Journal of neurotrauma
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Journal of neurotrauma · Jul 2017
HYPERTENSION-INDUCED ENHANCED MYOGENIC CONSTRICTION OF CEREBRAL ARTERIES IS PRESERVED AFTER TRAUMATIC BRAIN INJURY.
Traumatic brain injury (TBI) was shown to impair pressure-induced myogenic response of cerebral arteries, which is associated with vascular and neural dysfunction and increased mortality of TBI patients. Hypertension was shown to enhance myogenic tone of cerebral arteries via increased vascular production of 20-hydroxyeicosatrienoic acid (HETE). This adaptive mechanism protects brain tissue from pressure/volume overload; however, it can also lead to increased susceptibility to cerebral ischemia. ⋯ Therefore, we investigated the myogenic responses of isolated middle cerebral arteries (MCA) of normotensive and spontaneously hypertensive rats (SHR) after severe impact acceleration diffuse brain injury. TBI diminished myogenic constriction of MCAs isolated from normotensive rats, whereas the 20-HETE-mediated enhanced myogenic response of MCAs isolated from SHRs was not affected by TBI. These results suggest that the optimal cerebral perfusion pressure values and vascular signaling pathways can be different and, therefore, should be targeted differently in normotensive and hypertensive patients following TBI.
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Journal of neurotrauma · Jul 2017
Repetitive Closed-Head Impact Model of Engineered Rotational Acceleration induces long-term cognitive impairments with persistent astrogliosis and microgliosis in mice.
Repeated mild traumatic brain injury (rmTBI) has been identified by epidemiology as a high-risk factor for dementia at a later stage in life. Animal models to replicate complex features of human rmTBI and/or to evaluate long-term effects on brain function have not been established. In this study, we used a novel closed-head impact model of engineered rotational acceleration (CHIMERA) to investigate the long-term neuropathological and cognitive functional consequences of rmTBI. ⋯ Repeated CHIMERA (rCHIMERA) resulted in motor deficits at 3 days, and in learning and memory impairments that were sustained up to 6 months post injury. GFAP and TNF-α gene expression was increased within a week, whereas astrogliosis and microgliosis were induced starting from day 1 up to 6.5 months after rCHIMERA with upregulated GFAP and Iba-1 protein levels. rCHIMERA also induced APP deposition from day 1 to day 7, but this diminished by 1 month. In conclusion, rCHIMERA produces long-lasting cognitive impairments with astrogliosis and microgliosis in mice, suggesting that rCHIMERA can be a useful animal model to study the long-term complications, as well as the cellular and molecular mechanisms, of human rmTBI.
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Cogniphobia refers to avoidance of mental exertion out of a fear of developing or exacerbating a headache. Headaches are very common after mild traumatic brain injury (mTBI) and often become chronic. Cogniphobia is hypothesized to contribute to poor cognitive test performance and persistent disability in some patients with mTBI. ⋯ Cogniphobia was associated with lower performance on memory testing (but not other cognitive tests), independent of headache severity. Participants who avoided mental exertion also tended to avoid physical activity and traumatic stress triggers. The findings provide preliminary support for the role of cogniphobia in persistent cognitive difficulties after mTBI, and suggest that cogniphobia may reflect a broader avoidant coping style.