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Biomedical subjects

M S Scher

Publications and source records attributed to M S Scher.

At least 19 recordsLinked to original sources

Migraine headaches and sleep disturbances in children.

OBJECTIVE: The aim of the present study was to investigate the prevalence of sleep disturbances in children with migraine headaches and to describe individual differences in sleep behaviors based on headache features (eg, frequency, duration, intensity). BACKGROUND: A relationship between migraine headaches and sleep disturbances has been suggested in both children and adults, but there is a lack of research examining the relationship between specific headache features and the range of sleep behaviors in children. METHODS: One hundred eighteen children, aged 2 to 12 years (mean, 9.1; standard deviation, 2.3) were evaluated for headaches at two pediatric neurology departments. Parents completed the Children's Sleep Habits Questionnaire and a standardized questionnaire regarding headache characteristics. RESULTS: Parents reported a high rate of sleep disturbances in children, including sleeping too little (42%), bruxism (29%), child co-sleeping with parents (25%), and snoring (23%). Children with migraine headaches experienced more sleep disturbances compared to published healthy control norms. After controlling for child demographics, we found that the frequency and duration of migraine headaches predicted specific sleep disturbances, including sleep anxiety, parasomnias, and bedtime resistance. CONCLUSIONS: Children with migraine headaches have a high prevalence of sleep disturbances. The direction of the relationship between headaches and sleep is unknown. Regardless, interventions targeting sleep habits may improve headache symptoms, and effective treatment of headaches in children may positively impact sleep.

Child↗

Controversies regarding neonatal seizure recognition.

Recognition and classification of neonatal seizures remain problematic, particularly when clinicians rely only on clinical criteria. Physicians should utilize synchronized video-EEG-polygraphic recordings to correlate suspicious behaviors with electrographic seizures, to help limit misdiagnosis and overtreatment of either normal or abnormal nonepileptic behaviors. Since neonatal seizures, particularly status epilepticus, predict an increased risk for later epilepsy and other neurological sequelae, accurate diagnoses are needed for aggressive antiepileptic drug use in the NICU, as well as family counseling and anticipatory medical care after discharge. Neurophysiological documentation of neonatal seizures also must be integrated with an appreciation of pathophysiological mechanisms responsible for brain lesions that cause seizures. Maternal-fetal-placental diseases, as well as genetic vulnerabilities may be responsible for seizures long before diagnosis in the newborn period. Alternatively, the severity of seizures in neonates with perinatal asphyxia or other etiologies may be independently associated with brain injury. Seizures in the newborn are one of the few, neonatal neurological emergencies. While prompt diagnostic and therapeutic plans are necessary, unresolved medical issues continue to challenge the physician's evaluation of the newborn with suspected seizures (table I) [1-3]. Recognition of the seizure state remains the foremost challenge to overcome. Clinical and electroencephalographic manifestations of neonatal seizures vary dramatically from those of older children. This generalization is underscored by the brevity and subtlety of the clinical repertoire of the newborn's neurological examination. Environmental restrictions surrounding the sick infant in an intensive care setting, including confinement within an isolette, intubation and attachment to multiple catheters limit accessibility. Medication alters arousal and muscle tone, which further limit the clinician's ability to consider these clinical neurological signs as surrogate markers of underlying brain disorders. Brain injury from antepartum factors may later be expressed as neonatal seizures, as part of a postnatal, encephalopathic clinical picture which may only be precipitated by stress during the intrapartum and neonatal periods [4]. Alternatively, medical conditions during parturition or after birth may cause seizures, with coincident injury. For medication options to effectively treat seizures, new agents need to be designed for specific etiologies, timing of injury, and the unique cellular/molecular organization of the immature brain. This review addresses the challenges and controversies regarding neonatal seizure recognition in the context of current clinical practices. Experimental models of neonatal seizures elucidate the pathophysiological mechanisms and adverse consequences of seizures on brain development. Since 20% to 50% of children with neonatal seizures experience later epilepsy, diagnostic accuracy is essential [5, 6], particularly for the newborn who suffers a prolonged seizure state.

Brain↗

Automated detection of tracé alternant during sleep in healthy full-term neonates using discrete wavelet transform.

OBJECTIVE: To develop an automated procedure for scoring neonatal sleep states using signal processing which are based on visual pattern recognition techniques. METHODS: We are developing an automated computer system to study relationships among multiple non-cerebral physiologic measures and brain activity in newborn infants, and are evaluating the usefulness of a number of different time-frequency domain transforms as potential diagnostic tools. RESULTS: Wavelet transforms yield excellent results in the detection of all twenty tracé alternant quiet sleep segments for 6 full-term healthy infants. CONCLUSIONS: We suggest that this method will be useful for the automated detection of neonatal sleep states, and may help delineate when sleep cycle disturbances occur on either an environmental or disease basis. More accurate physiologic descriptions of neonatal state may improve the clinician's ability to assess functional brain organization for a given post-conceptional age as well as document functional brain maturation at progressively older corrected ages.

Algorithms↗

Fetal and neonatal neurologic consultations: identifying brain disorders in the context of fetal-maternal-placental disease.

Pediatric neurologists provide an important consultative role for the fetus or neonate with a suspected brain disorder. Although most consultations are initiated after birth, neonatal neurologic dysfunction may be reflective of fetal brain damage or maldevelopment. Maternal or placental/cord disease states can predispose the fetus or neonate to brain disorders during the antepartum, intrapartum, or early postpartum periods. Neurologists must therefore consider maternal, placental, and fetal conditions on which a neonatal encephalopathy may be superimposed, with or without recent brain injury. This review suggests how the pediatric neurologist can contribute more effectively to fetal and neonatal neurologic evaluations regarding etiologies and mechanisms of brain injury; their role will enhance diagnostic services composed of maternal-fetal specialists, placental and pediatric pathologists, neonatologists, neurosurgeons, geneticists, and other pediatric subspecialists. Selected examples of structural markers during fetal life, and functional markers during neonatal life, illustrate the wide spectrum of disease states that are highly dependent on the timing and location of brain injury. The pediatric neurologist has the opportunity to integrate these complementary lines of investigation into a responsive consultative opinion, which is both medically accurate and ethical, responsible to the welfare of the mother and child.

Adult↗

Effects of prenatal cocaine/crack and other drug exposure on electroencephalographic sleep studies at birth and one year.

OBJECTIVE: Little is known about the neurophysiologic effects of prenatal cocaine/crack use. The aim of this study, designed to overcome methodologic limitations of previous research, was to investigate the effects of prenatal cocaine use on electroencephalographic (EEG) sleep patterns, a marker of central nervous system development. METHODS: In a longitudinal study of prenatal cocaine/crack exposure, women were interviewed at the end of each trimester about cocaine, crack, alcohol, tobacco, marijuana, and other drug use. Two-hour paper- and computer-generated EEG sleep recordings were obtained on a sample of the full-term infants on the second day of life and at 1 year postpartum. Eligible newborns were full-term, had received no general anesthesia, and had a 5-minute Apgar score >5. All infants whose mothers used one or more lines of cocaine during their first trimester or any crack (n = 37) were selected. A comparison group was chosen randomly from the group of women who did not use cocaine or crack during their pregnancy (n = 34). RESULTS: Women who used cocaine/crack during the first trimester were older, less educated, less likely to be working, and used more tobacco, alcohol, marijuana, and other illicit drugs than women who did not use cocaine/crack during the first trimester. There were no differences in infant birth weight, length, head circumference, or gestational age between the two exposure groups. After controlling for the significant covariates, prenatal cocaine exposure was associated with less well developed spectral correlations between homologous brain regions at birth, and with lower spectral EEG power values at 1 year of age. Prenatal alcohol, marijuana, and tobacco use were found to affect state regulation and cortical activities. CONCLUSIONS: These results indicate that the neurotoxic effects of prenatal cocaine/crack use can be detected with quantitative EEG measures.

Adult↗

Phenobarbital compared with phenytoin for the treatment of neonatal seizures.

BACKGROUND: Seizures occur in 1 to 2 percent of neonates admitted to an intensive care unit. The treatment is usually with either phenobarbital or phenytoin, but the efficacy of the two drugs has not been compared directly. METHODS: From 1990 to 1995, we studied 59 neonates with seizures that were confirmed by electroencephalography. The neonates were randomly assigned to receive either phenobarbital or phenytoin intravenously, at doses sufficient to achieve free plasma concentrations of 25 microg per milliliter for phenobarbital and 3 microg per milliliter for phenytoin. Neonates whose seizures were not controlled by the assigned drug were then treated with both drugs. Seizure control was assessed by electroencephalographic criteria. RESULTS: Seizures were controlled in 13 of the 30 neonates assigned to receive phenobarbital (43 percent) and 13 of the 29 neonates assigned to receive phenytoin (45 percent; P=1.00). When combined treatment is considered, seizure control was achieved in 17 (57 percent) of the neonates assigned to receive phenobarbital first and 18 (62 percent) of those assigned to receive phenytoin first (P=0.67). The severity of the seizures was a stronger predictor of the success of treatment than was the assigned agent. Neonates with mild seizures or with seizures that were decreasing in severity before treatment were more likely to have their seizures end, regardless of the treatment assignment. CONCLUSIONS: Phenobarbital and phenytoin are equally but incompletely effective as anticonvulsants in neonates. With either drug given alone, the seizures were controlled in fewer than half of the neonates.

Anticonvulsants↗

Effects of prenatal substance exposure: altered maturation of visual evoked potentials.

We investigated the effects of prenatal substance use on visual evoked potentials (VEPs). Seventy-four children were tested at birth and 1 month of age with binocular flash VEPs and at 4, 8, and 18 months of age with binocular pattern VEPs. Regressions were run by trimester to assess the independent effects of substance exposure. Variables included in the regression model were alcohol, marijuana, tobacco, other drug use for each trimester, maternal age, education, income, race, marital status, infant sex, birthweight, and Dubowitz score. Changes in specific components of the binocular VEP were both substance- and trimester-specific. First trimester alcohol use was associated with prolonged P1 wave latencies at 1 month of age. Prolonged P1 wave latencies at birth and 18 months were associated with tobacco use during each of the three trimesters, at 1 and 18 months with third trimester marijuana use, and at 1 and 18 months with first trimester other illicit drug use. Although these women were moderate substance users during pregnancy, their offspring exhibited maturational changes in components of the VEP in the absence of neonatal behavioral disturbances.

Aging↗

Neonates with electrically confirmed seizures and possible placental associations.

Placental specimens were reviewed from 73 singleton pregnancies of women whose offspring received electroencephalogram (EEG) studies in the neonate period. A group of 43 neonates (postconception age [PCA] 23-44 weeks) with electrically confirmed seizures in the immediate neonate period were compared with 30 healthy preterm and term infants of comparable PCA who had no electrographic seizures. Pathologic placental changes were separated: Group A consisted of chorioamnionitis, edema, meconium staining, and/or retroplacental hematoma. Group B consisted of abnormal villous maturation, infarction, and/or chronic villitis. Logistic regression analyses calculated the odds ratio of having Group A or Group B placental lesions in each neonate group as a function of increasing PCA. For the seizure group, the odds of having Group B with or without Group A placental lesions increased by a factor of 1.2 for each postconception week up to 43 weeks PCA. For a 15-week interval the odds of having Group B lesions for the seizure group increased by a factor of 12.1 (P < 0.007). Ratios were not significant for Group A lesions alone in the seizure group or for either Group B or Group A findings in the neonate group without seizures. Pathophysiologic events in utero leading to Group B rather than Group A findings are associated with electrically confirmed seizures in near-term and term infants. Group A lesions were considered more likely to have intrapartum or peripartum associations, whereas Group B lesions were considered more likely to have antepartum associations.

Cerebral Cortex↗

Understanding sleep ontogeny to assess brain dysfunction in neonates and infants.

The ontogenetic framework onto which a child's sleep is constructed undergoes significant developmental alterations during early life. Sleep state behaviors, in large part, reflect continuities from fetal through neonatal time periods. Major changes in sleep organization subsequently occur throughout infancy. Maturational expressions of sleep behaviors must be understood by the pediatric neurologist before specific physiologic phenomena can be assessed as transient sleep disturbances or clinically relevant sleep disorders. The first part of this two-part review article focuses on the major aspects of developmental sleep physiology in the first few months of life. Recognition of age-specific electroencephalographic/polysomnographic patterns will facilitate the child neurologist's evaluation of the newborn with suspected seizures and interictal encephalopathies, as well as the prediction of neurologic sequelae.

Child Development↗

Applying classifications of sleep disorders to children with neurologic conditions.

Information concerning sleep ontogeny and sleep disorders in children is required by many pediatric specialists. Pediatric neurologists, for instance, frequently are called upon to assist in the evaluation of children with undiagnosed symptoms and signs during sleep, as well as to care for children and adolescents with specific neurologic diseases who also experience sleep disturbances. This review discusses pediatric sleep disturbances with specific reference to sleep in children with neurologic conditions.

Child↗

Stimulus-evoked electrographic patterns in neonates: an abnormal form of reactivity.

Stimulus-evoked electrographic patterns are described for 12 neonates, coincident with tactile or painful stimulation. Four newborns had stimulus-evoked electrographic seizures with and without concomitant clinical seizure behaviors. Eight neonates had generalized or focal stimulus-evoked discharges, with or without coincident movements, which did not evolve into electrographic seizures. Nine infants were less than 36 weeks estimated gestational age at the time stimulus-evoked discharges were noted. Eleven neonates were comatose or phamacologically paralyzed at the time the stimulus-evoked patterns were initially noted. All neonates had moderate or severe interictal EEG background abnormalities at the time these patterns were observed. All patients had brain lesions documented by either cranial imaging or neuropathological examinations. Eleven patients died or have significant neurological handicaps. These phenomena represent an abnormal form of cortical reactivity to sensory stimuli in the developing brain. Most neonates with these patterns have significant diffuse or multifocal damage to the neocortex.

Adolescent↗

Neurophysiological assessment of brain function and maturation. II. A measure of brain dysmaturity in healthy preterm neonates.

Severe brain disorders can be expressed as markedly abnormal encephalopathic EEG patterns in neonates who are usually neurologically depressed, with abnormal levels of reactivity and tone. This symptomatic group is now a minority of medically ill neonates as a result of more vigorous fetal and neonatal resuscitative efforts. Most neonates alternatively express brain dysfunction as more pervasive alterations in EEG-sleep organization or maturation, usually in the absence or after resolution of abnormal clinical signs. One form of dysfunction is expressed as neurophysiologic dysmaturity. Brain dysmaturity may reflect altered rates of development in infants who sustained prenatal or postnatal stresses, as discussed in the first part of this review. We now summarize our findings of dysmature EEG-sleep development at conceptional term ages in an asymptomatic preterm cohort during a prolonged extrauterine period before discharge from the nursery. Dysmaturity of EEG-sleep function was expressed as delayed and/or accelerated physiologic behaviors, as compared with behaviors expected for the conceptional age. Dysmature brain function at conceptional term ages was also associated with poorer neurodevelopmental performances at 12 and 24 months of age. Neuronal pathways which subserve state-specific neurophysiologic behaviors will functionally adapt to stress by either slowing or accelerating neurological maturation. Through ontogenetic brain adaptation, which continues during postnatal development, a balance is maintained between the needs of the present developmental stage and anticipated needs during subsequent stages of maturation. How medical complications and environmental influences interact to promote greater brain dysmaturity in the neonate is still unknown. EEG sleep study can serve as a useful neurophysiologic screening procedure for the child suspected of having a subclinical presentation of an emerging static encephalopathy; longitudinal studies will then document deviations from expected ontogeny in the vulnerable child who is later stressed by environmental and socioeconomic factors.

Adaptation, Physiological↗

Neurophysiological assessment of brain function and maturation: I. A measure of brain adaptation in high risk infants.

Neurophysiologic assessments using EEG/polysomnographic studies permit the clinician to recognize expected patterns of brain maturation in the healthy neonate. By comparison, one can detect encephalopathic behaviors of newborns who are medically at risk. Severe physiologic expressions of encephalopathy are associated with neuropathologic lesions on postmortem examinations, brain lesions documented on neuroimaging studies, and major neurodevelopmental sequelae of survivors. However, such patterns are observed for only a minority of high risk neonates; less severe encephalopathies occur more frequently in neonates without evidence of brain lesions on imaging studies who either recover from medical illness or who manifest no findings of neurological dysfunction. These subtle and persistent brain disorders are obviously more difficult to detect and grade. This is specifically relevant for preterm infants in whom various degrees of encephalopathy may exist, but whose physiologic behaviors must be distinguished form expected behavioral and neurophysiologic patterns of prematurity. Neonates may express brain dysfunction as altered rates of brain maturation, as compared with expected patterns for a given conceptional age. Neurophysiologic expressions of brain dysmaturity, either from prenatal and/or postnatal stresses, may actually occur in a substantially larger segment of the high risk neonatal population than has been anticipated. EEG-sleep studies can serve as a noninvasive neurophysiologic probe of brain organization and maturation to extend clinical observations to assess the severity and persistence of brain dysfunction in a neonate who may be at risk for later neurodevelopmental compromise.

Adaptation, Physiological↗

Regional differences in spectral EEG measures between healthy term and preterm infants.

State-specific spectral electroencephalographic (EEG) values were compared among 14 bipolar channel derivations between two healthy neonatal cohorts. Fifty-five healthy preterm neonates of < or = 32 weeks gestational age at birth were studied with 24-channel recordings over 3 hours at term conceptional age. These were compared with studies of 45 healthy term neonates. Five spectral measures for each channel (i.e., total spectral EEG, delta, theta, alpha, and beta frequency ranges) were calculated for each minute, which was identified as active or quiet sleep, based on visual analysis. Using multivariate analysis of variance, differences at each channel were assessed between neonatal cohorts for both states and cohorts; higher total EEG spectral values were noted during active sleep; whereas higher delta and theta spectral values were noted during quiet sleep. The term cohort had higher values for spectral theta, alpha, and beta power spectra in multiple channels, most significantly in the left central (i.e., C3O1) and sagittal regions (FzCz, CzPz) during both states (P < .0001, adj r2 > or = .2). Both interhemispheric and intrahemispheric differences in spectral values were present. For a healthy preterm cohort, lower spectral energies are expressed during sleep in specific head regions. Physiologic asymmetries exist in the newborn brain which are unique for the preterm infant, emphasizing functional alterations in brain development. How these asymmetries are altered by prenatal or postnatal stress or disease states needs to be explored.

Brain Mapping↗

Grating acuity and visual-field development in children with intraventricular hemorrhage.

Visual development was studied in 171 preterm children who had intraventricular hemorrhage (IVH) and in 73 healthy preterm (HPT) children who did not develop IVH. Binocular grating acuity was assessed at age 1 month; monocular grating acuity and binocular visual-field extent were assessed at 4, 8, 12, 17, 24, 30, 36, and 48 months; and monocular H, O, T, V letter recognition acuity was tested at 36 and 48 months. A significantly greater proportion of IVH subjects than HPT subjects had ocular abnormalities. IVH subjects had significantly poorer grating acuity than HPT subjects at 1, 4, 8, 36, and 48 months, poorer recognition acuity than HPT subjects at 36 and 48 months, and smaller average field extent than HPT subjects at 4, 12, and 17 months. Acuity deficits were not related to grade of IVH or to the presence of periventricular leukomalacia, but may have been associated with the presence of ocular abnormalities or cerebral palsy in some IVH subjects.

Case-Control Studies↗

Computer classification of state in healthy preterm neonates.

Nineteen electroencephalographic (EEG) sleep measures describing four physiologic aspects of sleep behavior (i.e. sleep continuity, EEG spectra, body and eye movements, and autonomic measures) were derived from visual and computer analyses of 71 24-channel, 3-hour EEG sleep recordings on 52 healthy preterm neonates from 28-36.5 weeks postconceptional age (PCA). Forty-eight subjects were neurodevelopmentally normal up to 2 years of age. Four electrographic states that comprise tracé discontinu of the preterm neonate were defined in terms of increasing seconds of EEG quiescence per minute. A regression analysis was performed after transformations of nonlinear data sets representing the 19 EEG sleep measures, with the four sleep states as outcome variables. Postconceptional age was also included in these analyses as the 20th explanatory variable. Four measures best defined the EEG sleep states, explaining 75% of the variance: decreasing rapid eye movements per minute, decreasing numbers of spontaneous arousals per minute, increasing spectral theta energies, and decreasing facial movements per minute. Other cerebral and noncerebral measures, including total spectral EEG energies, spectral EEG energies in three bandwidths (i.e. delta, alpha, beta), cardiac and respiratory measures, and body movements, did not contribute as significantly to the prediction. Inclusion of PCA into the regression equation with the four EEG measures, selected by the analysis procedure, indicated that its contribution to state prediction was also small; the effect of PCA on state was found to be explained by the four EEG sleep measures.

Electroencephalography↗

Seizures in the newborn infant. Diagnosis, treatment, and outcome.

Neonatal seizures remain an emergent clinical problem in the neonatal intensive care unit that requires prompt diagnosis and treatment. The electroencephalogram is the preferred tool by which a surface-recorded seizure can be documented. While a number of etiologic possibilities may occur, overlapping mechanisms result in a lower seizure threshold. The susceptibility to seizures shortly after birth, efficacy of antiepileptic medications to control seizures, as well as the prediction of outcome in patients with neonatal seizures remains controversial. Prospective studies are required to assess interactions among maternal, fetal, and neonatal conditions that contribute to the occurrence of neonatal seizures.

Anticonvulsants↗

Prediction of lower developmental performances of healthy neonates by neonatal EEG-sleep measures.

Previous neurophysiologic studies from our laboratory have demonstrated altered EEG-sleep behavior at conceptional term ages in healthy preterm infant compared with a term cohort. Developmental assessments at 12 and 24 months of age of 16 children in each cohort were compared using MANOVA. Differences were detected on MANOVA between each cohort on Bayley mental and motor performance scores, while social skills (Vineland) and temperament (Carey) were similar. Healthy preterm infants had lower scores at 12 months of age (P < .0001) and 24 months (P < .04) than term infants before adjustment for prematurity. No group differences were observed after adjustment. For the combined cohort of 32 healthy neonates, specific neonatal EEG-sleep measures were included as predictor variables in regression analyses with Bayley mental scores as outcome variables. Lower Bayley mental scores at 12 and 24 months were associated with higher spectral EEG correlations, lower spectral EEG energies in the beta frequency ranges, fewer arousals per minute, lower rapid eye movements per minute, and shorter sleep latencies from awake state to active sleep. Significant associations were observed before adjustment for prematurity at both 12 and 24 months, and after adjustment at 12 months of age for lower spectral beta EEG energies. Lower socioeconomic class also correlated with lower developmental scores. Even in the absence of major neonatal illnesses, brain adaptation to prematurity influences later developmental outcome. Adjustment for "age equivalency" may be required up to at least 24 months of age even in a healthy preterm population.

Analysis of Variance↗