Serum Amyloid A1/Toll-Like Receptor-4 Axis, an Important Link between Inflammation and Outcome of TBI Patients.

Traumatic brain injury (TBI) is one of the leading causes of mortality and disability worldwide without any validated biomarker or set of biomarkers to help the diagnosis and evaluation of the evolution/prognosis of TBI patients. To achieve this aim, a deeper knowledge of the biochemical and pathophysiological processes triggered after the trauma is essential. Here, we identified the serum amyloid A1 protein-Toll-like receptor 4 (SAA1-TLR4) axis as an important link between inflammation and the outcome of TBI patients. Using serum and mRNA from white blood cells (WBC) of TBI patients, we found a positive correlation between serum SAA1 levels and injury severity, as well as with the 6-month outcome of TBI patients. SAA1 levels also correlate with the presence of TLR4 mRNA in WBC. In vitro, we found that SAA1 contributes to inflammation via TLR4 activation that releases inflammatory cytokines, which in turn increases SAA1 levels, establishing a positive proinflammatory loop. In vivo, post-TBI treatment with the TLR4-antagonist TAK242 reduces SAA1 levels, improves neurobehavioral outcome, and prevents blood-brain barrier disruption. Our data support further evaluation of (i) post-TBI treatment in the presence of TLR4 inhibition for limiting TBI-induced damage and (ii) SAA1-TLR4 as a biomarker of injury progression in TBI patients.

Epidural Lipomatosis and Syringomyelia in Adulthood: Case Report and Literature Review.

BACKGROUND: We review 2 previously published cases of epidural lipomatosis associated with syringomyelia. We also present the case of a 42-year-old woman with a medullary syrinx from C1 to T3, initially only with upper limb paresthesias that presented after 10 years of follow-up for left hemiparesis and paresthesias in the tongue. Chiari malformation and cerebral or spinal space-occupying lesions were ruled out, as were other causes of syrinx except the presence of epidural lipomatosis extending from T1 to T12. CASE DESCRIPTION: Right laminotomies were performed from T1 to T12, removing excessive epidural fat tissue. After surgery the symptoms remained stable. At discharge the patient progressively recovered from the hemiparesis, and in follow-up magnetic resonance imaging the resolution of the syrinx was confirmed. CONCLUSIONS: This is the third case of a patient with a spinal syrinx and no other related causes except from spinal lipomatosis, although with only 3 cases it is not possible to completely state that lipomatosis caused the syrinx. Our case supports the trend established by the 2 previous cases. For treatment, initially patients should be managed conservatively, trying to correct the underlying etiologies of spinal lipomatosis. In case of failed conservative treatment, removal of adipose epidural excess in the most appropriate way is preferred.