Response to correspondence on "pilot study of efficacy of tongue and body acupuncture in children with visual impairment".
Response to correspondence on "pilot study of efficacy of tongue and body acupuncture in children with visual impairment". J Child Neurol. 2008 Jun;23(6):718-9 Authors: Wong V PMID: 18540003 [PubMed - in process] Correspondence on "pilot study of efficacy of tongue and body acupuncture in children with visual impairment".
Correspondence on "pilot study of efficacy of tongue and body acupuncture in children with visual impairment". J Child Neurol. 2008 Jun;23(6):717-8; author reply 718-9 Authors: Wong M PMID: 18540002 [PubMed - in process] Correspondence on "electroencephalography (EEG) with ocular compression in the diagnosis of breath-holding spells or syncope".
Correspondence on "electroencephalography (EEG) with ocular compression in the diagnosis of breath-holding spells or syncope". J Child Neurol. 2008 Jun;23(6):716-7 Authors: Khurana D, Valencia I, Kruthiventi S, Gracely E, Melvin J, Legido A, Kothare S PMID: 18540001 [PubMed - in process] Correspondence on "Plasma Interleukin-1beta Levels in Children With Febrile Seizures".
Correspondence on "Plasma Interleukin-1beta Levels in Children With Febrile Seizures". J Child Neurol. 2008 Jun;23(6):715; author reply 715-6 Authors: Mohebbi MR PMID: 18540000 [PubMed - in process] Response to Correspondence on "Plasma Interleukin-1{beta} Levels in Children With Febrile Seizures".
Response to Correspondence on "Plasma Interleukin-1{beta} Levels in Children With Febrile Seizures". J Child Neurol. 2008 Jun;23(6):715-6 Authors: Yahya Tomoum H PMID: 18539999 [PubMed - in process] Vanishing white matter disease: the first reported chinese patient.
Vanishing white matter disease: the first reported chinese patient. J Child Neurol. 2008 Jun;23(6):710-4 Authors: Wong SS, Luk DC, Wong VC, Scheper GC, van der Knaap MS Vanishing white matter disease is a rare neurological disease. The majority of patients reported are Caucasian individuals. We describe the first Chinese patient with typical clinical and radiological features genetically confirmed to have vanishing white matter disease for a mutation in EIF2B4, followed by a brief review of the disease. PMID: 18539998 [PubMed - in process] Successful management of refractory neonatal seizures with midazolam.
Successful management of refractory neonatal seizures with midazolam. J Child Neurol. 2008 Jun;23(6):706-9 Authors: Sirsi D, Nangia S, LaMothe J, Kosofsky BE, Solomon GE Seizures are indicative of underlying neurologic dysfunction in neonates. Repeated seizures may be deleterious to the brain even without disturbances of ventilation or perfusion. First-line antiepileptic drugs such as phenobarbital and phenytoin are not very effective in controlling seizures in neonates. Rapid control of status epilepticus with midazolam has been demonstrated in 2 previous studies with complete clinical and electrographic response in neonates who did not respond to phenobarbital and phenytoin. We report our experience with 3 neonates with status epilepticus. Seizures in all 3 neonates did not respond to phenobarbital and phenytoin but responded to midazolam infusion. Midazolam may be considered a safe and effective antiepileptic drug in refractory neonatal seizures of diverse etiologies. PMID: 18539997 [PubMed - in process] Severe infantile hypotonia with ethylmalonic aciduria: case report.
Severe infantile hypotonia with ethylmalonic aciduria: case report. J Child Neurol. 2008 Jun;23(6):703-5 Authors: Okuyaz C, Ezgü FS, Biberoglu G, Zeviani M, Tiranti V, Yilgör E An 8-month-old girl was admitted to an outpatient clinic with significant hypotonia and weakness. Organic acid analysis in urine revealed a significant increase in ethylmalonic acid. A deoxyribonucleic analysis revealed the presence of a 625G>A (G-to-A substitution at nucleotide 625) variant short-chain acyl-coenzyme A dehydrogenase gene polymorphism. With the clinical, biochemical and molecular findings, short-chain acyl-coenzyme A dehydrogenase deficiency was suspected. Because 625G>A and 511C>T (C-to-T substitution at nucleotide 511) genetic variations are also present in 14% of the general population, these are considered to be genetic sensitivity variations rather than causing a disease themselves and to result in possible short-chain acyl-coenzyme A dehydrogenase deficiency in the presence of environmental factors such as fever and hunger as well as cellular, biochemical, and other genetic factors. It was stressed that severe infantile hypotonia could also be the only manifestation of ethylmalonic aciduria spectrum disorders. PMID: 18539996 [PubMed - in process] Increased intracranial pressure in a case of pediatric multiple sclerosis.
Increased intracranial pressure in a case of pediatric multiple sclerosis. J Child Neurol. 2008 Jun;23(6):699-702 Authors: Williams BJ, Skinner HJ, Maria BL A 15-year-old girl presented to our emergency department with dizziness, anorexia, nausea, and malaise. Clinical examination and magnetic resonance imaging studies showed characteristic features of multiple sclerosis. Surprisingly, a diagnostic lumbar puncture showed significant intracranial hypertension in addition to numerous oligoclonal bands, elevated immunoglobulin G index and immunoglobulin G/albumin ratio in the cerebrospinal fluid. It is proposed that a large burden of active demyelinating disease may cause increased intracranial pressure, thus providing an additional sound rationale for prompt therapeutic administration of intravenous high-dose steroids. PMID: 18539995 [PubMed - in process] Diffuse multicystic encephalomalacia in a preterm baby due to homozygous methylenetetrahydrofolate reductase 677 C-->T mutation.
Diffuse multicystic encephalomalacia in a preterm baby due to homozygous methylenetetrahydrofolate reductase 677 C-->T mutation. J Child Neurol. 2008 Jun;23(6):695-8 Authors: Aygun C, Tanyeri B, Ceyhan M, Bagci H, Kucukoduk S Methylenetetrahydrofolate reductase catalyzes the formation of 5-methyltetrahydrofolate from 5,10-methylentetrahydrofolate and produces folate for the methylation of homocysteine to methionine. Due to insufficient conversion of homocysteine to methionine, plasma homocysteine levels increase in methylenetetrahydrofolate reductase deficiency. Homocysteine is an amino acid that contains a neurotoxic sulfur molecule and can induce neuronal apoptosis. Methylenetetrahydrofolate reductase deficiency is 1 of the etiological factors that causes neurological symptoms and signs in the newborn and childhood period. Here, we report a premature baby with prenatal onset diffuse multicystic encephalomalacia and cerebellar atrophy due to homozygous methylenetetrahydrofolate reductase mutation. PMID: 18539994 [PubMed - in process] Lucy Balian Rorke-Adams, MD: an autobiography.
Lucy Balian Rorke-Adams, MD: an autobiography. J Child Neurol. 2008 Jun;23(6):674-82 Authors: Rorke-Adams LB PMID: 18539993 [PubMed - in process] A personal autobiography.
A personal autobiography. J Child Neurol. 2008 Jun;23(6):669-73 Authors: Hagberg BA PMID: 18539992 [PubMed - in process] Brain lesions and IQ: recovery versus decline depends on age of onset.
Brain lesions and IQ: recovery versus decline depends on age of onset. J Child Neurol. 2008 Jun;23(6):663-8 Authors: Duval J, Braun CM, Montour-Proulx I, Daigneault S, Rouleau I, Bégin J A growing literature suggests that early lesions are associated with poorer IQ outcome. Those studies covered a restricted age range in pediatric populations only and did not control for important moderator variables. The present investigation studied IQ change in brain-lesioned children and adults (age 0 to 84 years). Altogether, 725 cases with a documented unilateral focal lesion were gathered from hospital charts and from published cases in the literature, including 240 with repeated IQ testing. Multiple regression analyses isolated the contribution of age at lesion onset to IQ change. Important mediator variables included were lesion side, site, volume, etiology, and so on. An early lesion was significantly associated with poorer postlesion IQ in time and with decline of IQ in time. Later onset lesions were associated with better postlesion IQ and recovery in time. The so-called Kennard principle is refuted, with regard to IQ. PMID: 18539991 [PubMed - in process] Ambulatory electroencephalography (EEG) in children: diagnostic yield and tolerability.
Ambulatory electroencephalography (EEG) in children: diagnostic yield and tolerability. J Child Neurol. 2008 Jun;23(6):655-62 Authors: Wirrell E, Kozlik S, Tellez J, Wiebe S, Hamiwka L Sixty-four children, aged 0-17 years, undergoing ambulatory electroencephalography (EEG) were prospectively recruited during a 12-month period. The diagnostic yield of ambulatory electroencephalography was determined for each of the following groups: group 1: differentiation of seizures from nonepileptic events; group 2: determination of seizure/interictal discharge frequency; and group 3: classification of seizure type or localization. The ambulatory electroencephalography answered the clinical question in 61% of group 1 (27/44) and 100% of groups 2 (16/16) and 3 (4/4). Of 44 cases in Group 1, clinical events were recorded in 61%; the ambulatory electroencephalography result changed the diagnosis from epileptic to nonepileptic or vice versa in 27%. When clinicians suspected that events were epileptic, ambulatory electroencephalography changed the clinical impression in 50%, whereas when events were suspected to be nonepileptic, ambulatory electroencephalography confirmed that impression in 83%. PMID: 18539990 [PubMed - in process] Melatonin for chronic insomnia in Angelman syndrome: a randomized placebo-controlled trial.
Melatonin for chronic insomnia in Angelman syndrome: a randomized placebo-controlled trial. J Child Neurol. 2008 Jun;23(6):649-54 Authors: Braam W, Didden R, Smits MG, Curfs LM Previous studies suggested that melatonin improves sleep in insomniac patients with Angelman syndrome. To assess the efficacy of melatonin, a randomized placebo-controlled study was conducted in 8 children with Angelman syndrome with idiopathic chronic insomnia. After a 1-week baseline period, patients received, depending on age, either melatonin 5 or 2.5 mg, or placebo, followed by 4 weeks of open treatment. Parents recorded lights off time, sleep onset time, wake-up time, and epileptic seizures in a diary. Salivary melatonin levels were measured at baseline and the last evening of the fourth treatment week. Melatonin significantly advanced sleep onset by 28 minutes, decreased sleep latency by 32 minutes, increased total sleep time by 56 minutes, reduced the number of nights with wakes from 3.1 to 1.6 nights a week, and increased endogenous salivary melatonin levels. Parents were satisfied with these results. Indications that melatonin dose in Angelman syndrome patients should be low, are discussed. PMID: 18539989 [PubMed - in process]
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