Correlation Between Fetal Heart Rate Evolution Patterns and Magnetic Resonance Imaging Findings in Severe Cerebral Palsy: A Longitudinal Study

Abstract

ABSTRACT The study of fetal heart rate (FHR) pattern evolution during labor is useful for evaluating the timing of perinatal brain injury that can lead to cerebral palsy (CP). Magnetic resonance imaging (MRI) is also useful for prospectively predicting neurological outcomes and retrospectively evaluating the pathophysiological types and patterns that affect brain injury. Using both FHR evolution studies and MRI findings of infants may help to evaluate the insult severity and pattern, as well as insult timing, of CP. Currently, studies on the association between these 2 tools are lacking. The aim of this study was to investigate the association between FHR patterns and MRI findings. This was a longitudinal cohort study using the nationwide database of the Recurrence Prevention Committee, Japan Obstetric Compensation System for Cerebral Palsy. Included were infants with severe CP at ≥34 weeks of gestation between 2009 and 2014. Severe CP was defined as equivalent to levels 3 to 5 of the Gross Motor Function Classification System. Excluded were infants with missing or uninterpretable cardiotocograph tracings or unavailable brain MRI findings after birth. Cardiotocograph strips were analyzed, and FHR patterns were categorized into 6 groups: bradycardia, persistently nonreassuring (NR-NR) pattern, reassuring-prolonged deceleration (R-PD), initially reassuring that progressed over time to a nonreassuring, or Hon pattern (R-Hon), persistent reassuring (R-R) pattern, and unclassified. Brain MRI patterns were classified based on the predominant site—basal ganglia–thalamus (BGT), white matter, watershed, stroke, normal, and unclassified—then described as mild, moderate, or severe. A total of 672 were included in the analysis. In the analysis of FHR patterns, 9% had bradycardia, 25% had NR-NR, 17% had R-PD, 17% had R-Hon, 13% had R-R, and 20% were unclassified. The majority had BGT injury (76%), indicating the cause as acute, profound hypoxia-ischemia. In infants in which the BGT region was spared, 5.4% had white matter injury, 1.2% had watershed injury, 1.6% had stroke, 1.9% had normal findings, and 14% were unclassified. In infants with BGT injury, common perinatal risk factors for CP included umbilical cord abnormality (>40%), placental abruption (23%), intrauterine infection (18%), and small for gestational age (13%). There was a significant increased risk of BGT injury in infants with placental abruption (adjusted odds ratio [aOR], 8.02; 95% confidence interval [CI], 1.53–41.95), but a decreased risk in small for gestational age infants (aOR, 0.38; 95% CI, 0.17–0.86). Basal ganglia–thalamus injury impacted a substantial proportion of infants across all FHR patterns, including bradycardia (97%), NR-NR (75%), R-PD (90%), R-Hon (76%), R-R (45%), and unclassified cases (45%). Most infants with BGT injury showed severe damage, with significant differences observed in the bradycardia group (aOR, 6.71; 95% CI, 1.26–35.75), NR-NR group (aOR, 2.51; 95% CI, 1.10–5.73), and R-PD group (aOR, 7.04; 95% CI, 2.24–22.10) compared with the R-R group after adjusting for clinical background. Cortical damage in the BGT accompanied most cases—with significantly more severe involvement in the bradycardia group (aOR, 5.61; 95% CI, 1.20–26.33), NR-NR group (aOR, 4.57; 95% CI, 1.33–15.68), and R-Hon group (aOR, 4.69; 95% CI, 1.22–18.00). Brainstem injuries were less frequent, with no difference in prevalence between groups. In summary, 76% of infants with severe CP developed BGT injury based on the analysis of brain MRI findings. Basal ganglia–thalamus injuries were more frequently characterized by severe neonatal asphyxia versus non-BGT injuries.