It is becoming increasingly clear that cerebrovascular hemodynamics are influenced by alterations in cardiopulmonary physiology. The work of Kety and Schmidt1 revealed that an increased cerebral blood flow occurs in hypercapnia and in hypoxia. It has also been shown that the increased cerebral blood flow in such situations is followed by increased cerebrospinal fluid pressure.2 The exact mechanism whereby these changes influence cerebral vascular dynamics is not clear. Clinical syndromes attesting the relationship between cardiopulmonary physiology and cerebrovascular dynamics have been described. Within the past two decades reports have appeared demonstrating signs and symptoms of intracranial disease in patients with primary pulmonary problems. These reports have been well reviewed by Conn et al.,3 who also added two cases of their own of patients with "emphysematous encephalopathy."
In recent months we have had the opportunity of studying two patients with pulmonary disease associated with clinical findings suggesting the