Reliable markers of neurological tissue injury could serve as biomarkers to assess injury severity, monitor disease resolution or deterioration, direct treatment, prognosticate, and as surrogate end points to help develop novel treatments. Direct markers of cerebral tissue injury are elevated in TBM but have not been examined in detail or in association with markers of inflammation. Inflammatory markers have been studied in TBM however, the extent of inflammation as detected by these markers may not correlate with the extent of cerebral tissue injury. Advanced tools to assess cerebral injury severity and prognosis are lacking. However, these have limited utility several reversible and irreversible factors influence clinical status and imaging findings usually manifest once the damage is already permanent. Quantification of the degree of cerebral injury is inexact: Disease severity is commonly evaluated by clinical and radiologic findings. The consequent raised intracranial pressure (ICP) aggravates the already decreased cerebral blood flow and increases the risk of brain ischemia and infarction. Additionally, it often obstructs the flow of cerebrospinal fluid (CSF), precipitating hydrocephalus. The prolific inflammatory process causes extensive basal subarachnoid exudate and vascular involvement, with external compression, vasospasm, and endovasculitis. The resulting cerebral tissue injury is an important determinant of poor outcome and is considered a consequence of the host immune response. Tuberculous meningitis (TBM) is a severe form of cerebral tuberculosis leading to high rates of death and disability in children. Pediatric tuberculous meningitis, biomarkers, S100B, NSE, GFAP Tuberculomas were associated with elevated interleukin (IL) 12p40, interferon-inducible protein 10, and monocyte chemoattractant protein 1 concentrations, whereas infarcts were associated with elevated tumor necrosis factor α, macrophage inflammatory protein 1α, IL-6, and IL-8. Cerebral infarcts were associated with highest overall neuromarker concentrations and an increasing profile over time. Combined neuromarker concentrations increased over time in patients who died, whereas inflammatory markers decreased. Initial and highest concentrations in week 1 of S100B and NSE were associated with poor outcome, as were highest concentration overall and an increasing profile over time in S100B, NSE, and GFAP. Neuromarkers and inflammatory markers were elevated in CSF on admission and for up to 3 weeks, but not in serum. Seven cases (16%) died and 16 (36%) had disabilities. Data were collected from 44 patients with TBM (cases median age, 3.3 years), 11 fatty filum controls (median age, 2.8 years) and 9 PTB controls (median age, 3.7 years).
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |