Hasil untuk "Neurology. Diseases of the nervous system"

Adeel S. Zubair, Lindsay Mcalpine, T. Gardin et al.

Importance Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in December 2019, causing human coronavirus disease 2019 (COVID-19), which has now spread into a worldwide pandemic. The pulmonary manifestations of COVID-19 have been well described in the literature. Two similar human coronaviruses that cause Middle East respiratory syndrome (MERS-CoV) and severe acute respiratory syndrome (SARS-CoV-1) are known to cause disease in the central and peripheral nervous systems. Emerging evidence suggests COVID-19 has neurologic consequences as well. Observations This review serves to summarize available information regarding coronaviruses in the nervous system, identify the potential tissue targets and routes of entry of SARS-CoV-2 into the central nervous system, and describe the range of clinical neurological complications that have been reported thus far in COVID-19 and their potential pathogenesis. Viral neuroinvasion may be achieved by several routes, including transsynaptic transfer across infected neurons, entry via the olfactory nerve, infection of vascular endothelium, or leukocyte migration across the blood-brain barrier. The most common neurologic complaints in COVID-19 are anosmia, ageusia, and headache, but other diseases, such as stroke, impairment of consciousness, seizure, and encephalopathy, have also been reported. Conclusions and Relevance Recognition and understanding of the range of neurological disorders associated with COVID-19 may lead to improved clinical outcomes and better treatment algorithms. Further neuropathological studies will be crucial to understanding the pathogenesis of the disease in the central nervous system, and longitudinal neurologic and cognitive assessment of individuals after recovery from COVID-19 will be crucial to understand the natural history of COVID-19 in the central nervous system and monitor for any long-term neurologic sequelae.

Yangyang Guo, Bingyang Zhang, Lianmei Zhong et al.

BackgroundIntracranial and/or extracranial atherosclerotic stenosis is a common etiology of acute ischemic stroke (AIS). This study aimed to evaluate the impact of intracranial or extracranial atherosclerotic stenosis on early neurological deterioration (END), hemorrhagic transformation (HT) and 90-day clinical outcomes in patients receiving intravenous thrombolysis.MethodsWe retrospectively enrolled patients with AIS who received intravenous alteplase (0.9 mg/kg) at the First Affiliated Hospital of Kunming Medical University between February 2019 and August 2022. Data on demographics, stroke risk factors, laboratory results, and neuroimaging findings were collected. Atherosclerotic stenosis (AS) was defined as >50% intracranial or extracranial arteries. Logistic regression was performed to identify independent predictors of clinical outcomes. END was defined as an increase of ≥4 points in the National Institutes of Health Stroke Scale (NIHSS) score within 24 h after stroke onset. HT was defined as any newly detected intracranial hemorrhage on follow-up cranial CT performed within 7 days after symptom onset.ResultsA total of 185 AIS patients receiving intravenous thrombolysis were included in this study, with 88 (47.6%) in the IEAS group and 97 (52.4%) in the non-stenosis group. There was no significant association between the incidence of END and the presence of IEAS. Multivariable regression analysis revealed that baseline NIHSS was an independent risk factor for HT (OR = 1.120, 95% CI 1.038–1.209, p = 0.003), 90-day poor clinical outcome (OR = 1.198, 95% CI 1.105–1.298, p = 0.001) and 90-day death (OR = 1.384, 95% CI 1.179–1.625, p = 0.001). Although IEAS was not significantly associated with the incidence of END or HT, it was significantly correlated with 90-day poor clinical outcome (OR = 1.350, 95% CI 1.108–1.644, p = 0.003).ConclusionsIn this cohort, IEAS was not associated with END or HT but emerged as an independent predictor of poor 90-day functional outcome after intravenous thrombolysis for AIS.

Fang Wang, Ying Liang, Qin-Wen Wang

Abstract Background Alzheimer’s disease (AD) is a complex neurodegenerative disorder with a largely unexplored epigenetic landscape. Objective This study employs an innovative approach that integrates multi-omics analysis and explainable machine learning to explore the epigenetic regulatory mechanisms underlying the epigenetic signature of PRRT1 implicated in AD. Methods Through comprehensive DNA methylation and transcriptomic profiling, we identified distinct epigenetic signatures associated with gene PRRT1 expression in AD patient samples compared to healthy controls. Utilizing interpretable machine learning models and ELMAR analysis, we dissected the complex relationships between these epigenetic signatures and gene expression patterns, revealing novel regulatory elements and pathways. Finally, the epigenetic mechanisms of these genes were investigated experimentally. Results This study identified ten epigenetic signatures, constructed an interpretable AD diagnostic model, and utilized various bioinformatics methods to create an epigenomic map. Subsequently, the ELMAR R package was used to integrate multi-omics data and identify the upstream transcription factor MAZ for PRRT1. Finally, experiments confirmed the interaction between MAZ and PRRT1, which mediated apoptosis and autophagy in AD. Conclusion This study adopts a strategy that integrates bioinformatics analysis with molecular experiments, providing new insights into the epigenetic regulatory mechanisms of PRRT1 in AD and demonstrating the importance of explainable machine learning in elucidating complex disease mechanisms.

Juanmei Gao, Yuan Liao, M. Qiu et al.

Neural stem/progenitor cells (NSCs) maintain the ability of self-renewal and differentiation and compose the complex nervous system. Wnt signaling is thought to control the balance of NSC proliferation and differentiation via the transcriptional coactivator β-catenin during brain development and adult tissue homeostasis. Disruption of Wnt signaling may result in developmental defects and neurological diseases. Here, we summarize recent findings of the roles of Wnt/β-catenin signaling components in NSC homeostasis for the regulation of functional brain circuits. We also suggest that the potential role of Wnt/β-catenin signaling might lead to new therapeutic strategies for neurological diseases, including, but not limited to, spinal cord injury, Alzheimer’s disease, Parkinson’s disease, and depression.

Meng-Yi Chen, Meng-Yi Chen, Qinge Zhang et al.

BackgroundA growing number of studies has implicated oxidative stress in the pathophysiology of psychiatric disorders including schizophrenia. The aim of this study was to explore the field of schizophrenia and oxidative stress-related research from a bibliometric perspective.MethodsAll relevant publications on schizophrenia and oxidative stress were obtained from Web of Science Core Collection (WOSCC) database from its inception date to November 8, 2022. VOSviewer software was used to examine co-authorships and co-occurring keywords. R software was used to present the main characteristics of publications and cooperation frequency among countries. CiteSpace was used to investigate keywords with the strongest citation bursts.ResultsA total of 3,510 publications on schizophrenia and oxidative stress were included. The United States had the largest number of publications (26.1%), and international collaborations. University of Melbourne was the most productive institution, while Schizophrenia Research was the most productive journal in this field. Apart from “schizophrenia” and “oxidative stress”, the terms “prefrontal cortex”, “brain” and “nitric oxide” were among the most frequently used keywords.ConclusionsIn conclusion, research on the association between oxidative stress and schizophrenia has received growing attention in the academic literature that is expected to continue its upward trajectory during the next two decades. Existing research suggests there has been a transition from research focused on pathways to animal models, and subsequently to clinical applications. Intervention studies on oxidative stress and schizophrenia are likely to be an important focus of related work in the near future.

Weihao Fan, Chunmei Liang, Mingqian Ou et al.

Progressive functional deterioration and loss of neurons underlies neurological diseases and constitutes an important cause of disability and death worldwide. The causes of various types of neurological diseases often share several critical nerve-related cellular mechanisms and pathological features, particularly the neuroinflammatory response in the nervous system. A rapidly growing body of evidence indicates that various microRNAs play pivotal roles in these processes in neurological diseases and might be viable therapeutic targets. Among these microRNAs, microRNA-146a (miR-146a) stands out due to the rapid increase in recent literature on its mechanistic involvement in neurological diseases. In this review, we summarize and highlight the critical role of miR-146a in neurological diseases. MiR-146a polymorphisms are associated with the risk of neurological disease. Alterations in miR-146a expression levels are crucial events in the pathogenesis of numerous neurological diseases that are spatially and temporally diverse. Additionally, the target genes of miR-146a are involved in the regulation of pathophysiological processes in neurological diseases, particularly the neuroinflammatory response. In summary, miR-146a mainly plays a critical role in neuroinflammation during the progression of neurological diseases and might be a prospective biomarker and therapeutic target. Understanding the mechanisms by which miR-146a affects the neuroinflammatory response in different neurological injuries, different cell types, and even different stages of certain neurological diseases will pave the way for its use as a therapeutic target in neurodegenerative diseases.

S. Lukehart, E. Hook, S. Baker-Zander et al.

Sheilagh Hodgins, Sheilagh Hodgins

The percentage of forensic psychiatric patients who are female varies from 5 to 13% in Europe, rises to 18% in England and Wales, and sits at 15% in Canada. Similarly, many fewer women than men are incarcerated in correctional facilities. While these statistics supposedly reflect less antisocial and aggressive behavior (AAB) among females than males, not all findings support this supposition. Data from prospective longitudinal studies show that aggressive and antisocial behavior onsets in childhood, and in a small group of females it remains stable across the life-span. Unlike similar males, few of these females are convicted of crimes. This article begins with a review of descriptive studies of females sentenced by criminal courts to treatment in forensic psychiatric hospitals and moves on to present evidence showing that most female AAB does not lead to criminal prosecution. Next, studies of female AAB are reviewed, noting that it onsets in early childhood and, that in a small group remains stable across the life-span. Subsequent sections of the article focus on the two most common mental disorders presented by female forensic patients, schizophrenia and borderline personality disorder, highlighting what is known about the sub-groups of women with these disorders who present AAB. The article concludes with recommendations for earlier identification by psychiatric services of women presenting mental disorders and AAB, treatments to reduce both the symptoms of their mental disorders and their life-long AAB, and the research that is needed in order to improve the effectiveness of these treatments. The real possibilities of prevention of the development of AAB, and even perhaps aspects of the mental disorders that plague female forensic patients, are described.

Ellen van der Plas, Jeffrey D. Long, Timothy R. Koscik et al.

IntroductionThe present study had four aims. First, neuronal injury markers, including neurofilament light (NF-L), total tau, glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase (UCH-L1), were compared between individuals with and without adult-onset myotonic dystrophy type 1 (DM1). Second, the impact of age and CTG repeat on brain injury markers was evaluated. Third, change in brain injury markers across the study period was quantified. Fourth, associations between brain injury markers and cerebral white matter (WM) fractional anisotropy (FA) were identified.MethodsYearly assessments, encompassing blood draws and diffusion tensor imaging on a 3T scanner, were conducted on three occasions. Neuronal injury markers were quantified using single molecule array (Simoa).ResultsThe sample included 53 patients and 70 controls. NF-L was higher in DM1 patients than controls, with individuals in the premanifest phases of DM1 (PreDM1) exhibiting intermediate levels (χ(2)2=38.142, P < 0.001). Total tau was lower in DM1 patients than controls (Estimate = −0.62, 95% confidence interval [CI] −0.95: −0.28, P < 0.001), while GFAP was elevated in PreDM1 only (Estimate = 30.37, 95% CI 10.56:50.19, P = 0.003). Plasma concentrations of UCH-L1 did not differ between groups. The age by CTG interaction predicted NF-L: patients with higher estimated progenitor allelege length (ePAL) had higher NF-L at a younger age, relative to patients with lower CTG repeat; however, the latter exhibited faster age-related change (Estimate = −0.0021, 95% CI −0.0042: −0.0001, P = 0.045). None of the markers changed substantially over the study period. Finally, cerebral WM FA was significantly associated with NF-L (Estimate = −42.86, 95% CI −82.70: −3.02, P = 0.035).InterpretationWhile NF-L appears sensitive to disease onset and severity, its utility as a marker of progression remains to be determined. The tau assay may have low sensitivity to tau pathology associated with DM1.

Emma A. Honkanen, Mikael Eklund, Simo Nuuttila et al.

Objective: To evaluate possible differences between brain dopamine transporter (DAT) binding in a group of symptomatic parkinsonism patients without dopaminergic degeneration and healthy individuals. Background: Dopaminergic neuroimaging studies of Parkinson’s disease (PD) have often used control groups formed from symptomatic patients with apparently normal striatal dopamine function. We sought to investigate whether symptomatic patients can be used to represent dopaminergically normal healthy controls. Methods: Forty healthy elderly individuals were scanned with DAT [123I]FP-CIT SPECT and compared to 69 age- and sex-matched symptomatic patients with nondegenerative conditions (including essential tremor, drug-induced parkinsonism and vascular parkinsonism). An automated region-of-interest based analysis of the caudate nucleus and the anterior/posterior putamen was performed. Specific binding ratios (SBR = [ROI-occ]/occ) were compared between the groups. Results: DAT binding in symptomatic patients was 8.6% higher in the posterior putamen than in healthy controls (p = 0.03). Binding correlated negatively with age in both groups but not with motor symptom severity, cognitive function or depression ratings. Conclusions: Putaminal DAT binding, as measured with [123I]FP-CIT SPECT, was higher in symptomatic controls than in healthy individuals. The reason for the difference is unclear but can include selection bias when DAT binding is used to aid clinical diagnosis and possible self-selection bias in healthy volunteerism. This effect should be taken into consideration when designing and interpreting neuroimaging trials investigating the dopamine system with [123I]FP-CIT SPECT.

Oriol Grau-Rivera, Irene Navalpotro-Gomez, Gonzalo Sánchez-Benavides et al.

Abstract Background Recognizing clinical manifestations heralding the development of Alzheimer’s disease (AD)-related cognitive impairment could improve the identification of individuals at higher risk of AD who may benefit from potential prevention strategies targeting preclinical population. We aim to characterize the association of body weight change with cognitive changes and AD biomarkers in cognitively unimpaired middle-aged adults. Methods This prospective cohort study included data from cognitively unimpaired adults from the ALFA study (n = 2743), a research platform focused on preclinical AD. Cognitive and anthropometric data were collected at baseline between April 2013 and November 2014. Between October 2016 and February 2020, 450 participants were visited in the context of the nested ALFA+ study and underwent cerebrospinal fluid (CSF) extraction and acquisition of positron emission tomography images with [18F]flutemetamol (FTM-PET). From these, 408 (90.1%) were included in the present study. We used data from two visits (average interval 4.1 years) to compute rates of change in weight and cognitive performance. We tested associations between these variables and between weight change and categorical and continuous measures of CSF and neuroimaging AD biomarkers obtained at follow-up. We classified participants with CSF data according to the AT (amyloid, tau) system and assessed between-group differences in weight change. Results Weight loss predicted a higher likelihood of positive FTM-PET visual read (OR 1.27, 95% CI 1.00–1.61, p = 0.049), abnormal CSF p-tau levels (OR 1.50, 95% CI 1.19–1.89, p = 0.001), and an A+T+ profile (OR 1.64, 95% CI 1.25–2.20, p = 0.001) and was greater among participants with an A+T+ profile (p < 0.01) at follow-up. Weight change was positively associated with CSF Aβ42/40 ratio (β = 0.099, p = 0.032) and negatively associated with CSF p-tau (β = − 0.141, p = 0.005), t-tau (β = − 0.147 p = 0.004) and neurogranin levels (β = − 0.158, p = 0.002). In stratified analyses, weight loss was significantly associated with higher t-tau, p-tau, neurofilament light, and neurogranin, as well as faster cognitive decline in A+ participants only. Conclusions Weight loss predicts AD CSF and PET biomarker results and may occur downstream to amyloid-β accumulation in preclinical AD, paralleling cognitive decline. Accordingly, it should be considered as an indicator of increased risk of AD-related cognitive impairment. Trial registration NCT01835717 , NCT02485730 , NCT02685969 .

Monica Daibert-Nido, Monica Daibert-Nido, Yulia Pyatova et al.

Background/Objectives: Visual field loss is frequent in patients with brain tumors, worsening their daily life and exacerbating the burden of disease, and no supportive care strategies exist. In this case series, we sought to characterize the feasibility and potential effectiveness of a home-based visual rehabilitation program in hemianopia patients using immersive virtual-reality stimulation.Subjects/Methods: Two patients, one with homonymous hemianopia and the other with bitemporal hemianopia, consecutive to pediatric brain tumors, with no prior visual rehabilitation performed 15 min of home-based audiovisual stimulation every 2 days for 6 weeks (case 2) and 7 weeks (case 1) between February and August 2020. Patients used a virtual-reality, stand-alone, and remotely controlled device loaded with a non-commercial audiovisual stimulation program managed in real time from the laboratory. Standard visual outcomes assessed in usual care in visual rehabilitation were measured at the clinic. Following a mixed method approach in this pragmatic study of two cases, we collected quantitative and qualitative data on feasibility and potential effectiveness and compared the results pre- and post-treatment.Results: Implementation and wireless delivery of the audiovisual stimulation, remote data collection, and analysis for cases 1 and 2 who completed 19/20 and 20/20 audiovisual stimulation sessions at home, respectively, altogether indicated feasibility. Contrast sensitivity increased in both eyes for cases 1 and 2. Visual fields, measured by binocular Esterman and monocular Humphrey full-field analyses, improved in case 1. A minor increase was observed in case 2. Cases 1 and 2 enhanced reading speed. Case 2 strongly improved quality of life scores.Conclusion: This is the first report of a home-based virtual-reality visual rehabilitation program for adult patients with hemianopia consecutive to a pediatric brain tumor. We show the feasibility in real-world conditions and potential effectiveness of such technology on visual perception and quality of life.

Laura Pajares, David Morillo, Joan Seguí et al.

Stephan Heinzel, Katharina Bey, Rosa Grützmann et al.

Studies have shown that people with obsessive–compulsive disorder (OCD) have impairments in spatial working memory (SWM) performance. However, it remains unclear whether this deficit represents a cognitive endophenotype preceding symptoms or a correlate of OCD. We investigated SWM in 69 people with OCD, 77 unaffected first-degree relatives of people with OCD and 106 healthy control participants. Taking age effects into account, SWM performance was best in healthy controls, intermediate in relatives and worst in OCD participants. However, since performance did not differ significantly between healthy controls and relatives, our study does not fully support SWM performance as a core cognitive endophenotype of OCD.

D. Leander Rimmele, Theresa Schrage, Lisa Lebherz et al.

Abstract Background We aimed to identify groups of patients with similar health status after stroke, assessed by patient reported outcome measures (PROMs), to improve initial risk stratification. Methods In a prospective study, inpatients were recruited during acute stroke treatment. Demographics, history, and cardio-vascular risk factors were assessed at baseline. Self-reported functional status, physical and mental health as well as anxiety and depressive symptoms were assessed 3 and 12 months after stroke and used to identify latent classes. The association of patient characteristics with latent class membership was investigated with multinomial logistic regression. Results Of the 650 patients included with a mean age of 75 years and 48% female, 70% had ischemic, 6% hemorrhagic strokes, and 24% transient ischemic attacks. Median NIHSS on admission was 2 (IQR:0,5). Values of PROMs remained comparable at 3 and 12 months. A three-class model was developed, differentiating between patients with mildly (75%), moderately (17%), and severely (8%) impaired self-reported health status. Adjusted for univariately significant baseline characteristics, initial NIHSS distinguished mild- from moderate-, and moderate- from severe-class-membership (p < 0.001). Length of inpatient stay (p < 0.001;OR = 1.1), diabetes (p = 0.021;OR = 1.91), and atrial fibrillation (p = 0.004;OR = 2.20) predicted allocation to the moderately vs. mildly affected class. Conclusions Grading stroke patients by a standard set of PROMs up to 1 year after stroke allows to distinguish the diverse impact of baseline characteristics on differently affected groups. In addition to initial stroke severity, longer inpatient stay, presence of diabetes and atrial fibrillation correlate with greater impairment of self-reported health in the less affected groups. Trial registration http://www.ClinicalTrials.gov ; Unique identifier: NCT03795948 .

Keane Lim, Sara-Ann Lee, Amy E. Pinkham et al.

Background: Converging evidence has indicated that deficits in social cognition may manifest as poor functioning; therefore, social cognition has emerged as an important research area and treatment target. However, few studies have examined the psychometrics of multiple social cognition measures in an Asian population. This study aims to evaluate the psychometrics of measures indexing the four core social cognition domains. Methods: Schizophrenia outpatients (n = 116) and healthy controls (n = 73) completed a battery of nine social cognitive measures, twice, four weeks apart. Psychometric properties were examined via test-retest reliability, internal consistency, utility as a repeated measure, time administration, and tolerability. Logistic regression was performed to identify psychometrically sound tasks that best discriminated case-control status. PCA was conducted to explore social cognition dimensional structure. Results: The Bell Lysaker Emotion Recognition Task (BLERT), Penn Emotion Recognition Task (ER40), and The Awareness of Social Inference Test, branch III (TASIT-3) showed strongest psychometrics. The Ambiguous Intentions and Hostility Questionnaire, Hostility Bias subscale (AIHQ-HB) showed slightly weaker properties, requiring further evaluation. The Hinting task, Mini Profile of Nonverbal Sensitivity (MiniPONS), Relationships Across Domains (RAD), Internal Personal and Situational Attributions Questionnaire (IPSAQ), and Mayer-Salovey-Caruso Emotional Intelligence Test (MSCEIT) showed poorer psychometrics in our sample. PCA revealed a two-factor solution comprising social cognition skills and attributional style/bias. Conclusion: Here, we examined the psychometric properties of a comprehensive social cognition battery based on the SCOPE study in an Asian schizophrenia population. Continued evaluation and standardization of social cognitive measures are needed to refine our understanding of this construct in schizophrenia. Keywords: Schizophrenia, Social cognition, Psychometric

Alicia Valiente-Gómez, Alicia Valiente-Gómez, Alicia Valiente-Gómez et al.

BackgroundPatients with a first episode psychosis (FEP) who are admitted for the first time to a psychiatric hospital frequently have experienced prior psychological trauma. Additionally, 40–80% develop posttraumatic stress symptoms, which are summarized as a post-psychotic post-traumatic syndrome (PPS). Eye Movement Desensitization and reprocessing (EMDR) therapy could be an effective psychotherapy to treat a PPS and prior psychological traumas in this population.ObjectivesTo assess if EMDR therapy leads to: 1) a reduction of relapses after intervention, 2) an improvement of trauma-related, psychotic and affective symptoms, 3) an improvement of overall functioning, and 4) an improvement in quality of life.MethodsThis is a multicenter phase II rater-blinded randomized controlled trial in which 80 FEP patients with a history of psychological trauma will be randomly assigned to EMDR (n = 40) or to TAU (n = 40). Traumatic events will be measured by the Global Assessment of Posttraumatic Stress Questionnaire, the Cumulative Trauma Screening, the Impact of Event Scale-Revised, the Dissociative Experiences Scale, the Childhood Trauma Scale, the Holmes–Rahe Life Stress Inventory, and the Dissociative Experiences Questionnaire. Clinical symptomatology will be evaluated using the Suicide and Drug Consumption module of the International Neuropsychiatric Interview, Structured Clinical Interview for Positive and Negative Syndrome Scale, Young’s Scale for Mania Evaluation, and Beck Depression II Questionnaire. Functionality will be assessed with the Global Assessment of Functioning and the Quality of Life with the Standardized Instrument developed by the EuroQol Group. The cognitive insight and adherence to the treatment will be assessed with the Beck Cognitive Insight Scale and the Drug Attitude Inventory. All variables will be measured at baseline, post-treatment and at 12-month follow-up.ConclusionThis study will provide evidence of whether EMDR therapy is effective in reducing trauma and clinical symptoms, reducing relapses and in improving functionality and quality of life in patients with FEP and a history of trauma.Clinical Trial Registrationwww.ClinicalTrials.gov, identifier: NCT03991377

Minoo Sharbafshaaer, Zabihollah Hashemzahi, Pravin Thomas et al.

ABSTRACT Objective: To exploring differences between degrees and causes of TBI in mental health impairment with comprising gender differences. Methods: The study was a cross-sectional observational study of TBI patients who bedded within 24 hours of presentation to the emergency department (ED), Khatam Hospital, located in Zahedan, Iran. Participants were randomized by a simple randomization technique. Information had been collected twice, first time screening patients by Glasgow Coma Scale score (GCS) and the second time was two months after discharging patients from the ED to estimate mental health impairment by using two separate clinical diagnostic tests. Results: The research considered 80 patients, with 66% being male and 34% female. The median age for both genders estimated 23.5 years. There was a statistically significant difference between degrees and causes of TBI on the total score of hospital anxiety and depression. In particular, degree and cause of TBI with depression in males (M = 14.54, SD = .22), and degrees of TBI on post-traumatic stress disorder in females (M = 87, SD = .7) were significant difference. Conclusion: The current investigation highlights the incidence of depression in male patients with severe levels of traumatic brain injury who injured by car accident multiple trauma; furthermore, this research found the remarkable rate of post-traumatic stress disorder in female patients with a mild degree of TBI. The researcher in traumatic brain injury should seriously deliberate and explore gender differences with the degree and cause of TBI in detail.

M. Maden

Setty M. Magaña, B. Keegan, B. Weinshenker et al.