This is not a vague theory. When researchers actually measured blood volume in postural orthostatic tachycardia syndrome, they found a real deficit in plasma volume, red cell volume, and total blood volume compared with healthy controls — and, strangely, the kidney hormones that should be screaming to retain salt and water (renin and aldosterone) were paradoxically low (Circulation). The body is under-filled and, at the hormonal level, doesn’t seem to know it.

Now layer hypermobility on top. In hypermobile Ehlers-Danlos syndrome and hypermobility spectrum disorder, the same collagen laxity that makes a shoulder slide out of place also makes veins more compliant — stretchier, easier to distend. Stretchy veins under gravity means blood pools in the legs, pelvis, and splanchnic bed instead of returning to the heart. Add a genuinely low plasma volume and you have a circulation with almost no reserve. A recent study of hEDS patients found reduced orthostatic cerebral blood flow velocity in 79% of them, along with mild widespread autonomic failure and frequent small fiber neuropathy (American Journal of Medicine Open). Comprehensive reviews of dysautonomia in the Ehlers-Danlos syndromes describe exactly this pattern of orthostatic intolerance and hypovolemia as a core feature, not a rare complication (PMC review).

If this is new territory for you, start with our primer on understanding dysautonomia and then come back — the rest of this article assumes that foundation.

When cerebral perfusion drops far enough and fast enough, the brain can produce jerking, stiffening, eye rolling, and even incontinence. This is convulsive syncope — and it is not epilepsy. The movements are the downstream consequence of global cerebral hypoperfusion, not abnormal electrical discharge (MedLink Neurology). It shows up in roughly one in eight patients presenting with syncope, and it is a well-documented cause of epilepsy misdiagnosis: between 10% and 25% of patients referred to epilepsy clinics turn out to have recurrent syncope instead (Epilepsy Society review chapter).

POTS patients are squarely in this group. A published case report describes a young patient carrying a seizure diagnosis for years — on antiepileptic medication — until tilt-table testing revealed POTS as the actual driver of the seizure-like episodes (case report, PubMed Central). I see the same story in clinic: a hypermobile patient, hot shower or long line or a bad night of hydration, a faint with convulsive movements, and then years of the wrong workup.

What tends to separate them. Hypovolemic, syncopal events usually have a warning — tunnel vision, ringing, nausea, sweating, that gray fading feeling — and they are triggered by position, heat, standing still, pain, or dehydration. The jerking is brief and irregular rather than a sustained rhythmic tonic-clonic sequence. Recovery is quick once you are flat, without the prolonged postictal confusion of a generalized seizure. Laboratory work supports the same split: creatine kinase typically rises within 24 hours of a generalized tonic-clonic seizure, and serum lactate two hours out is usually elevated after a true seizure but rarely after syncope. None of this is diagnostic on its own — it is why the workup matters.

The stroke-like presentation is less familiar to most clinicians, so it frightens people more. Patients describe transient one-sided weakness or heaviness, facial droop, difficulty finding words, blurred or blacked-out vision, or a limb that feels foreign — coming on with standing and easing when they lie down.

There are two overlapping mechanisms. The first is straightforward under-perfusion: cerebral blood flow velocity drops abnormally on standing. Neurologists have formally described orthostatic cerebral hypoperfusion syndrome, in which cerebral blood flow falls on tilt testing without any drop in blood pressure at all — meaning a normal blood pressure reading in the ER does not rule this out. In the original series, mean cerebral blood flow velocity fell 24% on tilt in these patients versus 4% in controls, with no orthostatic hypotension in either group (Frontiers in Aging Neuroscience).

The second is the one people miss: hypocapnia. When volume-depleted patients stand, stroke volume falls and they hyperventilate to compensate. Blowing off carbon dioxide constricts cerebral arterioles, which cuts brain blood flow further — a paradoxical self-defeating loop that was documented in orthostatic intolerance decades ago in Stroke (Stroke, AHA Journals) and has since been mapped in detail: reduced stroke volume and brain perfusion are what drive the postural hyperventilation in POTS in the first place (JACC: Basic to Translational Science). Brain SPECT imaging in POTS patients with cognitive dysfunction has now shown regional perfusion abnormalities directly (Scientific Reports).

Migraine physiology muddies the water further, and hypermobile patients have a lot of it — migraine is reported in up to three quarters of patients with symptomatic joint hypermobility, often with aura and earlier onset than the general population (Frontiers in Neurology). Aura itself can produce transient sensory, speech, and motor deficits. Hypoperfusion and migraine frequently travel together in the same episode.

Patients tell me their worst episodes happen in the air, at ski resorts, or in mountain towns — and the physiology backs them up. A commercial cabin is pressurized to roughly 6,000–8,000 feet, not sea level. In a controlled hypobaric chamber study of 502 volunteers published in the New England Journal of Medicine, oxygen saturation fell by up to 4.4 percentage points at 8,000 feet, and reported discomfort rose with altitude and became apparent after three to nine hours of exposure (NEJM). That is a healthy cohort. Now give that same exposure to someone already running low on plasma volume with stretchy veins.

Four things stack up on a flight, all in the wrong direction: mild hypobaric hypoxia, cabin humidity often in the single digits pulling insensible water out of you with every breath, hours of immobile dependent sitting letting blood pool, and the usual travel behavior of skipping salt and fluids because airplane bathrooms are miserable. Altitude also triggers a diuresis — you lose fluid faster at elevation, which is precisely the mechanism you cannot afford to lose. The same logic applies to a road trip over a mountain pass, a Denver conference, or a hot rooftop bar at altitude.

Gravity is the enemy in these episodes, so remove it. Lying down with the legs elevated is the single most effective intervention available in the first sixty seconds — it returns pooled blood to the central circulation and restores cerebral perfusion mechanically, no medication required. Do not try to “walk it off” and do not let someone prop you upright in a chair. On a plane, the aisle floor is better medicine than the seat.

This is the most underused tool in dysautonomia care, and the evidence is strong. In a randomized crossover tilt-table trial, compression lowered heart rate and improved symptoms in a dose-dependent way — full abdominal-plus-leg compression performed best, and stroke volume and systolic pressure were better maintained with abdominal coverage than with lower-leg stockings alone (JACC).

A 2025 follow-up showed that commercially available abdominal-only garments cut the orthostatic heart rate rise by about 14 bpm and reduced symptoms both acutely and over hours of wear (Canadian Journal of Cardiology).

Practical version: cover the abdomen, not just the calves — that is where the splanchnic pooling happens. Put it on before you get out of bed, and wear it for the entire flight.

In a randomized crossover study, six days of high sodium intake raised total blood volume and plasma volume, lowered standing norepinephrine, and reduced the orthostatic heart rate change in POTS patients compared with a low sodium diet (JACC). Salt is a treatment here, not a vice.

The practical failure point is compliance. Salty drinks taste awful, so people quietly stop. That is exactly why I formulated CoreSalt™ for my own patients as a taste-free capsule — sodium, magnesium, and potassium with tyrosine, taurine, and ginger — with a steady daily baseline and a higher breakthrough dose for heat, training, sauna, and travel days.

Practical version: pair sodium with water. Aim for roughly 250–500 mL of fluid for every extra gram of sodium, and have your dose set in clinic rather than guessed at.

Most of my hypermobile POTS patients are chronically under-hydrated in a way they have normalized. The target is deliberate, spread-out intake through the day — not one heroic bottle at 4 p.m. — with front-loading in the morning, when orthostatic symptoms are usually worst.

Oral hydration combined with sodium remains first-line; the review literature on oral and intravenous hydration in orthostatic intolerance is clear that water without salt does not accomplish sustained volume expansion (Autonomic Neuroscience).

Practical version: on a travel day, pre-load the night before and the morning of, bring your own bottle through security and fill it, and keep drinking on descent. Then add the fourth lever — hypermobility-safe strength work, especially legs and core, because muscle is the pump that makes all of this hold.

I want to be very direct here, because the reassurance in this article can be misused. These episodes are common in hypermobile patients — and they still need a proper workup the first time they happen. The whole point of knowing the pattern is to recognize it after the dangerous causes have been excluded, not instead of excluding them.

That matters especially in this population. Patients with hEDS and hypermobility spectrum disorders — particularly those with a migraine history — carry a heightened rate of unruptured intracranial aneurysm, spontaneous cervical artery dissection, and fibromuscular dysplasia (PubMed). Connective tissue disease is a reason to look harder at a stroke-like episode, not a reason to wave it off.

A reasonable evaluation usually includes orthostatic vital signs done properly, an ECG and cardiac rhythm assessment, tilt-table or autonomic testing, laboratory work for anemia, thyroid, and electrolytes, EEG and neuroimaging when the presentation warrants it, and cerebrovascular imaging if focal deficits or a dissection-type headache are part of the picture. Seizures, arrhythmia, structural heart disease, dissection, and hypoglycemia all have to be on the table.

Call emergency services now, don’t wait it out, if focal deficits persist after lying down, if this is a first-ever event, if there is a sudden severe or “worst ever” headache or neck pain, if convulsions last more than a couple of minutes or repeat, if there is confusion lasting beyond a few minutes, chest pain, or injury from the fall.

→ Understanding the Basics of Dysautonomia
→ Am I Hypermobile?
→ Safe Strength Training for Hypermobility & EDS
→ Choosing an Electrolyte for Dysautonomia & POTS
→ Book Your Hypermobility Appointment

This article is for educational purposes and is not medical advice. Seizure-like and stroke-like episodes require evaluation by a physician who can exclude epilepsy, arrhythmia, cerebrovascular disease, and other causes before attributing them to orthostatic hypoperfusion. Fluid, sodium, and compression recommendations should be individualized — they are not appropriate for everyone, particularly patients with heart failure, kidney disease, or uncontrolled hypertension. — Dr. J & The Fascia Institute Family