EEG Findings In Children Research Articles

Serum levels of cytokines and EEG findings in children with influenza associated with mild neurological complications

We studied the relation among serum cytokine levels, EEG changes, and mild neurological complications (delirium and febrile seizure) in children with influenza. The serum levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and soluble tumor necrosis factor receptor-1 (sTNFR-1) were measured in 27 children with proven influenza infection with mild neurological complications (10 patients with delirium and 17 with febrile seizures) and seven control children. EEG was recorded in 14 children with neurological complications. EEG showed focal slowing in four of nine patients with delirium and in four of five with febrile seizures. Generalized slowing was observed in one patient with delirium. The median serum IL-6 level was 31.2 ± 15.1 pg/ml (range, 7.5–64.5 pg/ml) in the delirium group, 42.3 ± 44.0 pg/ml (range, 8.0–196.0 pg/ml) in the febrile seizure group, and 15.4 ± 7.0 pg/ml (range, 7.2–28.0 pg/ml) in the control group. Serum TNF-α and sTNFR-1 levels were not different among three groups. Mild neurological complications associated with influenza were related to the mildly abnormal serum IL-6 levels and EEG findings. The combination of these parameters will be useful for early diagnosis and differentiation of neurological complications in children with influenza. Further studies will be necessary for investigating that IL-6 has the diagnostic value for differentiation between severe encephalopathy and mild neurological complications in children with influenza.

EEG AND VIDEO-EEG IN CHILDREN WITH AUTISM AND STARING SPELLS

Objectives: The prevalence of epilepsy in children with autism is approximately 30%. This increases the concerns of episodes of staring and abnormal behavior being epileptic in nature. We studied the incidence of abnormal EEG findings in children with diagnosis of autism referred to an epilepsy center for evaluation of staring spells.

Book Review

Book Review

Seizures and EEG Findings in Children With Autism Spectrum Disorder

AbstractAutism spectrum disorder (ASD) is a neurobiological developmental symptom complex characterized by early onset of deficits in verbal and nonverbal communication skills, socio-communicative function, and repetitive behaviors. The well-documented increased frequency of seizures and abnormal electroencephalographic (EEG) findings in ASD support the concept that the central nervous system dysfunction has a neurobiological basis. We review the prevalence of seizures and EEG abnormalities in children with ASD and explore the possible clinical significance of this correlation.

Cortical dysgenesis: serial EEG findings in children and adults

Cortical dysgenesis (CD) is becoming increasingly recognised as a cause of epilepsy in otherwise cryptogenic cases. We describe the serial EEG findings in 22 patients with focal/localised CD. The EEGs covered a minimum period of 5 years in each case (median = 13 years, range: 5–30 years), beginning in childhood. Median age at seizure onset was 3 years (range: 3 weeks–10 years, (n = 21). The EEG was normal in the one patient, a 6 year old, who did not have epilepsy. Background rhythms appropriate for age were preserved in the majority of patients ( 18 22 ). Slow activity localised to the area of CD was seen in 11 patients; in 3 patients, this did not appear until the second decade of life. Epileptiform discharges were seen in at least one EEG in 20 patients: these were continuous or near-continuous (6 patients) or occurred recurrently in short runs (6 patients). In 6 patients, these discharges appeared only after the second decade of life and in 11 patients, they became more widespread over time. In the remaining patients, the EEG changes did not evolve. Sleep failed to produce new abnormalities (n = 15). None of the patients showed EEG features characteristic of lissencephaly or evolution to the Lennox-Gastaut syndrome. Even in this selected cohort of patients who had undergone serial clinical EEGs, the EEG abnormalities in focal/localised CD appeared relatively stable and showed only moderate changes over time. CD must be included in the differential diagnosis of any patient who presents with localised slow activity on EEG.

EEG findings in children and adolescents with mitochondrial encephalomyopathies: A study of 25 cases

EEG was studied in 25 children and adolescents with mitochondrial encephalomyopathies, defined on the basis of clinical, biochemical and morphological criteria. Twenty cases conformed to well-known mitochondrial syndromes: Alpers syndrome [6], Leigh syndrome [2], MERRF (myoclonus epilepsy and ragged red fibers) syndrome [3], MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) syndrome [5] and Kearns-Sayre syndrome [4]. Many patients were followed for several years with repeated EEG. In all, 112 EEG records were included in the study. A common feature of all the mitochondrial encephalomyopathic syndromes was slowing of the alpha rhythm. Epileptic discharges were seen in most syndromes. In spite of the small number of cases in each group, in Alpers, MERRF and MELAS syndromes we found sequential EEG patterns which seemed to be typical of the respective syndromes. In contrast, in Kearns-Sayre syndrome, a slow background rhythm was the only consistent finding. We conclude that EEG, especially repeated recordings, may be of help in the diagnostic evaluation of mitochondrial encephalomyopathies.

Ambulatory EEG recordings in epileptic and nonepileptic children.

We examined the cassette-recorded 24-hour ambulatory EEG findings in children who had either clinically definite seizures or episodic behavioral disturbances not regarded as epileptic on clinical grounds. Among 40 epileptic patients, 22 had one or more attacks during the 24-hour recording session. In 15 of these patients all clinical attacks had appropriate ictal electrographic accompaniments; in another 6 some (but not all) attacks did so. Among 55 children with nonepileptic spells clinically, the 24-hour recording was uninterpretable for technical reasons in one, and in 30 it provided no relevant information because there were no recorded clinical or electrographic attacks. In the remaining 24 patients, one or more clinical attacks were captured, and in no instance was there any accompanying electrographic change. Our findings indicate that the absence of ictal EEG changes during attacks cannot be used in isolation to make a diagnosis of pseudoseizures, but support such a diagnosis made on clinical grounds. The more important role of the ambulatory EEG is to exclude a diagnosis of nonepileptic attacks by demonstrating electrographic seizure activity accompanying typical clinical attacks. Whether the technique will have a useful role in the evaluation of patients when the nature of an episodic disturbance of cerebral function is unclear clinically remains to be established, but will require long-term follow-up to validate any conclusions reached by the electrophysiologic technique.