neuropsychological function assessments. In the regional analysis, there were no statistically significant differences between patients and controls in apparent diffusion coefficient, while differences in sodium concentration and fractional anisotropy were found only in single regions. However, for each of the 12 regions, sodium concentration effect sizes were uni-directional, due to lower mean sodium concentration in patients compared to controls. Consequently, linear regression analysis found statistically significant lower global grey and white matter sodium concentrations in patients compared to controls. The strongest correlation with outcome was between global grey matter sodium concentration and the composite z-score from the neuropsychological testing. In conclusion, both sodium concentration and diffusion showed poor utility in differentiating patients from controls, and weak correlations with clinical presentation, when using a region-based approach. In contrast, sodium linear regression, capitalizing on partial volume correction and high sensitivity to global changes, revealed high effect sizes and associations with patient outcome. This suggests that well-recognized sodium imbalances in traumatic brain injury are (i) detectable non-invasively; (ii) non-focal; (iii) occur even when the antecedent injury is clinically mild. Finally, in contrast to our principle hypothesis, patients’ sodium concentrations were lower than controls, indicating that the biological effect of traumatic brain injury on the sodium homeostasis may differ from that in other neurological disorders.Note: This figure has been annotated.

Informal carer's knowledge of traumatic brain injury questionnaire: Initial development and validation.

AimTo develop and psychometrically test the instrument for measuring the knowledge of traumatic brain injury of informal carers.DesignInstrument development.MethodFocus group discussions were conducted among informal carers and healthcare specialists in March 2017. The content validity was determined by the mean of the item content validity index. A reliability test was performed by the Kuder‐Richardson 20 and Pearson's correlation coefficient among 40 informal carers of patients with a traumatic brain injury in the rehabilitation medicine department of a tertiary hospital from August–September 2017.ResultsThe final 34‐item questionnaire covers the nature of traumatic brain injury, the consequences of traumatic brain injury, the rehabilitation process, and the role of the caregiver. The item content means ranged from 0.8–1.00, and the difficulty of knowledge items ranged from 0.18–0.98. The internal consistency reliability and correlation coefficient were 0.70 and 0.84, respectively.

The Delayed Neuropathological Consequences of Traumatic Brain Injury in a Community-Based Sample.

The late neuropathological effects of traumatic brain injury have yet to be fully elucidated, particularly with respect to community-based cohorts. To contribute to this critical gap in knowledge, we designed a multimodal neuropathological study, integrating traditional and quantitative approaches to detect pathologic changes in 532 consecutive brain autopsies from participants in the Adult Changes in Thought (ACT) study. Diagnostic evaluation including assessment for chronic traumatic encephalopathy (CTE) and quantitative immunoassay-based methods were deployed to examine levels of pathological (hyperphosphorylated) tau (pTau) and amyloid (A) β in brains from ACT participants with (n = 107) and without (n = 425) history of remote TBI with loss of consciousness (w/LOC). Further neuropathological assessments included immunohistochemistry for α-synuclein and phospho-TDP-43 pathology and astro- (GFAP) and micro- (Iba1) gliosis, mass spectrometry analysis of free radical injury, and gene expression evaluation (RNA sequencing) in a smaller sub-cohort of matched samples (49 cases with TBI and 49 non-exposed matched controls). Out of 532 cases, only 3 (0.6%–none with TBI w/LOC history) showed evidence of the neuropathologic signature of chronic traumatic encephalopathy (CTE). Across the entire cohort, the levels of pTau and Aβ showed expected differences for brain region (higher levels in temporal cortex), neuropathological diagnosis (higher in participants with Alzheimer's disease), and APOE genotype (higher in participants with one or more APOE ε4 allele). However, no differences in PHF-tau or Aβ1−42 were identified by Histelide with respect to the history of TBI w/LOC. In a subset of TBI cases with more carefully matched control samples and more extensive analysis, those with TBI w/LOC history had higher levels of hippocampal pTau but no significant differences in Aβ, α-synuclein, pTDP-43, GFAP, Iba1, or free radical injury. RNA-sequencing also did not reveal significant gene expression associated with any measure of TBI exposure. Combined, these findings suggest long term neuropathological changes associated with TBI w/LOC may be subtle, involve non-traditional pathways of neurotoxicity and neurodegeneration, and/or differ from those in autopsy cohorts specifically selected for neurotrauma exposure.

C. elegans detects toxicity of traumatic brain injury generated tau

Traumatic brain injury (TBI) is associated with widespread tau pathology in about 30% of patients surviving late after injury. We previously found that TBI in mice induces the formation of an abnormal form of tau (tauTBI) which progressively spreads from the site of injury to remote brain regions. Intracerebral inoculation of TBI brain homogenates into naïve mice induced progressive tau pathology, synaptic loss and late cognitive decline, suggesting a pivotal role of tauTBI in post-TBI neurodegeneration. However, the possibility that tauTBI was a marker of TBI-associated neurodegeneration rather than a toxic driver of functional decline could not be excluded.Here we employed the nematode C. elegans as a biosensor to test the pathogenic role of TBI generated tau. The motility of this nematode depends on efficient neuromuscular transmission and is exceptionally sensitive to the toxicity of amyloidogenic proteins, providing a tractable model for our tests. We found that worms exposed to brain homogenates from chronic but not acute TBI mice, or from mice in which tauTBI had been transmitted by intracerebral inoculation, had impaired motility and neuromuscular synaptic transmission. Results were similar when worms were given brain homogenates from transgenic mice overexpressing tau P301L, a tauopathy mouse model, suggesting that TBI-induced and mutant tau have similar toxic properties. P301L brain homogenate toxicity was similar in wild-type and ptl-1 knock-out worms, indicating that the nematode tau homolog protein PTL-1 was not required to mediate the toxic effect. Harsh protease digestion to eliminate the protein component of the homogenates, pre-incubation with anti-tau antibodies or tau depletion by immunoprecipitation, abolished the toxicity. Homogenates of chronic TBI brains from tau knock-out mice were not toxic to C. elegans, whereas oligomeric recombinant tau was sufficient to impair their motility.This study indicates that tauTBI impairs motor activity and synaptic transmission in C. elegans and supports a pathogenic role of tauTBI in the long-term consequences of TBI. It also sets the groundwork for the development of a C. elegans-based platform for screening anti-tau compounds.

Effect of Growth Hormone on Neuropsychological Outcomes and Quality of Life of Patients with Traumatic Brain Injury: A Systematic Review.

One of the most devastating chronic consequences of traumatic brain injury (TBI) is cognitive impairment. One of the possible underlying causes is growth hormone deficiency (GHD) caused by TBI-induced hypopituitarism. Currently, TBI patients are not routinely screened for pituitary function, and there are no standard therapies when GHD is diagnosed. Further, the possible positive effects of GH replacement on cognitive function and quality of life after TBI are not well established. We aimed to assess the current knowledge regarding the effect of GH therapy on cognitive function and quality of life after TBI. We performed a literature search in PubMed, Embase, and Central® databases from inception to October 2019. We extracted data on each term of severity (mild-moderate-severe) of TBI with and without GHD, time since injury, parameters of growth hormone treatment (dosing, length), and cognitive outcomes in terms of verbal and non-verbal memory, and executive, emotional, and motor functions, and performed a meta-analysis on the results of a digit span test assessing working memory. We identified 12 studies (containing two randomized controlled trials) with 264 mild-to-moderate-to-severe TBI patients (Glasgow Coma Score [GCS] varied between 6 and 15) with (n = 255) or without (n = 9) GHD who received GH therapy. GH was administered subcutaneously in gradually increasing doses, monitoring serum insulin-like growth factor-I (IGF-I) level. After TBI, regardless of GCS, 6-12 months of GH therapy, started in the chronic phase post-TBI, induced a moderate improvement in processing speed and memory capacities, decreased the severity of depression, and led to a marked improvement in quality of life. Limitations include the relatively low number of patients involved and the divergent neuropsychological tests used. These results indicate the need for further multi-centric controlled studies to substantiate the use of GH replacement therapy as a potential tool to alleviate TBI-related cognitive impairment and improve quality of life.

COllaborative Neuropathology NEtwork Characterizing ouTcomes of TBI (CONNECT-TBI)

Efforts to characterize the late effects of traumatic brain injury (TBI) have been in progress for some time. In recent years much of this activity has been directed towards reporting of chronic traumatic encephalopathy (CTE) in former contact sports athletes and others exposed to repetitive head impacts. However, the association between TBI and dementia risk has long been acknowledged outside of contact sports. Further, growing experience suggests a complex of neurodegenerative pathologies in those surviving TBI, which extends beyond CTE. Nevertheless, despite extensive research, we have scant knowledge of the mechanisms underlying TBI-related neurodegeneration (TReND) and its link to dementia. In part, this is due to the limited number of human brain samples linked to robust demographic and clinical information available for research. Here we detail a National Institutes for Neurological Disease and Stroke Center Without Walls project, the COllaborative Neuropathology NEtwork Characterizing ouTcomes of TBI (CONNECT-TBI), designed to address current limitations in tissue and research access and to advance understanding of the neuropathologies of TReND. As an international, multidisciplinary collaboration CONNECT-TBI brings together multiple experts across 13 institutions. In so doing, CONNECT-TBI unites the existing, comprehensive clinical and neuropathological datasets of multiple established research brain archives in TBI, with survivals ranging minutes to many decades and spanning diverse injury exposures. These existing tissue specimens will be supplemented by prospective brain banking and contribute to a centralized route of access to human tissue for research for investigators. Importantly, each new case will be subject to consensus neuropathology review by the CONNECT-TBI Expert Pathology Group. Herein we set out the CONNECT-TBI program structure and aims and, by way of an illustrative case, the approach to consensus evaluation of new case donations.

Traumatic Brain Injury and Treatment of Behavioral Health Conditions.

Traumatic brain injury (TBI) is a common neurological condition that results from an external force altering normal brain function, whether temporarily or permanently. A concussion is one type of TBI. TBIs vary greatly in severity, which concomitantly creates tremendous variability in their manifestation. The fingerprint of TBI is damage to the frontal areas of the brain, which, with sufficient magnitude, results in impairment of a person's ability to regulate cognition, emotion, and behavior. These consequences of TBI make recognition in the context of treating behavioral health conditions of utmost importance. TBI not only causes behavioral health problems but also produces associated deficits that can undermine the effectiveness of treatment for a behavioral health condition. This overview delineates key characteristics of TBI and describes its association with behavioral health conditions. Mechanisms underlying the relationship between TBI and behavioral health are presented, and a series of recommendations for professionals are proposed. This article is intended to raise awareness about TBI and simultaneously introduce key concepts for accommodating the effects of TBI in behavioral health care.

In Vivo Detection of Extracellular Adenosine Triphosphate in a Mouse Model of Traumatic Brain Injury.

Traumatic brain injury (TBI) is traditionally characterized by primary and secondary injury phases, both contributing to pathological and morphological changes. The mechanisms of damage and chronic consequences of TBI remain to be fully elucidated, but synaptic homeostasis disturbances and impaired energy metabolism are proposed to be a major contributor. It has been proposed that an increase of extracellular (eATP) adenosine triphosphate (ATP) in the area immediately surrounding impact may play a pivotal role in this sequence of events. After tissue injury, rupture of cell membranes allows release of intracellular ATP into the extracellular space, triggering a cascade of toxic events and inflammation. ATP is a ubiquitous messenger; however, simple and reliable techniques to measure its concentration have proven elusive. Here, we integrate a sensitive bioluminescent eATP sensor known as pmeLUC, with a controlled cortical impact mouse model to monitor eATP changes in a living animal after injury. Using the pmeLUC probe, a rapid increase of eATP is observed proximal to the point of impact within minutes of the injury. This event is significantly attenuated when animals are pretreated with an ATP hydrolyzing agent (apyrase) before surgery, confirming the contribution of eATP. This new eATP reporter could be useful for understanding the role of eATP in the pathogenesis in TBI and may identify a window of opportunity for therapeutic intervention.

The Effects of Traumatic Brain Injury and Post-Traumatic Stress Disorder on Prison Adjustment and Recidivism among Military Veterans: Evidence from Minnesota.

The prevalence of, and link between, mental health disorders-such as traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD)-and antisocial behavior is well-documented among the military veteran population. Studies also show that TBI and PTSD account for variation in prison-based and re-entry outcomes. Despite this body of research, comparatively fewer studies have explicitly focused on how these factors affect prison adjustment for inmates with prior military experience. We used administrative data provided by the Minnesota Department of Corrections (MnDOC) and employed a series of survival analyses to examine how prior diagnoses of TBI and PTSD (among other risk factors) influence metrics of institutional adjustment and recidivism among a sample of military veterans. Our results indicate that the effects of TBI, PTSD, and other indicators of criminogenic risk are relevant when examining the experiences of justice-involved military veterans-especially with respect recidivism-based outcomes. The implications of our results are discussed and directions for future research are given.

ТРАВМА ЧЕРЕПА КАК ОДНА ИЗ ПРИЧИН РАЗВИТИЯ СУБДУРАЛЬНОЙ ГЕМАТОМЫ У РЕБЕНКА ГРУДНОГО ВОЗРАСТА С ГЛУТАРОВОЙ АЦИДУРИЕЙ 1-ГО ТИПА: КРАТКИЙ ОБЗОР ЛИТЕРАТУРЫ И КЛИНИЧЕСКОЕ НАБЛЮДЕНИЕ

The article presents a brief review of the literature and clinical observation of glutaric aciduria type 1 (GA1) in a child, manifested by encephalitis-like crisis and subdural hematomas, which were initially regarded as the consequences of traumatic brain injury. Based on the analysis of clinical and neuroimaging data, the diagnosis of GA1 was assumed, which was later confirmed by molecular genetic research. After therapy with the inclusion of a specialized diet with protein restriction, some improvement in motor activity was noted. The presence of bilateral subdural hematomas dictates the need for differential diagnosis with GA1. A highly informative method of diagnosing GA1 is brain MRI.

New insights in implicit sequence learning of adults with traumatic brain injury: As measured by an ocular serial reaction time (O-SRT) task.

Objective: We investigated the effect of traumatic brain injury (TBI) on implicit sequence learning (ISL) and its relation with demographic, clinical, and working memory (WM) capacity using an eye-tracked variant of the standard serial reaction time (RT; SRT) task. Besides RT, this ocular SRT (O-SRT) task enables generation of correct anticipations (CA) and stucks, reflecting other critical aspects of ISL. Method: ISL was tested in 26 individuals with TBI and 28 healthy controls using the O-SRT task. Mixed analyses of variance were conducted to analyze RT and CA in three phases: learning, interference, and recovery from interference. The average number of stucks was compared with an independent-samples t test. Finally, Pearson correlation analyses of ISL with demographic, clinical, and WM capacity measures were performed. Results: Based on RT, ISL was impaired in the TBI group. However, CA demonstrated improved learning, but with deficits in the interference and recovery from interference phases. Stucks were more frequent in the TBI group, which affected RT and CA measures. Neither demographic nor clinical factors were associated with ISL. Verbal, but not spatial, WM capacity was impaired in the TBI group, and spatial WM capacity positively correlated with ISL in controls only. Conclusion: We suggest that the high TBI group stuck rate can be attributed to lack of initiative and/or conservative response bias associated with TBI, and view it as a main cause leading to deficits in ISL. Unlike controls, the TBI group could not muster their relatively preserved spatial WM capacity to support their ISL performance. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Peculiarities of formation and clinical course of symptomatic epilepsy as a result of cranial injury

Post-traumatic epilepsy (PTE) is a formidable and frequent consequence of traumatic brain injury (TBI) in the long term. 41 patients with PTE were examined, mostly men of working age. The time of formation of PTE after was 14.3 ± 1.4 months, which decreased depending on the severity of brain injury, the average frequency of seizures was 2.93 ± 0.8 per month.Focal seizures were mainly registered (63.4%, p <0.05), and taking into account the focal onset in bilateral tonic-clonic seizures, this figure reached 90.2% (p <0.05). Among the selected syndromes, except for direct PTE, autonomic dysfunctions (87.8%) with paroxysmal course (58.5%) prevailed, especially in persons with moderate trauma (r = 0.51, p <0.05).Typical comorbid symptoms in people with PTE were cognitive deficits, which correlated with the severity of TBI, as well as depressive and anxiety symptoms. Depressive layers were more often observed in the presence of the focal component of seizures (94.7%, p <0.05), temporal localization of the pathological process and predominant vagotonia. Anxiety manifestations affected all types of attacks on the background of sympathicotonia (83.3%, p <0.05), which in our opinion improved the implementation of crisis conditions, which were observed in 66.7% of cases.

The Association of Early Electrocardiographic Abnormalities With Brain Injury Severity and Outcome in Severe Traumatic Brain Injury.

The aim of this study was to evaluate the frequency of electrocardiographic (ECG) abnormalities in the acute phase of severe traumatic brain injury (TBI) and the association with brain injury severity and outcome. In contrast to neurovascular diseases, sparse information is available on this issue. Data of adult patients with severe TBI admitted to the Intensive Care Unit (ICU) for intracranial pressure monitoring of a level-1 trauma center from 2002 till 2018 were analyzed. Patients with a cardiac history were excluded. An ECG recording was obtained within 24 h after ICU admission. Admission brain computerized tomography (CT)-scans were categorized by Marshall-criteria (diffuse vs. mass lesions) and for location of traumatic lesions. CT-characteristics and maximum Therapy Intensity Level (TILmax) were used as indicators for brain injury severity. We analyzed data of 198 patients, mean (SD) age of 40 ± 19 years, median GCS score 3 [interquartile range (IQR) 3–6], and 105 patients (53%) had thoracic injury. In-hospital mortality was 30%, with sudden death by cardiac arrest in four patients. The incidence of ECG abnormalities was 88% comprising ventricular repolarization disorders (57%) mostly with ST-segment abnormalities, conduction disorders (45%) mostly with QTc-prolongation, and arrhythmias (38%) mostly of supraventricular origin. More cardiac arrhythmias were observed with increased grading of diffuse brain injury (p = 0.042) or in patients treated with hyperosmolar therapy (TILmax) (65%, p = 0.022). No association was found between ECG abnormalities and location of brain lesions nor with thoracic injury. Multivariate analysis with baseline outcome predictors showed that cardiac arrhythmias were not independently associated with in-hospital mortality (p = 0.097). Only hypotension (p = 0.029) and diffuse brain injury (p = 0.017) were associated with in-hospital mortality. In conclusion, a high incidence of ECG abnormalities was observed in patients with severe TBI in the acute phase after injury. No association between ECG abnormalities and location of brain lesions or presence of thoracic injury was present. Cardiac arrhythmias were indicative for brain injury severity but not independently associated with in-hospital mortality. Therefore, our findings likely suggest that ECG abnormalities should be considered as cardiac mimicry representing the secondary effect of traumatic brain injury allowing for a more rationale use of neuroprotective measures.

The Connection between Traumatic Brain Injury (TBI) and Attention-Deficit/Hyperactivity Disorder, Therapeutic Approaches

A Traumatic Brain Injury (TBI) is an injury to the brain caused by an external force (vehicle, accidents, violence, sports injuries, industrial accidents, falls). Brain trauma can occur either from an object penetrating the skull or from rapid acceleration (speeding up), or deceleration (slowing down or stopping suddenly) of the brain. Traumatic Brain Injury (TBI) is a major cause of mortality and disability, especially in children and young adults. Based on the Glasgow Coma Scale (GCS), the neurological scale used to measure a person’s level of consciousness after a brain injury, traumatic brain injury is classified as: mild (GCS 13 - 15), moderate (GCS 9 - 12), severe (GCS 8 or less), and evaluates the following functions: Eye Opening (E), Motor Response (M), and Verbal Response (V), to determine a patient’s overall GCS, add together the scores from eye opening, motor response and verbal response. Scores range from 3 to 15. A score of 8 or less signifies coma. Symptoms can vary depending on the severity of the head injury. An individual with a mild traumatic brain injury can remain conscious, or may experience a loss of consciousness for a few seconds or minutes. Other symptoms may include headache, confusion, dizziness, vision changes, ringing in the ears or changes in hearing, fatigue or lethargy, a change in sleep patterns, behavioral or mood changes, and cognitive and/or executive functioning problems. People with a moderate or severe traumatic brain injury may show the same symptoms, but may also have a headache that gets worse, repeated vomiting or nausea, convulsions or seizures, an inability to awaken from sleep, dilation of one or both pupils of the eyes, slurred speech, weakness or numbness in the extremities, loss of coordination, and increased confusion, restlessness, or agitation. Attention-Deficit/Hyperactivity Disorder secondary to Traumatic Brain Injury (TBI) is one of the most common neurobehavioral consequences of Traumatic Brain Injury (TBI), occurring in 20% to 50% of individual’s post-injury (Irastorza, 2011). Some of the most persistent problems include impairment in memory, attention and concentration, language, executive skills, social judgment, social behavior, and impulsiveness. Previous studies have shown that Traumatic Brain Injury (TBI) is a major cause of mental health problems and increases the risk of Attention-Deficit/Hyperactivity Disorder (Schachar et al., 2015). According to studies (Ilie et al., 2015), physical brain injury contributes to the development of Attention-Deficit/Hyperactivity Disorder. Because the risk of Attention-Deficit/Hyperactivity Disorder development after Traumatic Brain Injury (TBI) remains high over an extended period, and some of the most persistent problems include impairment in memory, attention and concentration, language, executive skills, social judgment, social behavior, and impulsiveness; this master thesis shows the importance of an early prompt intervention after brain injury, and the need to establish a therapeutic plan in order to treat the Attention-Deficit/Hyperactivity Disorder development and evolution. The purpose of the present study is to investigate the association between Traumatic Brain Injury (TBI) and Attention-Deficit/Hyperactivity Disorder, and also to show the importance of prompt intervention and preventive therapy in order to stop the Attention-Deficit/Hyperactivity Disorder development and evolution.

Mentalizing deficit among patients with traumatic brain injury

Mentalization or theory of mind as an aspect of our social cognition, is our ability to infer mental states of others (intentions, desires, thoughts, emotions) and to predict their behavior accordingly. This function significantly affects our participation and orientation in the social world and plays an important role in conversational situations, social interactions, social integ-ration and adaptation. The brain regions that serve as the basis for mind-reading function can be damaged as a consequence of traumatic brain injury, which frequently occurs among the younger population. Traumatic brain injury can cause focal or diffuse cerebral injuries, often leading to theory of mind deficit. In this topic such publications were researched that compared theory of mind ability between traumatic brain injury patients and control subjects (comparative case-control studies). We searched for the studies in the following internet based/online databases: PubMed, Web of Science, ScienceDirect, Google Scholar, APA PsycNET (PsycARTICLES) and EBSCO Host. The search was performed using the following key word combinations: theory of mind or mentalizing or social cognition AND traumatic brain injury or head/brain injury or diffuse axonal injury. Based on the results of the included and processed studies (21 pc), traumatic brain injury often leads to mentalization deficit with different severity. With this present review we aim to draw attention to the fact that the appearance and severity of mind reading dysfunction can considerably affect the outcome of the disease, the length of rehabilitation time and the prognosis of traumatic brain injury patients. Besides this, with this review, we aim to take sides in whether theory of mind ability is domain-specific or domian-general based on studies including traumatic brain injury patients.

Aberrant modulation of brain activity underlies impaired working memory following traumatic brain injury

Impaired working memory is a common and disabling consequence of traumatic brain injury (TBI) that is caused by aberrant brain processing. However, little is known about the extent to which deficits are perpetuated by specific working memory subprocesses. Using a combined functional magnetic resonance imaging (fMRI) and working memory paradigm, we tested the hypothesis that the pattern of brain activation subserving working memory following TBI would interact with both task demands and specific working memory subcomponents: encoding, maintenance, and retrieval. Forty-three patients with moderate-severe TBI, of whom 25 were in the acute phase of recovery (M = 2.16 months, SD = 1.48 months, range = 0.69 – 6.64 months) and 18 in the chronic phase of recovery (M = 23.44 months, SD = 6.76 months, range = 13.35 – 34.82 months), were compared with 38 demographically similar healthy controls. Behaviourally, we found that working memory deficits were confined to the high cognitive load trials in both acute (P = 0.006) and chronic (P = 0.024) cohorts. Furthermore, results for a subset of the sample (18 chronic TBI and 17 healthy controls) who underwent fMRI revealed that the TBI group showed reduced brain activation when simply averaged across all task trials (regardless of cognitive load or subcomponent). However, interrogation of the subcomponents of working memory revealed a more nuanced pattern of activation. When examined more closely, patterns of brain activity following TBI were found to interact with both task demands and the working memory subcomponent: increased activation was observed during encoding in the left inferior occipital gyrus whereas decreased activation was apparent during maintenance in the bilateral cerebellum and left calcarine sulcus. Taken together, findings indicate an inability to appropriately modulate brain activity according to task demand that is specific to working memory encoding and maintenance.

The Changes in Brain Oxygenation During Transcranial Alternating Current Stimulation as Consequences of Traumatic Brain Injury: A Near-Infrared Spectroscopy Study.

The aim was to evaluate the changes in brain tissue oxygenation, assessed by near-infrared spectroscopy (NIRS), during transcranial alternating current stimulation (tACS) in patients with mild and moderate traumatic brain injury (TBI). Nineteen patients with diffuse, blunt, non-severe TBI (mean age 32.7±11.4years; 4 women and 15 men; Glasgow Coma Score before tACS 14.1±0.5) were treated by 10 Hz in-phase tACS applied for 30minutes to the left and right lateral prefrontal cortex at 21days after TBI. Regional cerebral tissue oxygen saturation (SctO2) in the frontal lobes was measured simultaneously by the cerebral oximeter. Significance was preset to P<0.05. The SctO2 values before tACS were not different between hemispheres ~65%. After 15minutes of tACS, a significant (p<0.05) decrease in regional SctO2 was observed with the minimum at the eighth minute of 53.4±3.2% and 53.4±3.2% in the left and right hemispheres, respectively. At the end of the stimulation (30minutes), the hemispheric differences in cerebral oxygen saturation became statistically insignificant again (p>0.05). Therefore, tACS causes a significant decrease in SctO2, probably, due to neuronal activation. Our data indicate that tACS may need to be supplemented with oxygen therapy. Further research is required.

Метаболические нарушения у пациентов, находящихся в хроническом критическом состоянии, обусловленном последствиями черепно-мозговой травмы

The problem of chronic critical illness therapy is relevant all over the world. Revealing the metabolic function in patients in chronic critical condition is an important link in the development of adequate treatment and rehabilitation tactics. The aim - identification of metabolic features in chronic critical patients after brain injury in the first 3 days from the moment of admission to the rehabilitation center. Material and methods. Single-center observational study included a group of 25 patients with chronic critical illness, aged 38.7±14.0 years with body mass index 20.8± 4.3 kg/m2 (min 14.5; max 29.7), who were on independent breathing through a tracheostomy tube, and who have pronounced neurological disorders in the form of depression of minimally conscious state, FOUR scale from 12 to 16 points, as well as bedsores 1-2 stage and polysegmental pneumonia. The patients underwent indirect calorimetry and analysis of biochemical parameters of protein, carbohydrate, fat and mineral metabolism, as well as the level of nitrogen excretion with urine. Results and discussion. The data obtained indicate that chronic critical ill patients with the consequences of traumatic brain injury had pronounced metabolic disorders, mainly of a protein component. Total protein level decreased up to 61.0±9.4 g/l (min 39.1; max 83.1), albumin up to 30.2±6.0 g/l (min 17.4; max 37.8), prealbumin up to 0.13± 0.06 g/l (min 0.04; max 0.23) and transferrin up to 147.7±37.7 mg/dl (min 84.0; max 209.0). The patients' requirement in protein was 106.4±38.5 g/day (min 57.1; max 160.5) or 1.55±0.46 g/kg/day (min 0.75; max 2.22). The level of resting energy expenditure measured by indirect calorimetry was 1549.1±421.8 kcal/day (min 673.0; max 2430.0) or in terms of body weight 24.8±7.6 kcal/kg/day (min 12.4; max 45.8). Conclusion. The data obtained indicate a continuing catabolic phase in patients more than 30 days after the primary injury, which led to their chronic critical condition.