Latency to first seizure after temporal lobectomy predicts long-term outcome.

PURPOSE: Temporal lobectomy is a well-established treatment for refractory temporal lobe epilepsy, yet many patients experience at least one seizure postoperatively. Little is known about the prognostic significance of the time from surgery to first seizure relapse in predicting long-term outcome. METHODS: In a retrospective analysis of patients who reported at least one complex partial seizure (CPS) or generalized tonic­clonic seizure (GTCS) after anterior temporal lobectomy (n = 268), we used a nominal response logistic model to predict the odds ratio (OR) of a seizure outcome based on length of the latency period from surgery to first postoperative seizure. A modified Engel outcome class scheme was used. We controlled for factors known to influence postoperative outcome, including history of tonic­clonic seizures, intelligence quotient (IQ), preoperative seizure frequency, magnetic resonance imaging (MRI) findings, and history of febrile convulsions. RESULTS: In the univariate analysis, the latency from surgery to the first postoperative disabling seizure was significantly associated with long-term outcome. Longer latency was associated with higher odds of being seizure-free or improved (modified Engel's classes 1, 2, and 3) relative to the unimproved state (class 4) (p < 0.001, 0.001 and 0.004, respectively). Conversely, a shorter latency increased the likelihood of achieving the worst prognosis (class 4) relative to class 1 (p < 0.001). Multivariate analysis yielded similar results. DISCUSSION: Latency to the first postoperative seizure predicts long-term outcome, with short latencies portending poor prognosis and long latencies portending a good prognosis. This information can be used for patient counseling and may influence decisions regarding reoperation.

Heparin stimulates Staphylococcus aureus biofilm formation.

Heparin, known for its anticoagulant activity, is commonly used in catheter locks. Staphylococcus aureus, a versatile human and animal pathogen, is commonly associated with catheter-related bloodstream infections and has evolved a number of mechanisms through which it adheres to biotic and abiotic surfaces. We demonstrate that heparin increased biofilm formation by several S. aureus strains. Surface coverage and the kinetics of biofilm formation were stimulated, but primary attachment to the surface was not affected. Heparin increased S. aureus cell-cell interactions in a protein synthesis-dependent manner. The addition of heparin rescued biofilm formation of hla, ica, and sarA mutants. Our data further suggest that heparin stimulation of biofilm formation occurs neither through an increase in sigB activity nor through an increase in polysaccharide intracellular adhesin levels. These finding suggests that heparin stimulates S. aureus biofilm formation via a novel pathway.