The King's Outcome Scale for Childhood Head Injury and injury severity and outcome measures in children with traumatic brain injury

The aim of this study was to relate discharge King's Outcome Scale for Childhood Head Injury (KOSCHI) category to injury severity and detailed outcome measures obtained in the first year post-traumatic brain injury (TBI). We used a prospective cohort study. Eighty-one children with TBI were studied: 29 had severe, 15 moderate, and 37 mild TBI. The male:female ratio was 1.8:1. The mean age was 11 years 10 months (SD 3.6, range 5-16y). Discharge KOSCHI categories were good (n=34), moderate (n=39), severe (n=6), and unclassifiable (n=2). KOSCHI category correlated strongly with admission Glasgow Coma Score, length of hospital stay, and post-traumatic amnesia. It also correlated significantly with Verbal IQ and Performance IQ (Wechsler); measures of attention; health status (Health Utilities Index [HUI]); health-related quality of life (Pediatric Quality of Life Inventory [PedsQL]); depressive symptoms (Birleson Depression Scale) assessed within 3 months postTBI; and with Verbal IQ, selective attention (map mission), and HUI and PedsQL domains assessed at least 6 months post-TBI discharge. KOSCHI did not correlate with behaviour or executive function. We conclude that the KOSCHI scored at hospital discharge correlates with severity of injury and some cognitive, health status, and HRQL outcomes early after TBI. It is not helpful at predicting later difficulties, or behavioural and emotional problems.     

Brain activation during working memory after traumatic brain injury in children

Eight children with moderate to severe traumatic brain injury (TBI) and eight matched, uninjured control children underwent fMRI during an N-back task to test effects of TBI on working memory performance and brain activation. Two patterns in the TBI group were observed. Patients whose criterion performance was reached at lower memory loads than control children demonstrated less extensive frontal and extrafrontal brain activation than controls. Patients who performed the same, highest (3-back) memory load as controls demonstrated more frontal and extrafrontal activation than controls. Our findings of performance and brain activation changes in children after TBI await longitudinal investigation.     

Brain Activation during Working Memory after Traumatic Brain Injury in Children

Eight children with moderate to severe traumatic brain injury (TBI) and eight matched, uninjured control children underwent fMRI during an N-back task to test effects of TBI on working memory performance and brain activation. Two patterns in the TBI group were observed. Patients whose criterion performance was reached at lower memory loads than control children demonstrated less extensive frontal and extrafrontal brain activation than controls. Patients who performed the same, highest (3-back) memory load as controls demonstrated more frontal and extrafrontal activation than controls. Our findings of performance and brain activation changes in children after TBI await longitudinal investigation.     

Depth of lesion model in children and adolescents with moderate to severe traumatic brain injury: use of SPGR MRI to predict severity and outcome

OBJECTIVES: The utility of a depth of lesion classification using an SPGR MRI sequence in children with moderate to severe traumatic brain injury (TBI) was examined. Clinical and depth of lesion classification measures of TBI severity were used to predict neurological and functional outcome after TBI. METHODS: One hundred and six children, aged 4 to 19, with moderate to severe TBI admitted to a rehabilitation unit had an SPGR MRI sequence obtained 3 months afterTBI. Acquired images were analyzed for location, number, and size of lesions. The Glasgow coma scale (GCS) was the clinical indicator of severity. The deepest lesion present was used for depth of lesion classification. Speed of injury was inferred from the type of injury. The disability rating scale at the time of discharge from the rehabilitation unit (DRS1) and at 1 year follow up (DRS2) were functional outcome measures. RESULTS: The depth of lesion classification was significantly correlated with GCS severity, number of lesions, and both functional measures, DRS1 and DRS2. This result was more robust for time 1, probably due to the greater number of psychosocial factors impacting on functioning at time 2. Lesion volume was not correlated with the depth of lesion model. In multivariate models, depth of lesion was most predictive of DRS1, whereas GCS was most predictive of DRS2. CONCLUSIONS: A depth of lesion classification of TBI severity may have clinical utility in predicting functional outcome in children and adolescents with moderate to severe TBI.     

Predictors of personality change due to traumatic brain injury in children and adolescents six to twenty-four months after injury

Phenomenology and predictive factors of personality change due to traumatic brain injury (TBI) 6 to 24 months after injury was investigated in children, ages 5 to 14 years, enrolled from consecutive admissions and followed prospectively for 2 years. Injury and preinjury psychosocial variables were assessed. Personality change occurred in 13% of participants between 6 and 12 months after injury and 12% in the second year after injury. Severity of injury consistently predicted personality change, and preinjury adaptive function predicted personality change only in the second year postinjury. Lesions of the superior frontal gyrus were associated with personality change between 6 and 12 months following injury, after controlling for severity of injury and the presence of other brain lesions. Only lesions in the frontal lobe white matter were significantly related to personality change in the second year after injury. After childhood TBI, neural correlates of personality change evolve between 6 and 12 months and 12 to 24 months after injury. The data implicate the dorsal prefrontal cortex and frontal lobe white matter in the emergence of personality change involving the effortful or conscious regulation of affective states.     

Functional reorganisation of memory after traumatic brain injury: a study with H(2)(15)0 positron emission tomography

OBJECTIVE: To study the effects of moderate to severe traumatic brain injury (TBI) on the functional neuroanatomy supporting memory retrieval. METHODS: Subjects were six patients who had sustained a moderate to severe TBI about four years before scanning and had since made a good recovery. Eleven healthy young adults matched to the patients for age and education served as controls. An established H(2)(15)0 positron emission tomography paradigm was used to elicit brain activations in response to memory retrieval. TBI patients' patterns of brain activation were compared statistically with those of control subjects. Both group and individual case data were analysed. RESULTS: Both TBI patients and controls engaged frontal, temporal, and parietal regions known to be involved in memory retrieval, yet the TBI patients showed relative increases in frontal, anterior cingulate, and occipital activity. The hemispheric asymmetry characteristic of controls was attenuated in patients with TBI. Reduced activation was noted in the right dorsomedial thalamus. Although local aspects of this pattern were affected by the presence of focal lesions and performance differences, the overall pattern was reliable across patients and comparable to functional neuroimaging results reported for normal aging, Alzheimer's disease, and other patients with TBI. CONCLUSIONS: The TBI patients performed memory tasks using altered functional neuroanatomical networks. These changes are probably the result of diffuse axonal injury and may reflect either cortical disinhibition attributable to disconnection or compensation for inefficient mnemonic processes.     

Cerebral correlates of declarative memory dysfunctions in early traumatic brain injury

We investigated residual brain damage in subjects who suffered severe traumatic brain injury (TBI) in childhood, and its relationship with declarative memory impairment. Magnetic resonance imaging (MRI) volumetric data and memory performance were compared between 16 adolescents with antecedents of severe TBI and 16 matched normal controls. Volumes of grey matter, white matter, cerebrospinal fluid (CSF), hippocampus, and caudate nuclei were measured. Verbal memory was assessed by the Rey's Auditory Verbal Learning test and visual memory by the Rey's Complex Figure. TBI patients performed significantly worse than controls in both verbal and visual memory. Patients presented decreased white matter volume and increased CSF. The hippocampus was reduced, but not the caudate nuclei. Memory performance correlated with CSF. Plasticity is incomplete for structural and functional deficits in children with TBI. Hippocampal atrophy, white matter loss, and memory impairment remain until adolescence. Memory sequelae are related more to diffuse brain injury, as reflected by MRI findings of increased CSF, than to hippocampal injury.     

Functional memory skills following traumatic brain injury in young children

Traumatic brain injury (TBI) may have a profound impact on a child's ongoing development. Various risk factors have been found to predict outcome, but considerable variability remains unexplained. This study used a prospective, longitudinal design to examine recovery of memory function following TBI within the pre-school period. Forty-four children with TBI were divided according to injury severity (mild, moderate, severe), and compared to age and SES matched healthy controls (n = 26). Children were evaluated acutely and at 12 months post-injury using the Rivermead Behavioural Memory Test for Children. Results failed to show a clear dose-response relationship between injury severity and memory function during the acute phase of recovery. However, this relationship developed over time, with greater memory impairments evident for children with more severe TBI by 12 months post-injury. Children with mild TBI exhibited few memory problems.     

Association between cognitive impairments and obsessive-compulsive spectrum presentations following traumatic brain injury

This study examined the association between self-reported obsessive-compulsive spectrum symptomatology and cognitive performance in a sample of patients with traumatic brain injury (TBI). Twenty-four adults with a moderate-severe TBI accessing a community brain injury rehabilitation service were recruited. Age ranged between 19 and 69 years. Participants completed a battery of neuropsychological tasks assessing memory, executive functioning, and speed of information processing. Self-report questionnaires assessing obsessive-compulsive (OC) symptoms and obsessive-compulsive personality disorder (OCPD) traits were also completed. Correlational analyses revealed that deficits in cognitive flexibility were associated with greater self-reported OC symptomatology and severity. Greater OC symptom severity was significantly related to poorer performance on a visual memory task. Verbal memory and speed of information processing impairments were unrelated to OC symptoms. Performance on tasks of memory, executive functioning, and speed of information processing were not associated with OCPD traits. Overall, results indicate that greater OC symptomatology and severity were associated with specific neuropsychological functions (i.e., cognitive flexibility, visual memory). OCPD personality traits were unrelated to cognitive performance. Further research is needed to examine the potential causal relationship and longer-term interactions between cognitive sequelae and obsessive-compulsive spectrum presentations post-TBI.     

The persistence of sleep disturbance and its correlates in children with moderate to severe traumatic brain injury: A longitudinal study

ObjectivesThe primary aim was to examine whether sleep disturbances persist in children in the chronic stage of recovery from moderate or severe traumatic brain injury (TBI). The secondary aim was to examine whether memory difficulties and/or other previously identified factors relate to sleep disturbances in children with moderate to severe TBI.MethodsThis longitudinal study included 21 children with moderate to severe TBI, 8–18 years old, recruited from an urban tertiary paediatric specialised brain injury rehabilitation unit. Participants were seen 5 years and again 7 years post-injury, on average. Sleep disturbances were assessed with Sleep Disturbance Scale for Children (SDSC). Correlates that were considered included indicators of TBI severity, and questionnaires assessing everyday memory, fatigue, internalizing and externalizing behaviors and pain intensity.ResultsThe SDSC scores of children with moderate to severe TBI indicated greater disturbances in initiating and maintaining sleep, arousal, sleep-wake transition, and excessive somnolence relative to the norms, at follow-up. The mean SDSC scores and the number of participants with subclinical to clinical sleep disturbances on the SDSC remained unchanged from baseline to follow-up. At follow-up, the SDSC initiating and maintaining sleep, and excessive somnolence scales were associated with poorer everyday memory and greater fatigue.ConclusionsChildren with moderate to severe TBI experience ongoing sleep disturbances for years post-injury. Greater sleep disturbances are associated with worse functional outcomes. Further research into sleep disturbances and development of treatments is important, as it could improve the outcomes of children with TBI.     

Recovery of content and temporal order memory for performed activities following moderate to severe traumatic brain injury

Few studies have investigated the complex nature of everyday activity memory following traumatic brain injury (TBI). This study examined recovery of content and temporal order memory for performed activities during the first year in individuals who suffered moderate to severe TBI. TBI and control participants completed eight different cognitive activities at baseline (i.e., acutely following injury for TBI) and then again approximately one year later (follow-up). Participants' free recall of the activities provided a measure of content memory. Temporal order memory was assessed with a reconstruction task. Self-report and informant report of everyday memory problems at follow-up were used to examine the relationship between activity memory performances and everyday memory. TBI participants showed significant recovery in both content and temporal order memory for activities during the first year. Despite showing significant recovery, the TBI group's activity memory performances remained poorer than that of controls at follow-up. Greater self- and informant report of everyday memory difficulties was associated with poorer temporal order memory but not content memory for activities. These findings demonstrate recovery in multiple memory processes that support activity memory following moderate to severe TBI. The findings also suggest a stronger link between everyday memory abilities and temporal order memory for activities than activity memory content in a TBI population.     

Depression in children and adolescents in the first 6 months after traumatic brain injury

The objective was to assess the nature, rate, predictive factors, and neuroimaging correlates of novel (new-onset) depressive disorders, both definite and subclinical, after traumatic brain injury (TBI). Children with TBI from consecutive admissions were enrolled and studied with psychiatric interviews soon after injury (baseline), and again 6 months post-injury. Novel definite/subclinical depressive disorders at 6-month follow up occurred in 11% (n=15) of the children and subsets of children with non-anxious depression (n=9) and anxious depression (n=6) were identified. Novel definite/subclinical depressive disorder was significantly associated with older age at the time of injury, family history of anxiety disorder, left inferior frontal gyrus (IFG) lesions, and right frontal white matter lesions. Non-anxious depressions were associated with older age at injury, left IFG and left temporal pole lesions. Anxious depressions were associated with family history of anxiety disorder, Personality Change due to TBI, right frontal white matter lesions, and left parietal lesions. These findings, which are similar to those reported after adult TBI, identify both similarities and differences in non-anxious and anxious depression following childhood TBI with respect to lesion laterality, genetic factors (in the form of family psychiatric history of anxiety disorder), age at injury, and more generalized affective dysregulation.     

Hippocampus, amygdala and global brain changes 10 years after childhood traumatic brain injury

Traumatic brain injury (TBI) in children results in damage to the developing brain, particularly in severely injured individuals. Little is known, however, of the long-term structural aspects of the brain following childhood TBI. This study investigated the integrity of the brain 10 years post-TBI using magnetic resonance imaging volumetrics in a sample of 49 participants with mild, moderate and severe TBI, evaluated against a normative sample of 20 individuals from a pediatric database with comparable age and gender distribution. Structural integrity was investigated in gray and white matter, and by manually segmenting two regions of interest (hippocampus, amygdala), potentially vulnerable to the effects of childhood TBI. The results indicate that more severe injuries caused a reduction in gray and white brain matter, while all TBI severity levels resulted in increased volumes of cerebrospinal fluid and smaller hippocampal volumes. In addition, enlarged amygdala volumes were detected in severely injured patients compared to their mild and moderate counterparts, suggesting that childhood TBI may disrupt the development of certain brain regions through diffuse pathological changes. The findings highlight the lasting impact of childhood TBI on the brain and the importance of monitoring brain structure in the long-term after early injury.     

New onset obsessive-compulsive symptoms in children and adolescents with severe traumatic brain injury

Traumatic brain injury (TBI) constitutes a major source of psychiatric morbidity and disability. This study examines new onset of obsessions and compulsions (OCS) within 1 year of severe pediatric TBI. Eighty children and adolescents ages 6-18 years with severe TBI were interviewed by a child psychiatrist using the Diagnostic Interview for Children and Adolescents-Revised to diagnose OCS and comorbidities. A brain magnetic resonance imaging used a 1.5 T scanner 3 months after injury with a T1-weighted spoiled gradient-recalled-echo sequence to provide high spatial resolution and T1- and T2(*)-contrast sensitivity. Race, sex, socioeconomic status, psychosocial adversity, and injury severity were used to predict new onset OCS. Psychiatric comorbidities and brain lesion volumes in orbitofrontal, mesial prefrontal, temporal lobe, basal ganglia, and thalamus were examined in relation to new onset OCS. Twenty-one children (21/72, 29.2%) had OCS after TBI. Most common were worries about disease, cleanliness, and inappropriate actions as well as excessive cleaning, doing things a certain way and ordering. Anxiety disorders, mania, dysthymia, depressive symptoms, and posttraumatic stress disorder were significantly associated with new onset OCS. Injury severity was not associated with new onset OCS. Greater psychosocial adversity (P=0.009), and being female (P=0.005) were associated with OCS while mesial prefrontal and temporal lobe lesions were associated with new onset obsessions (P<0.05). OCS are common after severe pediatric TBI and are associated with greater comorbidities. New onset obsessions are associated with female sex, psychosocial adversity, and mesial prefrontal and temporal lesions.     

Functional outcome in TBI II: verbal memory and information processing speed mediators

Following traumatic brain injury (TBI), patients often report memory difficulties, as well as reduced information processing speed. However, it remains unclear the extent to which these deficits contribute to functional impairment. In the present study, we compared the relative contribution of verbal memory and information processing speed to functional impairment at 12-month post-injury, in 87 patients with moderate-to-severe TBI. Employing structural equation modeling, we found that information processing speed, but not verbal memory functions, significantly mediated the relationship between TBI severity and post-TBI adaptive functioning. These findings suggest that despite the pervasive memory complaints among patients with TBI, it is the impact of neurotrauma on frontal systems that appears to be primarily responsible for patients' difficulties in social and occupational functioning.     

Memory Dysfunctions after Mild and Moderate Traumatic Brain Injury : Comparison between Patients with and without Frontal Lobe Injury

Objective

The purpose of this study was to assess memory dysfunction in patients with mild and moderate traumatic brain injury (TBI) with and without frontal lobe injury (FLI).

Methods

The subjects were 110 TBI patients, who had recovered from the acute clinical phase, and comprised 20 (18.2%) mild TBI (MTBI) patients with FLI, 16 (14.5%) MTBI patients without FLI, 51 (46.4%) moderate TBI (MOTBI) patients with FLI and 23 (20.9%) MTBI patients without FLI. All patients were administrated the Korean version of the Memory Assessment Scale (K-MAS).

Results

Almost all the Summary Scale scores on the K-MAS failed to show any differences between TBI patients with and without FLI, but differences did emerge by types at severities. TBI patients with FLI showed higher Global Memory ability than TBI patients without FLI if their TBI was only mild, but when their TBI was more severe, this finding was reversed, and TBI patients with FLI showed lower Verbal and Global Memory abilities than TBI patients without FLI.

Conclusion

Different kinds of assessment tools are needed for the measurement of memory abilities in TBI patients with FLI, and that the selection of the appropriate tool depends on the severity of the TBI.     

Relationship of calpain-mediated proteolysis to the expression of axonal and synaptic plasticity markers following traumatic brain injury in mice

The role of neuronal plasticity and repair on the final functional outcome following traumatic brain injury (TBI) remains poorly understood. Moreover, the relationship of the magnitude of post-traumatic secondary injury and neurodegeneration to the potential for neuronal repair has not been explored. To address these questions, we employed Western immunoblotting techniques to examine how injury severity affects the spatial and temporal expression of markers of axonal growth (growth-associated protein GAP-43) and synaptogenesis (pre-synaptic vesicular protein synaptophysin) following either moderate (0.5 mm, 3.5 M/s) or severe (1.0 mm, 3.5 M/s) lateral controlled cortical impact traumatic brain injury (CCI-TBI) in young adult male CF-1 mice. Moderate CCI increased GAP-43 levels at 24 and 48 h post-insult in the ipsilateral hippocampus relative to sham, non-injured animals. This increase in axonal plasticity occurred prior to maximal hippocampal neurodegeneration, as revealed by de Olmos silver staining, at 72 h. However, moderate CCI-TBI did not elevate GAP-43 expression in the ipsilateral cortex where neurodegeneration was extensive by 6 h post-TBI. In contrast to moderate injury, severe CCI-TBI failed to increase hippocampal GAP-43 levels and instead resulted in depressed GAP-43 expression in the ipsilateral hippocampus and cortex at 48 h post-insult. In regards to injury-induced changes in synaptogenesis, we found that moderate CCI-TBI elevated synaptophysin levels in the ipsilateral hippocampus at 24, 48, 72 h and 21 days, but this effect was not present after severe injury. Together, these data highlights the adult brain's ability for axonal and synaptic plasticity following a focal cortical injury, but that severe injuries may diminish these endogenous repair mechanisms. The differential effects of moderate versus severe TBI on the post-traumatic plasticity response may be related to the calpain-mediated proteolytic activity occurring after a severe injury preventing increased expression of proteins required for plasticity. Supporting this hypothesis is the fact that GAP-43 is a substrate for calpain along with our data demonstrating that calpain-mediated degradation of the cytoskeletal protein, alpha-spectrin, is approximately 10 times greater in ipsilateral hippocampal tissue following severe compared to moderate CCI-TBI. Thus, TBI severity has a differential effect on the injury-induced neurorestorative response with calpain activation being one putative factor contributing to neuroregenerative failure following severe CCI-TBI. If true, then calpain inhibition may lead to both neuroprotective effects and an enhancement of neuronal plasticity/repair mechanisms post-TBI.     

Longitudinal outcome and recovery of social problems after pediatric traumatic brain injury (TBI): Contribution of brain insult and family environment

Pediatric traumatic brain injury (TBI) can result in a range of social impairments, however longitudinal recovery is not well characterized, and clinicians are poorly equipped to identify children at risk for persisting difficulties. Using a longitudinal prospective design, this study aimed to evaluate the contribution of injury and non-injury related risk and resilience factors to longitudinal outcome and recovery of social problems from 12- to 24-months post-TBI. 78 children with TBI (injury age: 5.0–15.0 years) and 40 age and gender-matched typically developing (TD) children underwent magnetic resonance imaging including a susceptibility-weighted imaging (SWI) sequence 2–8 weeks post-injury (M = 39.25, SD = 27.64 days). At 12 and 24-months post- injury, parents completed questionnaires rating their child’s social functioning, and environmental factors including socioeconomic status, caregiver mental health and family functioning. Results revealed that longitudinal recovery profiles differed as a function of injury severity, such that among children with severe TBI, social problems significantly increased from 12- to 24-months post-injury, and were found to be significantly worse than TD controls and children with mild and moderate TBI. In contrast, children with mild and moderate injuries showed few problems at 12-months post-injury and little change over time. Pre-injury environment and SWI did not significantly contribute to outcome at 24-months, however concurrent caregiver mental health and family functioning explained a large and significant proportion of variance in these outcomes. Overall, this study shows that longitudinal recovery profiles differ as a function of injury severity, with evidence for late-emerging social problems among children with severe TBI. Poorer long-term social outcomes were associated with family dysfunction and poorer caregiver mental health at 24-months post injury, suggesting that efforts to optimize the child’s environment and bolster family coping resources may enhance recovery of social problems following pediatric TBI.     

Fatigue in the first year after traumatic brain injury: course,relationship with injury severity,and correlates

ABSTRACT

The objectives of this study were to document the evolution of fatigue in the first year after traumatic brain injury (TBI), and to explore correlates of fatigue. Participants were 210 adults who were hospitalised following a TBI. They completed questionnaires 4, 8, and 12 months post-injury, including the Multidimensional Fatigue Inventory (MFI). Participants with severe TBI presented greater mental and physical fatigue, and reduced activity compared to participants with moderate TBI. For all MFI subscales except reduced motivation, the general pattern was a reduction of fatigue levels over time after mild TBI, an increase of fatigue after severe TBI, and stable fatigue after moderate TBI. Fatigue was significantly associated with depression, insomnia, cognitive difficulties, and pain at 4 months; the same variables and work status at 8 months; and depression, insomnia, cognitive difficulties, and work status at 12 months. These findings suggest that injury severity could have an impact on the course of fatigue in the first year post-TBI. Depression, insomnia, and cognitive difficulties remain strong correlates of fatigue, while for pain and work status the association with fatigue evolves over time. This could influence the development of intervention strategies for fatigue, implemented at specific times for each severity subgroup.     

Disorders of Mood After Traumatic Brain Injury

Traumatic brain injury (TBI) of any severity can result in broad and persisting biopsychosocial sequelae. Post-TBI sequelae impact, to varying degrees, a person's ability to function at home and work, leading to added emotional distress. It is in the context of these biological, interpersonal, and social disruptions that mood disorders can arise. Mood disorders after TBI occur at a greater frequency than in the general population, with estimates approaching 25% to 50% for major depression, 15% to 30% for dysthymia, and 9% for mania. Post-TBI depression and mania appear to embrace a symptom presentation that is similar to non-TBI depression and mania, and the symptoms can be discerned from other neurobehavioral symptoms. TBI-related brain damage consistently involves regions of the brain that are increasingly recognized as important in the regulation of mood, including the frontal cortex, basal ganglia, and temporal lobes. However, there is insufficient information to postulate a specific neuroanatomic model for post-TBI depression and mania. It is the variable nature of TBI-related brain injury, occurring in the context of other relevant factors that limit the ability to make accurate models to predict who will develop a post-TBI mood disorder.