Young patients with sudden racing heart rates upon standing were routinely misdiagnosed with hysteria and panic attacks; Mayo Clinic neurologist Phillip Low proved that a damaged autonomic nervous system allows blood to pool in the legs, forcing the heart into frantic tachycardia. Published in Neurology in 1993, this landmark paper formally defined Postural Orthostatic Tachycardia Syndrome (POTS), providing the diagnostic foundation for millions of patients battling post-viral autonomic conditions and Long COVID today.

For decades, hundreds of thousands of young, previously athletic patients—predominantly young women—experienced debilitating dizziness, brain fog, and fainting whenever they stood up. Medical doctors repeatedly dismissed their symptoms as anxiety, panic disorders, or chronic hyperventilation.
Mayo Clinic neurologist Phillip Low discovered a clear physical neurological disorder: POTS. When a healthy person stands up, the autonomic nervous system automatically squeezes blood vessels in the legs to push blood up to the brain. In POTS patients, this reflex fails, allowing blood to pool in the lower body and forcing the heart to race by thirty to fifty beats a minute just to prevent the brain from fainting.
Low established the first objective tilt-table diagnostic criteria for autonomic dysfunction. By giving millions of dismissed patients a biological diagnosis, by guiding modern autonomic rehabilitation protocols, and by serving as the clinical foundation for post-viral Long COVID research, POTS neurology validates autonomic medicine.
Idiopathic postural orthostatic tachycardia syndrome
To characterize the idiopathic postural orthostatic tachycardia syndrome (POTS), we reviewed the records of all patients aged 20 to 51 who presented to the Mayo Autonomic Reflex Laboratory and who exhibited tachycardia at rest or during head-up tilt. These patients were usually women who experienced an acute onset of persistent lightheadedness and fatigue or gastrointestinal dysmotility. In seven patients, a viral illness may have preceded the onset of symptoms. In two instances, signs and symptoms of a small-fiber sensory neuropathy were present. Laboratory evaluation of autonomic function revealed increased diastolic blood pressure to tilt (5/16), increased Valsalva ratio, marked decrease in phase II of the Valsalva maneuver with normal phase IV overshoot, and normal forced respiratory sinus arrhythmia. Abnormal quantitative sudomotor axon reflex test and thermoregulatory sweat test and an excessive orthostatic increase of catecholamines were found in some patients. We conclude that in many instances POTS may be a manifestation of a mild form of acute autonomic neuropathy.
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