BACKGROUND: Individuals with mal de debarquement syndrome (MdDS) experience a 
chronic illusion of self-motion triggered by prolonged exposure to passive 
motion, such as from sea or air travel. The experience is one of rocking 
dizziness similar to when the individual was originally on the motion trigger 
such as a boat or airplane. MdDS represents a prolonged version of a normal 
phenomenon familiar to most individuals but which persists for months or years 
in others. It represents a natural example of the neuroplasticity of motion 
adaptation. However, the localization of where that motion adaptation occurs is 
unknown. Our goal was to localize metabolic and functional connectivity changes 
associated with persistent MdDS.
METHODS: Twenty subjects with MdDS lasting a median duration of 17.5 months were 
compared to 20 normal controls with (18)F FDG PET and resting state fMRI. 
Resting state metabolism and functional connectivity were calculated using age, 
grey matter volume, and mood and anxiety scores as nuisance covariates.
RESULTS: MdDS subjects showed increased metabolism in the left entorhinal cortex 
and amygdala (z>3.3). Areas of relative hypometabolism included the left 
superior medial gyrus, left middle frontal gyrus, right amygdala, right insula, 
and clusters in the left superior, middle, and inferior temporal gyri. MdDS 
subjects showed increased connectivity between the entorhinal cortex/amygdala 
cluster and posterior visual and vestibular processing areas including middle 
temporal gyrus, motion sensitive area MT/V5, superior parietal lobule, and 
primary visual cortex, while showing decreased connectivity to multiple 
prefrontal areas.
CONCLUSION: These data show an association between resting state metabolic 
activity and functional connectivity between the entorhinal cortex and amygdala 
in a human disorder of abnormal motion perception. We propose a model for how 
these biological substrates can allow a limited period of motion exposure to 
lead to chronic perceptions of self-motion.