Sleep disturbances following mild traumatic brain injury in childhood

OBJECTIVE: To examine objective and subjective reports of sleep disturbance in school-aged children who had sustained mild traumatic brain injury (TBI) at least 6 months prior to the study. METHODS: Eighteen children aged 7-12 years with a history of mild TBI (GCS 13-15. LOC < 15 min) were compared to 30 children with orthopedic injuries using actigraphy and parental and self-report sleep questionnaires. RESULTS: Parents reported greater sleep disturbance in the mild TBI group. No significant differences were found in parental ratings of daytime sleepiness, child-reported sleep difficulties, or objective (actigraph) sleep measures. CONCLUSIONS: The finding of greater parental reports of sleep disturbance following mild TBI 6 months after injury requires greater exploration and future research with a larger sample followed from the point of injury would seem appropriate.     

Long-term behavior problems following pediatric traumatic brain injury: prevalence,predictors, and correlates

OBJECTIVE: To study identified rates of long-term behavior problems in children with traumatic brain injury (TBI) compared to children with only orthopedic injuries and risk factors and correlates for new behavior problems following TBI. METHODS: Sample included children with severe TBI (n = 42), moderate TBI (n = 41), and orthopedic injuries only (ORTHO;n = 50). The baseline assessment measured child behavior, adaptation, and neuropsychological, academic, and family functioning. Follow-ups were conducted at 6 and 12 months and at an extended follow-up a mean of 4 years after injury. RESULTS: The prevalence of caseness, defined as elevated behavior problem ratings, was higher in one or both TBI groups than in the ORTHO group at each follow-up (e.g., 36% of severe TBI group, 22% of moderate TBI group, and 10% of ORTHO group at extended follow-up). Most instances of postinjury-onset caseness at the extended follow-up were evident within the first year after TBI. Predictors were severe TBI, socioeconomic disadvantage, and preinjury behavioral concerns. Concurrent correlates included weakness in working memory and adaptive behavior skills, poorer behavior and school competence, and adverse family outcomes. CONCLUSIONS: Postinjury-onset caseness is persistent, risks are multifactorial, and correlates include child dysfunction and family sequelae.     

Race as a moderator of parent and family outcomes following pediatric traumatic brain injury

OBJECTIVE: To use data from a prospective, longitudinal study to determine whether race moderates parent and family outcomes during the first year following pediatric traumatic brain injuries (TBI). METHOD: Participants included 73 white and 18 black children with moderate to severe TBI and their families, and 32 white and 23 black children with orthopedic injuries only (OI) and their families. Assessments of parent and family functioning occurred shortly after injury (baseline) and at 6- and 12-month follow-ups. RESULTS: Race was a significant moderator of group differences in parental psychological distress and perceived family burden, by and large independent of socioeconomic status. The negative consequences of TBI were relatively less pronounced for parents of black children than for parents of white children at baseline, but became more pronounced at the two follow-ups. Black and white parents differed in preferred coping strategies, which may partially account for their different reactions to their children's injuries. CONCLUSIONS: The sociocultural factors associated with race may moderate the effects of pediatric TBI and OI on parents and families.     

Long-term parental and family adaptation following pediatric brain injury

OBJECTIVE: To determine whether parents of children with traumatic brain injuries (TBI) report increased injury-related burden, distress, and family dysfunction and to examine the effects of attrition on the results. METHODS: Children with severe TBI, moderate TBI, and orthopedic injuries were followed at six time points from baseline to 6 years after injury. Parents completed measures of injury-related burden, psychological distress, and family functioning at each assessment. Mixed model analysis was used to examine long-term changes. RESULTS: Attrition was higher among families in the severe TBI group with lower burden thereby amplifying group differences. The severe TBI group reported higher injury-related burden over time after injury than the other groups. Family functioning was moderated by social resources. Families of children with severe TBI and low resources reporting deteriorating functioning over the follow-up interval. CONCLUSIONS: Although environmental advantages moderate long-term effects on family functioning, families of children with severe TBI experience long-standing injury-related burden.     

Impaired emotional contagion following severe traumatic brain injury

Empathy deficits are widely-documented in individuals after severe traumatic brain injury (TBI). This study examined the relationship between empathy deficits and psychophysiological responsivity in adults with TBI to determine if impaired responsivity is ameliorated through repeated emotional stimulus presentations. Nineteen TBI participants (13 males; 41 years) and 25 control participants (14 males; 31 years) viewed five repetitions of six 2-min film clip segments containing pleasant, unpleasant, and neutral content. Facial muscle responses (zygomaticus and corrugator), tonic heart rate (HR) and skin conductance level (SCL) were recorded. Mean responses for each viewing period were compared to a pre-experiment 2-min resting baseline period. Self-reported emotional empathy was also assessed. TBI participants demonstrated identical EMG response patterns to controls, i.e. an initial large facial response to both pleasant and unpleasant films, followed by habituation over repetitions for pleasant films, and sustained response to unpleasant films. Additionally, an increase in both arousal and HR deceleration to stimulus repetitions was found, which was larger for TBI participants. Compared to controls, TBI participants self-reported lower emotional empathy, and had lower resting arousal, and these measures were positively correlated. Results are consistent with TBI producing impairments in emotional empathy and responsivity. While some normalisation of physiological arousal appeared with repeated stimulus presentations, this came at the cost of greater attentional effort.     

Excessive sleep need following traumatic brain injury: a case–control study of 36 patients

Increased sleep need following traumatic brain injury, referred to in this study as post‐traumatic pleiosomnia, is common, but so far its clinical impact and therapeutic implications have not been characterized. We present a case–control study of 36 patients with post‐traumatic pleiosomnia, defined by an increased sleep need of at least 2 h per 24 h after traumatic brain injury, compared to 36 controls. We assessed detailed history, sleep‐activity patterns with sleep logs and actigraphy, nocturnal sleep with polysomnography and daytime sleep propensity with multiple sleep latency tests. Actigraphy recordings revealed that traumatic brain injury (TBI) patients had longer estimated sleep durations than controls (10.8 h per 24 h, compared to 7.3 h). When using sleep logs, TBI patients underestimated their sleep need. During nocturnal sleep, patients had higher amounts of slow‐wave sleep than controls (20 versus 13.8%). Multiple sleep latency tests revealed excessive daytime sleepiness in 15 patients (42%), and 10 of them had signs of chronic sleep deprivation. We conclude that post‐traumatic pleiosomnia may be even more frequent than reported previously, because affected patients often underestimate their actual sleep need. Furthermore, these patients exhibit an increase in slow‐wave sleep which may reflect recovery mechanisms, intrinsic consequences of diffuse brain damage or relative sleep deprivation.     

Sleep and wake disturbances following traumatic brain injury

Traumatic brain injury (TBI) is a major health concern in industrialised countries. Sleep and wake disturbances are among the most persistent and disabling sequelae after TBI. Yet, despite the widespread complaints of post-TBI sleep and wake disturbances, studies on their etiology, pathophysiology, and treatments remain inconclusive. This narrative review aims to summarise the current state of knowledge regarding the nature of sleep and wake disturbances following TBI, both subjective and objective, spanning all levels of severity and phases post-injury. A second goal is to outline the various causes of post-TBI sleep-wake disturbances. Globally, although sleep-wake complaints are reported in all studies and across all levels of severity, consensus regarding the objective nature of these disturbances is not unanimous and varies widely across studies. In order to optimise recovery in TBI survivors, further studies are required to shed light on the complexity and heterogeneity of post-TBI sleep and wake disturbances, and to fully grasp the best timing and approach for intervention.     

Eliciting parental report following pediatric traumatic brain injury: preliminary findings on the Pediatric Inventory of Neurobehavioral Symptoms.

The current article presents preliminary normative data for the Pediatric Inventory of Neurobehavioral Symptoms (PINS), a parent rating scale consisting of symptoms associated with post-traumatic cerebral dysfunction, such as disinhibition, perseveration, reduced spontaneity, inappropriate affective responses, episodic phenomena, and disruptions of biologic function. Comparison data from a sample of 50 elementary age children who had sustained traumatic brain injury (TBI) reveals significant differences on the PINS total score and each of five subscale scores. Two of the 5 PINS subscales (Episodic Symptoms, Biologic Signs) significantly differentiated the TBI and Attention Deficit Hyperactivity Disorder (n = 35) groups, suggesting that these may be clinical features that distinguish post-traumatic cerebral dysfunction from developmental psychopathology. Despite the need for additional research, the PINS appears to be a promising new measure in advancing our understanding of the neurobehavioral sequelae of pediatric traumatic brain injury.     

Long-term potentiation deficits and excitability changes following traumatic brain injury

The effects of traumatic brain injury (TBI) on hippocampal long-term potentiation (LTP) and cellular excitability were assessed at postinjury days 2, 7, and 15. TBI was induced using a well-characterized central fluid-percussion model. LTP of the Schaffer collateral/commissural system was assessed in vivo in urethane-anesthetized rats. Significant LTP of the population excitatory postsynaptic potential (EPSP) slope was found only in controls, and no recovery to control levels was observed for any postinjury time point. Four measurement parameters reflecting pyramidal cell discharges (population spike) indicated that TBI significantly increased cellular excitability at postinjury day 2: (1) pretetanus baseline recording showed that TBI reduced population spike threshold and latency; (2) tetanic stimulation (400 Hz) increased population spike amplitudes to a greater degree in injured animals than in control animals; (3) tetanus-induced population spike latency shifts were greater in injured cases; and (4) tetanic stimulation elevated EPSP to spike ratios (E-S potentiation) to a greater degree in injured animals. These parameters returned to control levels, as measured on postinjury days 7 and 15. These results suggest that TBI-induced excitability changes persist at least through 2 days postinjury and involve a differential impairment of mechanisms subserving LTP of synaptic efficacy and mechanisms related to action potential generation     

Error-related processing following severe traumatic brain injury: An event-related functional magnetic resonance imaging (fMRI) study

Continuous monitoring of one's performance is invaluable for guiding behavior towards successful goal attainment by identifying deficits and strategically adjusting responses when performance is inadequate. In the present study, we exploited the advantages of event-related functional magnetic resonance imaging (fMRI) to examine brain activity associated with error-related processing after severe traumatic brain injury (sTBI). fMRI and behavioral data were acquired while 10 sTBI participants and 12 neurologically-healthy controls performed a task-switching cued-Stroop task. fMRI data were analyzed using a random-effects whole-brain voxel-wise general linear model and planned linear contrasts. Behaviorally, sTBI patients showed greater error-rate interference than neurologically-normal controls. fMRI data revealed that, compared to controls, sTBI patients showed greater magnitude error-related activation in the anterior cingulate cortex (ACC) and an increase in the overall spatial extent of error-related activation across cortical and subcortical regions. Implications for future research and potential limitations in conducting fMRI research in neurologically-impaired populations are discussed, as well as some potential benefits of employing multimodal imaging (e.g., fMRI and event-related potentials) of cognitive control processes in TBI.     

Autonomic and neural correlates of dysregulated arousal in severe traumatic brain injury

Severe traumatic brain injury (TBI) in adults is associated with abnormalities in arousal and emotional responsivity, which are observed physiologically, behaviourally and via self-report measures. While an accurate measure of physiological arousal is debated, ,  and  have consistently shown an inverse relationship between skin conductance level (SCL), and mean alpha power (alpha) during an eyes-closed resting condition (EC), accompanied by an increase in SCL and corresponding decrease in alpha during eyes-open (EO). Thus, alpha may provide a novel index of autonomic arousal. This study aimed to elucidate the neural and autonomic correlates of arousal disturbances in TBI.     

综合性护理在重症颅脑损伤患者术后护理中的应用

目的：探讨综合性护理在重症颅脑损伤患者术后护理中的应用价值。方法：将60例重症颅脑损伤的患者用随机数字表法分为观察组和对照组,对照组围手术期采用常规护理,观察组术后采用综合护理,比较两组患者的并发症、生命体征、住院时间以及护理满意度。结果：观察组护理后的SOFA、APACHEII评分低于对照组,GCS评分高于对照组,有统计学意义(P<0.05)。观察组的并发症少于对照组,焦虑评分低于对照组,入住ICU、住院时间短于对照组,护理满意度高于对照组,有统计学意义(P<0.05)。结论：综合性护理能减少重症颅脑手术患者术后并发症,改善预后。     

Changes in resting connectivity during recovery from severe traumatic brain injury

In the present study we investigate neural network changes after moderate and severe traumatic brain injury (TBI) through the use of resting state functional connectivity (RSFC) methods. Using blood oxygen level dependent functional MRI, we examined RSFC at 3 and 6 months following resolution of posttraumatic amnesia. The goal of this study was to examine how regional off-task connectivity changes during a critical period of recovery from significant neurological disruption. This was achieved by examining regional changes in the intrinsic, or “resting”, BOLD fMRI signal in separate networks: 1) regions linked to goal-directed (or external-state) networks and 2) default mode (or internal-state) networks. Findings here demonstrate significantly increased resting connectivity internal-state networks in the TBI sample during the first 6 months following recovery. The most consistent finding was increased connectivity in both internal and external state networks to the insula and medial temporal regions during recovery. These findings were dissociable from repeat measurements in a matched healthy control sample.     

Regional difference of reactive astrogliosis following traumatic brain injury revealed by hGFAP-GFP transgenic mice

Reactive astrocytes greatly influence the wound healing and neuronal regeneration processes following brain injury. However, the origin and fate of reactive astrocytes appear to be different depending on the type, severity and duration of brain injury. Using the cryogenic traumatic brain injury model, here we comprehensively addressed the regional differences of reactive astrocytes in the injured cortex. In the proximal region of injury site, NG2-expressing and cytoplasmic Olig2-labeled cells were densely localized 3 days after the injury. Next to this proximal layer, most of reactive astrocytes did not express NG2 but exhibited radial glia-like shape with elongated processes. Accordingly, they expressed the progenitor or radial glial markers, such as vimentin, brain lipid binding protein (BLBP) and the green fluorescent protein (GFP) under the control of the human GFAP (hGFAP) promoter. However, only few glial fibrillary acidic protein (GFAP) expressing astrocytes were found in this layer. Distal to the injury site, most of astrocytes strongly expressed GFAP with hypertonic morphology. At day 15 after injury, all layers expressing GFAP and other marker expressions disappeared, indicating the termination of reactive astrogliosis. Taken together, our data suggest that reactive astrogliosis occurs in a regionally segregated manner in the early phase of brain injury.     

Brief report: sleep in parents of children with autism spectrum disorders

OBJECTIVE: To examine sleep quality and sleep-wake patterns in parents of children with autism spectrum disorders (ASDs) and parents of typically developing (TD) children. METHODS: Thirty-five mothers and 22 fathers completed the Pittsburgh Sleep Quality Index, a 7-day sleep diary, and wore an actigraph for 1 week. RESULTS: Parents of children with ASDs reported poorer sleep quality compared to the TD group. In addition, parents of children with ASDs had objectively different sleep patterns, with an earlier wake time and shorter total sleep time than parents of TD children. Finally, regardless of group, fathers had significantly shorter sleep time compared to mothers. CONCLUSIONS: This study is one of the first to demonstrate poorer sleep quality and shorter sleep quantity in parents of children with ASDs using validated measures of sleep. Future studies should examine the relationship between chronic sleep loss and stress in parents of children with ASDs.     

Genetic and histologic evidence implicates role of inflammation in traumatic brain injury-induced apoptosis in the rat cerebral cortex following moderate fluid percussion injury

Traumatic brain injury (TBI) causes massive brain damage. However, the secondary injury and temporal sequence of events with multiple mechanisms after the insult has not been elucidated. Here, we examined the occurrence of apoptosis and a causal relationship between inflammation and apoptosis in the TBI brain. Following a lateral moderate fluid percussion injury model of TBI in adult rats, microarray analyses detected apparent changes in the expression levels of apoptosis-related genes which revealed time-dependent expression patterns for 23 genes in the lateral cortex. The upregulated 23 genes included inflammatory cytokines such as interleukin 1 (IL-1) α, IL-1β, and tumor necrotic factor (TNF) which immediately increased at 3 h following the injury. Time-dependent gene expression profile analyses showed that apoptosis was subsequently induced following inflammation. These results taken together suggested changes in expression of apoptosis-related genes may be associated with inflammatory response. Accompanying this surge of cell death genes after TBI was a neurostructural pathologic hallmark of apoptosis characterized by leakage of cytochrome c into cytoplasm, DNA fragmentation and apoptotic cells in the lateral cortex of the impacted hemisphere. Caspase-3 positive cells in the TBI brain were initially sporadic after 3 h, but these apoptotic cells subsequently increased and populated the cerebral cortex at 6 and 12 h, and gradually reached a plateau by 48 h. Interestingly, the expression profile of CD68 macrophage labeled cells closely resembled that of apoptotic cells after TBI, including the role of inflammatory signaling pathway in the progression of apoptotic cell death. These results taken together suggest that TBI induced upregulation of apoptosis-related genes, concomitant with the detection of apoptotic brain pathology during the 3-48 h post-injury period, which may be likely mediated by inflammation. Therapies designed at abrogating apoptosis and/or inflammation may prove effective when initiated at this subacute TBI phase.     

Slow wave activity moderates the association between new learning and traumatic brain injury severity

Study ObjectivesSleep–wake complaints and difficulties in making new learning are among the most persistent and challenging long-term sequelea following moderate to severe traumatic brain injury (TBI). Yet, it is unclear whether, and to what extent, sleep characteristics during the chronic stage of TBI contribute to sleep–wake and cognitive complaints. We aimed to characterize sleep architecture in chronic moderate to severe TBI adults and assess whether non-rapid eye movement slow wave activity (SWA) is associated to next day performance in episodic memory tasks according to TBI severity.MethodsForty-two moderate to severe TBI participants, 12–47 months post-injury, and 38 healthy controls were tested with one night of in-laboratory polysomnography, followed the next morning by questionnaires (sleep quality, fatigue, and sleepiness) and neuropsychological assessment. We used multiple regression analyses to assess the moderator effect of SWA power on TBI severity and next-day memory performance.ResultsWe found that TBI participants reported worse sleep quality and fatigue, and had worse cognitive performance than controls. No between group differences were found on macro- and micro-architecture of sleep. However, SWA significantly interacted with TBI severity to explain next-day memory performance: higher SWA was more strongly associated to better memory performance in more severe TBI compared to milder TBI.ConclusionsThis study provides evidence that the injured brain is able to produce macro- and micro-architecture of sleep comparable to what is seen in healthy controls. However, with increasing TBI severity, lower non-rapid eye movement SWA power is associated with reduced ability to learn and memorise new information the following day.     

The influence of attention and arousal on emotion perception in adults with severe traumatic brain injury

Many people with traumatic brain injury (TBI) have poor emotion recognition, with negative emotions more frequently impaired. They can also display abnormal affective responses to emotionally charged material, however, the mechanisms underpinning such deficits are unclear. This study examined whether affective responsivity can be improved by focusing attention and whether responsivity is associated with perception accuracy. Eighteen adults with moderate-to-severe TBI and 18 control participants viewed facial expressions while skin conductance (SCR) and evoked cardiac deceleration (ECD) (used as indices of orientation) and skin conductance levels (SCL) (used as an index of phasic arousal) were monitored. They viewed two blocks of faces (8 angry and 8 happy per block), passively in the first block and with the instruction to identify the emotional expression in the second. No differences between conditions, emotions or groups were found using SCR. Both groups demonstrated increasing ECD for the attend condition relative to the passive condition. For the passive task the control group showed increasing SCL (sensitisation) over trials when viewing angry faces and decreasing SCL (habituation) to happy faces. No differences between emotions were shown for the TBI group who rapidly habituated to both expressions. For the attend task, there was no evidence of habituation for either expression for either the control or TBI participants. Physiological measures did not correlate to accuracy in recognising emotions. The results suggest that increasing attentional demands improves orientation and emotional engagement (arousal) to emotional faces following TBI. However, the relationship to this and emotion perception accuracy remains unclear.