Visuospatial Attention Allocation as an Indicator of Cognitive Deficit in Traumatic Brain Injury: A Systematic Review and Meta-Analysis.
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SUBMITTER: Walz JA
PROVIDER: S-EPMC8329082 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ImportanceThere are conflicting accounts about the risk for attention-deficit/hyperactivity disorder (ADHD) following traumatic brain injury (TBI), possibly owing to variations between studies in acute TBI severity or when ADHD was assessed postinjury. Analysis of these variations may aid in identifying the risk.ObjectiveTo conduct a meta-analysis of studies assessing ADHD diagnoses in children between ages 4 and 18 years following concussions and mild, moderate, or severe TBI.Data sourcesPubMed, PsycInfo, and Cochrane Central Register of Controlled Trials (1981-December 19, 2019) were searched including the terms traumatic brain injury, brain injuries, closed head injury, blunt head trauma, concussion, attention deficit disorders, ADHD, and ADD in combination with childhood, adolescence, pediatric, infant, child, young adult, or teen.Study selectionLimited to English-language publications in peer-reviewed journals and patient age (4-18 years). Differences about inclusion were resolved through consensus of 3 authors.Data extraction and synthesisMOOSE guidelines for abstracting and assessing data quality and validity were used. Odds ratios with 95% credible intervals (CrIs) are reported.Main outcomes and measuresThe planned study outcome was rate of ADHD diagnoses.ResultsA total of 12 374 unique patients with TBI of all severity levels and 43 491 unique controls were included in the 24 studies in this review (predominantly male: TBI, 61.8%; noninjury control, 60.9%; other injury control, 66.1%). The rate of pre-TBI ADHD diagnoses was 16.0% (95% CrI, 11.3%-21.7%), which was significantly greater than the 10.8% (95% CrI, 10.2%-11.4%) incidence of ADHD in the general pediatric population. Compared with children without injuries, the odds for ADHD were not significantly increased following concussion (≤1 year: OR, 0.32; 95% CrI, 0.05-1.13), mild TBI (≤1 year: OR, 0.56; 0.16-1.43; >1 year: OR, 1.07; 95% CrI, 0.35-2.48), and moderate TBI (≤1 year: OR, 1.28; 95% CrI, 0.35-3.34; >1 year: OR, 3.67; 95% CrI, 0.83-10.56). The odds for ADHD also were not significantly increased compared with children with other injuries following mild TBI (≤1 year: OR, 1.07; 95% CrI, 0.33-2.47; >1 year: OR, 1.18; 95% CrI, 0.32-3.12) and moderate TBI (≤1 year: OR, 2.34; 95% CrI, 0.78-5.47; >1 year: OR, 3.78; 95% CrI, 0.93-10.33). In contrast, the odds for ADHD following severe TBI were increased at both time points following TBI compared with children with other injuries (≤1 year: OR, 4.81; 95% CrI, 1.66-11.03; >1 year: OR, 6.70; 95% CrI, 2.02-16.82) and noninjured controls (≤1 year: OR, 2.62; 95% CrI, 0.76-6.64; >1 year: OR, 6.25; 95% CrI, 2.06-15.06), as well as those with mild TBI (≤1 year OR, 5.69; 1.46-15.67: >1 year OR, 6.65; 2.14-16.44). Of 5920 children with severe TBI, 35.5% (95% CrI, 20.6%-53.2%) had ADHD more than 1 year postinjury.Conclusions and relevanceThis study noted a significant association between TBI severity and ADHD diagnosis. In children with severe but not mild and moderate TBI, there was an association with an increase in risk for ADHD. The high rate of preinjury ADHD in children with TBI suggests that clinicians should carefully review functioning before a TBI before initiating treatment.
| S-EPMC8276124 | biostudies-literature
Project description:ObjectivesTo measure the clinical, structural and functional changes of an individualised structured cognitive rehabilitation in mild traumatic brain injury (mTBI) population.SettingA single centre study, Malaysia.ParticipantsAdults aged between 18 and 60 years with mTBI as a result of road traffic accident, with no previous history of head trauma, minimum of 9 years education and abnormal cognition at 3 months will be included. The exclusion criteria include pre-existing chronic illness or neurological/psychiatric condition, long-term medication that affects cognitive/psychological status, clinical evidence of substance intoxication at the time of injury and major polytrauma. Based on multiple estimated calculations, the minimum intended sample size is 50 participants (Cohen's d effect size=0.35; alpha level of 0.05; 85% power to detect statistical significance; 40% attrition rate).InterventionsIntervention group will receive individualised structured cognitive rehabilitation. Control group will receive the best patient-centred care for attention disorders. Therapy frequency for both groups will be 1 hour per week for 12 weeks.Outcome measuresPrimary: Neuropsychological Assessment Battery-Screening Module (S-NAB) scores. Secondary: Diffusion Tensor Imaging (DTI) parameters and Goal Attainment Scaling score (GAS).ResultsResults will include descriptive statistics of population demographics, CogniPlus cognitive program and metacognitive strategies. The effect of intervention will be the effect size of S-NAB scores and mean GAS T scores. DTI parameters will be compared between groups via repeated measure analysis. Correlation analysis of outcome measures will be calculated using Pearson's correlation coefficient.ConclusionThis is a complex clinical intervention with multiple outcome measures to provide a comprehensive evidence-based treatment model.Ethics and disseminationThe study protocol was approved by the Medical Research Ethics Committee UMMC (MREC ID NO: 2016928-4293). The findings of the trial will be disseminated through peer-reviewed journals and scientific conferences.Trial registration numberNCT03237676.
| S-EPMC6756424 | biostudies-literature
Project description:Importance:After traumatic brain injury (TBI), children often experience impairment when faced with tasks and situations of increasing complexity. Studies have failed to consider the potential for attention problems to develop many years after TBI or factors that may predict the development of secondary attention-deficit/hyperactivity disorder (SADHD). Understanding these patterns will aid in timely identification of clinically significant problems and appropriate initiation of treatment with the hope of limiting additional functional impairment. Objective:To examine the development of SADHD during the 5 to 10 years after TBI and individual (sex, age at injury, and injury characteristics) and environmental (socioeconomic status and family functioning) factors that may be associated with SADHD. Design, Setting, and Participants:Concurrent cohort/prospective study of children aged 3 to 7 years hospitalized overnight for TBI or orthopedic injury (OI; used as control group) who were screened at 3 tertiary care children's hospitals and 1 general hospital in Ohio from January 2003 to June 2008. Parents completed assessments at baseline (0-3 months), 6 months, 12 months, 18 months, 3.4 years, and 6.8 years after injury. A total of 187 children and adolescents were included in the analyses: 81 in the TBI group and 106 in the OI group. Main Outcomes and Measures:Diagnosis of SADHD was the primary outcome. Assessments were all completed by parents. Secondary ADHD was defined as an elevated T score on the DSM-Oriented Attention-Deficit/Hyperactivity Problems Scale of the parent-reported Child Behavior Checklist, report of an ADHD diagnosis, and/or current treatment with stimulant medication not present at the baseline assessment. The Family Assessment Device-Global Functioning measurement was used to assess family functioning; scores ranged from 1 to 4, with greater scores indicating poorer family functioning. Results:The analyzed sample included 187 children with no preinjury ADHD. Mean (SD) age was 5.1 (1.1) years; 108 (57.8%) were male, and 50 (26.7%) were of nonwhite race/ethnicity. Of the 187 children, 48 (25.7%) met our definition of SADHD. Severe TBI (hazard ratio [HR], 3.62; 95% CI, 1.59-8.26) was associated with SADHD compared with the OI group. Higher levels of maternal education (HR, 0.33; 95% CI, 0.17-0.62) were associated with a lower risk of SADHD. Family dysfunction was associated with increased risk of SADHD within the TBI group (HR, 4.24; 95% CI, 1.91-9.43), with minimal association within the OI group (HR, 1.32; 95% CI, 0.36-4.91). Conclusions and Relevance:Early childhood TBI was associated with increased risk for SADHD. This finding supports the need for postinjury monitoring for attention problems. Consideration of factors that may interact with injury characteristics, such as family functioning, will be important in planning clinical follow-up of children with TBI.
| S-EPMC5875309 | biostudies-literature
Project description:Being able to focus on a complex task and inhibit unwanted actions or interfering information (i.e., inhibitory control) are essential human cognitive abilities. However, it remains unknown the extent to which mild traumatic brain injury (mTBI) may impact these critical functions. In this study, seventeen patients and age-matched healthy controls (HC) performed a variant of the Stroop task and attention-demanding 4-choice response tasks (4CRT) with identical stimuli but two contexts: one required only routine responses and the other with occasional response conflicts. The results showed that mTBI patients performed equally well as the HC when the 4CRT required only routine responses. However, when the task conditions included occasional response conflicts, mTBI patients with even a single concussion showed a significant slow-down in all responses and higher error rates relative to the HC. Results from event-related functional magnetic resonance imaging (efMRI) revealed altered neural activity in the mTBI patients in the cerebellum-thalamo-cortical and the fronto-basal-ganglia networks regulating inhibitory control. These results suggest that even without apparent difficulties in performing complex attention-demanding but routine tasks, patients with mTBI may experience long-lasting deficits in regulating inhibitory control when situations call for rapid conflict resolutions.
| S-EPMC5668274 | biostudies-literature
Project description:Objective: To quantitatively aggregate effects of cognitive training (CT) on cognitive and functional outcome measures in patients with traumatic brain injury (TBI) more than 12-months post-injury. Design: We systematically searched six databases for non-randomized and randomized controlled trials of CT in TBI patients at least 12-months post-injury reporting cognitive and/or functional outcomes. Main Measures: Efficacy was measured as standardized mean difference (Hedges' g) of post-training change. We investigated heterogeneity across studies using subgroup analyses and meta-regressions. Results: Fourteen studies encompassing 575 patients were included. The effect of CT on overall cognition was small and statistically significant (g = 0.22, 95%CI 0.05 to 0.38; p = 0.01), with low heterogeneity (I2 = 11.71%) and no evidence of publication bias. A moderate effect size was found for overall functional outcomes (g = 0.32, 95%CI 0.08 to 0.57, p = 0.01) with low heterogeneity (I2 = 14.27%) and possible publication bias. Statistically significant effects were also found only for executive function (g = 0.20, 95%CI 0.02 to 0.39, p = 0.03) and verbal memory (g = 0.32, 95%CI 0.14 to 0.50, p < 0.01). Conclusion: Despite limited studies in this field, this meta-analysis indicates that CT is modestly effective in improving cognitive and functional outcomes in patients with post-acute TBI and should therefore play a more significant role in TBI rehabilitation.
| S-EPMC5081379 | biostudies-literature
Project description:BACKGROUND:Attention-deficit/hyperactivity disorder (ADHD) is a major sequela of traumatic brain injury (TBI) in youths. The objective of this study was to examine whether ADHD symptoms are differentially associated with genetic risk and brain structure in youths with and without a history of TBI. METHODS:Medical history, ADHD symptoms, genetic data, and neuroimaging data were obtained from a community sample of youths. ADHD symptom severity was compared between those with and without TBI (TBI n = 418, no TBI n = 3193). The relationship of TBI history, genetic vulnerability, brain structure, and ADHD symptoms was examined by assessing 1) ADHD polygenic score (discovery sample ADHD n = 19,099, control sample n = 34,194), 2) basal ganglia volumes, and 3) fractional anisotropy in the corpus callosum and corona radiata. RESULTS:Youths with TBI reported greater ADHD symptom severity compared with those without TBI. Polygenic score was positively associated with ADHD symptoms in youths without TBI but not in youths with TBI. The negative association between the caudate volume and ADHD symptoms was not moderated by a history of TBI. However, the relationship between ADHD symptoms and structure of the genu of the corpus callosum was negative in youths with TBI and positive in youths without TBI. CONCLUSIONS:The identification of distinct ADHD etiology in youths with TBI provides neurobiological insight into the clinical heterogeneity in the disorder. Results indicate that genetic predisposition to ADHD does not increase the risk for ADHD symptoms associated with TBI. ADHD symptoms associated with TBI may be a result of a mechanical insult rather than neurodevelopmental factors.
| S-EPMC6330150 | biostudies-literature
Project description: Not available
| S-EPMC2575660 | biostudies-literature
Project description:Dopaminergic stimulation has been proposed as a treatment strategy for post-traumatic brain injured patients in minimally conscious state based on a clinical trial using amantadine, a weak dopamine transporter blocker. However, a specific contribution of dopaminergic neuromodulation in minimally conscious state is undemonstrated. In a phase 0 clinical trial, we evaluated 13 normal volunteers and seven post-traumatic minimally conscious state patients using 11C-raclopride PET to estimate dopamine 2-like receptors occupancy in the striatum and central thalamus before and after dopamine transporter blockade with dextroamphetamine. If a presynaptic deficit was observed, a third and a fourth 11C-raclopride PET were acquired to evaluate changes in dopamine release induced by l-DOPA and l-DOPA+dextroamphetamine. Permutation analysis showed a significant reduction of dopamine release in patients, demonstrating a presynaptic deficit in the striatum and central thalamus that could not be reversed by blocking the dopamine transporter. However, administration of the dopamine precursor l-DOPA reversed the presynaptic deficit by restoring the biosynthesis of dopamine from both ventral tegmentum and substantia nigra. The advantages of alternative pharmacodynamic approaches in post-traumatic minimally conscious state patients should be tested in clinical trials, as patients currently refractory to amantadine might benefit from them.
| S-EPMC6598636 | biostudies-literature
Project description:Deficits in attention are a common and devastating consequence of traumatic brain injury (TBI), leading to functional impairments, rehabilitation barriers, and long-term disability. While such deficits are well documented, little is known about their underlying pathophysiology hindering development of effective and targeted interventions. Here we evaluate the integrity of brain systems specific to attentional functions using quantitative assessments of electroencephalography recorded during performance of the Attention Network Test (ANT), a behavioral paradigm that separates alerting, orienting, and executive components of attention. We studied 13 patients, at least 6 months post-TBI with cognitive impairments, and 24 control subjects. Based on performance on the ANT, TBI subjects showed selective impairment in executive attention. In TBI subjects, principal component analysis combined with spectral analysis of the EEG after target appearance extracted a pattern of increased frontal midline theta power (2.5-7.5 Hz) and suppression of frontal beta power (12.5-22.5 Hz). Individual expression of this pattern correlated (r = - 0.67, p < 0.001) with executive attention impairment. The grading of this pattern of spatiotemporal dynamics with executive attention deficits reflects impaired recruitment of anterior forebrain resources following TBI; specifically, deafferentation and variable disfacilitation of medial frontal neuronal populations is proposed as the basis of our findings.
| S-EPMC5288490 | biostudies-literature
Project description:The purpose of this multicenter, prospective, randomized, placebo-controlled study was to evaluate and compare the efficacy of two cognitive rehabilitation interventions (Memory and Attention Adaptation Training (MAAT) and Attention Builders Training (ABT)), with and without pharmacological enhancement (ie, with methylphenidate (MPH) or placebo), for treating persistent cognitive problems after traumatic brain injury (TBI). Adults with a history of TBI at least 4 months before study enrollment with either objective cognitive deficits or subjective cognitive complaints were randomized to receive MPH or placebo and MAAT or ABT, yielding four treatment combinations: MAAT/MPH (N=17), ABT/MPH (N=19), MAAT/placebo (N=17), and ABT/placebo (N=18). Assessments were conducted pre-treatment (baseline) and after 6 weeks of treatment (post treatment). Outcome measures included scores on neuropsychological measures and subjective rating scales. Statistical analyses used linear regression models to predict post-treatment scores for each outcome variable by treatment type, adjusting for relevant covariates. Statistically significant (P<0.05) treatment-related improvements in cognitive functioning were found for word-list learning (MAAT/placebo>ABT/placebo), nonverbal learning (MAAT/MPH>MAAT/placebo and MAAT/MPH>ABT/MPH), and auditory working memory and divided attention (MAAT/MPH>ABT/MPH). These results suggest that combined treatment with metacognitive rehabilitation (MAAT) and pharmacotherapy (MPH) can improve aspects of attention, episodic and working memory, and executive functioning after TBI.
| S-EPMC5520776 | biostudies-literature