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Background: Severe post-caesarean pain remains an important issue associated with persistent pain and postpartum depression. Women's sleep quality prior to caesarean delivery and its influence on postoperative pain and analgesic intake have not been evaluated yet.Methods: Women undergoing caesarean delivery with spinal anaesthesia (bupivacaine 12 mg, fentanyl 20 μg, morphine 100 μg) were evaluated preoperatively for sleep quality using the Pittsburgh Sleep Quality Index (PSQI) questionnaire (PSQI 0-5 indicating good sleep quality, PSQI 6-21 poor sleep quality). Peak and average postoperative pain scores at rest, movement and uterine cramping were evaluated during 24 h using a verbal numerical pain score (VNPS; 0 indicating no pain and 100 indicating worst pain imaginable), and analgesic intake was recorded. Primary outcome was peak pain upon movement during the first 24 h.Results: Seventy-eight of 245 women reported good sleep quality (31.2%; average PSQI 3.5 ± 1.2) and 167 poor sleep quality (68.2%; average PSQI 16.0 ± 3.4; p < 0.001). Women with poor sleep quality had significantly higher peak pain scores upon movement (46.7 ± 28.8 vs. 36.2 ± 25.6, respectively; p = 0.006). With multivariable logistic regression analysis, poor sleep quality significantly increased the risk for severe peak pain upon movement (VNPS ≥70; OR 2.64; 95% CI 1.2-6.0; p = 0.02).Discussion: A significant proportion of women scheduled for caesarean delivery were identified preoperatively as having poor sleep quality, which was associated with more severe pain and increased analgesic intake after delivery. The PSQI score may therefore be a useful tool to predict increased risk for acute post-caesarean pain and higher analgesic requirements, and help tailor anaesthetic management.Significance: Multiple studies have evaluated predictors for severe acute pain after caesarean delivery that may be performed in a clinical setting, however, sleep quality prior to delivery has not been included in predictive models for post-caesarean pain. The PSQI questionnaire, a simple test to administer preoperatively, identified that up to 70% of women report poor sleep quality before delivery, and poor sleep quality was associated with increased post-caesarean pain scores and analgesic intake, indicating that PSQI could help identify preoperatively women at risk for severe pain after caesarean delivery. [ABSTRACT FROM AUTHOR]

Background: Quantitative sensory testing (QST) measures response to painful stimuli and has been used to predict post-caesarean pain. Pain reported upon intravenous cannulation was shown to predict epidural analgesic use and pain intensity during labour. We hypothesized that pain intensity reported by women upon local anaesthesia injection (ILA) for spinal anaesthesia may predict acute pain after caesarean delivery (CD).Methods: In a prospective observational trial, 229 women undergoing elective CD under spinal anaesthesia were enrolled. Using standardized script before ILA, women received ILA (lidocaine 1% 2.5 mL via 25 G needle), and provided an ILA score after the injection [verbal numeric pain scale (VNPS); 0-100]. Demographic data, average, peak pain (at rest, with movement and uterine cramping) and analgesic requests were recorded for the first 24 h.Results: Fourteen percent of women experienced severe pain (VNPS ≥70) upon ILA. Good correlation was noted between ILA and pain scores at rest and upon mobilization during the 24 h following surgery (average resting pain r = 0.529, p < 0.001, average pain at mobilization r = 0.483, p < 0.0001). Severe acute postoperative pain (VNPS ≥70) was predicted by severe ILA pain with a sensitivity of 91.6% and specificity of 93.3%.Conclusion: This is the first study evaluating a clinical measure to predict post-caesarean pain. Our main findings were that 14% of women experience severe pain upon ILA, which was associated with increased pain during the first 24 h. [ABSTRACT FROM AUTHOR]

SCN1A is the most clinically relevant epilepsy gene and is associated with generalized epilepsy and febrile seizure plus (GEFS+) and Dravet syndrome. We postulated that earlier onset of febrile seizures in the febrile seizure (FS) and febrile seizure plus (FS+) phenotypes may occur in the presence of a SCN1A mutation. This was because of the age-related onset of Dravet syndrome, which typically begins in the first year of life. We found that patients with FS and FS+ with SCN1A mutations had earlier median onset of febrile seizures compared to the population median. Patients with GABRG2 mutations had a similar early onset in contrast to patients with SCN1B mutations where onset was later. This study is the first to demonstrate that a specific genetic abnormality directly influences the FS and FS+ phenotype in terms of age of onset. [ABSTRACT FROM AUTHOR]

Purpose: In families with idiopathic generalized epilepsy (IGE), multiple IGE subsyndromes may occur. We performed a genetic study of IGE families to clarify the genetic relation of the IGE subsyndromes and to improve understanding of the mode(s) of inheritance. Methods: Clinical and genealogic data were obtained on probands with IGE and family members with a history of seizures. Families were grouped according to the probands' IGE subsyndrome: childhood absence epilepsy (CAE), juvenile absence epilepsy (JAE), juvenile myoclonic epilepsy (JME), and IGE with tonic-clonic seizures only (IGE-TCS). The subsyndromes in the relatives were analyzed. Mutations in genes encoding α1 and γ2 γ,-aminobutyric acid (GABA)-receptor subunits, α1 and β1 sodium channel subunits, and the chloride channel CLC-2 were sought. Results: Fifty-five families were studied. 122 (13%) of 937 first- and second-degree relatives had seizures. Phenotypic concordance within families of CAE and JME probands was 28 and 27%, respectively. JAE and IGE-TCS families had a much lower concordance (10 and 13%), and in the JAE group, 31% of relatives had CAE. JME was rare among affected relatives of CAE and JAE probands and vice versa. Mothers were more frequently affected than fathers. No GABA-receptor or sodium or chloride channel gene mutations were identified. Conclusions: The clinical genetic analysis of this set of families suggests that CAE and JAE share a close genetic relation, whereas JME is a more distinct entity. Febrile seizures and epilepsy with unclassified tonic-clonic seizures were frequent in affected relatives of all IGE individuals, perhaps representing a nonspecific susceptibility to seizures. A maternal effect also was seen. Our findings are consistent with an oligogenic model of inheritance. [ABSTRACT FROM AUTHOR]