Dr. Schofield: It is exciting that there has been increasing publications in the field of dysautonomia over the last few years. I would like to see more research into the underlying causes of dysautonomia, including the
- clinically apparent link between dysautonomia and mast cell activation syndrome;
- utility of the novel/early Sjogren’s panel (since we know that SS-A and SS-B have very poor sensitivity in patients with autonomic neuropathy/dysautonomia due to Sjogren’s syndrome) in association with lip (minor salivary) biopsy;
- incidence of criteria and non-criteria antiphospholipid antibodies in patients with dysautonomia, since this diagnosis may be associated with severe complications if missed
- presence of autoimmune conditions to cause dysautonomia by triggering the production of the adrenergic and muscarinic antibodies that have been found in many patients with dysautonomia
Dr. Plotnikoff: The correlation of POTS with hypermobility as well as with mast cell activation is fascinating and needs to be better understood. Additional topics where more data is needed include
- autoimmune drivers of POTS
- infectious or toxic triggers for POTS
- POTS as a function of unbalanced membrane composition/receptor dysfunction
Dr. Goodkin: There are some interesting non-invasive potential treatments that need to be investigated, including
- A randomized trial of cranial osteopathic manipulation in children that directly modulates the autonomic nervous system. One physician believes POTS is caused by abnormal sensory processing and has had excellent results with cranial nerve stimulation using a tuning fork, vagus nerve stimulator and eye movements called saccades;
- Use of a vagus nerve stimulator to improve gastrointestinal hypomotility symptoms in pediatric patient;
- Randomized trial of Xyrem (powerful inducer of phase 4 sleep) to improve sleep quality, even in those with a normal polysomnograms;
- The role of specific exercise training on POTS symptomology;
- The role of iron for improving POTS symptoms. Anecdotal data suggests that patients with a ferritin less than 40 feel better with treatment independent of hemoglobin.