Introduction:The variability and complexity of handgrip forces in various modulations were investigated to identify post-stroke changes in force modulation, and extend our understanding of stroke-induced deficits. Methods: Eleven post-stroke subjects and ten age-matched controls performed voluntary grip force control tasks (power-grip tasks) at three contraction levels, and stationary dynamometer holding tasks (stationary holding tasks). Variability and complexity were described with root mean square jerk (RMS-jerk) and fuzzy approximate entropy (fApEn), respectively. Force magnitude, Fugl-Meyer upper extremity assessment and Wolf motor function test were also evaluated. Results: Comparing the affected side with the controls, fApEn was significantly decreased and RMS-jerk increased across the three levels in power-grip tasks, and fApEn was significantly decreased in stationary holding tasks. There were significant strong correlations between RMS-jerk and clinical scales in power-grip tasks. Discussion: Abnormal neuromuscular control, altered mechanical properties, and atrophic motoneurons could be the main causes of the differences in complexity and variability in post-stroke subjects.
Posters 622of sampling were 1500 (370-3660) g, 30 (25-40) wks, 6/91, 54/91 and 3 (2-23) days respectively. Significant correlations between 17-OHP and BW (r = -0.69, p < 0.001) and GA (r= -0.67, p < 0.001) were observed. Median 17-OHP was higher in cases treated with betamethason (85.5 vs 57 umol/L, p< 0.0001). In a multiple regression model, GA remained the only independent variable. To further elaborate the association between betamethason and 17OHP, a case-control (GA) study was performed. No significant difference (paired) in incidence of betamethasone administration was observed (54/91 vs 37/91, p=0.2). Conclusions:Maternal betamethasone administration is associated with raised 17-OHP at screening, but can be explained by the lower gestational age. Gestational age is the only independent variable associated with further raised 17OHP in a cohort of false positive screening samples. Background: Ketanserin, a selective serononin 2 -receptor antagonist, is used for the treatment of severe hypertensive disorders during pregnancy. High concentrations are found in umbilical cord after maternal treatment. However, the effect on the circulation of the infant has not been investigated. KETANSERIN: USE FOR THE TREATMENT OF HYPERTENSIVE DISORDERS DURING PREGNANCY AND THE EFFECT ON THE CIRCULATION OF THE INFANT Methods: From May 2007 through December 2009, we prospectively studied 58 infants who in utero were exposed to ketanserin, by monitoring heart rate and blood pressure during the first 24 hours of life. We analyzed the effect of infant-related, medication-related (cumulative dosage, therapy duration and last dosage rate) and maternal factors. The primary outcome was hypotension.Results: Eight infants (13.8%) became hypotensive during the first eight hours of life with need for treatment. Last dosage rate (p=.005) as well as mean dosage rate of ketanserin (cumulative dosage divided by therapy duration , p=.002) were significantly higher in the group with hypotension. Every hypotensive infant was exposed to a last dosage rate of at least 8mg/hour. Maternal HELLPsyndrome was diagnosed more often in hypotensive compared to normotensive infants (p=.048).Discussion: This study provides evidence that maternal ketanserin use has a blood pressure lowering effect in the infant. The risk of hypotension is determined by the last dosage rate of ketanserin and the co-existence of maternal HELLP-syndrome.Monitoring of blood pressure after delivery only seems necessary when an infant is exposed to a dosage rate of at least 8mg/hour. Observation of the infant during the first 12 hours of life seems to be sufficient to detect problems in blood pressure regulation.
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