POTS is not a new problem, only a newly named one. For over a century doctors described young people who fainted or raced their hearts on standing, calling it "soldier's heart" or "effort syndrome." Not until the 1990s did Mayo Clinic researchers formally define Postural Orthostatic Tachycardia Syndrome and give the condition a name.
Where did POTS come from before it had a name?
Descriptions of POTS-like symptoms reach back more than 150 years. During the American Civil War, physician Jacob Mendez Da Costa documented soldiers with racing hearts, breathlessness, and exhaustion, and the picture became known as "soldier's heart," "Da Costa's syndrome," or "effort syndrome" (Wooley, 1976). Similar patients were later labeled with "neurocirculatory asthenia."
These early labels captured a real, repeatable pattern: otherwise healthy young people who felt awful when upright or under exertion. What the labels lacked was a measurable definition, so the condition was often dismissed or misattributed to nerves.
When did POTS get its modern name?
The term Postural Orthostatic Tachycardia Syndrome was formally introduced in 1993, when Dr. Ron Schondorf and Dr. Phillip Low at the Mayo Clinic described patients with orthostatic intolerance whose heart rate jumped dramatically on standing without the expected drop in blood pressure (Schondorf & Low, 1993). This unifying definition gave clinicians a concrete, testable criterion and finally organized research around a condition that had long been misunderstood. If you are exploring a possible diagnosis, our overview of POTS walks through what the pattern looks like today.
What have we learned about POTS since then?
Research since the 1990s shows POTS is not a single disease but a syndrome with several overlapping drivers (Lei et al., 2019). Four insights stand out:
- Hypovolemia (low blood volume): up to 70% of patients have reduced circulating blood volume, feeding fatigue and dizziness.
- Hyperadrenergic states: roughly half live in a heightened "fight-or-flight" mode, with adrenaline surges driving symptoms.
- Deconditioning: prolonged inactivity can shrink cardiac reserve and reduce stroke volume, worsening the cycle.
- Exercise responsiveness: graded, structured activity has been shown to reverse much of this imbalance over time (Fu & Levine, 2015).
Together these findings moved care away from "it's just anxiety" toward real, measurable physiology. Because the drivers overlap with symptoms like brain fog and dizziness, a careful workup matters.
Why does this history matter for patients?
Because POTS is heterogeneous, treatment has to be personalized. Some patients improve most with fluids, salt, and compression, while others need gradual exercise retraining or strategies that calm an overactive nervous system (Lei et al., 2019). There is no single right protocol.
At its core, progress often depends on empowerment: learning to pace, self-regulate, and slowly rebuild tolerance. That means meaningful long-term improvement is possible, even when the path looks different for each person.
How does the upper neck connect to POTS?
At Cerebral, we also pay attention to the craniocervical junction (CCJ), where the top of the spine meets the base of the skull. This region surrounds the brainstem, which helps regulate blood pressure, heart rate, and vagal tone. In our clinical experience, even subtle misalignment or irritation here may disrupt that autonomic balance.
That can amplify the very challenges POTS patients already face, such as poor blood-flow regulation, excess sympathetic drive, and reduced vagal calming. By restoring alignment, upper cervical care may help lower brainstem stress and support healthier self-regulation. It is not a standalone cure, but it can be one part of a comprehensive plan alongside hydration, exercise, and education. You can read more in our articles on how upper cervical care may help POTS patients and hydration, blood flow, and the upper neck.
References
- Wooley CF. Where are the diseases of yesteryear? DaCosta's syndrome, soldiers heart, the effort syndrome, neurocirculatory asthenia — and the mitral valve prolapse syndrome. *Circulation*. 1976. https://www.ahajournals.org/doi/10.1161/01.cir.53.5.749
- Schondorf R, Low PA. Idiopathic postural orthostatic tachycardia syndrome: an attenuated form of acute pandysautonomia? *Neurology*. 1993. https://www.neurology.org/doi/10.1212/WNL.43.1_Part_1.132
- Lei LY, Chew DS, Sheldon RS, Raj SR. Evaluating and managing postural tachycardia syndrome. *Cleveland Clinic Journal of Medicine*. 2019. https://www.ccjm.org/content/86/5/333
- Fu Q, Levine BD. Exercise in the postural orthostatic tachycardia syndrome. *Autonomic Neuroscience: Basic and Clinical*. 2015. https://www.sciencedirect.com/science/article/abs/pii/S1566070214002021