In 1961, Greutzner and Geletneky1 reported a high incidence of abnormal electroencephalograms in adult and pediatric patients with cystic fibrosis. Their study also revealed a correspondingly high incidence among the relatives of these patients. In addition, abnormal slowing in brain wave frequency occurred in 50% of the patients with elevated sweat chloride and sodium concentrations. Their findings suggested central nervous system involvement to be a systemic manifestation of the disease, and it was postulated that this involvement was secondary either to a primary genetic defect or to a metabolic disturbance.
Approximately 95% of all patients with cystic fibrosis of the pancreas manifest pulmonary symptoms which may result in severe pulmonary dysfunction with pulmonary insufficiency and respiratory acidosis. Since it is known that pulmonary insufficiency can contribute to hypoxia as well as to cerebral symptoms,2 an attempt was made to investigate the relationship of the electroencephalograms to arterial