5; CI: 1.2‐1.9) of having severe neuromotor alteration between 18 and 22 months.6 Kohlendorfer et al.9 also investigated the association of potential risk factors for neurodevelopmental disorders. Children who developed neonatal sepsis were three times more likely to have neuromotor and cognitive development alterations (PDI and MDI < 85)

at 12 months of corrected age. Conversely, a recent study10 on neurodevelopment alterations in a cohort of preterm infants assessed at 24 months of corrected age included 136 children with confirmed sepsis, 169 BEZ235 with suspected sepsis, and 236 without infection. Children with confirmed sepsis were three times more likely to have cerebral palsy when compared with those without sepsis. It was observed that children with clinical infection were almost twice as likely to have cerebral palsy, but there was no statistical significance. Clinical sepsis and confirmed sepsis showed no association with cognitive delay.10 Although the blood culture is considered to be the gold standard for sepsis diagnosis, its sensitivity is less than 50%.25 In the present study, it was important to include clinical sepsis, as due to the low sensitivity of blood cultures, children

who had infection could fail to be included as exposed to sepsis, and thus underestimate its effects on neuromotor development. Several authors have considered clinical sepsis in their recently published articles, either alone Sclareol or in combination26, see more 27 and 28 with confirmed sepsis, and employed similar criteria to those of the present study for the classification of clinical sepsis.6, 10 and 28 Neuromotor alterations in preterm infants with neonatal infection may be mediated by white matter lesions.5 and 29 However, it is not known which mechanism generates the white matter lesions. It appears that such lesions can be attributed to the susceptibility of oligodendrocyte precursors to inflammation, hypoxia, and ischemia.28 Helmes et al.30 observed no association between late‐onset sepsis

and white matter lesions, and found no adverse effects on development at 15 months of age in preterm children. It should be considered that part of the observed neuromotor alterations may be due to transient neurological abnormalities observed in preterm infants up to 18 months of corrected age. Brandt et al.31 observed abnormal neurological signs, mainly in the first year of life, and concluded that it is not possible to predict whether an early abnormal neurological sign is transient, and thus a longitudinal follow‐up of these children is required, emphasizing the importance of follow‐up in this population. Gianní et al.32 emphasized the importance of early stimulation and intervention in these children to promote better neuropsychomotor development. In the present study, the families of children with any alteration were instructed to perform exercises at home and/or physical therapy.