Articles: traumatic-brain-injuries.
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Brain injury : [BI] · Jan 2017
Temporal profile of care following mild traumatic brain injury: predictors of hospital admission, follow-up referral and six-month outcome.
To investigate the clinical management and medical follow-up of patients with mild traumatic brain injury (mTBI) presenting to emergency departments (EDs). ⋯ Clinical factors modulate triage to admission, while demographic/socioeconomic elements modulate follow-up care acquisition; six-month functional disability associates with both clinical and demographic/socioeconomic variables. Improving triage to acute and outpatient care requires further investigation to optimize resource allocation and outcome after mTBI. ClinicalTrials.gov registration: NCT01565551.
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The Western Cape Province of South Africa has a great shortage of diagnostic expertise, rehabilitative infrastructure, and support services for patients with traumatic brain injury (TBI). The neurosurgical outpatient setting is busy and often chaotic, and patients are frequently lost to follow-up. This study sought to continue with the design and development of a comprehensive, yet brief tool to aid patient referrals and ensure that no consequence of TBI is left unidentified and unaddressed. ⋯ The findings further highlight the prevalence of the cognitive, behavioral, and psychological consequences of TBI and shed additional light on the particular types of problems that patients with TBI face. Following the identified changes, the questionnaire and algorithm combination are now ready to be validated in the neurosurgical clinical setting.
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The delayed diagnosis of adrenal insufficiency is relatively common because its symptoms are non-specific. One of the causes of adrenal insufficiency is isolated adrenocorticotropic hormone deficiency (IAD), which is sometimes caused by traumatic brain injury. ⋯ However, the relationship between milder head trauma-such as chronic subdural hematoma - and the occurrence of hormonal deficiency is uncertain. We herein report the case of a 79-year-old man with IAD who presented with leg edema and pain in his extremities following a recent history of chronic subdural hematoma.
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Journal of neurotrauma · Jan 2017
Human Mesenchymal Stem Cell Treatment Normalizes Cortical Gene Expression after Traumatic Brain Injury.
Traumatic brain injury (TBI) results in a progressive disease state with many adverse and long-term neurological consequences. Mesenchymal stem cells (MSCs) have emerged as a promising cytotherapy and have been previously shown to reduce secondary apoptosis and cognitive deficits associated with TBI. Consistent with the established literature, we observed that systemically administered human MSCs (hMSCs) accumulate with high specificity at the TBI lesion boundary zone known as the penumbra. ⋯ Pathway analysis using the KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway database revealed that TBI regulated a large number of genes belonging to pathways involved in metabolism, receptor-mediated cell signaling, neuronal plasticity, immune cell recruitment and infiltration, and neurodegenerative disease. Remarkably, hMSC treatment was found to normalize 49% of all genes disrupted by TBI, with notably robust normalization of specific pathways within the categories mentioned above, including neuroactive receptor-ligand interactions (57%), glycolysis and gluconeogenesis (81%), and Parkinson's disease (100%). These data provide evidence in support of the multi-mechanistic nature of stem cell therapy and suggest that hMSC treatment is capable of simultaneously normalizing a wide variety of important molecular pathways that are disrupted by brain injury.
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To discuss the clinical case of a patient with transsynaptic retrograde degeneration (TRD) demonstrated by progressive retinal nerve fiber layer loss documented by serial spectral domain optical coherence tomography secondary to traumatic brain injury after 2 months post-trauma. ⋯ TRD can occur as soon as 2 months after severe TBI with damage posterior to the lateral geniculate nucleus. Progressive RNFL loss can be tracked with SD-OCT, and the rate of thinning may slowly stabilize over time. Visual field defects can improve months after the trauma but may not correspond to the progressive RNFL loss detected by SD-OCT.