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Medical Sciences	100%

Selected Abstracts

The Relative Influence of Epileptic EEG Discharges, Short Nonconvulsive Seizures, and Type of Epilepsy on Cognitive Function

EPILEPSIA, Issue 1 2004
Albert Aldenkamp
Summary: Purpose: This study addressed whether cognitive impairment in children with epilepsy is caused by disease-related stable factors, such as the type of epilepsy, or by acute effects of paroxysmal epileptic activity such as epileptic EEG discharges. We studied a nonselected group with short nonconvulsive seizures, as these seizures may elude detection and may therefore persist over a longer period. In this group, the diagnostic issue is to differentiate between the combined effects of several epilepsy-related factors on cognition. Methods: All children were assessed with 32-channel EEG, synchronized with a computerized cognitive test system and a video-monitoring system. Recording time was 2 h. The primary inclusion criteria were unclear seizures and fluctuations in cognitive performance and/or frequent epileptic EEG discharges in a recent EEG. Results: One hundred fifty-two patients met the inclusion criteria; 31 patients appeared not to have a diagnosis of epilepsy and were used as a nonepilepsy control group. Our results show that type of epilepsy has an impact on stable cognitive functions, such as educational achievement. Paroxysmal epileptic activity (acute effects of seizures and epileptic EEG discharges) affects primarily transient mechanistic cognitive processes (alertness, mental speed). Conclusions: These results suggest that the effects of paroxysmal epileptic activity on transient cognitive mechanisms may accumulate over time and consequently affect the more stable aspects of cognitive function such as educational achievement. The clinical relevance is that early detection of the cognitive impact of seizure-related activity and subsequent treatment may prevent its detrimental impact on cognitive and educational development. [source]

35 Electrogastrography in healthy participants: comparison of children and adults

NEUROGASTROENTEROLOGY & MOTILITY, Issue 6 2006
CA FRIESEN
The current study examined whether electrogastrogram (EGG) patterns differ between children/adolescents and adults, including whether EGG recordings obtained from healthy children would be considered normal by standards established for adults. Twenty-eight healthy children (54% females; ages 8,17, M = 12.4 years) were evaluated and compared to 15 healthy adults. EGGs were recorded for 30 min in the fasting state and for 1 h following a standard meal. For both pediatric and adult participants, there was a significant increase in both the dominant frequency and the dominant power from the pre- to the post , prandial period (p < 0.001 for each). There was a significant post-prandial increase in the %normal slow waves in pediatric participants only (81.5 vs. 89.0% vs. p < 0.001). Children demonstrated a significantly lower mean fasting %normal slow waves (81.5% vs. 94.2%) and a significantly greater fasting % tachygastria (8.9% vs. 2.3%) than did adults. Other parameters did not differ. Using adult standards, the %normal slow waves were ,70% of recording time in 96% children in the fasting state and in 100% in the postprandial period. A postprandial power increase was seen in 89% of the children. In conclusion, while adults should not be used as controls in pediatric studies of EGG, our data would indicate that American Motility Society (AMS) consensus adult criteria for a normal EGG are appropriate to apply to children and adolescents when utilizing methodology and meal challenge similar to that used to establish the adult norms. [source]

Episodes of hypoxemia during synchronized intermittent mandatory ventilation in ventilator-dependent very low birth weight infants

PEDIATRIC PULMONOLOGY, Issue 1 2005
Steve R.E. Firme MD
Abstract Distinct patterns of asynchrony, and episodes of hypoxemia, may occur in a spontaneously breathing preterm infant during conventional intermittent mandatory ventilation (IMV) on traditional time-cycled, pressure-limited ventilators. Synchronized IMV (SIMV) and assist/control ventilation are frequent modes of patient-triggered ventilation used with infant ventilators. The objective of this study was to use computerized pulse oximetry to quantify the occurrence of episodes of hypoxemia (oxygen desaturation) during SIMV vs. IMV, in preterm infants ,1,250 g who required mechanical ventilation at ,14 days of age. We performed a randomized, crossover study with each infant being randomized to IMV or SIMV (Infant Star ventilator) for initial testing for a 1-hr period. Patients were subsequently tested on the alternate modality after a stabilization period of 10 min at the same ventilator and fractional inspired oxygen concentration (FiO2) settings. Pulse oximetry data were obtained with a Nellcor N-200 monitor, a microcomputer, and a software program (SatMaster). An investigator blinded to the randomized assignment evaluated all measurements. Eighteen very low birth weight (VLBW) infants with a birth weight of 777,±,39 g (mean,±,SEM) and gestational age 25.1,±,0.3 weeks were studied. The average pulse oximeter oxygen saturation (SaO2) was higher on SIMV than IMV (P,<,0.01). During SIMV, these infants had significantly fewer episodes of hypoxemia (duration of episodes of oxygen desaturation as a percentage of scorable recording time) to 86,90% SaO2 (P,<,0.01), 81,85% SaO2 (P,<,0.01), and 76,80% SaO2 (P,<,0.05) when compared to IMV. There was also a significant decrease in percentage of time of desaturation to SaO2,<,90% (P,=,0.002),,<,85% SaO2 (P,=,0.003), and <80% SaO2 (P,=,0.02) during SIMV vs. IMV. Our preliminary findings indicate that the use of SIMV in a population of VLBW ventilator-dependent infants (,14 days of age) results in better oxygenation and decreased episodes of hypoxemia as compared to IMV. © 2005 Wiley-Liss, Inc. [source]

Recurrent spreading depolarizations after subarachnoid hemorrhage decreases oxygen availability in human cerebral cortex

ANNALS OF NEUROLOGY, Issue 5 2010
Bert Bosche MD
Objective Delayed ischemic neurological deficit (DIND) contributes to poor outcome in subarachnoid hemorrhage (SAH) patients. Because there is continuing uncertainty as to whether proximal cerebral artery vasospasm is the only cause of DIND, other processes should be considered. A potential candidate is cortical spreading depolarization (CSD)-induced hypoxia. We hypothesized that recurrent CSDs influence cortical oxygen availability. Methods Centers in the Cooperative Study of Brain Injury Depolarizations (COSBID) recruited 9 patients with severe SAH, who underwent open neurosurgery. We used simultaneous, colocalized recordings of electrocorticography and tissue oxygen pressure (ptiO2) in human cerebral cortex. We screened for delayed cortical infarcts by using sequential brain imaging and investigated cerebral vasospasm by angiography or time-of-flight magnetic resonance imaging. Results In a total recording time of 850 hours, 120 CSDs were found in 8 of 9 patients. Fifty-five CSDs (,46%) were found in only 2 of 9 patients, who later developed DIND. Eighty-nine (,75%) of all CSDs occurred between the 5th and 7th day after SAH, and 96 (80%) arose within temporal clusters of recurrent CSD. Clusters of CSD occurred simultaneously, with mainly biphasic CSD-associated ptiO2 responses comprising a primary hypoxic and a secondary hyperoxic phase. The frequency of CSD correlated positively with the duration of the hypoxic phase and negatively with that of the hyperoxic phase. Hypoxic phases significantly increased stepwise within CSD clusters; particularly in DIND patients, biphasic ptiO2 responses changed to monophasic ptiO2 decreases within these clusters. Monophasic hypoxic ptiO2 responses to CSD were found predominantly in DIND patients. Interpretation We attribute these clinical ptiO2 findings mainly to changes in local blood flow in the cortical microcirculation but also to augmented metabolism. Besides classical contributors like proximal cerebral vasospasm, CSD clusters may reduce O2 supply and increase O2 consumption, and thereby promote DIND. ANN NEUROL 2010;67:607,617 [source]