Boyettegordon7448
Post-partum relapse occurred in 31 women (26%). There was no association between obstetric or anaesthetic characteristics and post-partum relapse. Both the occurrence and number of relapses prior to and during pregnancy, and the time between last relapse and delivery, were significantly associated with post-partum relapse in univariate analysis. The occurrence of relapse within the year preceding the pregnancy was the sole independent factor associated with post-partum relapse.
Neuraxial procedures were not associated with increased rate of post-partum relapse; only disease activity prior to pregnancy was predictive of post-partum relapse.
Neuraxial procedures were not associated with increased rate of post-partum relapse; only disease activity prior to pregnancy was predictive of post-partum relapse.
In urgent situations, preoperative full stomach assessment mostly relies on clinical judgment. Our primary objective was to assess the diagnostic performance of clinical judgment for the preoperative assessment of full stomach in urgent patients compared to gastric point-of-care ultrasound (PoCUS). Our secondary objective was to identify risk factors associated with PoCUS full stomach in urgent patients.
We led a prospective observational study at our Hospital, between January and July 2016. Adult patients admitted for urgent surgery were eligible. Patients with altered gastric sonoanatomy, interventions reducing stomach content, impossible lateral decubitus were excluded. Clinical judgment and risk factors of full stomach were collected before gastric PoCUS measurements. Ultrasonographic full stomach was defined by solid contents or liquid volume ≥ 1.5 ml kg
. Diagnostic performance was assessed through sensitivity, specificity, accuracy, positive and negative predictive value.
The prevalence of clinical and PoCUS full stomach in 196 included patients was 29% and 27%, respectively. Positive and negative predictive values were 42% (95% CI 32.3-52.6%) and 79% (95% CI 74.9-83.4%), respectively. Patients with PoCUS full stomach were clinically misdiagnosed in 55% of cases. PoCUS full stomach was associated with abdominal or gynaecological-obstetrical surgery (OR 3.6, 95% CI 1.5-8.8, P < 0.01) but not with fasting durations. Positive solid intake after illness onset with respect to 6-h solid fasting rule was associated with PoCUS low-risk gastric content (OR 0.4, 95% CI 0.2-0.9, P = 0.03).
Clinical judgment showed poor-to-moderate performance in urgent surgical patients for the diagnosis of full stomach. Gastric PoCUS should be used to assess risk of full stomach in this population.
Clinical judgment showed poor-to-moderate performance in urgent surgical patients for the diagnosis of full stomach. Gastric PoCUS should be used to assess risk of full stomach in this population.This study examines changes in synaptic transmission with progression of the chronic epileptic state. Male Sprague-Dawley rats (P40-45) were injected with either saline or pilocarpine. In rats injected with pilocarpine, status epilepticus ensued. Hippocampal slices were cut 20-60 days or 80-110 days post-treatment. Evoked and miniature EPSCs (mEPSCs) were recorded from CA1 pyramidal neurons using whole-cell voltage-clamp. Fiber volleys were also recorded from stratum radiatum. Evoked EPSCs from the pilocarpine-treated cohort showed enhanced amplitudes 20-60 days post-treatment compared to the saline-treated cohort, whereas mEPSCs recorded from the same age group showed no change in event frequency and a slight but significant decrease in mEPSC amplitude distribution. In contrast, comparing evoked EPSCs and mEPSCs recorded 80-110 days after treatment indicated reduced amplitudes from pilocarpine-treated animals compared to controls. mEPSC inter-event interval decreased. This could be explained by a partial depletion of the ready releasable pool of neurotransmitter vesicles in Schaffer collateral presynaptic terminals of the pilocarpine-treated rats. In both saline- and pilocarpine-treated cohorts, concomitant decreases in mEPSC amplitudes as time after treatment progressed suggest that age-related changes in CA1 circuitry may be partially responsible for changes in synaptic transmission that may influence the chronic epileptic state.Pallidal deep brain stimulation (DBS) is an important option for patients with severe dystonias, which are thought to arise from a disturbance in striatal control of the globus pallidus internus (GPi). The mechanisms of GPi-DBS are far from understood. Although a disturbance of striatal function is thought to play a key role in dystonia, the effects of DBS on cortico-striatal function are unknown. We hypothesised that DBS, via axonal backfiring, or indirectly via thalamic and cortical coupling, alters striatal function. We tested this hypothesis in the dtsz hamster, an animal model of inherited generalised, paroxysmal dystonia. Hamsters (dystonic and non-dystonic controls) were bilaterally implanted with stimulation electrodes in the GPi. DBS (130 Hz), and sham DBS, were performed in unanaesthetised animals for 3 h. Synaptic cortico-striatal field potentials, as well as miniature excitatory postsynaptic currents (mEPSC) and firing properties of medium spiny striatal neurones were recorded in brain slice preparations obtained immediately after EPN-DBS. The main findings were as follows a. DBS increased cortico-striatal evoked responses in healthy, but not in dystonic tissue. b. Commensurate with this, DBS increased inhibitory control of these evoked responses in dystonic, and decreased inhibitory control in healthy tissue. c. Further, DBS reduced mEPSC frequency strongly in dystonic, and less prominently in healthy tissue, showing that also a modulation of presynaptic mechanisms is likely involved. d. Cellular properties of medium-spiny neurones remained unchanged. We conclude that DBS leads to dampening of cortico-striatal communication, and restores intrastriatal inhibitory tone.The pathophysiology of extensive cortical tissue destruction observed in hemispheric hypodensity, a severe type of brain injury observed in young children, is unknown. Here, we utilize our unique, large animal model of hemispheric hypodensity with multifactorial injuries and insults to understand the pathophysiology of this severe type of traumatic brain injury, testing the effect of different stages of development. Piglets developmentally similar to human infants (1 week old, "infants") and toddlers (1 month old, "toddlers") underwent injuries and insults scaled to brain volume cortical impact, creation of mass effect, placement of a subdural hematoma, seizure induction, apnea, and hypoventilation or a sham injury while anesthetized with a seizure-permissive regimen. Piglets receiving model injuries required overnight intensive care. https://www.selleckchem.com/products/remodelin.html Hemispheres were evaluated for damage via histopathology. The pattern of damage was related to seizure duration and hemorrhage pattern in "toddlers" resulting in a unilateral hemispheric pattern of damage ipsilateral to the injuries with sparing of the deep brain regions and the contralateral hemisphere.
