Aims: Phobic postural vertigo (PPV) is also referred to as secondary somatoform vertigo
because it is often followed by organic vertigo disease such as vestibular neuritis,
Meniere's disease, vestibular migraine, benign paroxysmal positional vertigo, etc.
Although it is a very common and disabling condition its pathophysiology is still
incompletely understood. It was hypothesized that hypersensitivity to movement perception
is one important mechanism leading to somatoform vertigo. This may be due to central
sensitization as described in other chronic conditions (e.g. primary headaches).
Methods: 76 patients (mean age: 38.7 y) suffering from PPV were recruited prospectively from
a tertiary dizziness center between 12/2010 and 06/2011. We performed VBM using 1.5T
high-resolution MRI and compared them to 74 healthy controls (mean age: 35.8 y).
Results: Patients showed a gray matter decrease in multiple brain areas such as the left middle
temporal gyrus, right anterior insular cortex, secondary visual cortex, right superior
temporal gyrus, cerebellum, different areas of the prefrontal cortex, left posterior
hippocampus and left anterior cingulate cortex.
Conclusions: The regions with GM changes observed may reflect different aspects of the condition.
While some are known to play a central role in vestibular and motion processing (cerebellum,
middle temporal gyrus, anterior insular cortex, right superior temporal gyrus) other
changes might be a structural correlate for malfunctioning vestibular processing.
Furthermore, gray matter decrease in the left posterior hippocampus might indicate
impairment of spatial memory leading to impaired orientation in space and navigation.
Other regions (ACC and prefrontal area) are known to represent the connection between
the somatosensory and emotional processing. These areas may play a central role in
the pathophysiology, development and chronification of PPV as seen in other chronic
disease (i.e., chronic pain disorders).
