Slow pupillary light responses in infants at high risk of cerebral palsy were associated with periventricular leukomalacia and neurological outcome. (19th August 2016)

• Record Type: Journal Article
• Authors: Hamer, Elisa G.; Vermeulen, R. Jeroen; Dijkstra, Linze J.; Hielkema, Tjitske; Kos, Claire; Bos, Arend F.; Hadders‐Algra, Mijna
• Is Part Of: Acta pædiatrica. Volume 105:Number 12(2016)
• Page Start: 1493
• Page End: 1501
• Publication Date: 2016-08-19
• Subjects: Cerebral palsy -- Infants -- Neuroimaging -- Periventricular leukomalacia -- Pupillary light response; Pediatrics -- Periodicals; Pediatrics; 618.92
• DOI: 10.1111/apa.13532
• Languages: English
• ISSNs: 0803-5253

Abstract

Abstract: Aim: Having observed slow pupillary light responses (PLRs) in infants at high risk of cerebral palsy, we retrospectively evaluated whether these were associated with specific brain lesions or unfavourable outcomes. Methods: We carried out neurological examinations on 30 infants at very high risk of cerebral palsy five times until the corrected age of 21 months, classifying each PLR assessment as normal or slow. The predominant reaction during development was determined for each infant. Neonatal brain scans were classified based on the type of brain lesion. Developmental outcome was evaluated at 21 months of corrected age with a neurological examination, the Bayley Scales of Infant Development Second Edition and the Infant Motor Profile. Results: Of the 30 infants, 16 developed cerebral palsy. Predominantly slow PLRs were observed in eight infants and were associated with periventricular leukomalacia (p = 0.007), cerebral palsy (p = 0.039), bilateral cerebral palsy (p = 0.001), poorer quality of motor behaviour (p < 0.0005) and poorer cognitive outcome (p = 0.045). Conclusion: This explorative study suggested that predominantly slow PLR in infants at high risk of cerebral palsy were associated with periventricular leukomalacia and poorer developmental outcome. Slow PLR might be an expression of white matter damage, resulting in dysfunction of the complex cortico‐subcortical circuitries.