Abstract

Objective To explore possible spinal cord dysfunction in clinically unaffected newborns emerging from fetal distress, using H-Reflex. Methods This cross-sectional study comprised 48 full-term newborn infants investigated between 8 h and 10 days after birth. Twenty-one (21) had fetal distress defined by late-decelerations in fetal heart rate, out of which 11 had also meconium release in utero; 5 passed meconium in utero with normal FHR patterns; and 22 normal controls had uneventful birth. All had normal birth-weight and Apgar scores. All were found normal on neurological examination, except one showing hypotonia following fetal distress. Soleus H-reflex was studied in right lower limb. Results Newborns delivered with fetal distress showed significant reduction in H-reflex excitability ( H/ M ratio) within 2 days of birth. Tests performed closer to the birth event revealed more severe depression. Meconium did not contribute to this effect. Conclusions Fetal distress can lead to transient, subclinical depression of spinal motoneurons in the newborn. Significance This neonatal H-reflex study focuses on excitability of a spinal motoneuron pool rather than conduction parameters (reflecting myelination) available in literature. It reveals excitability changes missed on clinical examination of newborns apparently unaffected by intrapartum hypoxic-ischemic spells. It also draws attention towards spinal cord dysfunction in birth-hypoxia.

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