Risk factors, management, and outcomes in isolated parafalcine or tentorial subdural hematomas.

INTRODUCTION: Indications for hospitalization in patients with parafalcine or tentorial subdural hematomas (SDH) remain unclear. This study derived and validated a clinical decision rule to identify patients at low risk for complications such that hospitalization can be avoided. METHODS: A multicenter retrospective medical record review of adult patients with parafalcine or tentorial SDHs was completed. The primary outcome was significant injury, defined as injury that led to neurosurgery, discharge to another facility, or death. A multivariable logistic regression was performed to identify variables independently associated with the outcome in the derivation cohort. These variables were then validated on a separate cohort from a different institution abstracted without knowledge of the identified variables. RESULTS: In the derivation cohort, 134 patients with parafalcine/tentorial SDHs were identified. The mean age was 63 ± 19 years with 82 (61%) male. Seventy-one (53%) had significant injuries. Variables independently associated with significant injury included: age over 60, adjusted odds ratio (aOR) 3.46 (95% CI 1.24, 9.62), initial Glasgow Coma Scale score below 15, aOR =7.92 (95% CI 2.78, 22.5), and additional traumatic brain injuries (TBIs) on computerized tomography (CT), aOR =5.97 (95% CI 2.48, 14.4). These three variables had a sensitivity of 71/71 (100%, 95% CI 96, 100%) and specificity of 12/63 (19%, 95% CI 10, 31%). The validation cohort (n = 83) had a mean age of 62 ± 22 years with 50 (60%) male. The three variables had a sensitivity of 36/36 (100%, 95% CI 92, 100%) and specificity of 7/47 (15%, 95% CI 6.2, 28%). All 39 (100%, 95% CI 93, 100%) patients from both cohorts who underwent neurosurgery had additional TBI findings on their CT scan. CONCLUSIONS: Patients with parafalcine/tentorial SDHs who are under 60 years with initial GCS scores of 15 and no addition TBIs on CT are at low risk and may not need hospitalization. Furthermore, patients with isolated parafalcine/tentorial SDHs are unlikely to undergo neurosurgery. Prospective, external validation with a larger sample size is now recommended. STUDY TYPE: Retrospective Cohort Study.

Wounding induces motility in sheets of corneal epithelial cells through loss of spatial constraints: role of heparin-binding epidermal growth factor-like growth factor signaling.

Cellular responses to wounding have often been studied at a molecular level after disrupting cell layers by mechanical means. This invariably results in damage to cells at the edges of the wounds, which has been suggested to be instrumental for initiating wound healing. To test this, we devised an alternative procedure to introduce gaps in layers of corneal epithelial cells by casting agarose strips on tissue culture plates. In contrast to mechanical wounding, removal of the strips did not lead to detectable membrane leakage or to activation of the stress-activated kinase JNK. Nonetheless, cells at the edge underwent the typical morphological transition to a highly motile phenotype, and the gaps closed at rates similar to those of mechanically induced wounds. To allow biochemical analysis of cell extracts, a procedure was devised that makes cell-free surface area acutely available to a large proportion of cells in culture. Rapid activation of the epidermal growth factor receptor (EGFR) was detected by immunoblotting, and the addition of an EGFR-blocking antibody completely abolished wound healing. In addition, wound healing was inhibited by agents that block signaling by the heparin-binding epidermal growth factor-like growth factor (HB-EGF). Cells stimulated with cell-free tissue culture surface released a soluble factor that induced activation of the EGFR, which was distinct from HB-EGF. These studies suggest that the triggering event for the induction of motility in corneal epithelial cells is related to the sudden availability of permissive surface area rather than to mechanical damage, and they demonstrate a central role of signaling through HB-EGF.