Seizures, hypoxic-ischemic brain injury, and intraventricular hemorrhage in the newborn

The review deals with neonatal seizures, perinatal hypoxic-ischemic brain injury, and neonatal intraventricular hemorrhage. neonatal seizures are the most prominent signals of the largest number of neonatal neurological disorders. The convulsive phenomena may be subtle. The predominant etiological process is hypoxic-ischemic encephalopathy. Prognosis is related primarily to the neurological disease responsible for the seizures. Treatment may be specific for the underlying disorder (e.g., glucose or calcium) or less specific (i.e., therapy with anticonvulsant drugs). Prompt control of the seizures is important to avoid brain injury secondary to the effects of the seizures on ventilation, perfusion, and brain metabolism. Hypoxic-ischemic encephalopathy in the newborn most often is a consequence of intrauterine asphyxia. Diagnosis depends primarily on recognition of the clinical syndrome but also on a variety of neurodiagnostic techniques, including radionuclide and CT brain scans. Prognosis is estimated best by a combination of clinical analysis and specialized neurodiagnostic studies. management is based principally on vigorous support, particularly of ventilation and perfusion, maintenance of adequate glucose influx, and control of seizures. Intraventricular hemorrhage is the most common type of neonatal intracranial hemorrhage. The neuropathology is characterized by bleeding from capillaries of the subependymal germinal matrix. Secondary rupture of the ependymal lining then causes intraventricular hemorrhage. Pathogenesis relates to the anatomy of the germinal matrix, the distribution and regulation of cerebral blood flow, and the structure and vulnerability of periventricular capillaries. Precise diagnosis requires a brain imaging procedure; portable, real-time ultrasound is the preferred approach for critically ill infants. Prognosis relates to the severity of the hemorrhage as well as any preceding hypoxic-ischemic insults and the subsequent occurrence of hydrocephalus. Choice of therapy for posthemorrhagic ventricular dilatation depends upon severity and rapidity of progression and ranges from close observation only to ventriculoperitoneal shunting.