Aetiological Factors

The aetiology of cerebral palsy (CP) is heterogeneous, multifactorial and only partially understood. The brain development begins with neurulation (3 weeks of gestation) and makes further important steps during the first 2 years of life, in particular in the first 12–15 months. CP can result from brain injury occurring during the prenatal, perinatal or postnatal periods. This chapter discusses the aetiological mechanisms that underpin the development of CP. For some, e.g. iodine, perinatal arterial ischaemic stroke (maternal, placental, fetal, neonatal), head injury, coagulation defects and haemorrhage, the relationship with the development of disability is clear. But for others, sometimes considered risk factors rather than aetiological factors, for example, premature birth, small for gestational age, and multiple pregnancies, despite strong evidence of an association, the aetiological mechanisms remain obscure. The potential mechanisms underlying the relationship between hypoxia and the role of neonatal encephalopathy in the development of CP are explored, and the role of genetic and familiar factors associated with CP is identified and discussed. In summary, the aetiological factors associated with CP are complex and diverse, and the precise causal mechanisms underpinning the development of CP for several of the associated risk factors are still unknown

Helicobacter pylori infection has no impact on manometric and pH-metric findings in adolescents and young adults with gastroesophageal reflux and antral gastritis: eradication results to no significant clinical improvement

The relationship between <em>Helicobacter pylori </em>(Hp) gastritis and gastroesophageal reflux disease (GERD) remains controversial. The aim was to investigate the association between Hp infection and gastroesophageal reflux (GER) and the impact of Hp eradication on esophageal acid exposure and motility in adolescents and young adults with Hp gastritis and GERD. Sixty-four patients with symptoms suggestive for GERD, of which 40 Hp-positive (group A) and 24 Hp-negative (group B), underwent endoscopy-biopsy, esophageal manometry and 24-hour pH-metry. All group A patients received eradication treatment and were re-evaluated six months later again with 24-hour pH-metry, esophageal manometry, endoscopy-biopsy and clinical assessment. At inclusion, there were no significant differences between the two groups regarding sex, age, grade of endoscopic esophagitis, manometric and pH-metry findings. All Hp-positive patients had an antral predominant gastritis. Eradication of Hp was successful in all patients, and gastritis and esophagitis were healed in all patients. The mean lower esophageal sphincter pressure (LESP) increased significantly from 11.25 mmHg before to 11.71 mmHg after eradication (P&lt;0.05). A significant decrease in reflux index was observed (mean RI 6.02% before versus 4.96% after eradication (P&lt;0.05). However clinical symptoms of GER improved not significantly after 6 months follow up. Conclusively, in children and young adults with GER symptoms and GERD, the presence or absence of Hp has no impact on manometric and pH-metric findings. Eradication of Hp infection results in increase in LESP with a consequent decrease in esophageal acid exposure but not significant clinical improvement