Child Neurology Open

2. Autism Spectrum Disorder and Neonatal Serum Magnesium Levels in Preterm Infants

   Amanda V. Bakian, PhD¹, Deborah A. Bilder, MD¹, E. Kent Korgenski, MS², Joshua L. Bonkowsky, MD, PhD³
   Child Neurology Open, vol. 5, First Published September 18, 2018.
   Abstract

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   Abstract

   Premature birth is associated with increased risk of autism spectrum disorder. Antenatal maternal magnesium administration is known to reduce subsequent risk of cerebral palsy including among premature infants, suggesting a potentially broader neuroprotective role for magnesium. Our objective was to determine whether magnesium could be protective against autism spectrum disorders in premature infants. A cohort of 4855 preterm children was identified, magnesium levels from 24 to 48 hours of life recorded, and subsequent autism spectrum disorder status determined. Adjusted relative risk of autism spectrum disorder with each 1 mg/dL increase in neonatal magnesium level was 1.15 (95% confidence interval: 0.86-1.53). Analysis of variance indicated that magnesium levels varied by gestational age and maternal antenatal magnesium supplementation, but not autism spectrum disorder status (F_1,4824 = 1.43, P = .23). We found that neonatal magnesium levels were not associated with decreased autism spectrum disorder risk. Future research into autism spectrum disorder risks and treatments in premature infants is needed.
    
3. 

   Functional Gains in Children With Spastic Hemiplegia Following a Tendon Achilles Lengthening Using Computerized Adaptive Testing—A Pilot Study

   Eli Saleh, MD¹, Noémi Dahan-Oliel, PhD, OT², Kathleen Montpetit, MSc, OT³, Thierry Benaroch, MD³, Rita Yap, MSc, PT³, Nadia Barakat, PhD⁴, M. J. Mulcahey, PhD, OT⁵
   Child Neurology Open, vol. 5, First Published November 14, 2018.
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   Abstract

   Purpose:

   This pilot study evaluated the outcomes of tendon Achilles lengthening in 12 children (mean age: 11.2 years) with spastic hemiplegia.

   Methods:

   Cerebral Palsy Computer Adaptive Tests, the timed up-and-go, the Gross Motor Function Measure, the Gillette Functional Assessment Questionnaire, and the Pediatric Outcomes Data Collection Instrument were administered at baseline and at 6, 12, and 24 months postsurgery.

   Results:

   Significant improvement at the latest follow-up (12-24 months following surgery) was seen in all domains of the Cerebral Palsy Computer Adaptive Test: activity (P = .017), lower extremity (P = .005), global (P = .005), pain (P = .005), and fatigue (P = .028), as well as in the Gross Motor Function Measure-standing domain (P = .02) and the mobility domain of the Pediatric Outcomes Data Collection Instrument (P = .04).

   Conclusion:

   These findings indicate that the tendon Achilles lengthening improved functional outcome in these children as measured by tests of physical function, walking speed, and activity performance.
    
4. 

   Clinical Profile of Pediatric Neurological Disorders: Outpatient Department, Khartoum, Sudan

   Inaam Noureldyme Mohamed, MD¹, Maha Abdelmoneum Elseed, MRCPCH¹, Ahlam Abdalrhman Hamed, MD¹
   Child Neurology Open, vol. 3, First Published April 4, 2016.
   Abstract

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   Abstract

   Background:

   There is no available data from Sudan reflecting the magnitude of the neurological disorders and disabilities in the pediatric age-group. This study aims to evaluate the pattern of neurological disorders among Sudanese children.

   Patients and Methods:

   This is a retrospective survey of children with epilepsy and other neurodisability disorders seen at pediatric neurology outpatient clinic, during the period from January 2007 to August 2013. The data of 9600 patients were analyzed.

   Results:

   A total of 6019 patients were included in the study. The majority of the patients had epilepsy that amounted to 52.8%, followed by cerebral palsy (19.1%), congenital anomalies of the central nervous system (6.2%), neuromuscular disorders (3.2%), stroke (2.4%), ataxia and movement disorders (1.9%), assumed genetic syndromes (1.2%), and others.

   Conclusion:

   Neurological disorders constitute a major cause of chronic morbidity in pediatric age-group.
    
5. 

   A New Observation of an Atypical and Severe Variant of the Guillain-Barre Syndrome in a Child: Remaining Challenges for Diagnosis, Nosologic Classification, and Therapeutic Course

   Linda Pons¹²³⁴, Véronique Manel, MD², Dorothée Ville, MD³, Etienne Javouhey, MD, PhD¹⁴, Fabienne Bordet, MD¹
   Child Neurology Open, vol. 2, 4, First Published October 26, 2015.
   Abstract

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   Abstract

   Guillain-Barré syndrome is a rare acute polyradiculoneuropathy. Several variants and unusual presentations have been described, particularly in pediatrics. In most cases, making an early diagnosis is challenging due to the treatments that consist in the rapid administration of intravenous immunoglobulin or plasma exchange. The authors present the case of a 7-year-old boy with an atypical and severe axonal Guillain-Barré syndrome, associated with Mycoplasma pneumonia. When he was admitted, febrile respiratory failure was the main focus, and then he presented signs of acute polyneuropathy with cranial nerve palsy and brief hyperreflexia. Mechanical ventilation was required for 48 days as well as 2 cycles of intravenous immunoglobulin. The authors describe all the medical challenges that the authors encountered. This case highlights the fact that respiratory distress can be the main clinical symptom in children. This delays the establishment of a correct diagnosis, even more so when neurological manifestations are abundant and unusual.
    
6. 

   Assessing Children With Disabilities Using WHO International Classification of Functioning, Disability and Health Child and Youth Version Activities and Participation D Codes

   Niels Ove Illum, MD¹, Kim Oren Gradel, PhD²³
   Child Neurology Open, vol. 2, 4, First Published October 28, 2015.
   Abstract

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7. 

   Newly Identified Characteristics and Suggestions for Diagnosis and Treatment of Diffuse Leptomeningeal Glioneuronal/Neuroepithelial Tumors: A Case Report and Review of the Literature

   Megan R. Lyle, DO¹, Jaydevsinh N. Dolia, MD², Jonathan Fratkin, MD³, Todd A. Nichols, MD⁴, Betty L. Herrington, MD⁵
   Child Neurology Open, vol. 2, 1, First Published February 16, 2015.
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   Abstract

   Diffuse leptomeningeal glioneuronal tumor is unique for communicating hydrocephalus, diffuse leptomeningeal enhancement, cystic changes, absence of tumor cells in cerebral spinal fluid, and a cell population of both glial and neuronal copositivity. It has likely been misdiagnosed as mixed glioneuronal tumors, oligodendrogliomas, and neuroepithelial tumors. Children with signs of this tumor are often worked up for infection, rheumatologic disease, or disseminated primary malignancy, resulting in unnecessary testing and treatment. We describe a 14-year-old female with recurrent headaches, hydrocephalus, and diffuse leptomeningeal enhancement discovered to be neoplastic 1 year after initial presentation, owing to extensive and unrevealing infectious and immunologic workups. Biopsies revealed atypical cells with markers of both glial and neuronal cells, positivity for OLIG-2, and focal p53 positivity. Great response was seen with temozolomide and craniospinal irradiation. Additionally, we postulate additional diagnostic indicators that may aid in earlier diagnosis and treatment decisions.
    
8. 

   Connexin 43 and Its Hemichannels Mediate Hypoxia–Ischemia-Induced Cell Death in Neonatal Rats

   Jingwei Wang, MD¹, Aihua Ma, MD, PhD¹, Jiashui Xi, MD¹, Yulin Wang, MD, PhD¹, Bojun Zhao, MD, PhD²
   Child Neurology Open, vol. 1, 1, First Published August 26, 2014.
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   Abstract

   Wistar rat pups had the left common carotid artery cut, and they were exposed to 8% oxygen with free access to food and water until they were killed at 1, 12, 24, and 48 hours after the hypoxia–ischemia (HI) insult. Connexin 43 (Cx43), hemichannel (HC1), and caspase 3 (Casp3) in cerebral HI tissues were examined by immunohistochemistry and Western blot analyses. Astrocytes cell line, astrocytes transduced with a retroviral empty vector (Psup astrocyte), or a Cx43-specific small hairpin RNA (shRNA) construct (shRNA astrocytes) was treated with oxygen–glucose deprivation (OGD) insult. The viability of astrocytes was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The results showed the expression of Cx43, HC1, and Casp3 in rats' brain, and astrocytes and Psup astrocytes increased significantly after 24 hours of HI/OGD insult. Cell viability decreased after 24 hours of the insult. The results suggest that Cx43 and hemichannel are likely to mediate the astrocytic death after HI insult.