Journal of neurotrauma
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Journal of neurotrauma · Jul 2012
Traumatic brain injury in young rats leads to progressive behavioral deficits coincident with altered tissue properties in adulthood.
Traumatic brain injury (TBI) affects many infants and children, and results in enduring motor and cognitive impairments with accompanying changes in white matter tracts, yet few experimental studies in rodent juvenile models of TBI (jTBI) have examined the timeline and nature of these deficits, histologically and functionally. We used a single controlled cortical impact (CCI) injury to the parietal cortex of rats at post-natal day (P) 17 to evaluate behavioral alterations, injury volume, and morphological and molecular changes in gray and white matter, with accompanying measures of electrophysiological function. At 60 days post-injury (dpi), we found that jTBI animals displayed behavioral deficits in foot-fault and rotarod tests, along with a left turn bias throughout their early developmental stages and into adulthood. ⋯ The final lesion constituted only ∼3% of brain volume, and morphological tissue changes were evaluated using MRI, as well as immunohistochemistry for neuronal nuclei (NeuN), myelin basic protein (MBP), neurofilament-200 (NF200), and oligodendrocytes (CNPase). White matter morphological changes were associated with a global increase in MBP immunostaining and reduced compound action potential amplitudes at 60 dpi. These results suggest that brain injury early in life can induce long-term white matter dysfunction, occurring in parallel with the delayed development and persistence of behavioral deficits, thus modeling clinical and longitudinal TBI observations.
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Journal of neurotrauma · Jul 2012
ReviewManagement of cardiovascular disease risk factors in individuals with chronic spinal cord injury: an evidence-based review.
Clinical scenario: A 37-year-old man suffered a complete spinal cord injury (C8, American Spinal Injury Association Impairment Scale [ASIA] score A) 10 years ago in a car accident. Should primary prevention of cardiovascular disease be a priority in this patient? In order to answer this question, we performed a systematic review of the literature to inform an evidence-based clinical review. The objective was to provide a comprehensive and up-to-date review of the clinical management of cardiovascular disease (CVD) and risk factors for individuals with spinal cord injury (SCI). ⋯ These limitations notwithstanding, we present a series of contemporary practice suggestions with regard to CVD event risk modification in SCI patients. For optimal outcomes, health care providers should be cognizant of these heightened CVD risk factors and the resultant increased CVD morbidity and mortality in SCI patients. Despite the absence of high-quality evidence-based treatment strategies, clinicians should re-examine their own CVD risk factor treatment strategies to better reflect contemporary practice in similar high-CVD-event-risk patients and populations.
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Journal of neurotrauma · Jul 2012
Cerebrospinal fluid levels of high-mobility group box 1 and cytochrome C predict outcome after pediatric traumatic brain injury.
High-mobility group box 1 (HMGB1) is a ubiquitous nuclear protein that is passively released from damaged and necrotic cells, and actively released from immune cells. In contrast, cytochrome c is released from mitochondria in apoptotic cells, and is considered a reliable biomarker of apoptosis. Thus, HMGB1 and cytochrome c may in part reflect the degree of necrosis and apoptosis present after traumatic brain injury (TBI), where both are felt to contribute to cell death and neurological morbidity. ⋯ Peak cytochrome c levels were independently associated with abusive head trauma (AHT; 24.29 [1.77-334.03]) and inversely and independently associated with favorable GOS scores (0.42 [0.18-0.99]). In conclusion, increased CSF levels of HMGB1 and cytochrome c were associated with poor outcome after TBI in infants and children. These data are also consistent with the designation of HMGB1 as a "danger signal." Distinctly increased CSF cytochrome c levels in infants and children with AHT and poor outcome suggests that apoptosis may play an important role in this unique patient population.
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Journal of neurotrauma · Jul 2012
Case ReportsBurr-hole drainage for the treatment of acute epidural hematoma in coagulopathic patients: a report of eight cases.
Craniotomy has been accepted as the treatment of choice for the management of acute epidural hematomas (AEDH). However, in practice, it seems possible to evacuate AEDH via a single burr hole instead of the traditional craniotomy in certain circumstances. Among 160 patients with AEDH meeting criteria for evacuation admitted to the emergency and accident division of our center between 2006 and 2009, we found 8 cases of hematoma appearing isodense to brain parenchyma on computed tomography (CT), who had concomitant coagulopathy. ⋯ In all 8 patients, AEDH was evacuated successfully via burr-hole placement over the site of hematoma. The level of consciousness and other symptoms improved within the first day, and no patient required an additional routine craniotomy. For patients with slowly-developing AEDH in the context of impaired coagulation, burr-hole evacuation and drainage might be a less invasive method of treatment compared to conventional craniotomy.
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Journal of neurotrauma · Jul 2012
Traumatic brain injury increased IGF-1B mRNA and altered IGF-1 exon 5 and promoter region epigenetic characteristics in the rat pup hippocampus.
Traumatic brain injury (TBI) is a major cause of acquired cognitive disability in childhood. Such disability may be blunted by enhancing the brain's endogenous neuroprotective response. An important endogenous neuroprotective response is the insulin-like growth factor-1 (IGF-1) mRNA variant, IGF-1B. ⋯ We report for the first time that hippocampal IGF-1B mRNA increased after developmental TBI. We speculate that epigenetic modifications at the P2 and exon 5/ESE regions are important in the regulation of IGF-1B mRNA expression. The exon 5/ESE region may present a means for future therapies to target IGF-1B transcription after TBI.