The Alberta Infant Motor Scale (AIMS) is widely used to screen for delays in motor development in high-risk infants, but its reliability and validity in Chinese infants have not been investigated. To examine the reliability and concurrent validity of AIMS in high-risk infants aged 0-9 months in China, this single-center study enrolled 50 high-risk infants aged 0-9 months (range, 0.17-9.27; average, 4.14±2.02), who were divided into two groups: 0-3 months (n=23) and 4-9 months (n=27). A physical therapist evaluated the infants with AIMS, with each evaluation video-recorded. To examine interrater reliability, two other evaluators calculated AIMS scores by observing the videos. To measure intrarater reliability, the two evaluators rescored AIMS after >1 month, using the videos. Concurrent validity was assessed by comparing results between AIMS and the Peabody Developmental Motor Scale-2 (PDMS-2). For all age groups analyzed (0-3, 4-9, and 0-9 months), intraclass correlation coefficients (ICCs) for AIMS total score were high for both intrarater comparisons (0.811-0.995) and interrater comparisons (0.982-0.997). AIMS total scores were well correlated with all PDMS-2 subtest scores (ICC=0.751-0.977 for reflexes, stationary, locomotion, grasping, and visual-motor integration subsets). However, the fifth percentile of AIMS total score was only moderately correlated with the gross motor quotient, fine motor quotient, and total motor quotient subtests of PDMS-2 (kappa=0.580, 0.601, and 0.724, respectively). AIMS has acceptable reliability and concurrent validity for screening of motor developmental delay in high-risk infants in China.

Background B‐Cell CLL/Lymphoma 11B (BCL11B) is a C 2 H 2 zinc finger transcription factor that has broad biological functions and is essential for the development of the immune system, neural system, cardiovascular system, dermis, and dentition. Variants of BCL11B have been found in patients with neurodevelopmental disorders and immunodeficiency. Materials and Methods Whole‐exome sequencing (WES) and clinical examinations were performed to identify the etiology of our patient. A variant in the BCL11B gene, NM_138576.4: c.1206delG (p.Phe403Serfs*2) was found and led to frameshift truncation. Results We reported a male patient with developmental delay and cerebral palsy who carried the BCL11B variant. The detailed clinical features, such as brain structure and immune detection, were described and reviewed in comparison to previous patients. Conclusions The BCL11B‐related neurodevelopmental disorders are rare, and only 17 variants in 25 patients have been found to date. Our report expands the variants spectrum of BCL11B and increases the case of neurodevelopmental abnormalities.