Postictal generalized electroencephalographic suppression following electroconvulsive therapy: Temporal characteristics and impact of anesthetic regimen.

OBJECTIVE: Postictal generalized electroencephalographic suppression (PGES) has been defined as electroencephalographic (EEG) activity of less than 10 microvolts following a generalized seizure. PGES is associated with an increased risk of sudden unexplained death in epilepsy, as well as treatment efficacy of electroconvulsive therapy (ECT). We investigated the impact of anesthetic on PGES expression and temporal characteristics. METHODS: We recorded postictal EEG in 50 ECT sessions in 11 patients with treatment resistant depression (ClinicalTrials.gov NCT02761330). For each participant, repeated sessions included either ketamine or etomidate general anesthesia during ECT. An automated algorithm was employed to detect PGES within 5 minutes after seizure termination. RESULTS: PGES was detected in 31/50 recordings, with intermittent epochs recurring up to five minutes after seizure termination. PGES total duration was greater following ketamine than etomidate anesthesia (p = 0.04). PGES expression declined loglinearly as a function of time (r = -0.89, p < 10-4). EEG amplitude during PGES did not vary linearly with time. CONCLUSIONS: PGES can occur intermittently for several minutes following seizure termination. Anesthetic effects should be considered when correlating PGES duration to clinical outcomes. SIGNIFICANCE: Prolonged EEG monitoring several minutes following seizure termination may be necessary to fully evaluate the presence and total duration of PGES.

Urinary retention rates after intravesical onabotulinumtoxinA injection for idiopathic overactive bladder in clinical practice and predictors of this outcome.

AIMS: The purpose of this study was to find the rate of urinary retention in clinical practice after treatment with onabotulinumtoxinA (BTN/A) for refractory overactive bladder (OAB) symptoms and determine factors that predict this outcome. METHODS: This is a retrospective study of BTN/A for treatment of non-neurogenic, refractory OAB symptoms. Patients were analyzed with respect to their first and second BTN/A injections. The primary outcome measure was postoperative urinary retention. Statistical significance was assessed with multivariate logistic regression. RESULTS: Based on inclusion and exclusion criteria, the study population was 160. Mean age was 64 ± 13.2 years and 24% of the patients were men. The rate of urinary retention was 35% (n = 56). For the first BTN/A treatment, multivariate analysis revealed that preoperative PVR (post-void residual volume) (OR 1.27, 95% CI 1.13-1.43, P < 0.001) and preoperative bladder capacity (OR 1.05, 95% CI 1.01-1.08, P = 0.005) were associated with postoperative urinary retention. In patients with a preoperative PVR of ≥100 ml, 94% (n = 17) went into urinary retention. For those who underwent a second BTN/A treatment, preoperative PVR, BTN/A units injected and retention after the first BTN/A were associated with an increased rate of postoperative retention. CONCLUSIONS: Increased preoperative PVR was associated with urinary retention. The retention rate is higher than that reported in recent clinical trials. The inclusion of patients with a preoperative PVR ≥100 ml and a lower threshold to initiate clean intermittent catheterization contributed to this high rate of retention.

KCNE1 enhances phosphatidylinositol 4,5-bisphosphate (PIP2) sensitivity of IKs to modulate channel activity.

Phosphatidylinositol 4,5-bisphosphate (PIP(2)) is necessary for the function of various ion channels. The potassium channel, I(Ks), is important for cardiac repolarization and requires PIP(2) to activate. Here we show that the auxiliary subunit of I(Ks), KCNE1, increases PIP(2) sensitivity 100-fold over channels formed by the pore-forming KCNQ1 subunits alone, which effectively amplifies current because native PIP(2) levels in the membrane are insufficient to activate all KCNQ1 channels. A juxtamembranous site in the KCNE1 C terminus is a key structural determinant of PIP(2) sensitivity. Long QT syndrome associated mutations of this site lower PIP(2) affinity, resulting in reduced current. Application of exogenous PIP(2) to these mutants restores wild-type channel activity. These results reveal a vital role of PIP(2) for KCNE1 modulation of I(Ks) channels that may represent a common mechanism of auxiliary subunit modulation of many ion channels.