--- title: "Neuropathic POTS: Symptoms, Causes & Treatment" description: Neuropathic POTS is one of the more common POTS subtypes, often triggered by viral illness, autoimmunity, or brain injury. 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Neuropathic POTS: Symptoms, Causes & Treatment # Neuropathic POTS: Symptoms, Causes & Treatment ![Image of Lynn Gaufin](https://www.cognitivefxusa.com/hubfs/ATeam%20Headshots/Headshots-Cut/Lynn-Guafin.jpg) Lynn Gaufin • Updated on 01 June, 2026 • Medically Reviewed by [Dr. Alina Fong](https://www.cognitivefxusa.com/blog/author/dr-alina-fong-phd) [mailto:?subject=Check%20out%20https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment%20&body=Check%20out%20https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment&media=https://2921058.fs1.hubspotusercontent-na1.net/hubfs/2921058/POTS%20Vessel%20Image.jpg](mailto:?subject=Check%20out%20https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment%20&body=Check%20out%20https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment&media=https://2921058.fs1.hubspotusercontent-na1.net/hubfs/2921058/POTS%20Vessel%20Image.jpg) Neuropathic POTS: Symptoms, Causes & Treatment 32:41 Neuropathic POTS is the most common subtype of [Postural Orthostatic Tachycardia Syndrome](https://www.cognitivefxusa.com/blog/what-is-pots-a-complete-guide-to-postural-orthostatic-tachycardia-syndrome), affecting roughly 50% of all diagnosed patients. It is caused by damage to the small nerve fibers (called small fiber neuropathy) that control blood vessel constriction in the legs and abdomen. When these nerves fail, blood pools in the lower body every time you stand, and the heart races to compensate. The result is not just tachycardia. It is a full-body regulatory breakdown that produces brain fog, fatigue, GI dysfunction, neuropathic pain, and disability levels that match congestive heart failure. If you have been diagnosed with POTS, or suspect you have it, understanding whether the neuropathic subtype is driving your symptoms changes what treatment looks like and how likely you are to recover. Neuropathic POTS Symptoms Neuropathic POTS Symptoms ## More Than a Racing Heart: The Full Symptom Picture POTS affects virtually every organ system. Symptoms highlighted in gold are particularly characteristic of the neuropathic subtype and help distinguish it from other forms of POTS. Neuropathic marker (helps confirm the subtype) Common across all POTS subtypes All Symptoms 14 Cardiovascular 3 Neurological 4 GI / Digestive 2 Peripheral Nerve 3 General 2 Orthostatic tachycardia Heart rate jumps 30+ bpm within 10 minutes of standing. The defining feature of POTS across all subtypes. 100% of patients (diagnostic criterion) Acrocyanosis Neuropathic Marker Dark blue-purple discoloration of the feet and lower legs on standing. Cold to touch. Caused by impaired sympathetic vasoconstriction in the skin. 40-50% of POTS patients Lightheadedness and presyncope Reduced cerebral blood flow on standing produces dizziness, visual graying, and the sensation of nearly fainting. Some patients do faint. ~90% of patients Brain fog and cognitive dysfunction Deficits in attention, processing speed, executive function, and working memory. In neuropathic POTS, cognitive problems worsen when upright and improve when lying down or drinking water. 95%+ report it; 67% daily Headache Often positional (worse standing, better lying down). May overlap with migraine. Driven by reduced cerebral perfusion and autonomic dysregulation. ~75% of patients Vision changes Blurred vision, tunnel vision, or visual graying on standing. Reduced retinal blood flow and visual-vestibular mismatch both contribute. ~60% of patients Sleep disturbances Difficulty falling or staying asleep, unrefreshing sleep. Nocturnal tachycardia and sympathetic overactivation interfere with normal sleep architecture. ~32% of patients Nausea and GI dysmotility Nausea, bloating, constipation, abdominal pain, and early satiety. In the neuropathic subtype, GI symptoms may reflect autonomic denervation of the enteric nervous system. 96% have at least 1 GI symptom Postprandial worsening Symptoms spike after meals, especially large or high-carb ones. Digestion diverts blood to the splanchnic circulation, worsening the orthostatic deficit. Common across subtypes Neuropathic pain Neuropathic Marker Burning, tingling, numbness, or electric-shock sensations in the hands and feet. Caused directly by the small fiber damage that defines the neuropathic subtype. Variable; strongly suggests SFN Sudomotor dysfunction Neuropathic Marker Patchy loss of sweating (anhidrosis), particularly in the lower extremities. The sweat glands are innervated by the same small fibers damaged in neuropathic POTS. Detectable on QSART or thermoregulatory sweat test. ~50% of POTS patients Temperature dysregulation Heat intolerance is near-universal. Heat causes vasodilation, worsening blood pooling and tachycardia. Cold extremities are common from poor peripheral circulation. Very common Exercise intolerance and chronic fatigue Even mild exertion triggers disproportionate symptoms. Reduced stroke volume during upright exercise produces an exaggerated heart rate response and early exhaustion. Nearly universal Functional disability Quality of life scores match congestive heart failure. About 25% are unable to work. 70.5% report lost income. Many patients describe being unable to stand long enough to cook a meal or take a shower. 25% functionally disabled The Real-World Impact Report cognitive impairment95% Have at least one GI symptom96% Report lost income70.5% Initially misdiagnosed with anxiety69% Maintain employment48% If these symptoms sound familiar and you have not been evaluated for POTS, a proper autonomic assessment is the first step toward understanding what is driving them. [Schedule a Consultation](https://www.cognitivefxusa.com/start-here-paperwork) [![POTS QUIZ](https://no-cache.hubspot.com/cta/default/2921058/interactive-207378670679.png) ](https://www.cognitivefxusa.com/hs/cta/wi/redirect?encryptedPayload=AVxigLKO%2FwuXN8XHu4%2F51lU3NnrqiwLIkkEZGh%2BcSEnH3NIf%2BMGVkOTLTqMpM7fnYemWsaVdFNrkbtyNpaZ4DWrb7R4hSS3pr0HjDVLIZhYx9rUBW96Pw%2BYH5mD55jQaEEXN%2FFniXDwQP7cxIEjmrBPIP1VMwp32%2FAKm1yt%2FFiqmpOE4mFCyB8WYRISoVUuyWw0ud7ouqBFk3zdBO0JboHpohVrP%2Bz8ydKAWGb6wWn3S4%2BMcspMikAdID%2FO%2BTSibwbWMeJ0J07KZ&webInteractiveContentId=207378670679&portalId=2921058) ## What is neuropathic POTS and how does it differ from other subtypes? POTS is not one condition. It is a syndrome with multiple underlying drivers, and the treatment that works depends on which driver is primary. [If you are still learning about POTS generally, start with our complete guide.](https://www.cognitivefxusa.com/blog/what-is-pots-a-complete-guide-to-postural-orthostatic-tachycardia-syndrome) Neuropathic POTS results from damage to thin, unmyelinated C-fibers, the sympathetic postganglionic nerves that tell blood vessels to constrict. These are the same nerves measured in a skin punch biopsy. When they are working properly, they release norepinephrine at the vascular wall to tighten vessels and push blood upward against gravity. When they are damaged, vessels in the legs and abdomen stay too relaxed. Blood falls and stays low. The heart detects the drop in venous return and races to keep cardiac output up. A landmark Vanderbilt University study published in the *New England Journal of Medicine* (Jacob et al., 2000) confirmed this by measuring norepinephrine release separately in the arms and legs. POTS patients had significantly lower norepinephrine in the leg veins (135 vs. 215 pg/mL in controls, P = 0.001), while arm measurements looked normal. The nerve damage follows a length-dependent pattern. The longest fibers fail first, which is why the legs are hit hardest. The other major subtypes work differently: **Hyperadrenergic POTS** involves excessive sympathetic activation rather than denervation. Standing norepinephrine shoots above 600 pg/mL (often above 1,000), blood pressure spikes alongside heart rate, and patients report intense anxiety, tremor, and cold sweaty hands. [Read more about hyperadrenergic POTS here.](https://www.cognitivefxusa.com/blog/hyperadrenergic-pots-symptoms-causes-and-how-to-treat-the-subtype-most-doctors-miss) [**Hypovolemic POTS**](https://www.cognitivefxusa.com/blog/hypovolemic-pots-symptoms-causes-and-treatment-for-low-blood-volume-pots) stems from abnormally low blood volume, roughly a 13% plasma deficit, caused by a paradoxical suppression of the renin-aldosterone system. These subtypes overlap. A neuropathic POTS patient often develops hyperadrenergic features as the brain ramps up sympathetic drive to compensate for the peripheral nerve failure. This is not a contradiction. It is the nervous system doing its job with broken tools. ## What does neuropathic POTS feel like? The symptoms extend far beyond a fast heartbeat. POTS produces disability across virtually every organ system, and the neuropathic subtype carries some distinct markers that help clinicians identify it. **Acrocyanosis** is the most visually obvious sign. Present in 40-50% of POTS patients, it shows up as a dark red-blue or purple discoloration of the feet and lower legs within minutes of standing. The skin feels cold to the touch. This happens because damaged sympathetic nerves cannot constrict the cutaneous vessels, so blood stagnates in the superficial veins. If your feet turn purple when you stand, that is a strong signal pointing toward neuropathic POTS specifically. **Brain fog** is often the most disabling symptom. More than 95% of POTS patients report cognitive impairment, with 67% experiencing it daily. Testing reveals deficits in attention, processing speed, executive function, and working memory. In neuropathic POTS, a key finding is that working memory deficits occur only when upright and improve with something as simple as drinking water (Rodriguez et al., 2019). This confirms the cognitive problems are hemodynamically driven: the brain is not getting enough blood. [We cover POTS brain fog in depth here.](https://www.cognitivefxusa.com/blog/pots-brain-fog-causes-and-treatment) **GI dysfunction** affects 96% of POTS patients. Nausea (79-86%), constipation (70%), bloating (55-67%), and abdominal pain (59-70%) are the most common complaints. In the neuropathic subtype, these symptoms may result from the same small fiber damage affecting the gut's enteric nervous system. Other hallmark symptoms include exercise intolerance and chronic fatigue (nearly universal), neuropathic pain with burning, tingling, or numbness in the hands and feet, patchy loss of sweating, particularly in the lower extremities (present in about 50% and highly suggestive of the neuropathic subtype), temperature dysregulation and heat intolerance, and sleep disturbances. Quality of life data puts this in perspective. POTS patients score as impaired as people with congestive heart failure on standardized measures (Benrud-Larson et al., 2002). About 25% are functionally disabled. Only 48% maintain employment, and 70.5% report lost income. ## What causes neuropathic POTS? The small fiber damage driving neuropathic POTS does not happen randomly. Four categories of triggers account for the vast majority of cases. ### Autoimmune attack on autonomic nerves The evidence for autoimmunity in POTS is building rapidly, though the picture is more nuanced than early reports suggested. Multiple research groups have found autoantibodies targeting the receptors that control autonomic function. The most compelling evidence comes from functional studies. Li and colleagues (2014, 2021) demonstrated that POTS patient serum actively binds and disrupts adrenergic receptors in lab assays. When they immunized rabbits with adrenergic receptor peptides, the animals developed POTS-like physiology that resolved when the autoantibodies were cleared. That is direct causal evidence. ![POTS Vessel Image](https://www.cognitivefxusa.com/hs-fs/hubfs/POTS%20Vessel%20Image.jpg?width=1408&height=768&name=POTS%20Vessel%20Image.jpg) The clinical testing picture is more complicated. Standard blood tests (ELISA) for these autoantibodies have not reliably distinguished POTS patients from healthy controls in well-designed studies (Raj et al., 2022, *Circulation*). This does not mean autoimmunity is not involved. It means the commercially available tests are not sensitive or specific enough to use as clinical diagnostics yet. Functional bioassays that measure what the antibodies *do* rather than just whether they are present appear to be more informative. About 20% of POTS patients have an identifiable autoimmune comorbidity (Hashimoto's, Sjogren's, celiac disease). In pediatric patients with confirmed small fiber neuropathy, the odds of positive autoimmune markers are 3 times higher than in those without nerve damage (Moak et al., 2024). ### Post-viral and post-infectious triggers Over half of POTS patients (50-60%) trace their symptom onset to a viral illness. [Long COVID](https://www.cognitivefxusa.com/blog/covid-can-cause-long-term-problems) has become the single largest trigger. A 2025 Norwegian study using objective tilt table testing found that 31% of highly symptomatic Long COVID patients met full POTS criteria (*Circulation: Arrhythmia and Electrophysiology*). The proposed mechanisms include molecular mimicry (the immune system confuses viral proteins with autonomic nerve proteins), direct viral invasion of autonomic neurons, and persistent neuroinflammation. An encouraging finding: one longitudinal study found POTS prevalence in Long COVID patients dropped from 71% in the first year to 0% after two years, suggesting many post-viral cases resolve over time. Other established viral triggers include Epstein-Barr virus, [Lyme disease](https://www.cognitivefxusa.com/blog/post-treatment-lyme-disease-treatment-ptld-specialist-care), and influenza. Post-vaccination POTS has been reported but is significantly less common than post-infection POTS. A *Nature Cardiovascular Research* analysis found POTS risk was five times higher after COVID-19 infection than after vaccination. ### Ehlers-Danlos Syndrome and the genetic connection About 80% of patients with [hypermobile Ehlers-Danlos Syndrome (hEDS)](https://www.cognitivefxusa.com/blog/pots-and-ehlers-danlos-syndrome-why-they-travel-together-and-what-that-means) also have POTS. The connection runs through the connective tissue: weakened vessel walls allow excessive venous pooling, and fragile connective tissue may leave small nerve fibers more vulnerable to damage. Since hEDS follows autosomal dominant inheritance, this represents a clear genetic pathway for POTS susceptibility. About 15% of POTS patients have a first-degree relative with the condition. The clinical triad of hEDS, POTS, and Mast Cell Activation Syndrome (MCAS) has been described with increasing frequency. A 2025 study of 392 patients (Yao et al., *Frontiers in Neurology*) confirmed the overlap is real and coined the term "autonomic neuro-immune axis dysfunction." ### Brain injury and concussion This is where the neuropathic POTS story intersects with [post-concussion syndrome](https://www.cognitivefxusa.com/blog/post-concussion-syndrome-and-post-concussion-symptoms-pcs), and the overlap has significant treatment implications. [We have written extensively about post-concussion autonomic dysfunction.](https://www.cognitivefxusa.com/blog/post-concussion-autonomic-dysfunction-dysautonomia) The brain contains a distributed network of autonomic control centers called the Central Autonomic Network (CAN). This network includes the insular cortex, hypothalamus, nucleus tractus solitarius (NTS) in the brainstem, and the ventrolateral medulla. Together, these structures coordinate every cardiovascular adjustment your body makes when you change position. TBI can damage any of them directly, or sever the white matter connections between them, creating what researchers have called a "disconnection syndrome" (Meyfroidt et al., 2017, *The Lancet Neurology*). The prevalence numbers are striking. Heyer and colleagues (2016) found that 70.6% of youth with persistent post-concussion symptoms had abnormal tilt table results, and 41% met full POTS criteria. Miranda et al. (2018) found 11.4% of POTS patients at a large pediatric center reported onset within three months of a concussion. The critical problem is recognition. POTS symptoms after concussion ([dizziness](https://www.cognitivefxusa.com/blog/post-concussion-syndrome-dizziness), [brain fog](https://www.cognitivefxusa.com/blog/post-concussion-brain-fog-months-later), [fatigue](https://www.cognitivefxusa.com/blog/post-concussion-syndrome-extreme-fatigue-how-to-recover), [exercise intolerance](https://www.cognitivefxusa.com/blog/exercise-after-a-concussion), tachycardia, [nausea](https://www.cognitivefxusa.com/blog/post-concussion-nausea-what-to-do)) look identical to standard post-concussion symptoms. Clinicians attribute everything to the head injury and never check for POTS. [This is part of why POTS is so often misdiagnosed as anxiety.](https://www.cognitivefxusa.com/blog/why-pots-is-so-often-misdiagnosed-as-anxiety-and-what-you-can-do) Post-concussion autonomic dysfunction appears to be reversible. Heyer et al. showed that 75% of PCS patients with POTS had normal tilt table results once their concussion symptoms improved. The autonomic disruption can resolve when the underlying brain dysfunction is treated. Neuropathic POTS Overview Understanding the Most Common POTS Subtype ## What Is Neuropathic POTS? Neuropathic POTS is caused by damage to the small nerve fibers that control blood vessel constriction. When these nerves fail, blood pools in the lower body every time you stand, and the heart races to compensate. ~50% of all POTS cases are neuropathic 80-85% of patients are female 5.9 yrs average time to diagnosis How Neuropathic POTS Works Tap each step to see the detail. The cascade starts with nerve damage and ends with a body-wide regulatory breakdown. Small fiber neuropathy damages sympathetic nerves The thin, unmyelinated C-fibers that release norepinephrine at blood vessel walls are injured. This damage follows a length-dependent pattern: the longest fibers (in the legs) fail first, while arm innervation stays relatively normal. Blood vessels in the legs lose their ability to constrict Without adequate norepinephrine release, the vessels in the lower extremities and splanchnic circulation stay too relaxed. Vanderbilt researchers confirmed femoral vein norepinephrine was 37% lower in POTS patients vs. controls. Blood pools in the lower body on standing Gravity pulls blood downward, but the impaired nerves cannot tighten the vessels to push it back up. Venous return to the heart drops. Stroke volume falls. The visible sign: feet and legs turn blue-purple (acrocyanosis) within minutes of standing. The heart races to maintain cardiac output The cardiovascular system detects the drop in preload and launches a compensatory sympathetic response. Heart rate jumps 30+ bpm (the diagnostic threshold for POTS). The heart itself retains normal innervation, so it responds by racing. Brain, gut, and whole-body symptoms follow Reduced cerebral blood flow produces brain fog and cognitive deficits. Autonomic denervation of the gut causes nausea, bloating, and dysmotility. Sudomotor nerve damage causes patchy anhidrosis. The compensatory sympathetic surge causes fatigue, anxiety-like symptoms, and exercise intolerance. POTS Is Not One Condition Three major subtypes, each with a different primary driver. Most patients have overlapping features. Neuropathic Hyperadrenergic Hypovolemic Most Common (~50%) Neuropathic POTS **Primary mechanism:** Small fiber neuropathy impairs vasoconstriction in the legs. Blood pools, heart compensates. **Key distinguishing features:** Acrocyanosis (blue/purple feet on standing), patchy loss of sweating in the legs, neuropathic pain (burning, tingling), normal or low standing norepinephrine from the legs specifically. **Best confirmed by:** Skin punch biopsy (IENFD), QSART, tilt table test. Denervation driven Length-dependent Often autoimmune Post-viral trigger common 30-60% of Patients Hyperadrenergic POTS **Primary mechanism:** Excessive sympathetic nervous system activation. May be primary (central overactivation) or secondary (compensating for another subtype). **Key distinguishing features:** Standing norepinephrine above 600 pg/mL (often above 1,000), blood pressure surges on standing, prominent anxiety/tremor/palpitations, cold sweaty hands, sensitivity to stimulation. **Best confirmed by:** Supine and standing catecholamine levels, tilt table with beat-to-beat BP monitoring. Sympathetic overdrive BP spikes on standing NE > 600 pg/mL Often overlaps with neuropathic Up to 70% of Patients Hypovolemic POTS **Primary mechanism:** Abnormally low blood volume (~13% plasma deficit) due to paradoxical suppression of the renin-aldosterone system despite low volume. **Key distinguishing features:** Symptoms worsen significantly with dehydration, heat, or missed meals. Often improves markedly with IV saline. May have low red blood cell volume even with normal plasma volume. **Best confirmed by:** Direct blood volume measurement (DAXOR BVA-100), plasma renin activity and aldosterone levels, response to volume expansion. Low blood volume Renin-aldosterone paradox Salt/fluid responsive Co-occurs with other subtypes Effective treatment depends on identifying which subtype, or combination, is driving your symptoms. A proper evaluation is the first step. [Schedule a Consultation](https://www.cognitivefxusa.com/start-here-paperwork) ## How is neuropathic POTS diagnosed? Confirming POTS requires demonstrating the characteristic heart rate response. Confirming the neuropathic subtype requires a second layer of testing to identify the small fiber damage. [Our full diagnostic guide covers this in detail.](https://www.cognitivefxusa.com/blog/how-is-pots-diagnosed-tests-timelines-and-what-to-expect) **[Tilt table test](https://www.cognitivefxusa.com/blog/pots-tilt-table-test) or active standing test** confirms POTS: a sustained heart rate increase of 30 bpm or more within 10 minutes of standing (40 bpm or more for ages 12-19), without orthostatic hypotension, with symptoms lasting at least 3-6 months. **Skin punch biopsy** is the gold standard for confirming small fiber neuropathy. A 3mm biopsy from the lower leg is stained to count the density of nerve fibers crossing into the epidermis. Results below the 5th percentile for age and sex confirm SFN. Sensitivity ranges from 74-90%, specificity from 64-90%. **QSART (Quantitative Sudomotor Axon Reflex Test)** measures sweat nerve function. About 56% of POTS patients have abnormal QSART results. Importantly, biopsy and QSART results often disagree in the same patient, meaning they identify different subsets of nerve damage and should be used together. **Blood testing** screens for autoimmune drivers and treatable causes: ANA, antithyroid antibodies, celiac panel, HbA1c, B12, CRP/ESR, thyroid function, and catecholamine levels (supine and standing). The diagnostic journey is notoriously long. POTS patients wait an average of nearly 6 years and see 7 different doctors before getting a correct diagnosis. Sixty-nine percent are initially told they have anxiety. After proper diagnosis, only 37% continue to carry a psychiatric label. ## What treatments work for neuropathic POTS? Treatment for neuropathic POTS works best when it addresses the underlying nervous system dysfunction rather than just suppressing symptoms. The strongest evidence supports exercise reconditioning, but the most complete recovery comes from programs that combine physical rehabilitation with targeted neurological inputs. ### Exercise reconditioning is the single most effective intervention The Levine protocol (also called the Dallas protocol) is the gold standard. A 2011 study in *Hypertension* compared three months of structured exercise to propranolol in 19 POTS patients. Exercise produced a 12% increase in heart mass, a 7% increase in blood volume, and 53% of participants no longer met POTS criteria. Quality of life improved significantly (physical functioning score: 33 to 50). Propranolol reduced heart rate but did not improve quality of life at all (34 to 36, P = 0.63). The protocol starts with recumbent exercise only (swimming, rowing, recumbent bike) for the first 1-3 months. This is critical because it eliminates the orthostatic stress that makes upright exercise intolerable. Upright exercise is introduced gradually after cardiovascular reconditioning has begun to restore stroke volume. Community-based data showed 71% remission among completers, though only 41% completed the full program. The dropout rate reflects the fundamental challenge: the treatment requires doing the thing the disease makes hardest. ### Compression and hydration form the baseline A 2021 randomized study found full abdominal-leg compression reduced standing heart rate from 109 bpm to 92 bpm (P < 0.001). Abdominal compression alone outperformed leg-only compression because the abdomen holds a larger blood volume. Waist-high garments at 30-40 mmHg are recommended over knee-high stockings. Fluid intake of 2-3 liters daily, salt loading (6-10g daily based on clinician guidance), and small frequent low-carb meals form the nutritional foundation. These expand plasma volume and reduce the orthostatic deficit that drives symptoms. ### Neurological rehabilitation targets the brain-level dysfunction Salt, compression, and exercise address what is happening downstream. They expand blood volume, physically prevent pooling, and recondition the heart. But for patients whose POTS involves central autonomic dysregulation (particularly after brain injury, concussion, or viral illness affecting the brainstem), the upstream regulation problem also needs direct attention. The nucleus tractus solitarius in the brainstem is not receiving, integrating, or responding to baroreceptor signals accurately. The vestibular system is sending imprecise gravity and position data. Breathing chemistry is off. Until those inputs are corrected, the autonomic system keeps misfiring no matter how much salt you consume. The research supports this layered approach. Vestibular rehabilitation (which is in direct communication with autonomic cardiovascular centers) produced clinically significant improvement in 63% of POTS patients in a 2025 tertiary clinic study. Resonance frequency breathing at approximately 6 breaths per minute is the strongest non-invasive amplifier of baroreflex gain in the research literature, directly training the NTS to respond more accurately to orthostatic challenges. HRV biofeedback after TBI improved baroreflex engagement and cognitive outcomes in a 2025 randomized controlled trial (Talbert et al.). Isometric wall sits were ranked as 90.5% effective for blood pressure reduction across a 2023 meta-analysis of 270 trials, improving the autonomic control of vascular tone that neuropathic POTS patients lack. ### Medications manage symptoms but do not reverse the condition No FDA-approved medications exist for POTS. All drug treatments are off-label and considered second-line. Ivabradine (a heart rate reducer that does not affect blood pressure) is the most promising, with 78% of patients reporting improvement in retrospective data. Low-dose propranolol (10-20 mg) reduces tachycardia, but higher doses worsen fatigue. Midodrine directly promotes vasoconstriction and is particularly logical for the neuropathic subtype. For patients with confirmed autoimmune-driven neuropathic POTS, IVIG has been explored, though a 2024 randomized trial found no clear benefit over albumin placebo. ## Treating POTS as a Neurological Condition at Cognitive FX At Cognitive FX, the [POTS/ANS Therapy Program](https://www.cognitivefxusa.com/pots-treatment) combines these evidence-based interventions into an intensive, individualized format. The program runs across multiple days. Day 1 is a full evaluation: heart rate, blood pressure, and oxygen saturation measured seated and standing, tilt table testing, vestibular assessment, cranial nerve and NTS assessment, supplement screening, and goal setting. This evaluation identifies your specific POTS profile (neuropathic, hyperadrenergic, hypovolemic, post-viral, post-concussive, or a combination) and determines which systems are the primary drivers. Treatment days run approximately six hours each of individualized, protocol-driven therapy targeting five key systems: ### **Cranial nerve activation** The NTS is where all baroreceptor input from cranial nerves IX and X converges before the autonomic response is coordinated. In POTS, the NTS is not lesioned. It is dysregulated: intact circuitry that is poorly calibrated. The program uses a sequenced cranial nerve stacking protocol that progressively loads the NTS through its accessible afferent inputs. Carotid sinus activation delivers baroreceptor signaling through CN IX. The dive reflex (cold applied to the face) triggers the trigeminovagal pathway through CN V to boost cardiac vagal output. Resonance frequency breathing at each patient's individual resonance rate (typically 4.5 to 7 breaths per minute) entrains baroreflex oscillations at their natural frequency of approximately 0.1 Hz. A salt water gargle activates CN IX pharyngeal mechanoreceptors while simultaneously delivering a sodium-sensing signal to the rostral NTS. The sequence finishes with a graded orthostatic transition (lying to sitting to standing with resonance breaths at each stage), applying the primed NTS state to the functional challenge that POTS makes hardest: standing up. ### **Vestibular recalibration** The vestibular organs detect gravity, linear acceleration, and rotation, and they are in constant direct communication with the autonomic nervous system. When vestibular processing is inaccurate or delayed, the cardiovascular adjustments needed to maintain brain perfusion misfire. The program trains both the saccule (vertical linear acceleration, activated through controlled vertical oscillation exercises progressing from supine to seated to standing) and the utricle (horizontal linear acceleration, trained through anterior-posterior and mediolateral sway drills). VOR (vestibulo-ocular reflex) training recalibrates the fastest reflex in the body, reducing the dizziness, nausea, and visual instability that compound POTS symptoms. Each vestibular exercise is performed with a fixed gaze target, and progression follows a strict symptom threshold: challenge without exceeding a 3-4/10 symptom increase. ### **Breathing chemistry and CO2 tolerance** Carbon dioxide is what breaks the bond between oxygen and hemoglobin so that oxygen can enter cells. If CO2 is too low (a common finding in POTS patients who chronically hyperventilate), tissue oxygenation suffers even when blood oxygen levels look normal. This produces brain fog, cold extremities, dizziness, and anxiety that overlap with and amplify POTS symptoms. The program retrains breathing mechanics from the ground up: nasal breathing as the default (mouth breathing activates sympathetic fight-or-flight signaling with every breath), diaphragmatic initiation, extended exhale techniques that shift the system toward parasympathetic dominance, and progressive CO2 tolerance training using breath holds and precision CO2 delivery devices. The goal is to raise the brainstem's CO2 set point so the respiratory drive stops triggering unnecessary sympathetic activation. ### **NeuroCardio interval training** Standard exercise reconditioning (like the Levine protocol) rebuilds cardiovascular capacity gradually over months. The program's NeuroCardio interval training (NCT) works a different angle: it forces the sympathetic and parasympathetic systems to cycle between full effort and complete rest within a single session, retraining the autonomic switching that is dysregulated in POTS. Sessions run 20 minutes. Each interval is 30 seconds of maximal effort followed by full recovery (breathing returns to baseline, heart rate drops) before the next round. The number of intervals is determined by recovery time, not a target count. If you only complete 1-2 rounds with full recovery, that is the right dose. The training effect comes from the recovery, not the exertion. ### **Isometric training and spinal autonomic support** Isometric wall sits and hand grip exercises improve autonomic control of vascular tone with as few as three sessions per week. Thoracic spine mobility work targets blood flow and sensory input to the intermediolateral (IML) nucleus, the column of preganglionic sympathetic neurons spanning T1-L2 that governs downstream vascular output. Progressive muscle relaxation and autogenic training build interoceptive awareness and parasympathetic access on demand, giving patients a tool to actively shift their autonomic state rather than being at its mercy. Patients leave with a structured home program covering all of these systems, organized into morning, midday, evening, and bedtime blocks. Compression garments, salt and fluid loading, head-of-bed elevation, and physical counter-maneuvers (squatting, leg crossing with tensing, pre-standing hand grip) are integrated as the foundational support layer underneath the neurological work. The home program is designed to be progressive: start with the morning cranial nerve stack and breathing work, add isometrics and vestibular training as those become stable, layer in NCT intervals once breathing baseline has improved. Published outcomes from Cognitive FX's EPIC Treatment protocol for post-concussion patients show an 80% average reduction in objective brain dysfunction scores, with results stable at one-year follow-up. For patients with concurrent POTS and post-concussion syndrome, addressing the brain-level dysfunction often resolves the autonomic symptoms that standard POTS treatments could not reach. *To learn whether you’re a candidate for our five-day neurological POTS treatment program, *[*take our quiz*](https://cognitivefxusa.typeform.com/pots-intake)* to see if you’re a fit for treatment* ## Can neuropathic POTS go away? Roughly 50% of patients improve significantly within 1-3 years, and about 80% show [meaningful improvement over time](https://www.cognitivefxusa.com/blog/will-pots-go-away). Complete remission rates range from 19-33%, with better outcomes in younger patients and those who maintain consistent exercise. After the Levine exercise protocol specifically, 53% no longer meet POTS diagnostic criteria. The factors that predict better outcomes include younger age at onset, consistent exercise (the single strongest modifiable factor), early diagnosis and treatment, identification and treatment of the underlying cause (autoimmune, post-viral, post-concussion), and for post-concussion patients, targeted rehabilitation addressing the brain systems that regulate autonomic function. The neuropathy itself may persist on testing even as symptoms improve. Functional adaptation and cardiovascular reconditioning can compensate substantially for residual nerve damage. For patients whose POTS involves central autonomic dysregulation, correcting the upstream brain-level dysfunction can restore regulation even when some peripheral nerve damage remains. ## The research pipeline is moving faster than ever The post-COVID surge in POTS cases has accelerated research investment dramatically. The NIH RECOVER-AUTONOMIC trials (the largest coordinated POTS treatment study ever) are testing IVIG, ivabradine, and non-drug care across 380 participants at 50 U.S. sites. Regeneron has initiated the first pharmaceutical company-sponsored Phase 2 trial for POTS (REGN7544, an NPR1 antagonist antibody). The first candidate blood biomarkers for POTS were identified in a 2025 proteomic analysis. And the NIH formally prioritized POTS through a 2024 Notice of Special Interest calling for biomarker, wearable technology, and genetic studies. For patients living with neuropathic POTS right now, the trajectory is clear: meaningful recovery is achievable for the majority, and the treatment landscape is expanding faster than at any point in the condition's history. ## See if our POTS treatment program is right for you Most POTS treatment stops at symptom management: salt, compression, and medications to blunt the heart rate response. Those tools matter, and we use them. But if your autonomic nervous system is misfiring because the brainstem, vestibular system, or cranial nerve pathways that regulate it are dysregulated, no amount of salt loading will fix that. The nervous system needs the right inputs to recalibrate. If you have POTS, especially if it developed after a concussion, viral illness, or brain injury, and you have tried the standard approaches without lasting improvement, [take our quiz](https://cognitivefxusa.typeform.com/pots-intake) to see if you’re a fit for our neurologic-based treatment. Not medical advice, informational purpose only. [![Schedule Free Consult](https://no-cache.hubspot.com/cta/default/2921058/interactive-205476243731.png) ](https://www.cognitivefxusa.com/hs/cta/wi/redirect?encryptedPayload=AVxigLJSda6X5CqV2c8XoZ%2BGDkdevQMLg%2FBaG9dqANF2U8Egwwcld%2BzA0eQtU87sunaOpLolPR6rA5ci7uyW1qjkyjgA%2BZXwg0rjULCCOfcjVWMHo4KYUBVVIW17CE%2FO1qyE0gVyrGNfaW1HHrT02GoxcrrX3c7i8gWoDogLEsGQA%2BwmStQs1rlzSNAqUjwtfb67PMwt&webInteractiveContentId=205476243731&portalId=2921058) --- ### References 1. Jacob G, Costa F, Shannon JR, et al. The neuropathic postural tachycardia syndrome. *N Engl J Med*. 2000;343(14):1008-1014. [PubMed](https://pubmed.ncbi.nlm.nih.gov/11018167/) 2. Gibbons CH, Bonyhay I, Benson A, Wang N, Freeman R. Structural and functional small fiber abnormalities in the neuropathic postural tachycardia syndrome. *PLoS One*. 2013;8(12):e84716. [PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC3874039/) 3. Haensch CA, Tosch M, Katona I, Weis J, Isenmann S. Small-fiber neuropathy with cardiac denervation in postural tachycardia syndrome. *Muscle Nerve*. 2014;50(6):956-961. [PubMed](https://pubmed.ncbi.nlm.nih.gov/24647968/) 4. Arnold AC, Ng J, Raj SR. Postural tachycardia syndrome: Diagnosis, physiology, and prognosis. *Auton Neurosci*. 2018;215:3-11. [PubMed](https://pubmed.ncbi.nlm.nih.gov/29523389/) 5. Thieben MJ, Sandroni P, Sletten DM, et al. Postural orthostatic tachycardia syndrome: the Mayo Clinic experience. *Mayo Clin Proc*. 2007;82(3):308-313. [PubMed](https://pubmed.ncbi.nlm.nih.gov/17352367/) 6. Gunning WT III, Kvale H, Kramer PM, Karabin BL, Grubb BP. POTS is associated with elevated G-protein coupled receptor autoantibodies. *J Am Heart Assoc*. 2019;8(18):e013602. [JAHA](https://www.ahajournals.org/doi/10.1161/JAHA.119.013602) 7. Raj SR, Guzman JC, Harvey P, et al. Detection of G protein-coupled receptor autoantibodies in POTS using standard methodology. *Circulation*. 2022;146(8):613-622. [Circulation](https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.122.059971) 8. Li H, Yu X, Liles C, et al. Autoimmune basis for postural tachycardia syndrome. *J Am Heart Assoc*. 2014;3(1):e000755. [PubMed](https://pubmed.ncbi.nlm.nih.gov/24572257/) 9. Vernino S, Bryarly M, Hopkins S, et al. Ganglionic acetylcholine receptor antibodies in postural tachycardia syndrome. *Neurol Clin Pract*. 2021;11(5):e686-e691. [PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC8382391/) 10. Moak JP, Leong D, Gurbani N, et al. Small fiber neuropathy in children and young adults with POTS. *Auton Neurosci*. 2024;252:103157. [PubMed](https://pubmed.ncbi.nlm.nih.gov/38537312/) 11. Ormiston CK, Swendseid B, et al. Prevalence and clinical impact of POTS in highly symptomatic Long COVID. *Circ Arrhythm Electrophysiol*. 2025;18(1):e013629. [PubMed](https://pubmed.ncbi.nlm.nih.gov/41025260/) 12. Fedorowski A, et al. Cardiovascular autonomic dysfunction in post-COVID-19 syndrome. *Nat Rev Cardiol*. 2024;21(6):379-395. [Nature](https://www.nature.com/articles/s41569-023-00946-3) 13. Kwan AC, Ebinger JE, Wei J, et al. The risks of POTS after COVID-19 vaccination and SARS-CoV-2 infection. *Nat Cardiovasc Res*. 2022;1:1101-1103. [Nature](https://www.nature.com/articles/s44161-022-00180-z) 14. Meyfroidt G, Baguley IJ, Menon DK. Paroxysmal sympathetic hyperactivity: the storm after acute brain injury. *Lancet Neurol*. 2017;16(9):721-729. [PubMed](https://pubmed.ncbi.nlm.nih.gov/28816118/) 15. Khalid F, Yang GL, McGuire JL, et al. Autonomic dysfunction following traumatic brain injury: translational insights. *Neurosurg Focus*. 2019;47(5):E8. [JNS](https://thejns.org/focus/view/journals/neurosurg-focus/47/5/article-pE8.xml) 16. Heyer GL, Fischer A, Wilson J, et al. Orthostatic intolerance and autonomic dysfunction in youth with persistent postconcussion symptoms. *Clin J Sport Med*. 2016;26(1):40-45. [PubMed](https://pubmed.ncbi.nlm.nih.gov/25706663/) 17. Miranda NA, Boris JR, Kouvel KM, Stiles L. Activity and exercise intolerance after concussion: Identification and management of POTS. *J Neurol Phys Ther*. 2018;42(3):163-171. [LWW](https://journals.lww.com/jnpt/fulltext/2018/07000/activity_and_exercise_intolerance_after.8.aspx) 18. Kanjwal K, Karabin B, Grubb BP. Autonomic dysfunction presenting as POTS following traumatic brain injury. *Cardiol J*. 2010;17(5):482-487. [PubMed](https://pubmed.ncbi.nlm.nih.gov/20865679/) 19. Bilan A, Chen D, Siddiqui T, Shen WK, Singer W. Skin biopsy and QSART in patients with POTS. *Auton Neurosci*. 2022;244:103060. [PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC9629858/) 20. Shaw BH, Stiles LE, Bourne K, et al. The face of postural tachycardia syndrome. *J Intern Med*. 2019;286(4):438-448. [PMC](https://pmc.ncbi.nlm.nih.gov/articles/PMC6790699/) 21. Fu Q, VanGundy TB, Shibata S, Auchus RJ, Williams GH, Levine BD. Exercise training versus propranolol in the treatment of POTS. *Hypertension*. 2011;58(2):167-175. [PubMed](https://pubmed.ncbi.nlm.nih.gov/21690484/) 22. George SA, Bivens TB, Howden EJ, et al. The international POTS registry: Evaluating exercise training in a community setting. *Heart Rhythm*. 2016;13(4):943-950. [PubMed](https://pubmed.ncbi.nlm.nih.gov/26690066/) 23. Bourne KM, Sheldon RS, Hall J, et al. Abdominal compression as a treatment for POTS. *J Am Heart Assoc*. 2021;10(4):e017610. [JAHA](https://www.ahajournals.org/doi/10.1161/JAHA.120.017610) 24. Benrud-Larson LM, Dewar MS, Sandroni P, et al. Quality of life in patients with POTS. *Mayo Clin Proc*. 2002;77(6):531-537. [PubMed](https://pubmed.ncbi.nlm.nih.gov/12059122/) 25. Raj SR, Black BK, Biaggioni I, et al. Propranolol decreases tachycardia and improves symptoms in POTS: less is more. *Circulation*. 2009;120(9):725-734. [PubMed](https://pubmed.ncbi.nlm.nih.gov/19687359/) 26. Yao B, Maxwell CR, et al. Association of POTS, hypermobility spectrum disorders, and mast cell activation syndrome. *Front Neurol*. 2025;16:1513199. [Frontiers](https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2025.1513199/full) 27. Fedorowski A. Postural orthostatic tachycardia syndrome: clinical presentation, aetiology and management. *J Intern Med*. 2019;285(4):352-366. [PubMed](https://pubmed.ncbi.nlm.nih.gov/30372565/) 28. Dysautonomia International. Diagnostic delay in POTS. [Link](https://www.dysautonomiainternational.org/page.php?ID=184) --- ![Image of Lynn Gaufin](https://www.cognitivefxusa.com/hs-fs/hubfs/ATeam%20Headshots/Headshots-Cut/Lynn-Guafin.jpg?height=150&name=Lynn-Guafin.jpg) ### About the author [Lynn Gaufin](https://www.cognitivefxusa.com/blog/author/lynn-gaufin) Dr. Lynn Gaufin graduated from the University of Utah and then attended medical school at Cornell University in New York City. After medical school he join the Army and was a surgeon in the military before finishing his Neurological Residency at University of California Los Angeles. Dr. Gaufin specializes in cervical and lumbar spine surgery, brain tumors, brain hemorrhages, and treatment of traumatic brain injuries. Dr. Gaufin is one of the emergency trauma neurosurgeons on call at Utah Valley Hospital. Before he began his practice in Utah he saw a significant amount of traumatic brain injuries during his career in the Army and his residency in Los Angeles. As a surgeon who treats individuals who suffer from mild to severe traumatic brain injuries he recognized a problem in the post operative rehabilitation. Individuals who suffered severe trauma would be admitted into speciality facilities where they would receive months of care. But patients who had a more mild trauma would be released and would largely be on their own when it came to restoring their cognitive function. That problem is what lead Dr. Gaufin to team up with Dr. Fong and Dr. Allen in the creation of Cognitive FX. Cognitive FX was able to take the research that Dr. Fong and Dr. Allen started in their Phd programs and bring it into the clinical environment. ## Related Posts ![](https://www.cognitivefxusa.com/hs-fs/hubfs/Hypovolemic%20Pots%20Infographic.jpg?height=175&name=Hypovolemic%20Pots%20Infographic.jpg) ### Hypovolemic POTS: Symptoms, Causes, & Treatment for Low Blood Volume POTS ![Image of Lynn Gaufin](https://www.cognitivefxusa.com/hs-fs/hubfs/ATeam%20Headshots/Headshots-Cut/Lynn-Guafin.jpg?height=70&name=Lynn-Guafin.jpg) [Lynn Gaufin](https://www.cognitivefxusa.com/blog/author/lynn-gaufin) {% module_block module "widget_de9dcb5c-04ce-424d-a847-5e60bab8d8e0" %}{% module_attribute "child_css" is_json="true" %}{}{% end_module_attribute %}{% module_attribute "css"... [Read the full article ](https://www.cognitivefxusa.com/blog/hypovolemic-pots-symptoms-causes-and-treatment-for-low-blood-volume-pots) ![](https://www.cognitivefxusa.com/hs-fs/hubfs/Hyperadrenergic%20POTS.jpg?height=175&name=Hyperadrenergic%20POTS.jpg) ### Hyperadrenergic POTS: Symptoms, Causes, & Treating the Subtype Most Doctors Miss ![Image of Lynn Gaufin](https://www.cognitivefxusa.com/hs-fs/hubfs/ATeam%20Headshots/Headshots-Cut/Lynn-Guafin.jpg?height=70&name=Lynn-Guafin.jpg) [Lynn Gaufin](https://www.cognitivefxusa.com/blog/author/lynn-gaufin) Hyperadrenergic POTS affects an estimated 30 to 60% of all POTS patients, yet most are never told which subtype they have. That matters because the hyperadrenergic form requires a fundamentally... [Read the full article ](https://www.cognitivefxusa.com/blog/hyperadrenergic-pots-symptoms-causes-and-how-to-treat-the-subtype-most-doctors-miss) ![POTS-Related Brain Fog: Causes and Treatment](https://www.cognitivefxusa.com/hs-fs/hubfs/pots-brain-fog-causes-and-treatment.jpg?height=175&name=pots-brain-fog-causes-and-treatment.jpg) ### POTS-Related Brain Fog: Causes and Treatment ![Image of Andy Clower, ATC](https://www.cognitivefxusa.com/hs-fs/hubfs/Andy_150px.webp?height=70&name=Andy_150px.webp) [Andy Clower, ATC](https://www.cognitivefxusa.com/blog/author/lynn-gaufin) Brain fog is an extremely common symptom for people with Postural Orthostatic Tachycardia Syndrome (POTS). [Over 95%](https://pubmed.ncbi.nlm.nih.gov/23999934/) of patients report feeling forgetful, mentally slow, and having difficulty with... [Read the full article ](https://www.cognitivefxusa.com/blog/pots-brain-fog-causes-and-treatment) ![](https://www.cognitivefxusa.com/hs-fs/hubfs/POTS%20QUIZ.jpeg?height=175&name=POTS%20QUIZ.jpeg) ### Do I Have POTS? Self-Assessment Quiz, Symptoms & 4 Types Explained ![Image of Lynn Gaufin](https://www.cognitivefxusa.com/hs-fs/hubfs/ATeam%20Headshots/Headshots-Cut/Lynn-Guafin.jpg?height=70&name=Lynn-Guafin.jpg) [Lynn Gaufin](https://www.cognitivefxusa.com/blog/author/lynn-gaufin) ## Take the POTS Self-Assessment Quiz {% module_block module "widget_8cf032e3-6b31-4c5a-96f7-4cf9fac5ce7d" %}{% module_attribute "child_css" is_json="true" %}{}{%... [Read the full article ](https://www.cognitivefxusa.com/blog/do-i-have-pots-self-assessment-quiz-symptoms-4-types-explained) ![](https://www.cognitivefxusa.com/hs-fs/hubfs/POTS%20ISSUES.jpeg?height=175&name=POTS%20ISSUES.jpeg) ### What Is POTS? Postural Orthostatic Tachycardia Syndrome Explained Simply ![Image of Dr. Alina Fong, Ph.D.](https://www.cognitivefxusa.com/hs-fs/hubfs/Alina_150px.webp?height=70&name=Alina_150px.webp) [Dr. Alina Fong, Ph.D.](https://www.cognitivefxusa.com/blog/author/lynn-gaufin) If you've ever stood up and felt your heart start racing, felt lightheaded out of nowhere, or experienced brain fog so thick you couldn't finish a sentence, you might be dealing with something called... [Read the full article ](https://www.cognitivefxusa.com/blog/what-is-pots-a-complete-guide-to-postural-orthostatic-tachycardia-syndrome) ![](https://www.cognitivefxusa.com/hs-fs/hubfs/POTS%20Anxiety%20Image.jpeg?height=175&name=POTS%20Anxiety%20Image.jpeg) ### Why POTS Is So Often Misdiagnosed as Anxiety (And What You Can Do) ![Image of Lynn Gaufin](https://www.cognitivefxusa.com/hs-fs/hubfs/ATeam%20Headshots/Headshots-Cut/Lynn-Guafin.jpg?height=70&name=Lynn-Guafin.jpg) [Lynn Gaufin](https://www.cognitivefxusa.com/blog/author/lynn-gaufin) {% module_block module "widget_feba32f8-8dae-4a1d-bf17-f0de98dfde9f" %}{% module_attribute "child_css" is_json="true" %}{}{% end_module_attribute %}{% module_attribute "css"... 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All Rights Reserved. | [Privacy Policy](https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment#) ```json { "@context" : "https://schema.org", "@type" : "BlogPosting", "author" : { "@type" : "Person", "name" : "Lynn Gaufin", "url" : "https://www.cognitivefxusa.com/blog/author/lynn-gaufin" }, "dateModified" : "2026-06-01T16:52:00.944Z", "datePublished" : "2026-04-16T15:27:56.000Z", "headline" : "Neuropathic POTS: Symptoms, Causes & Treatment", "image" : [ "https://www.cognitivefxusa.com/hubfs/POTS%20Vessel%20Image.jpg" ], "mainEntityOfPage" : { "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment", "@type" : "WebPage" }, "publisher" : { "@type" : "Organization", "logo" : { "@type" : "ImageObject", "url" : "https://www.cognitivefxusa.com/hubfs/Cognitive-Final-Logo-BlBlk-Med.png" }, "name" : "Cognitive FX" } } ``` ```json { "@context" : "https://schema.org", "@type" : "Article", "about" : { "@type" : "MedicalCondition", "name" : "" }, "audience" : { "@type" : "Audience", "audienceType" : [ "patient", "caregiver" ] }, "author" : { "@type" : "Person", "affiliation" : { "@type" : "MedicalOrganization", "name" : "Cognitive FX", "url" : "https://www.cognitivefxusa.com" }, "name" : "Lynn Gaufin" }, "dateModified" : "01 June, 2026", "datePublished" : "2026-04-16 15:27:56", "description" : "Neuropathic POTS is one of the more common POTS subtypes, often triggered by viral illness, autoimmunity, or brain injury. Symptoms, diagnosis, and treatment explained.", "headline" : "Neuropathic POTS: Symptoms, Causes & Treatment", "image" : "", "mainEntityOfPage" : { "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment", "@type" : [ "MedicalWebPage" ], "breadcrumb" : { "@type" : "BreadcrumbList", "itemListElement" : [ { "@type" : "ListItem", "item" : "https://www.cognitivefxusa.com", "name" : "Cognitive FX Home", "position" : 1 }, { "@type" : "ListItem", "item" : "https://www.cognitivefxusa.com/blog", "name" : "Blog Home", "position" : 2 }, { "@type" : "ListItem", "item" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment", "name" : "Neuropathic POTS: Symptoms, Causes & Treatment", "position" : 3 } ] }, "lastReviewed" : "1780332720950", "reviewedBy" : { "@type" : "Person", "name" : "" } }, "publisher" : { "@type" : "Organization", "brand" : { "@type" : "Organization", "name" : "Cognitive FX", "sameAs" : [ "https://www.linkedin.com/in/cognitive-fx-usa/", "https://www.instagram.com/cognitive_fx/", "https://twitter.com/cognitivefx", "https://www.facebook.com/cognitivefx/", "https://www.pinterest.com/cognitivefx/", "https://www.tiktok.com/@cognitivefx" ] }, "name" : "Cognitive FX", "url" : "https://www.cognitivefxusa.com" } } ``` ```json { "@context" : "https://schema.org", "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment#webpage", "@type" : "MedicalWebPage", "about" : { "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment#condition" }, "breadcrumb" : { "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment#breadcrumb" }, "dateModified" : "2026-04-16", "datePublished" : "2024-09-01", "description" : "Neuropathic POTS is the most common POTS subtype, affecting roughly 50% of patients. Caused by small fiber neuropathy damaging the nerves that constrict leg vessels. Learn the symptoms, diagnostic tests, and treatments that actually work.", "headline" : "Neuropathic POTS: Symptoms, Causes & Treatment", "inLanguage" : "en-US", "isPartOf" : { "@id" : "https://www.cognitivefxusa.com/blog#website" }, "lastReviewed" : "2026-04-16", "mainContentOfPage" : { "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment#article" }, "medicalAudience" : [ { "@type" : "MedicalAudience", "audienceType" : "Patient" }, { "@type" : "MedicalAudience", "audienceType" : "Caregiver" } ], "name" : "Neuropathic POTS: Symptoms, Causes & Treatment", "primaryImageOfPage" : { "@type" : "ImageObject", "height" : 768, "url" : "https://www.cognitivefxusa.com/hs-fs/hubfs/POTS%20Vessel%20Image.jpg", "width" : 1408 }, "publisher" : { "@id" : "https://www.cognitivefxusa.com/#organization" }, "reviewedBy" : { "@id" : "https://www.cognitivefxusa.com/blog/author/dr-alina-fong-phd#person" }, "specialty" : { "@type" : "MedicalSpecialty", "name" : "Neurology" }, "url" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment" } ``` ```json { "@context" : "https://schema.org", "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment#condition", "@type" : "MedicalCondition", "alternateName" : [ "Neuropathic POTS", "POTS neuropathic subtype", "Small fiber neuropathy POTS" ], "cause" : [ { "@type" : "MedicalCause", "description" : "Autoantibodies targeting adrenergic and muscarinic receptors disrupt autonomic function. About 20% of POTS patients have an identifiable autoimmune comorbidity such as Hashimoto's thyroiditis, Sjogren's syndrome, or celiac disease.", "name" : "Autoimmune attack on autonomic nerves" }, { "@type" : "MedicalCause", "description" : "50-60% of POTS patients trace onset to a viral illness. Long COVID has become the single largest trigger, with 31% of highly symptomatic Long COVID patients meeting full POTS criteria. Other triggers include Epstein-Barr virus, Lyme disease, and influenza.", "name" : "Post-viral and post-infectious triggers" }, { "@type" : "MedicalCause", "description" : "About 80% of patients with hEDS also have POTS. Weakened vessel walls allow excessive venous pooling, and fragile connective tissue may leave small nerve fibers more vulnerable to damage.", "name" : "Hypermobile Ehlers-Danlos Syndrome (hEDS)" }, { "@type" : "MedicalCause", "description" : "TBI can damage the Central Autonomic Network including the insular cortex, hypothalamus, nucleus tractus solitarius, and ventrolateral medulla. 70.6% of youth with persistent post-concussion symptoms have abnormal tilt table results, and 41% meet full POTS criteria.", "name" : "Traumatic brain injury and concussion" } ], "code" : [ { "@type" : "MedicalCode", "code" : "G90.A", "codingSystem" : "ICD-10-CM" }, { "@type" : "MedicalCode", "code" : "I49.8", "codingSystem" : "ICD-10-CM" } ], "description" : "A subtype of Postural Orthostatic Tachycardia Syndrome caused by damage to small unmyelinated nerve fibers that control blood vessel constriction in the legs and abdomen. When these sympathetic postganglionic nerves fail, blood pools in the lower body on standing and the heart races to compensate. Affects roughly 50% of diagnosed POTS patients.", "epidemiology" : "Affects an estimated 1 to 3 million Americans. 80-85% of patients are female. Neuropathic subtype accounts for roughly 50% of POTS cases. Patients wait an average of 5.9 years and see 7 different doctors before receiving a correct diagnosis, with 69% initially misdiagnosed with anxiety.", "name" : "Neuropathic Postural Orthostatic Tachycardia Syndrome", "possibleComplication" : [ "Functional disability matching congestive heart failure on quality of life measures", "Loss of employment (only 48% maintain employment)", "Cognitive impairment interfering with work and daily tasks", "Deconditioning cycle from exercise intolerance" ], "possibleTreatment" : [ { "@type" : "MedicalTherapy", "description" : "Structured recumbent exercise (swimming, rowing, recumbent bike) progressing to upright training over months. The single most effective intervention: 53% of participants no longer meet POTS criteria after three months, with 71% remission among completers in community data.", "name" : "Exercise reconditioning (Levine/Dallas protocol)" }, { "@type" : "MedicalTherapy", "description" : "Full abdominal-leg compression at 30-40 mmHg reduces standing heart rate from 109 bpm to 92 bpm in randomized trials. Abdominal compression outperforms leg-only compression.", "name" : "Compression garments" }, { "@type" : "MedicalTherapy", "description" : "2-3 liters of fluid daily and 6-10g salt daily expand plasma volume and reduce the orthostatic deficit. Small frequent low-carb meals minimize postprandial worsening.", "name" : "Salt and fluid loading" }, { "@type" : "MedicalTherapy", "description" : "Targeted therapy for the nucleus tractus solitarius, vestibular system, breathing chemistry, and vascular tone. Particularly important for POTS driven by brainstem, vestibular, or cranial nerve dysregulation after concussion or viral illness.", "name" : "Neurological rehabilitation" }, { "@type" : "MedicalTherapy", "description" : "Produced clinically significant improvement in 63% of POTS patients in a 2025 tertiary clinic study. Trains the saccule, utricle, and vestibulo-ocular reflex to recalibrate gravity and position sensing that drives autonomic adjustments.", "name" : "Vestibular rehabilitation" }, { "@type" : "MedicalTherapy", "description" : "Breathing at approximately 6 breaths per minute is the strongest non-invasive amplifier of baroreflex gain, directly training the nucleus tractus solitarius to respond more accurately to orthostatic challenges.", "name" : "Resonance frequency breathing" }, { "@type" : "MedicalTherapy", "description" : "Wall sits and hand grip exercises improve autonomic control of vascular tone with as few as three sessions per week. Ranked 90.5% effective for blood pressure regulation in a 2023 meta-analysis of 270 trials.", "name" : "Isometric exercise training" }, { "@type" : "DrugClass", "description" : "Heart rate reducer that does not affect blood pressure. Off-label for POTS; 78% of patients report improvement in retrospective data.", "name" : "Ivabradine" }, { "@type" : "DrugClass", "description" : "Promotes vasoconstriction directly. Particularly logical for the neuropathic subtype where peripheral vasoconstriction is impaired.", "name" : "Midodrine" }, { "@type" : "DrugClass", "description" : "10-20 mg reduces tachycardia without worsening fatigue. Higher doses worsen fatigue in POTS patients.", "name" : "Low-dose propranolol" } ], "riskFactor" : [ { "@type" : "MedicalRiskFactor", "name" : "Female sex" }, { "@type" : "MedicalRiskFactor", "name" : "Recent viral illness including COVID-19" }, { "@type" : "MedicalRiskFactor", "name" : "Hypermobile Ehlers-Danlos Syndrome" }, { "@type" : "MedicalRiskFactor", "name" : "Recent concussion or traumatic brain injury" }, { "@type" : "MedicalRiskFactor", "name" : "Personal or family history of autoimmune disease" } ], "signOrSymptom" : [ { "@type" : "MedicalSignOrSymptom", "description" : "Heart rate increase of 30 or more bpm within 10 minutes of standing (40 bpm for ages 12-19). The defining feature of POTS across all subtypes.", "name" : "Orthostatic tachycardia" }, { "@type" : "MedicalSignOrSymptom", "description" : "Dark blue-purple discoloration of the feet and lower legs on standing, cold to the touch. Present in 40-50% of POTS patients and a key marker of the neuropathic subtype.", "name" : "Acrocyanosis" }, { "@type" : "MedicalSignOrSymptom", "description" : "Dizziness, visual graying, and near-fainting caused by reduced cerebral blood flow on standing. Reported by approximately 90% of patients.", "name" : "Lightheadedness and presyncope" }, { "@type" : "MedicalSignOrSymptom", "description" : "Deficits in attention, processing speed, executive function, and working memory. More than 95% of POTS patients report cognitive impairment, with 67% experiencing it daily. Symptoms worsen when upright and improve when lying down.", "name" : "Brain fog and cognitive dysfunction" }, { "@type" : "MedicalSignOrSymptom", "description" : "Burning, tingling, numbness, or electric-shock sensations in the hands and feet caused by small fiber nerve damage. Strongly suggestive of the neuropathic subtype.", "name" : "Neuropathic pain" }, { "@type" : "MedicalSignOrSymptom", "description" : "Patchy loss of sweating (anhidrosis), particularly in the lower extremities. Present in approximately 50% of POTS patients and detectable on QSART or thermoregulatory sweat testing.", "name" : "Sudomotor dysfunction" }, { "@type" : "MedicalSignOrSymptom", "description" : "Nausea, bloating, constipation, abdominal pain, and early satiety. Affects 96% of POTS patients, with nausea reported by 79-86%.", "name" : "Gastrointestinal dysmotility" }, { "@type" : "MedicalSignOrSymptom", "description" : "Even mild exertion triggers disproportionate symptoms. Reduced stroke volume during upright exercise produces an exaggerated heart rate response and early exhaustion.", "name" : "Exercise intolerance and chronic fatigue" }, { "@type" : "MedicalSignOrSymptom", "description" : "Near-universal in POTS. Heat causes vasodilation, worsening blood pooling and tachycardia.", "name" : "Heat intolerance" }, { "@type" : "MedicalSignOrSymptom", "description" : "Often positional (worse standing, better lying down). Affects approximately 75% of patients and may overlap with migraine.", "name" : "Headache" } ] } ``` ```json { "@context" : "https://schema.org", "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment#article", "@type" : [ "Article", "MedicalScholarlyArticle" ], "about" : { "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment#condition" }, "articleSection" : "POTS Treatment", "author" : { "@id" : "https://www.cognitivefxusa.com/blog/author/lynn-gaufin#person", "@type" : "Person", "name" : "Lynn Gaufin", "url" : "https://www.cognitivefxusa.com/blog/author/lynn-gaufin" }, "citation" : [ { "@type" : "ScholarlyArticle", "author" : "Jacob G, Costa F, Shannon JR, et al.", "datePublished" : "2000", "name" : "The neuropathic postural tachycardia syndrome", "publisher" : "New England Journal of Medicine", "url" : "https://pubmed.ncbi.nlm.nih.gov/11018167/" }, { "@type" : "ScholarlyArticle", "author" : "Gibbons CH, Bonyhay I, Benson A, Wang N, Freeman R", "datePublished" : "2013", "name" : "Structural and functional small fiber abnormalities in the neuropathic postural tachycardia syndrome", "publisher" : "PLoS One", "url" : "https://pmc.ncbi.nlm.nih.gov/articles/PMC3874039/" }, { "@type" : "ScholarlyArticle", "author" : "Fu Q, VanGundy TB, Shibata S, Auchus RJ, Williams GH, Levine BD", "datePublished" : "2011", "name" : "Exercise training versus propranolol in the treatment of POTS", "publisher" : "Hypertension", "url" : "https://pubmed.ncbi.nlm.nih.gov/21690484/" }, { "@type" : "ScholarlyArticle", "author" : "Heyer GL, Fischer A, Wilson J, et al.", "datePublished" : "2016", "name" : "Orthostatic intolerance and autonomic dysfunction in youth with persistent postconcussion symptoms", "publisher" : "Clinical Journal of Sport Medicine", "url" : "https://pubmed.ncbi.nlm.nih.gov/25706663/" }, { "@type" : "ScholarlyArticle", "author" : "Bourne KM, Sheldon RS, Hall J, et al.", "datePublished" : "2021", "name" : "Abdominal compression as a treatment for POTS", "publisher" : "Journal of the American Heart Association", "url" : "https://www.ahajournals.org/doi/10.1161/JAHA.120.017610" }, { "@type" : "ScholarlyArticle", "author" : "Ormiston CK, Swendseid B, et al.", "datePublished" : "2025", "name" : "Prevalence and clinical impact of POTS in highly symptomatic Long COVID", "publisher" : "Circulation: Arrhythmia and Electrophysiology", "url" : "https://pubmed.ncbi.nlm.nih.gov/41025260/" }, { "@type" : "ScholarlyArticle", "author" : "Moak JP, Leong D, Gurbani N, et al.", "datePublished" : "2024", "name" : "Small fiber neuropathy in children and young adults with POTS", "publisher" : "Autonomic Neuroscience", "url" : "https://pubmed.ncbi.nlm.nih.gov/38537312/" }, { "@type" : "ScholarlyArticle", "author" : "Li H, Yu X, Liles C, et al.", "datePublished" : "2014", "name" : "Autoimmune basis for postural tachycardia syndrome", "publisher" : "Journal of the American Heart Association", "url" : "https://pubmed.ncbi.nlm.nih.gov/24572257/" } ], "dateModified" : "2026-04-16", "datePublished" : "2024-09-01", "description" : "A comprehensive clinical guide to neuropathic POTS, the most common subtype of Postural Orthostatic Tachycardia Syndrome. Covers symptoms, mechanism, diagnosis, evidence-based treatments, and recovery prognosis.", "headline" : "Neuropathic POTS: Symptoms, Causes & Treatment", "image" : { "@type" : "ImageObject", "height" : 768, "url" : "https://www.cognitivefxusa.com/hs-fs/hubfs/POTS%20Vessel%20Image.jpg", "width" : 1408 }, "inLanguage" : "en-US", "isPartOf" : { "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment#webpage" }, "keywords" : [ "neuropathic POTS", "POTS subtypes", "small fiber neuropathy", "postural orthostatic tachycardia syndrome", "acrocyanosis", "dysautonomia treatment", "POTS diagnosis", "QSART test", "skin punch biopsy", "Levine protocol", "POTS exercise program", "post-concussion POTS", "long COVID POTS" ], "mainEntityOfPage" : { "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment#webpage" }, "mentions" : [ { "@type" : "MedicalCondition", "name" : "Hyperadrenergic POTS", "url" : "https://www.cognitivefxusa.com/blog/hyperadrenergic-pots-symptoms-causes-and-how-to-treat-the-subtype-most-doctors-miss" }, { "@type" : "MedicalCondition", "name" : "Hypovolemic POTS", "url" : "https://www.cognitivefxusa.com/blog/hypovolemic-pots-symptoms-causes-and-treatment-for-low-blood-volume-pots" }, { "@type" : "MedicalCondition", "name" : "Hypermobile Ehlers-Danlos Syndrome" }, { "@type" : "MedicalCondition", "name" : "Mast Cell Activation Syndrome" }, { "@type" : "MedicalCondition", "name" : "Post-concussion syndrome", "url" : "https://www.cognitivefxusa.com/blog/post-concussion-syndrome-and-post-concussion-symptoms-pcs" }, { "@type" : "MedicalCondition", "name" : "Long COVID" }, { "@type" : "MedicalCondition", "name" : "Small fiber neuropathy" } ], "name" : "Neuropathic POTS: Symptoms, Causes & Treatment", "publisher" : { "@id" : "https://www.cognitivefxusa.com/#organization" }, "reviewedBy" : { "@id" : "https://www.cognitivefxusa.com/blog/author/dr-alina-fong-phd#person", "@type" : "Person", "affiliation" : { "@id" : "https://www.cognitivefxusa.com/#organization" }, "jobTitle" : "Clinical Neuropsychologist", "name" : "Dr. Alina Fong", "url" : "https://www.cognitivefxusa.com/blog/author/dr-alina-fong-phd" }, "timeRequired" : "PT33M", "url" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment", "wordCount" : 4500 } ``` ```json { "@context" : "https://schema.org", "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment#faq", "@type" : "FAQPage", "mainEntity" : [ { "@type" : "Question", "acceptedAnswer" : { "@type" : "Answer", "text" : "Neuropathic POTS is the most common subtype of Postural Orthostatic Tachycardia Syndrome, accounting for roughly 50% of diagnosed cases. It is caused by damage to the small unmyelinated nerve fibers (sympathetic postganglionic C-fibers) that tell blood vessels in the legs and abdomen to constrict. When these nerves fail, blood pools in the lower body every time you stand, and the heart races to compensate for the drop in venous return." }, "name" : "What is neuropathic POTS?" }, { "@type" : "Question", "acceptedAnswer" : { "@type" : "Answer", "text" : "Neuropathic POTS involves nerve damage causing vessels that will not constrict. Hyperadrenergic POTS involves excessive sympathetic activation with standing norepinephrine above 600 pg/mL, blood pressure spikes on standing, and prominent anxiety and tremor. Hypovolemic POTS stems from abnormally low blood volume (about a 13% plasma deficit) caused by paradoxical suppression of the renin-aldosterone system. These subtypes overlap frequently. A neuropathic POTS patient often develops hyperadrenergic features as the brain ramps up sympathetic drive to compensate for peripheral nerve failure." }, "name" : "How is neuropathic POTS different from other POTS subtypes?" }, { "@type" : "Question", "acceptedAnswer" : { "@type" : "Answer", "text" : "The hallmark sign is acrocyanosis: dark blue-purple discoloration of the feet and lower legs within minutes of standing, with cold skin. Brain fog affects more than 95% of patients and is often the most disabling symptom. Gastrointestinal symptoms affect 96% of patients, including nausea, constipation, bloating, and abdominal pain. Other common features include exercise intolerance, burning or tingling pain in the hands and feet, patchy loss of sweating (especially in the lower legs), heat intolerance, and sleep disturbances. Quality of life scores match those of congestive heart failure patients." }, "name" : "What does neuropathic POTS feel like?" }, { "@type" : "Question", "acceptedAnswer" : { "@type" : "Answer", "text" : "Four major triggers account for the majority of cases. Autoimmune attack on autonomic nerves, supported by research showing autoantibodies targeting adrenergic and muscarinic receptors. Post-viral onset, which affects 50-60% of POTS patients. Long COVID has become the largest single trigger, with 31% of highly symptomatic Long COVID patients meeting full POTS criteria. Ehlers-Danlos Syndrome, since roughly 80% of hEDS patients also have POTS. Traumatic brain injury and concussion, which can damage the Central Autonomic Network in the brainstem. Studies show 70.6% of youth with persistent post-concussion symptoms have abnormal tilt table results, and 41% meet POTS criteria." }, "name" : "What causes neuropathic POTS?" }, { "@type" : "Question", "acceptedAnswer" : { "@type" : "Answer", "text" : "POTS itself is confirmed by a tilt table test or active standing test showing a sustained heart rate increase of 30 bpm or more within 10 minutes of standing (40 bpm for ages 12 to 19), without orthostatic hypotension, with symptoms lasting at least 3 to 6 months. The neuropathic subtype specifically requires additional testing to identify small fiber nerve damage. Skin punch biopsy is the gold standard, using a 3mm biopsy from the lower leg to count intraepidermal nerve fiber density. QSART (Quantitative Sudomotor Axon Reflex Test) measures sweat nerve function and is abnormal in about 56% of POTS patients. Skin biopsy and QSART often identify different subsets of nerve damage, so they complement rather than replace each other. Blood testing screens for autoimmune drivers and catecholamine levels." }, "name" : "How is neuropathic POTS diagnosed?" }, { "@type" : "Question", "acceptedAnswer" : { "@type" : "Answer", "text" : "Exercise reconditioning is the single most effective intervention. The Levine protocol starts with recumbent exercise only (swimming, rowing, recumbent bike) for the first 1 to 3 months to avoid orthostatic stress, then progresses to upright training. A 2011 study found 53% of participants no longer met POTS criteria after three months. Compression garments at 30-40 mmHg covering the abdomen and legs reduce standing heart rate significantly. Salt loading (6-10g daily) and fluid intake of 2-3 liters daily expand plasma volume. Neurological rehabilitation targeting the nucleus tractus solitarius, vestibular system, breathing chemistry, and vascular tone is particularly important when POTS follows concussion or viral illness. Off-label medications include ivabradine, midodrine, and low-dose propranolol." }, "name" : "What treatments work for neuropathic POTS?" }, { "@type" : "Question", "acceptedAnswer" : { "@type" : "Answer", "text" : "Roughly 50% of patients improve significantly within 1 to 3 years, and about 80% show meaningful improvement over time. Complete remission rates range from 19 to 33%, with better outcomes in younger patients and those who maintain consistent exercise. After the Levine exercise protocol specifically, 53% no longer meet POTS diagnostic criteria. The factors predicting better outcomes include younger age at onset, consistent exercise, early diagnosis, and identification and treatment of the underlying cause. For post-concussion POTS patients, 75% had normal tilt table results once their concussion symptoms improved, suggesting post-TBI autonomic dysfunction can resolve when the underlying brain dysfunction is treated." }, "name" : "Can neuropathic POTS go away?" }, { "@type" : "Question", "acceptedAnswer" : { "@type" : "Answer", "text" : "They are closely related but not identical. Small fiber neuropathy (SFN) is the underlying nerve damage, which can be confirmed by skin punch biopsy showing reduced intraepidermal nerve fiber density. Neuropathic POTS is the clinical syndrome that results when that small fiber damage specifically affects the sympathetic nerves controlling vascular tone, producing the orthostatic tachycardia pattern that defines POTS. Not everyone with SFN develops POTS, and not everyone with neuropathic POTS has biopsy-confirmed SFN, partly because current tests have 74-90% sensitivity." }, "name" : "Is neuropathic POTS the same as small fiber neuropathy?" }, { "@type" : "Question", "acceptedAnswer" : { "@type" : "Answer", "text" : "The medical term is acrocyanosis. In neuropathic POTS, damaged sympathetic nerves cannot constrict the cutaneous blood vessels in the legs, so blood stagnates in the superficial veins when you stand. The pooled blood has lower oxygen content, which gives the skin the characteristic blue-purple appearance. The feet and lower legs also feel cold to the touch. Acrocyanosis is present in 40-50% of POTS patients and is one of the most specific visual markers pointing toward the neuropathic subtype." }, "name" : "Why do my feet turn purple when I stand up?" }, { "@type" : "Question", "acceptedAnswer" : { "@type" : "Answer", "text" : "Yes. Traumatic brain injury can damage the Central Autonomic Network, a distributed system in the brain that includes the insular cortex, hypothalamus, nucleus tractus solitarius in the brainstem, and ventrolateral medulla. These structures coordinate every cardiovascular adjustment your body makes when you change position. Research shows 70.6% of youth with persistent post-concussion symptoms have abnormal tilt table results, and 41% meet full POTS criteria. Post-concussion autonomic dysfunction appears to be largely reversible, with 75% of PCS patients with POTS showing normal tilt table results once their concussion symptoms improved." }, "name" : "Can a concussion cause neuropathic POTS?" } ] } ``` ```json { "@context" : "https://schema.org", "@id" : "https://www.cognitivefxusa.com/blog/neuropathic-pots-symptoms-causes-treatment#breadcrumb", "@type" : "BreadcrumbList", "itemListElement" : [ { "@type" : "ListItem", "item" : "https://www.cognitivefxusa.com", "name" : "Home", "position" : 1 }, { "@type" : "ListItem", "item" : "https://www.cognitivefxusa.com/blog", "name" : "Blog", "position" : 2 }, { "@type" : "ListItem", "name" : "Neuropathic POTS: Symptoms, Causes & Treatment", "position" : 3 } ] } ``` ```json { "@context" : "https://schema.org", "@id" : "https://www.cognitivefxusa.com/#organization", "@type" : [ "Organization", "MedicalOrganization" ], "address" : { "@type" : "PostalAddress", "addressCountry" : "US", "addressLocality" : "Provo", "addressRegion" : "UT", "postalCode" : "84604", "streetAddress" : "280 W River Park Drive Suite 110" }, "alternateName" : "CFX", "description" : "Specialized brain rehabilitation clinic treating post-concussion syndrome, POTS, autonomic dysfunction, long COVID, and related neurological conditions using functional brain imaging (fNCI) and the EPIC Treatment protocol.", "email" : "hello@cognitivefxusa.com", "foundingDate" : "2014", "logo" : { "@type" : "ImageObject", "height" : 152, "url" : "https://www.cognitivefxusa.com/hubfs/Main_Logo_500px.png", "width" : 500 }, "medicalSpecialty" : [ "Neurology", "Rehabilitation" ], "name" : "Cognitive FX", "sameAs" : [ "https://www.facebook.com/cognitivefx", "https://www.instagram.com/cognitive_fx" ], "telephone" : "+1-385-446-4161", "url" : "https://www.cognitivefxusa.com" } ``` ```json { "@context" : "https://schema.org", "@id" : "https://www.cognitivefxusa.com/blog#website", "@type" : "WebSite", "description" : "Research-backed articles on brain injury, POTS, dysautonomia, long COVID, and TMS treatment from the clinical team at Cognitive FX.", "inLanguage" : "en-US", "name" : "Cognitive FX Blog", "publisher" : { "@id" : "https://www.cognitivefxusa.com/#organization" }, "url" : "https://www.cognitivefxusa.com/blog" } ```