Chronic Respiratory Acidosis Due to Brain Disease: Reversal of Normal Electroencephalographic Response to Hyperventilation

I. Introduction  In recent years attention has been directed to the alteration in the chemical constituents of the extracellular fluid resulting from cerebral lesions other than those located in the hypophysis. It is the purpose of this communication to report yet another type of metabolic abnormality—chronic respiratory acidosis—due to disease of the central nervous system.The effect of cerebral lesions on the excretion of sodium and chloride ions was first reported by Allott¹ in 1939. The syndrome which he described consists of severe hypernatremia and hyperchloremia associated with moderate azotemia, hyperchloruria, and hypopotassemia in a patient without dehydration. Other reports of similar nature have been published by MacCarty and Cooper,² Sweet et al.,³ and McLardy.⁴ It seems likely that this chemical pattern results from damage to the hypothalamic nuclei in the distribution of the anterior cerebral arteries. There are many reports of sodium and chloride disturbances