Postural Orthostatic Tachycardia Syndrome (POTS) is the most common form of dysautonomia seen in chronic Lyme and tick-borne disease patients, particularly those with Bartonella. POTS is characterized by an excessive heart rate increase (≥30 bpm in adults, ≥40 bpm in adolescents) upon standing, accompanied by symptoms of cerebral hypoperfusion such as lightheadedness, brain fog, coat-hanger pain (neck/shoulder), palpitations, exercise intolerance, and profound fatigue.
Overlapping forms of dysautonomia frequently co-occur in the Lyme and related infection population, including orthostatic hypotension, neurocardiogenic syncope (vasovagal), inappropriate sinus tachycardia, small-fiber neuropathy-related autonomic dysfunction, and complex multisystem dysautonomia driven by autoimmunity against adrenergic, muscarinic, and angiotensin II receptors. These autonomic nervous system disturbances are triggered or dramatically worsened by the infections themselves, especially Bartonella, which has a particular tropism for endothelial cells and autonomic ganglia.
Dysautonomia is often a reason Lyme and co-infection patients remain profoundly disabled even after aggressive antimicrobial treatment—the infections initiate an autoimmune and inflammatory cascade that damages autonomic nerves and blood vessels, leading to chronic volume dysregulation, impaired vasoconstriction, and central sensitization. According to Dr. Tania Dempsey, MD, Bartonella is her most frequently implicated trigger, followed by Babesia and Lyme Borrelia, with many patients experiencing dramatic flares of POTS symptoms during treatment as dying bacteria release neurotoxins that further activate mast cells and sympathetic nerves. Successful management, in her experience, requires simultaneous treatment of the underlying infections, aggressive mast cell stabilization (H1/H2 blockers, cromolyn, ketotifen, low-histamine diet), volume expansion (salt, fluids, compression), and targeted autonomic therapies (beta-blockers, ivabradine, midodrine, pyridostigmine, IVIG in autoimmune cases), without which patients plateau or relapse despite microbiologic improvement.
