The degree of Wallerian degeneration (WD) in the corticospinal tracts seen with magnetic resonance imaging (MRI) was correlated with the distribution and severity of congenital hemiplegia in 20 children aged nine months to nine years. All the children had hemispheric lesions diagnosed with ultrasound in the neonatal period: MRI and clinical assessment were performed from nine months to nine years of age. Hemiplegia was graded as mild, moderate or severe and into predominantly upper or lower limb distribution. WD was assessed by the presence or absence of signal intensity changes in the internal capsule on inversion recovery and spin echo sequences and by the asymmetry of the upper brainstem. The degree of asymmetry was estimated by measuring the cross sectional area (CSA) of the brainstem at three levels and calculating the ratio of the measurements between the side of the lesion and the unaffected side. Infarct size was estimated from the CSA of the infarct at the maximum site of the lesion. Both measurements were correlated with the severity of outcome and the site of involvement. There was a better correlation between severity of outcome and brainstem asymmetry (p = 0.003) than severity of outcome and infarct size (p = 0.02). There was also a significant correlation between upper limb involvement and brainstem asymmetry (p = 0.01). As WD estimated by brainstem asymmetry appears early and is easy to measure, it may be a good marker to estimate later impairment in infants with predominantly unilateral hemispheric haemorrhagic/ischaemic lesions diagnosed in the neonatal period.

Clinical and laboratory investigations of neonatal pain suggest that preterm neonates are more vulnerable to stress and painful procedures and have heightened responses to successive stimuli. Preterm infants receiving intensive care are subjected to frequent invasive and stressful procedures as well as more chronic environmental influences. Acute episodic pain may cause early neurologic injury. Repeated and prolonged exposure to pain may alter subsequent psychokinetic development, as well as affect long-term neurodevelopmental, behavioral and social-emotional outcome. Several pain measures exist to assess pain in full-term and preterm neonates, including behavioral indicators and physiological indicators of pain. Therapeutic interventions can provide comfort and analgesia in preterm neonates. Guidelines for preventing or treating neonatal pain and its adverse consequences include recognition of the sources of pain and routine assessments of neonatal pain, avoidance of recurrent painful stimuli and the use of specific non-pharmacological and pharmacological interventions.

Neonates with unilateral hemispheric lesions detected by imaging in the newborn period are at risk for developing hemiplegia. Five full-term infants with predominantly unilateral lesions identified by cranial ultrasound in the neonatal period and confirmed with MRI were examined clinically at regular intervals in order to establish the development, incidence and evolution of later hemiplegia and the evolution of hemiplegic signs. In the neonatal period the infants had either a normal examination or subtle transient abnormalities. Abnormalities were not seen until 6 months of age in infants who developed hemiplegia. The number of hemiplegic signs in each child increased with time, the earlier the signs appeared the more severe the hemiplegia. In some infants deterioration with loss of preexisting skills was observed. At 24 months two of the infants were normal, one had a mild and two a moderate hemiplegia.

Clinical and laboratory investigations of neonatal pain suggest that preterm neonates are more vulnerable to stress and painful procedures and have heightened responses to successive stimuli. Preterm infants receiving intensive care are subjected to frequent invasive and stressful procedures as well as more chronic environmental influences. Acute episodic pain may cause early neurologic injury. Repeated and prolonged exposure to pain may alter subsequent psychokinetic development, as well as affect long-term neurodevelopmental, behavioral and social-emotional outcome. Several pain measures exist to assess pain in full-term and preterm neonates, including behavioral indicators and physiological indicators of pain. Therapeutic interventions can provide comfort and analgesia in preterm neonates. Guidelines for preventing or treating neonatal pain and its adverse consequences include recognition of the sources of pain and routine assessments of neonatal pain, avoidance of recurrent painful stimuli and the use of specific non-pharmacological and pharmacological interventions.

Aim: To investigate whether the factor V Leiden mutation (FVL), the prothrombin gene G20210A variant or the methylenetetrahydrofolate reductase (MTHFR) C677T genotype are risk factors for central nervous system (CNS) thrombosis or intraventricular hemorrhage (IVH) in neonates. Methods: Thirteen full‐term infants with cerebral infarct documented with magnetic resonance imaging were assessed with the whole spectrum of assays for thrombophilia including the three DNA‐based prothrombotic factors. The frequency of congenital defects was compared with that observed in 38 healthy full‐term infants. The genetic defects were also assessed in 55 premature neonates, gestational age <32wk, 17 of whom developed IVH, grade II‐IV. The remaining 38 premature neonates without IVH were used as controls. Results: In the CNS thrombosis group: a prothrombotic factor was detected in 53% of patients and an underlying disease or a triggering event in 61.5%. The frequency of FVL in thrombosed neonates was higher (23%) than in the group of healthy full‐term infants (10.5%), although it did not reach statistical significance. IVH developed in 30.9% of premature neonates. Apart from several maternal or neonatal risk factors for IVH, FII G20210A was found in a considerably higher prevalence in the cohort of neonates with IVH (12%) than in those without (2%), although the difference was not statistically significant. Conclusion: The pathogenesis of cerebral thrombosis or IVH in neonates is multifactorial. Along with underlying diseases or triggering events, congenital prothrombotic factors (FVL or FII G20210A) showed a trend towards a higher frequency in full‐term infants with CNS thrombosis or premature neonates with IVH than in controls. However, their contribution to neonatal cerebral thrombosis or IVH remains to be determined.