Congenital nystagmus protects against motion sickness

What is it about?

Motion sickness is provoked when ambiguity or ‘conflict’ within vestibular signals or within visual vestibular interactions challenge the constancy of ‘uprightness’, the parsing of tilt versus translation and the interpretation of self-versus environmental motion. Frequently, such conflicts pit the ‘slow phase’ visual mechanisms of pursuit and optikokinesis against the slow phase vestibular ocular reflex (VOR); as when reading in a car the VOR evoked by car motion is opposed by pursuit to maintain fixation on the text: the effort is rarely satisfactory and nausea ensues. The implication of slow phase eye movements in motion sickness provocation raises the question of motion sickness susceptibility in subjects with abnormal slow phase eye movements. A near-ideal population to test are subjects with ‘CN’ type congenital nystagmus who are normal in other respects relevant to nauseogenesis. During fixation of a stationary or moving target, both with and without head movement, the visual and vestibular slow phase eye movements of CN take the eyes ‘off target’ with exponentially increasing velocity. Frequent resetting saccades return the eyes to target creating a nystagmus. We recruited 34 CN subjects who consented to being filmed and completed a validated motion sickness susceptibility questionnaire ‘MSSQ’ and a visually induced motion sickness susceptibility questionnaire ‘VIMSSQ’. CN MSSQ scores were significantly lower (p<.01) for both childhood and adult motion sickness versus standard population norms. CN VIMSSQ scores were also lower for ‘nausea’ (p<.01) and ‘headache’ (p<.05) factors, marginally lower for ‘dizziness’ (p=.08), but similar to normal for ‘fatigue’, ‘eye strain’ and ‘avoidance’.

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Photo by Wonderlane on Unsplash

Photo by Wonderlane on Unsplash

Why is it important?

The classical ‘nausea’ of motion sickness and the frequent secondary feature of ‘headache’ are absent or significantly low in the CN population. Evident explanations are twofold. Firstly, CN subjects could be highly adapted to motion from early life because their visual world is unstable from birth. Secondly, slow phase eye movements are an important component of visual-vestibular tonic control of balance and orientation. They are organised in a brainstem-cerebellar neural network. A disorder of the network, as in ‘CN’, prevents the occurrence of ’conflicts’ which provoke motion sickness.