The exact mechanism for the induction of the<unk>  is still unknown; however, a leading theory asserts that the<unk>  (and perhaps motion sickness in general) is somehow related to the reticular formation, an area of the brainstem associated with arousal. A study of motion-induced effects on the P50 potential (a measure of arousal) showed that subjects exposed to motion environments experience decreased sensory gating, which involves the filtering of information in the brain. In the case of Space Motion Sickness, the unweighting of otolith organs can lead to a sensory mismatch between the visual, vestibular, and somatosensory systems. Motion studies in which the subjects lacked vestibular systems did not experience symptoms of the<unk>  or other manifestations of motion sickness. Vestibular system The role of the vestibular system in the inducement of the<unk>  or related symptoms may be difficult to ascertain. Researchers must compare the results of test subjects experiencing a motion environment to a control environment lacking motion. Experimental subjects who suffered increased fatigue in a rotating environment apparently recovered from this side effect when the same environment ceased motion. In similar studies, control subjects lacking vestibular function did not experience the motion-induced drowsiness associated with the<unk> , while subjects with normal-functioning vestibular systems did experience increased fatigue in the rotating environments. Visual stimulus The relation of the visual-vestibular stimulus to the<unk>  may be observed when comparing airline cockpit crew with cabin crew. While the former typically experience more confined conditions, the airline cabin crew tend to experience more symptoms associated with<unk> ; this effect may be attributed to the lack of visual validation and increased movement of the cabin crew. Biochemicals Certain hormones or biochemicals likely affect the pathways associated with motion sickness in general and the<unk>  in particular. Studies reported by Kennedy, Drexler and Kennedy (2010) have investigated the role of cortisol and melatonin (a hormone associated with the maintenance of circadian rhythms) in motion-induced drowsiness. Subjects were exposed to vection-producing environments (virtual reality, for example) and symptoms were evaluated using a Simulator Sickness Questionnaire.<unk>  symptoms were also measured using a developed scale. The levels of endogenous cortisol and melatonin were then compared with levels before the subjects were tested in the vection environments. Most subjects showed increased levels of endogenous cortisol and melatonin post-vection. Melatonin may therefore be involved in the drowsy state associated with the<unk> . Noradrenergic pathways The inhibition of noradrenergic pathways has also been associated with symptoms of the<unk> . Studies have shown that animals exposed to motion environments commonly exhibit drowsiness and disinclination for activity. These animals show slowed electroencephalography waves, which are involved in the firing of neurons in the brain. The locus coeruleuses of these animals are apparently deactivated. The<unk>  is therefore linked to inhibition of the locus coeruleus-noradrenergic pathways. As such, noradrenaline releasers may be useful in counteracting these symptoms.
Sopite syndrome
Larsen syndrome
Jeavons syndrome
Roemheld syndrome
Dressler syndrome
Feingold syndrome
Reynolds syndrome
Crome syndrome