Although once a widely speculated about and largely theoretical topic, spaceflightinduced intracranial hypertension is more accepted as a distinct clinical phenomenon; yet, the underlying physiological mechanisms are still poorly understood. In the past, many terms were used to describe the symptoms of malaise, nausea, vomiting, and vertigo though longer duration spaceflights have increased the prevalence of overlapping symptoms of headache and visual disturbance. Spaceflight-induced visual pathology is thought to be a manifestation of increased intracranial pressure (ICP) because of its similar presentation to cases of known intracranial hypertension on Earth as well as the documentation of increased ICP by lumbar puncture in symptomatic astronauts upon return to gravity. The most likely mechanisms of spaceflight-induced increased ICP include a cephalad shift of body fluids, venous outflow obstruction, blood-brain barrier breakdown, and disruption to CSF flow. The relative contribution of increased ICP to the symptoms experienced during spaceflight is currently unknown though as other factors recently posited to contribute include local effects on ocular structures, individual differences in metabolism, and the vasodilator effects of carbon dioxide. Spaceflight-induced intracranial hypertension must be distinguished from other pathologies with similar symptomatology. The following chapter discusses the proposed physiologic causes and the pathological manifestations of increased ICP in the spaceflight environment and provides considerations for future long-term space travel.
Part of the book: Into Space