MS-Children
What it found
A paper reports the results; we have not read it yet. See Papers below.
What was tested
Treatment tested
- Exposure to methylprednisolone during pregnancy
What it measured
Main measures
General cognitive ability - Reynolds Intellectual Assessment Scales and Screening (RIAS)
approx. 30 - 40 min.
Thinking and memory
Other measures (12)
Structural brain development - BrainAge score
approx. 20 min.
MRI lesionsBlood or spinal fluid markersSalivary cortisol decay curve
approx. 5 min. per swab
Salivary alpha-amylase
approx. 5 min. per swab
Heart rate variability
approx. 75 min.
Spectral edge frequency in the EEG
approx. 75 min.
Nerve conduction testsExternal assessment sheet for attention deficit / hyperactivity disorder (FBB-ADHS, German Version)
approx. 15 - 20 min.
Thinking and memoryChild Behavior Checklist (CBCL/6-18R)
approx. 15 - 20 min.
Thinking and memoryMood and sleepStrengths and Difficulties Questionnaire (SDQ-Deu-S)
approx. 15 - 20 min.
Thinking and memoryPhysical functionContinuous Performance Test (CPT)
approx. 15 min.
Thinking and memoryEmotional excitability scale from Personality questionnaire for children between 9 and 14 years (PFK 9-14, German Version)
approx. 15 min.
Who could take part
MS (type not specified) · 8 to 18
Inclusion Criteria: * MS diagnosis was made based on the McDonald criteria valid at the time of diagnosis * Written consent by the legal guardians of the participating child following a detailed oral and written education * Exposed group (n=40): Children and adolescents (aged 8 to 18 years) of mothers with prenatal exposition to MP in the context of a MS relapse therapy * Non-exposed group (n=40): Children and adolescents of mothers suffering from MS without MP therapy during pregnancy (aged 8 to 18 years) matched for age, gender and social background Exclusion Criteria: * Perinatal complications such as cerebral bleeding, neonatal intensive care with ventilation, prenatal therapy with glucocorticoids except for an MS relapse * Maternal abuse of noxious agents during pregnancy * Long-term glucocorticoid medication (e.g. asthma) * Preterm births (before 36 weeks of pregnancy) * Severe disease making an examination impossible (e.g. mental retardation) * disease-modifying therapy during pregnancy
As registered. Criteria can change, so ask the trial team or your neurologist.
About this trial
In the sponsor's words
Introduction: Fetal exposure to glucocorticoids (GCs) used to induce fetal lung maturation in women threatened by premature labour is known to induce aberrations in brain development and stress sensitivity, cognitive dysfunction and neuro-psychiatric disorders in later life which all predict early brain ageing. Another common source of fetal GC exposure is the treatment of relapses in multiple sclerosis (MS), the most common neurological disease in young women. Despite the lack of studies, the 300-fold higher dosage of GCs for MS relapse treatment compared to obstetric indications is considered harmless for the fetus . Objectives: To examine the effects of GCs for MS relapse treatment during pregnancy on offspring structural and functional brain development, stress sensitivity, and cognitive and behavioural performance. Methods: Epidemiological multi-centre cohort study in 80 children and adolescents aged 8 to 18 years whose mothers received GCs to treat a MS relapse during pregnancy compared to unexposed participants. Expected Impact: Creating a guideline-changing evidence-based risk-benefit assessment regarding benefits of the MS relapse therapy for the mother and potential harm to the child.
Papers
Results
Kozik V, Schwab M, Thiel S, Hellwig K, Rakers F, Dreiling M. Protocol for a Cross-Sectional Study: Effects of a Multiple Sclerosis Relapse Therapy With Methylprednisolone on Offspring Neurocognitive Development and Behavior (MS-Children). Front Neurol. 2022 Apr 26;13:830057. doi: 10.3389/fneur.2022.830057. eCollection 2022.Background
Moisiadis VG, Matthews SG. Glucocorticoids and fetal programming part 1: Outcomes. Nat Rev Endocrinol. 2014 Jul;10(7):391-402. doi: 10.1038/nrendo.2014.73. Epub 2014 May 27.Background
Bloom SL, Sheffield JS, McIntire DD, Leveno KJ. Antenatal dexamethasone and decreased birth weight. Obstet Gynecol. 2001 Apr;97(4):485-90. doi: 10.1016/s0029-7844(00)01206-0.Background
Uno H, Eisele S, Sakai A, Shelton S, Baker E, DeJesus O, Holden J. Neurotoxicity of glucocorticoids in the primate brain. Horm Behav. 1994 Dec;28(4):336-48. doi: 10.1006/hbeh.1994.1030.Background
Antonow-Schlorke I, Helgert A, Gey C, Coksaygan T, Schubert H, Nathanielsz PW, Witte OW, Schwab M. Adverse effects of antenatal glucocorticoids on cerebral myelination in sheep. Obstet Gynecol. 2009 Jan;113(1):142-151. doi: 10.1097/AOG.0b013e3181924d3b.Background
van Dijk AE, van Eijsden M, Stronks K, Gemke RJ, Vrijkotte TG. Prenatal stress and balance of the child's cardiac autonomic nervous system at age 5-6 years. PLoS One. 2012;7(1):e30413. doi: 10.1371/journal.pone.0030413. Epub 2012 Jan 17.Background
Glover V, O'Connor TG, O'Donnell K. Prenatal stress and the programming of the HPA axis. Neurosci Biobehav Rev. 2010 Sep;35(1):17-22. doi: 10.1016/j.neubiorev.2009.11.008. Epub 2009 Nov 13.Background
Raikkonen K, Gissler M, Kajantie E. Associations Between Maternal Antenatal Corticosteroid Treatment and Mental and Behavioral Disorders in Children. JAMA. 2020 May 19;323(19):1924-1933. doi: 10.1001/jama.2020.3937.Background
Eriksson JG. The fetal origins hypothesis--10 years on. BMJ. 2005 May 14;330(7500):1096-7. doi: 10.1136/bmj.330.7500.1096. No abstract available.Background
Erhart M, Dopfner M, Ravens-Sieberer U; BELLA study group. Psychometric properties of two ADHD questionnaires: comparing the Conners' scale and the FBB-HKS in the general population of German children and adolescents--results of the BELLA study. Eur Child Adolesc Psychiatry. 2008 Dec;17 Suppl 1:106-15. doi: 10.1007/s00787-008-1012-1.
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History
Started
Oct 2020
Main results due
Dec 2023
Finished
Dec 2024
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