Traumatic Brain Injury

Physiological monitoring of the severe traumatic brain injury patient in the intensive care unit

Authors: Le Roux P.

Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Despite encouraging animal research, pharmacological agents and neuroprotectants have disappointed in the clinical environment. Current TBI management therefore is directed towards identification, prevention, and treatment of secondary cerebral insults that are known to exacerbate outcome after injury. This strategy is based on a variety of monitoring techniques that include the neurological examination, imaging, laboratory analysis, and physiological monitoring of the brain and other organ systems used to guide therapeutic interventions. Recent clinical series suggest that TBI management informed by multimodality monitoring is associated with improved patient outcome, in part because care is provided in a patient-specific manner. In this review we discuss physiological monitoring of the brain after TBI and the emerging field of neurocritical care bioinformatics.

The Expression Changes of Cystathionine-β-synthase in Brain Cortex After Traumatic Brain Injury

Authors: Zhang M, Shan H, Wang Y, Wang T, Liu W, Wang L, Zhang L, Chang P, Dong W, Chen X, Tao L.

Cystathionine-β-synthase (CBS) catalyzes the condensation of serine with homocysteine to form cystathionine and occupies a crucial regulatory position between the methionine cycle and the biosynthesis of cysteine by transsulfuration. It was reported that CBS was a novel marker of both differentiation and proliferation for certain cell types, suggesting that CBS represents a survival-promoting protein. However, its expression and function in the central nervous system lesion are not well understood. To investigate changes of CBS after traumatic brain injury (TBI) and its possible role, mice TBI model was established by controlled cortical impact system, and the expression and cellular localization of CBS after TBI was investigated in the present study. Western blot analysis revealed that CBS was present in normal mice brain cortex. It gradually decreased, reached a valley at the third day after TBI, and then restored to basal level. Importantly, more CBS was colocalized with neuron. In addition, Western blot detection showed that the third day postinjury was also the apoptosis peak indicated by the elevated expression of caspase-3. Importantly, immunohistochemistry analysis revealed that injury-induced expression of CBS was colabeled by Bcl-2 and had no co-localization with caspase-3. These data suggested that CBS may be implicated in the apoptosis of neuron and involved in the pathophysiology of brain after TBI.

Blast traumatic brain injury in the rat using a blast overpressure model

Authors: Yarnell AM, Shaughness MC, Barry ES, Ahlers ST, McCarron RM, Grunberg NE.

Traumatic brain injury (TBI) is a serious health concern for civilians and military populations, and blast-induced TBI (bTBI) has become an increasing problem for military personnel over the past 10 years. To understand the biological and psychological effects of blast-induced injuries and to examine potential interventions that may help to prevent, attenuate, and treat effects of bTBI, it is valuable to conduct controlled animal experiments. This unit discusses available paradigms to model traumatic brain injury in animals, with an emphasis on the relevance of these various models to study blast-induced traumatic brain injury (bTBI). This paper describes the detailed methods of a blast overpressure (BOP) paradigm that has been used to conduct experiments with rats to model blast exposure. This particular paradigm models the pressure wave created by explosions, including improvised explosive devices (IEDs). Curr. Protoc. Neurosci. 62:9.41.1-9.41.14. © 2013 by John Wiley & Sons, Inc.

Reduced complexity of intracranial pressure observed in short time series of intracranial hypertension following traumatic brain injury in adults

Authors: Soehle M, Gies B, Smielewski P, Czosnyka M.

Physiological parameters, such as intracranial pressure (ICP), are regulated by interconnected feedback loops, resulting in a complex time course. According to the decomplexification theory, disease is characterised by a loss of feedback loops resulting in a reduced complexity of the time course of physiological parameters. We hypothesized that complexity of the ICP time series is decreased during periods of intracranial hypertension (IHT) following adult traumatic brain injury. In an observational retrospective cohort study, ICP was continuously monitored using intraparenchymally implanted probes and stored using ICM + -software. Periods of IHT (ICP > 25 mmHg for at least 1,024 s), were compared with preceding periods of intracranial normotension (ICP < 20 mmHg) and analysed at 1 s-intervals. ICP data (length = 1,024 s) were normalised (mean = 0, SD = 1) and complexity was estimated using the scaling exponent α (as derived from detrended fluctuation analysis), sample entropy (SampEn, m = 1, r = 0.2 × SD) and multiscale entropy. 344 episodes were analysed in 22 patients. During IHT (ICP = 31.7 ± 7.8 mmHg, mean ± SD), α was significantly elevated (α = 1.02 ± 0.22, p < 0.001) and SampEn significantly reduced (SampEn = 1.45 ± 0.46, p = 0.004) as compared to before IHT (ICP = 15.7 ± 3.2 mmHg, α = 0.81 ± 0.14, SampEn = 1.81 ± 0.24). In addition, MSE revealed a significantly (p < 0.05) decreased entropy at scaling factors ranging from 1 to 10. Both the increase in α as well as the decrease in SampEn and MSE indicate a loss of ICP complexity. Therefore following traumatic brain injury, periods of IHT seem to be characterised by a decreased complexity of the ICP waveform.

Dietary omega-3 deficiency from gestation increases spinal cord vulnerability to traumatic brain injury-induced damage

Authors: Ying Z, Feng C, Agrawal R, Zhuang Y, Gomez-Pinilla F.

Although traumatic brain injury (TBI) is often associated with gait deficits, the effects of TBI on spinal cord centers are poorly understood. We seek to determine the influence of TBI on the spinal cord and the potential of dietary omega-3 (n-3) fatty acids to counteract these effects. Male rodents exposed to diets containing adequate or deficient levels of n-3 since gestation received a moderate fluid percussion injury when becoming 14 weeks old. TBI reduced levels of molecular systems important for synaptic plasticity (BDNF, TrkB, and CREB) and plasma membrane homeostasis (4-HNE, iPLA2, syntaxin-3) in the lumbar spinal cord. These effects of TBI were more dramatic in the animals exposed to the n-3 deficient diet. Results emphasize the comprehensive action of TBI across the neuroaxis, and the critical role of dietary n-3 as a means to build resistance against the effects of TBI.

Cognitive, affective, and conative theory of mind (ToM) in children with traumatic brain injury

Authors: Dennis M, Simic N, Bigler ED, Abildskov T, Agostino A, Taylor HG, Rubin K, Vannatta K, Gerhardt CA, Stancin T, Yeates KO.

We studied three forms of dyadic communication involving theory of mind (ToM) in 82 children with traumatic brain injury (TBI) and 61 children with orthopedic injury (OI): Cognitive (concerned with false belief), Affective (concerned with expressing socially deceptive facial expressions), and Conative (concerned with influencing another's thoughts or feelings). We analyzed the pattern of brain lesions in the TBI group and conducted voxel-based morphometry for all participants in five large-scale functional brain networks, and related lesion and volumetric data to ToM outcomes. Children with TBI exhibited difficulty with Cognitive, Affective, and Conative ToM. The perturbation threshold for Cognitive ToM is higher than that for Affective and Conative ToM, in that Severe TBI disturbs Cognitive ToM but even Mild-Moderate TBI disrupt Affective and Conative ToM. Childhood TBI was associated with damage to all five large-scale brain networks. Lesions in the Mirror Neuron Empathy network predicted lower Conative ToM involving ironic criticism and empathic praise. Conative ToM was significantly and positively related to the package of Default Mode, Central Executive, and Mirror Neuron Empathy networks and, more specifically, to two hubs of the Default Mode Network, the posterior cingulate/retrosplenial cortex and the hippocampal formation, including entorhinal cortex and parahippocampal cortex.

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