Although CNH is typically characterized by the presence of lesions in the brainstem region, the mechanism by which these lesions create uninhibited stimulation of the expiratory and inhalatory centers is still poorly understood. These lesions typically arise after cancerous cells from another location of the body metastasize and move to the brain. The mechanism by which CNH was originally thought to occur involved the separation of the pontine and medullary respiratory centers by infiltrative tumors. Animal models mimicking this separation, however, do not exhibit CNH. A secondary postulated mechanism by which CNH may function is that the lesions produce lactate which consequently serves as a stimulator for the chemoreceptors of the medullary region of the brainstem. Previous studies of CNH patients have verified the presence of lactic acid in cerebral spinal fluid.
Central neurogenic hyperventilation
Central sleep apnea
Exercise-induced bronchoconstriction
Hypoxic ventilatory response
Hypoxic pulmonary vasoconstriction
Central hypoventilation syndrome
Intermittent hypoxia
Histotoxic hypoxia