No abstract

There is uncertainty about the level of systemic blood pressure required to maintain adequate cerebral oxygen delivery and organ integrity. This prospective, observational study on 35 very low birth weight infants aimed to determine the mean blood pressure (MBP) below which cerebral electrical activity, peripheral blood flow (PBF), and cerebral fractional oxygen extraction (CFOE) are abnormal. Digital EEG, recorded every day on the first 4 d after birth, were analyzed a) by automatic spectral analysis, b) by manual measurement of interburst interval, and c) qualitatively. CFOE and PBF measurements were performed using near-infrared spectroscopy and venous occlusion. MBP was measured using arterial catheters. The median (range) of MBP recorded was 32 mm . The EEG became abnormal at MBP levels below 23 mm Hg: a) the relative power of the delta (0.5-3.5 Hz) frequency band was decreased, b) interburst intervals were prolonged, and c) all four qualitatively abnormal EEG (low amplitude and prolonged interburst intervals) from four different patients were recorded below this MBP level. The only abnormally high CFOE was measured at MBP of 20 mm Hg. PBF decreased at MBP levels between 23 and 33 mm Hg. None of the infants in this study developed cystic periventricular leukomalacia. One infant (MBP, 22 mm Hg) developed ventricular dilatation after intraventricular hemorrhage. The EEG and CFOE remained normal at MBP levels above 23 mm Hg. It would appear that cerebral perfusion is probably maintained at MBP levels above 23 mm Hg. (Pediatr Res 59: 314-319, 2006) S everal authors have described an association between systemic hypotension in premature infants and neurologic morbidity (1-3), and, in some centers, clinical practice is to support blood pressure by inotropes and volume expanders when the MBP level falls below 30 mm Hg. The likely mechanism by which hypotension causes neurologic damage is by diminished oxygen delivery through decreased cerebral perfusion. However, the relationship between MBP and cerebral blood flow is unclear in premature infants (4 -8). Some authors have argued that cerebral blood flow is pressure passive and dependent on MBP in infants between 28 and 39 wk gestation (5,7). Others, who have studied infants between 24 and 34 wk gestation, observed that cerebral blood flow is independent of MBP (4,8). Furthermore, the critical level of MBP at which cerebral perfusion becomes compromised has not been clearly determined.In spite of a lack of evidence linking systemic hypotension to brain damage in very low birth weight infants, it is well known that older subjects lose consciousness when MBP falls to a seriously low level. A change in the level of consciousness may not be recognized in sick newborn infants who are heavily sedated while being ventilated, but it may be associated with recognizable changes in the EEG pattern. Using a cerebral function monitor, Greisen et al. (9) showed that reduced blood flow to the neonatal brain correlated with decreased amplitude of the EEG. There have bee...

Continuous EEG monitoring has not been used widely in neonatal intensive care, especially in the care of extremely premature infants, probably in part because of a lack of a reliable quantitative method. The purpose of this study was to quantify the EEG of the very premature infants just after birth by using spectral analysis and to describe the characteristics of the spectral signal when infants were clinically stable. Digital EEG recordings were performed on 53 infants who were Յ30 wk gestation for 75 min each day during the first 4 d after birth. Artefact was rejected manually after visual inspection of trace. The EEG was analyzed by manual measurement of interburst interval and automatically by spectral analysis using Fast Fourier Transformation. Spectral analysis generated the normal ranges of the relative power of the ␦ (0.5-3.5 Hz), (4 -7.5 Hz), ␣ (8 -12.5 Hz), and ␤ (13-30 Hz) frequency bands, spectral edge frequency, and symmetry. The median (range) relative power of the ␦ band increased significantly from 68% (62-76%) on day 1 to 81% (72-89%) on day 4 (p ϭ 0.001). The interburst intervals became progressively shorter between days 1 [14s (10 -25)] and 3 [8s (6 -12)]; there were no significant differences between days 3 and 4. The relative power of the ␦ band seemed to be the most useful and repeatable spectral measurement for continuous long-term monitoring. However, automatic artefact rejection software needs to be developed before continuous quantitative EEG monitoring can be used in the neonatal intensive care environment. The hemodynamic status of extremely premature infants is particularly labile during the first days after birth. Intensive interventions for such infants are intended to maintain an adequate tissue oxygen supply, particularly to the brain. Because clinical management is aimed at preserving cerebral integrity in these infants, it would be helpful to have some form of continuous neuromonitoring to guide clinical interventions. EEG provides a useful, noninvasive technique for monitoring cerebral electrical activity, and advances in digital technology have made it possible to record high-quality EEG even in an electrically noisy intensive care environment and have done away with the necessity of using large amounts of recording paper. However, interpretation of the EEG is generally considered to be highly specialized, and this is at least one reason that continuous EEG monitoring is not used widely in neonatal intensive care.There are three major issues to be considered for the automatic and reliable analysis of the EEG signal of premature infants and for data to be presented in a manner that is useful to clinicians. First, the EEG of these infants consists predominantly of high-amplitude slow waves (1,2). Bell et al. (3) showed that the relative power of slow waves with frequency Ͻ1 Hz might be as high as 90% in infants at 28 wk gestation. A recent study using DC EEG on infants between 34 and 37 wk gestation found that the spontaneous EEG activity of sleeping preterm infants consiste...

Decreased arterial carbon dioxide tension (PaCO 2 ) results in decreased cerebral blood flow, which is associated with diminished cerebral electrical activity. In such a situation, cerebral fractional oxygen extraction (CFOE) would be expected to increase to preserve cerebral oxygen delivery. This study aimed to determine whether changes in blood gases in infants less than 30 wk' gestation were associated with changes in background electroencephalograms (EEG) and CFOE. Thirty-two very low birth weight infants were studied daily for the first three days after birth. Digital EEG recordings were performed for 75 min each day. CFOE, mean blood pressure and arterial blood gases were measured midway through each recording. EEG was analysed by (a) spectral analysis and (b) manual calculation of interburst interval. Blood pressure, pH and PaCO 2 did not have any effect on the EEG. On day one, only PaCO 2 showed a relationship with the relative power of the delta frequency band (0.5-3.5 Hz) and the interburst interval. The relative power of the delta band remained within normal limits when PaCO 2 was between 24 and 55 mm Hg on day one. There was a negative association between PaCO 2 and CFOE. The associations between PaCO 2 and EEG measurements were strongest on day one, weaker on day two, and absent on day three. The slowing of EEG and increased CFOE at lower levels of PaCO 2 are likely to be due to decreased cerebral oxygen delivery induced by hypocarbia. When PaCO 2 was higher, there was suppression of the EEG. Periventricular leukomalacia is an important cause of neurologic morbidity in very low birth weight infants (1) and has been associated with severe hypocarbia during the first 24 h after birth. This effect of arterial carbon dioxide tension (PaCO 2 ) on the brain is likely to be mediated through its effect on cerebral blood flow, which is decreased by hypocarbia. In such a situation, cerebral fractional oxygen extraction (CFOE) would be expected to increase, as cerebral oxygen delivery is reduced (8). Decreased cerebral oxygen delivery would also be expected to be associated with reduced cerebral electrical activity. A positive relationship between cerebral blood flow and integrated amplitude of the EEG has been demonstrated on a group of infants between 27 and 33 wk' gestation (9). However, no studies have described the relationship between background cerebral electrical activity and PaCO 2 in very low birth weight infants.Electroencephalography provides a noninvasive technique for monitoring cerebral electrical activity. The normal EEG pattern of infants less than 30 wk' gestation is markedly discontinuous and consists of long isoelectric periods called interburst intervals, interspersed with bursts of high voltage and mixed frequency activity (10). Two separate studies have linked adverse neurologic outcome of such infants with an abnormal background EEG activity characterised by prolonged Received February 18, 2004; accepted November 16, 2004

Photosensitivity is reported to occur in approximately 40% of patients with juvenile myoclonic epilepsy. Our experience suggests that the prevalence is higher and may be related to both the duration of intermittent photic stimulation and also the age at which the procedure is undertaken. A two-year retrospective review of all EEGs was undertaken on all children attending a paediatric EEG department to identify those with juvenile myoclonic epilepsy. Photosensitivity was defined as a generalized spike or spike-wave paroxysm occurring at least twice during intermittent photic stimulation. Sixty-one children with a diagnosis of juvenile myoclonic epilepsy with a median age of 13 (range 7-16) years were identified, 55 (90%) of whom were photosensitive. Eighteen of these 55 patients showed photosensitivity only after four minutes of continuous photic stimulation. The prevalence of photosensitivity in juvenile myoclonic epilepsy is likely to be higher than previously reported. When a diagnosis of juvenile myoclonic epilepsy is being considered, the initial diagnostic EEG should include intermittent photic stimulation for up to five minutes, or less if the patient shows evidence of photosensitivity. The identification of photosensitivity may have important management implications.