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PURPOSE: To assess the clinical effectiveness of treating acute seizures with midazolam and lidocaine infusion. METHODS: This single-center historical cohort study included 39 term neonates with electrographic seizures who underwent treatment with midazolam (1st line) and lidocaine (2nd line). Therapeutic response was measured using continuous video-EEG monitoring. The EEG measurements included total seizure burden (minutes), maximum ictal fraction (minutes/hour), and EEG-background (normal/slightly abnormal vs. abnormal). Treatment response was considered good (seizure control with midazolam infusion), intermediate (need to add lidocaine to the control), or no response. Using clinical assessments supplemented by BSID-III and/or ASQ-3 at 2 to 9 years old age, neurodevelopment was classified as normal, borderline, or abnormal. RESULTS: A good therapeutic response was obtained in 24 neonates, an intermediate response in 15, and no response in any of the neonates. Babies with good response showed lower values in maximum ictal fraction compared with those with intermediate response (95% CI: 5.85-8.64 vs. 9.14-19.14, P = 0.002). Neurodevelopment was considered normal in 24 children, borderline in five, and abnormal in other 10 children. Abnormal neurodevelopment was significantly associated with an abnormal EEG background, maximum ictal fraction >11 minutes, and total seizure burden >25 minutes (odds ratio 95% CI: 4.74-1708.52, P = 0.003; 1.72-200, P = 0.016; 1.72-142.86, P = 0.026, respectively) but not with the therapeutic response. Serious adverse effects were not recorded. CONCLUSIONS: This retrospective study suggests that the midazolam/lidocaine association could potentially be efficacious in decreasing seizure burden in term neonates with acute seizures. These results would justify testing the midazolam/lidocaine combination as a first-line treatment for neonatal seizures in future clinical trials.
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This report presents a case of superficial siderosis of the central nervous system secondary to repeated intraventricular and subarachnoid bleeding of a newborn infant with neonatal alloimmune thrombocytopenia. In addition, this infant manifested Dandy-Walker variant. To date, the few known cases of superficial siderosis in neonates have not been associated with neonatal alloimmune thrombocytopenia or Dandy-Walker complex. We believe that repeated bleeding in the central nervous system from early fetal life, especially in the posterior fossa, may produce cerebellar atrophy as occurs in adults with superficial siderosis of the central nervous system.
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Hemorragia Cerebral/etiologia , Síndrome de Dandy-Walker/complicações , Siderose/etiologia , Trombocitopenia/complicações , Cerebelo/anormalidades , Hemorragia Cerebral/diagnóstico por imagem , Hemorragia Cerebral/patologia , Síndrome de Dandy-Walker/diagnóstico por imagem , Síndrome de Dandy-Walker/patologia , Humanos , Recém-Nascido , Imageamento por Ressonância Magnética , Masculino , Siderose/diagnóstico por imagem , Siderose/patologia , Trombocitopenia/diagnóstico por imagem , Trombocitopenia/patologia , UltrassonografiaRESUMO
OBJECTIVE: Clinical significance of neonatal positive temporal sharp waves (PTS) is controversial. The aim of this work is to study (1) PTS incidence in preterm infants with or without major ultrasound lesion (MUL) per gestational age (GA), and (2) the relationship between PTS in both sleep states and other electroencephalographic (EEG) findings with poor prognoses. METHODS: 97 preterm infants of <27-36 weeks GA, and 12 full-term healthy infants were presented. Prospective study included (1) neurodevelopmental assessment at 40-42 weeks conceptional age (CA), (2) serial neurosonography, and (3) EEG recording at postnatal week 1, 2, 4 and at 40-42 weeks CA. RESULTS: In 50 neonates without MUL, peak PTS was at 31-32 weeks GA. In 47 neonates with MUL, PTS increased significantly from week 2 after birth, descending at the 4th. Neonates of <33 weeks GA with MUL showed significantly increased PTS at term. A significant relationship was found between PTS and other EEG abnormalities with poor neurologic prognoses. PTS incidence varied with sleep states, being predominant in indeterminate sleep in neonates with MUL. CONCLUSIONS: PTS increased significantly in infants with MUL, mainly at week 2 of postnatal life, persisting high until term CA, and correlated with other abnormal EEG findings. SIGNIFICANCE: PTS are highly sensitive to MUL.
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Encefalopatias/diagnóstico por imagem , Encefalopatias/fisiopatologia , Encéfalo/fisiopatologia , Ecoencefalografia , Eletroencefalografia , Recém-Nascido Prematuro , Estudos de Casos e Controles , Idade Gestacional , Humanos , Recém-Nascido , Fases do Sono , Fatores de TempoRESUMO
OBJECTIVE: To determine whether full-term newborn infants of diabetic mothers (IDM) present immature/disorganised EEG patterns in the immediate neonatal period, and whether there was any relationship with maternal glycaemic control. DESIGN AND SETTING: Cohort study with an incidental sample performed in a tertiary hospital neonatal unit. PATIENTS: 23 IDM and 22 healthy newborns born between 2010 and 2013. INTERVENTIONS: All underwent video-EEG recording lasting >90 min at 48-72 h of life. MAIN OUTCOME MEASURES: We analysed the percentage of indeterminate sleep, transient sharp waves per hour and mature-for-gestational age EEG patterns (discontinuity, maximum duration of interburst interval (IBI), asynchrony, asymmetry, δ brushes, encoches frontales and α/θ rolandic activity). The group of IDM was divided into two subgroups according to maternal HbA1c: (1) HbA1c≥6% and (2) HbA1c<6%. RESULTS: Compared with healthy newborns, IDM presented significantly higher percentage of indeterminate sleep (57% vs 25%; p<0.001), discontinuity (2.5% vs 0%; p=0.044) and δ brushes in the bursts (6% vs 3%; p=0.024); higher duration of IBI (0.3 s vs 0 s; p=0.017); fewer encoches frontales (7/h vs 35/h; p<0.001), reduced θ/α rolandic activity (3/h vs 9/h; p<0.001); and more transient sharp waves (25/h vs 5/h; p<0.001). IDM with maternal HbA1c≥6% showed greater percentage of δ brushes in the burst (14% vs 4%; p=0.007). CONCLUSIONS: Full-term IDM newborns showed video-EEG features of abnormal development of brain function. Maternal HbA1c levels<6% during pregnancy could minimise the risk of cerebral dysmaturity.
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Encefalopatias/diagnóstico , Diabetes Mellitus Tipo 1/diagnóstico , Diabetes Gestacional/diagnóstico , Eletroencefalografia , Glicemia/metabolismo , Encéfalo/fisiopatologia , Encefalopatias/sangue , Encefalopatias/fisiopatologia , Desenvolvimento Infantil , Estudos de Coortes , Diabetes Mellitus Tipo 1/sangue , Diabetes Gestacional/sangue , Eletroencefalografia/métodos , Feminino , Idade Gestacional , Hemoglobinas Glicadas/metabolismo , Humanos , Recém-Nascido , Mães , Gravidez , Estatística como Assunto , Nascimento a Termo , Gravação em Vídeo/estatística & dados numéricosRESUMO
We present 2 term newborn infants with apneic seizure originating in the occipital lobe that was diagnosed by video-EEG. One infant had ischemic infarction in the distribution of the posterior cerebral artery, extending to the cingulate gyrus. In the other infant, only transient occipital hyperechogenicity was observed by using neurosonography. In both cases, although the critical EEG discharge was observed at the occipital level, the infants presented no clinical manifestations. In patient 1, the discharge extended to the temporal lobe first, with subtle motor manifestations and tachycardia, then synchronously to both hemispheres (with bradypnea/hypopnea), and the background EEG activity became suppressed, at which point the infant experienced apnea. In patient 2, background EEG activity became suppressed right at the end of the focal discharge, coinciding with the appearance of apnea. In neither case did the clinical description by observers coincide with video-EEG findings. The existence of connections between the posterior limbic cortex and the temporal lobe and midbrain respiratory centers may explain the clinical symptoms recorded in these 2 cases. The novel features reported here include video-EEG capture of apneic seizure, ischemic lesion in the territory of the posterior cerebral artery as the cause of apneic seizure, and the appearance of apnea when the epileptiform ictal discharge extended to other cerebral areas or when EEG activity became suppressed. To date, none of these clinical findings have been previously reported. We believe this pathology may in fact be fairly common, but that video-EEG monitoring is essential for diagnosis.