Cerebrospinal fluid constituents of cat vary with susceptibility to motion sickness.

Six female cats, varying in susceptibility to motion sickness, were implanted with chronic cannulae in the rostral portion of the fourth ventricle. The cats were then challenged with a motion sickness-inducing stimulus. Samples of cerebrospinal fluid were withdrawn before and after emesis or 30 min of motion if emesis did not occur and again on control (no motion) days. The samples were analyzed by HPLC with an array of 16 coulometric detectors. Thirty-six compounds were identified in the samples. Baseline levels of DOPAC, MHPGSO4, uric acid, DA, 5-HIAA and HVA were lower on motion and control days in cats which became motion sick when compared with cats which did not become motion sick. None of the identified compounds varied as a function of either exposure to motion or provocation of emesis. It is concluded that susceptibility to motion sickness is a manifestation of individual differences related to fundamental neurochemical composition.

Hormonal status and fluid electrolyte metabolism in motion sickness.

In the first experimental series, 10 healthy male test subjects with a high susceptibility to motion sickness showed a significant increase of ACTH, cortisol, STH, prolactin, ADH, aldosterone concentrations, and plasma renin activity after vestibular tests. The 10 subjects with a moderate susceptibility exhibited a still higher increase of the hormones, except plasma renin. The 8 test subjects with a low susceptibility displayed a considerable increase in ACTH, cortisol, and STH after vestibular stimulation. In the second experimental series, the increase of STH, cortisol, ADH, aldosterone and renin occurred immediately after rotation in the moderate susceptibility subjects and an hour after exposure in the high susceptibility subjects. This may be indicative of specific immediate adaptation mechanisms or excitation transfer in the CNS in high susceptibility persons. In the third experimental animal series, the permeability of the blood-brain barrier for 125I and IgG increased after rotation. Greater concentrations of potassium, chloride, and urea in CSF are suggestive of an inhibition process activation in the CNS and, probably, of an active urea transport by the vascular plexus epithelium which maintains constant osmotic pressure of cerebral extracellular fluid and prevents hyper-hydration of CNS neurons.

Neurohumoral hypothesis of motion-induced vomiting. Communication.

The current status and implications of the neurohumoral hypothesis of motion-induced vomiting are reviewed. Data show that squirrel monkey subjects vomit only once if horizontal rotation is terminated immediately on the occurrence of the emetic response. Refractory periods for multiple vomiting episodes concurrent with continued rotation are sufficiently brief to suggest that the expected presence of the hypothetical neurochemical agent in the cerebrospinal fluid of the fourth ventricle should continue to evoke more than one vomiting response even after cessation of motion stimulation. In its present form, the hypothesis is conceptually vague and should be developed further to account for a mechanism by which the expected recurrent emesis is inhibited during the period when the alleged agent is a potentially effective stimulant.

Evidence for a motion sickness agent in cerebrospinal fluid.

The possibility that there might be a neurohumoral cerebrospinal fluid (CSF) link in motion sickness was directly tested in cats by blocking the flow of CSF from the third into the fourth ventricle. Evidence obtained thus far is consistent with the hypothesis. Cats with demonstrably sound blocks did not vomit in response to an accelerative motion sickness stimulus, whereas cats with imperfect 'leaky' blocks vomited with little or no increase in latency. Although there are several putative candidates, the identification of a humoral motion sickness substance is a matter of conjecture.