Brain Fog in EDS, POTS and Long COVID: Causes and Practical Ways to Cope

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Adam Foster

Director at The Fibro Guy

Adam Foster is the founder of The Fibro Guy and one of the leading voices in hypermobility, EDS, and chronic pain rehabilitation. A former Reconnaissance Soldier, he developed chronic pain after an IED blast in Afghanistan and built his approach from the ground up when the medical system had no answers. Since 2009 he has worked with thousands of people across eight countries, drawing on pain neuroscience, motor learning, and sensorimotor rehabilitation. He co-authored "No Pain, No Pain" with trauma psychologist Dr Mairi Harper, directed the documentary "Invisible Monster," and has been featured in Forbes, BBC Radio 4, ITV News, LiveScience, and The Telegraph.

Latest posts by Adam Foster (see all)

• Teeth, Gums and Jaw Pain in hEDS, and How to Get Through a Dental Appointment - 28 September 2026
• Why ADHD and Hypermobility Keep Turning Up Together - 16 September 2026
• Hypermobility and Early Development: Milestones, Motor Delay, and Predictions - 12 September 2026

Brain fog is a rubbish name for something a lot of people are living with. It’s probably a fair part of why it keeps getting waved off at appointments. What you’re describing when you reach for it, is the loss of the things you need in order to hold a chat, follow a set of instructions, or write an email that makes any sense at all.

Across POTS, hEDS and long COVID, the objective work keeps pointing at the same handful of things: blood vessels, the automatic nervous system, inflammation, and the small nerve fibres ^[1]. Those findings sit in three groups that are linked to each other: the blood flow and autonomic side, the inflammatory and immune side. And the things that amplify the whole lot, which are pain, fatigue, broken sleep and low mood ^[2].

Which of those is hits hardest in you, however, is what decides whether anything on offer has a chance of working. In POTS and hEDS, the biggest one tends to be how much blood is getting to your brain while you’re upright, along with an automatic control system that’s running too hot, for lack of a better word. Long COVID brings a longer list along with it, and on that list sits the lining that keeps blood and brain apart, and inflammation.

It Gets Worse Upright, and It Shows Up on a Scan

You can think perfectly well lying in bed, but then lose the thread of a sentence twenty minutes after standing up, and that observation is the one the measurements keep finding. In POTS, the explanation that holds up the most consistently, is that less blood is reaching the brain during the stress of being upright, or during a long stretch of concentrating ^[3]. It’s been looked at head on, with a scan that maps blood flow through the brain, in a group of people with POTS and cognitive symptoms: about six in ten of them had abnormal flow, and it clustered in the front of the brain, and in the areas that handle movement and sensation ^[1].

Standing up is a plumbing problem. The tap on the top floor is the one that goes quiet first when the mains pressure drops: when you’re upright, your head is the outlet furthest above the pump.

Your heart pushes out less blood with each beat when you stand (not the same thing as the heart rate everybody fixates on), and the carbon dioxide level in your blood falls, which matters because that level is what sets how wide the brain’s own blood vessels are. Squeezing the lower body with compression blunted all three of those during a head up tilt in women with POTS: the drop in output per beat, the drop in carbon dioxide, and the drop in the speed of blood through one of the main arteries feeding the brain ^[4].

The alertness chemistry gets far less attention though. In the type of POTS that comes with nerve damage, working memory upright got worse in step with how bad people’s symptoms were, and noradrenaline, the alertness and stress chemical, was already high and then rose too far on standing, in a pattern that ran parallel to the fog itself ^[5].

A Normal Reading in a Chair Doesn’t Settle It

One finding has to sit alongside the upright picture, or the rest of it will mislead you. Resting and seated blood flow readings don’t reliably come out abnormal, and that caveat is a real one ^[6]. In one small group measured sitting down, flow through an artery at the back of the brain came out normal, while short term memory and alertness were worse, which suggests some of the cognitive trouble can carry on even when the particular flow number being measured in that position looks fine ^[6]. A reading taken while you’re sitting comfortably in a chair is not the reading that describes your actual afternoon, so if a normal one has been used to shut you down, that’s the thing worth reopening.

In hEDS, the Label and the Physiology Come Apart

Plenty of people reading this have hEDS and no POTS diagnosis, and have been told that the fog is the fatigue, or the pain, or the bad sleep, and left there with it. The hEDS work is newer than the POTS work and a fair bit of it is indirect, though the autonomic and nerve findings keep landing in the same place ^[7]. When a large group of people diagnosed with hEDS had all of this measured properly, four things came out ^[7]:

• about eight in ten had reduced blood flow to the brain on standing
• a third met the criteria for POTS
• nine in ten had a mild, widespread failure of the automatic control system
• about two thirds had damage to the smallest nerve fibres, the ones that carry temperature, nociceptive input and the automatic signals

Those first two are the pair to hold: most of that group had less blood reaching the brain on standing, and only a third of them met the criteria for POTS ^[7]. So, the label and the physiology came apart, which is handy to have in your pocket if a heart rate that didn’t rise by enough has been used to tell you the upright side of this is fine. Alongside that, attention comes out impaired in hEDS, executive function shifts depending on what position the body is in, and the cognitive problems people report about themselves track their fatigue, pain, anxiety, depression and sleep difficulties ^[8]. Which is to say the test result moves when the position does, and most cognitive assessment is done sitting down.

Mast cells come up a lot in hEDS and POTS circles, and usually with far more confidence than anybody should use The activation story often gets discussed in both conditions, and the evidence sitting under it is uneven ^[9]. Reviews of the hEDS, POTS and mast cell triad are clear that a common unifying mechanism hasn’t been established, and that some of the literature tying the three together leans on overlapping symptoms and loose diagnostic criteria ^[9]. What has been measured, in people with mast cell disorders including hereditary alpha-tryptasemia and MCAS, is reduced blood flow to the brain on standing, damage to the small nerve fibres, and an automatic system that isn’t regulating properly ^[10]. So the overlap turns up in the body, and it turns up without the tidy single explanation that usually gets sold alongside it.

Long COVID Adds a Leaking Barrier and a List of Maybes

If your fog started after a COVID infection, you’ve had both extremes thrown at you by now: that it’s all in your head, and that it’s microclots and nothing else. The imaging and molecular work supports two things in people whose main long COVID problems are cognitive, which is that the lining keeping blood and brain apart is disrupted, and that inflammation in the body hasn’t settled down yet ^[11]. That leak was measured directly, with an MRI using a dye that shows where the lining is letting things go through it. In people with brain fog associated with long COVID, the blood work in the same group pointed at an activated immune system and at clotting behaving abnormally ^[11].

Beyond that one, these are the mechanisms with the broadest agreement behind them ^[12]:

• inflammation inside the brain
• an inner lining of the blood vessels that isn’t working properly
• damage in the smallest vessels
• an automatic system out of regulation
• the parts of the cell that make energy running under strain

The routes proposed from there to your actual symptoms, include the brain’s own immune cells switching on, inflammatory chemicals being released, the barrier leaking, tiny clots, and less oxygen getting through to the cells that need it ^[12].

There’s a far stranger one as well, and I’d not have guessed it. After a viral infection, serotonin in the body fell, through tryptophan being absorbed less well from the gut, platelets over activating, and an enzyme clearing serotonin faster than it should, with knock on effects on the messages travelling up the vagus nerve and on memory ^[13].

The list you’ll actually have read about on forums runs through virus persisting in the body, the gut brain connection, Epstein-Barr waking back up, and microclots. Those get proposed over and over, though the reviews keep pointing out that a lot of the evidence is measured at a single moment, or is mechanistic, or is contested ^[14]. There’s no harm at all in reading about any of them, but there is a fair bit of harm in paying somebody for a treatment aimed at one.

Pain, Fatigue, Sleep and Mood Sit on Top of All Three

This is the part that usually goes wrong, because the second anybody mentions sleep or mood in the same breath as fog, it gets heard as being told the fog is psychological (and there’s a fair chance you’ve been told exactly that). That isn’t the claim. Psychological symptoms, fatigue, sleep disruption and dizziness appear to amplify the experience of the fog without fully explaining it ^[15]. Amplify and explain are different words, and the difference between them is the whole argument, because something can be loaded by your sleep and your pain and still be a physical problem in its own right. In long COVID, fog goes strongly along with fatigue, trouble finding words, memory complaints, aching muscles, depression and being slower to react and move, and because all of it was measured at one moment, none of it can tell you which came first ^[15].

In hEDS, the same thing shows up: how badly people rate their own thinking tracks their fatigue, pain, anxiety, depression and sleep difficulties ^[16]. Some of that chain is workable, though, because insomnia and depression come out as strong predictors of fatigue in hEDS, and the fatigue itself is tightly linked to trouble concentrating ^[17]. In long COVID, disturbed sleep is common, and it’s usually tangled up with the fatigue and the mood symptoms ^[18].

What Helps Depends on Which Driver Is Loudest

What you’d want is something aimed at the fog itself, and what’s on offer is aimed at the drivers behind it, so you go at whichever driver is loudest. Where the upright symptoms and the POTS physiology are the prominent part of it, these all have evidence behind them for improving the upright physiology and the overall symptom load, with some indirect support for a cognitive benefit on top ^[5]:

• drinking a large glass of water fairly quickly
• compression on the lower body
• exercise reconditioning
• raising the fluid and salt in circulation
• selected heart rate lowering drugs

Named individually, that’s water, compression, exercise and volume expansion, ivabradine and beta blockers, and each of them can improve either the upright measurements or quality of life ^[19].

One thing to keep in mind though. In POTS, treatments that improve the upright physiology often bring the overall symptom load down, and thinking is rarely the main thing being measured, so the direct evidence on fog specifically is limited ^[2]. And how much of any of it is right for you is a conversation with whoever manages your care, because the amounts are individual, and they aren’t numbers to take off a blog (including this one).

CBT, Cognitive Training and the Trial That Came Out Even

The long COVID side has the biggest pile of trials behind it, and the results are messier than either the optimists or the cynics will tell you. Pooling the trials that have been run, online CBT probably reduces fatigue and improves concentration, and supervised rehabilitation that combines physical work with mental health work probably improves overall health, depression and quality of life ^[20]. That isn’t the same as CBT or rehab reversing a single biological cause of brain fog, and what it does mean is that they currently have some of the clearest trial evidence for improving the symptoms people report, concentration included ^[21]. If you’ve had CBT offered for a physical symptom, you’ll have assumed, reasonably enough, that you were being managed instead of treated (I would have), and that’s worth keeping separate from what those trials actually measured.

Structured practice at thinking tasks came out as the strongest area of this work, with CBT on moderate support, and neurostimulation and the other approaches on weaker ground ^[22]. In adults with long COVID, that practice and structured rehabilitation are where the current evidence points hardest, and the benefits are still inconsistent from one trial and one outcome to the next ^[22].

Smaller work reported improvements in people’s own ratings of their thinking, and in day to day function, after structured cognitive practice and after a version of it that forces you to use the impaired skill instead of working round it ^[23]. But when computerised cognitive training, structured cognitive behavioural rehabilitation and passing a weak electrical current through the skull were tested in a much larger group, none of the three came out better than what it was compared against by the end of treatment ^[24]. It’s the finding that tends not to make it into the advertising.

Low dose naltrexone comes up a lot, and it tends to come up by name. Small observational work suggests possible benefit for fatigue, pain, brain fog, sleep and function ^[25]. When that evidence got pooled together though, none of what went into the pool was a study where people had been randomly assigned ^[26].

The hEDS Advice Is Borrowed From Somewhere Else

If you’ve got hEDS and somebody’s handed you a brain fog protocol, here’s where it came from. For hEDS and EDS there’s very little direct trial evidence on treating brain fog, and the ideas in circulation are largely carried across from the work on dysautonomia, pain, fatigue and sleep ^[16]. What that leaves is indirect, and indirect isn’t nothing: managing the upright symptoms, the pain, the sleep, the fatigue, the mood and the everyday function ^[16]. The multidisciplinary models suggest assessing thinking, sleep, psychological factors and possible inflammation in the brain together, instead of handling the fog as an isolated cognitive complaint ^[27]. The trials aimed specifically at brain fog through sleep are limited, and sleep is still a plausible thing to aim at ^[28].

Work Out Which One Is Yours, Then Start There

So, if the worst of it arrives twenty minutes after you stand up, that’s a plumbing problem, and it’s one where compression and fluid have something behind them. If it arrived after an infection and came with the inflammation, that’s a different conversation with a different list. And if it’s riding on top of three hours of sleep and a fortnight of bad pain, then sleep and pain are where the work goes first, because those are the parts of this that anybody can actually get hold of.

Adam

References

[1] Seeley, M.C., O’Brien, H., Wilson, G., Coat, C., Smith, T., Hickson, K. et al. (2025) ‘Novel brain SPECT imaging unravels abnormal cerebral perfusion in patients with postural orthostatic tachycardia syndrome and cognitive dysfunction’, Scientific Reports. https://doi.org/10.1038/s41598-025-87748-4

[2] Prassanna, A.R. (2026) ‘Persistent Cognitive Dysfunction in Postural Orthostatic Tachycardia Syndrome: A Scoping Review of Neural Mechanisms, Interventions, and Critical Research Gaps’, Cureus. https://doi.org/10.7759/cureus.112862

[3] Ocon, A.J., Medow, M.S., Taneja, I., Clarke, D. and Stewart, J.M. (2009) ‘Decreased upright cerebral blood flow and cerebral autoregulation in normocapnic postural tachycardia syndrome’, American Journal of Physiology-Heart and Circulatory Physiology. https://doi.org/10.1152/ajpheart.00138.2009