Understanding symptoms from the sympathetic nervous system and parasympathetic nervous system

At Caring Medical, we see patients whose symptoms do not fit neatly into one diagnosis. A person may have persistent neck or back pain along with dizziness, palpitations, digestive problems, abnormal sweating, temperature intolerance, fatigue, headaches, visual disturbances, urinary symptoms, or episodes of feeling faint. Many have accumulated numerous consultations, tests, and medications without finding one explanation for the whole symptom pattern.

Some of these patients have been diagnosed with dysautonomia, an umbrella term for disorders or disturbances affecting the autonomic nervous system. Others have symptoms suggestive of autonomic dysfunction but have not undergone formal testing. New research strengthens the case for considering autonomic symptoms during the evaluation of chronic musculoskeletal pain. It does not, however, show that every patient with chronic pain has a neurological disorder or that spinal instability is the cause in every case.

What does the autonomic nervous system control?

The autonomic nervous system regulates many functions that occur without conscious effort, including:

  • heart rate and blood pressure;
  • blood-vessel constriction and dilation;
  • digestion and intestinal movement;
  • sweating and temperature regulation;
  • breathing patterns;
  • bladder function;
  • pupil responses; and
  • aspects of immune and inflammatory regulation.

The two best-known divisions are the sympathetic nervous system and the parasympathetic nervous system. The sympathetic system helps the body respond to physical or emotional demands—the familiar “fight or flight” response. The parasympathetic system supports recovery, digestion, energy conservation, and the return toward a resting state. These systems do not simply switch on and off. They continually adjust to posture, movement, exertion, meals, temperature, stress, hydration, and illness.

When regulation becomes impaired, symptoms can appear in several organ systems at the same time. This is why dysautonomia may initially look like separate cardiac, neurological, gastrointestinal, hormonal, or psychological problems.

Symptoms that may warrant an autonomic evaluation

Possible autonomic symptoms include:

  • lightheadedness or near-fainting after standing;
  • an excessive or uncomfortable rise in heart rate;
  • unexplained blood-pressure fluctuations;
  • exercise intolerance or prolonged worsening after exertion;
  • abnormal sweating or poor temperature tolerance;
  • nausea, early fullness, bloating, constipation, or diarrhea;
  • urinary urgency, difficulty initiating urination, or incomplete emptying;
  • blurred vision or difficulty adjusting to changes in light;
  • tremulousness, weakness, fatigue, or “brain fog”; and
  • symptoms that improve when lying down.

These symptoms are not specific to dysautonomia. Anemia, dehydration, medication effects, thyroid disease, heart rhythm disorders, diabetes, infection, vestibular disorders, migraine, anxiety, sleep disorders, and other medical problems can produce overlapping complaints. Appropriate evaluation is therefore essential.

What are we seeing in this image?

We see how the nerves and the ganglia, (the ganglia are displayed by the arrows), run around, through, and in between the vertebrae of the spine. What you are seeing is the hard wiring of your nervous system and its communication system. If the spine is unstable, if pressure is exerting on the nerves and ganglia, the communication system starts “dropping calls,” the conversation then becomes garbled, hard to understand. These communication problems lead to symptoms, diseases, and a myriad of diagnoses.

We see how the nerves and the ganglia, (the ganglia are displayed by the arrows), run around, through and in between the vertebrae of the spine. What you are seeing is the hard wiring of your nervous system and its communication system. If the spine is unstable, if pressure is exerting on teh nerves and ganglia, the communication system starts "dropping calls," the conversation becomes garbled, hard to understand. These communication problems lead to symptoms, diseases and a myriad of diagnosis.

New 2026 research: Dysautonomia is common in chronic musculoskeletal pain

A 2026 systematic review and meta-analysis examined 17 studies involving 1,003 adults with chronic musculoskeletal pain and 417 healthy controls. The studies included patients with fibromyalgia, Ehlers-Danlos syndrome, and rheumatoid arthritis. The pooled prevalence of dysautonomia was 64%, although the estimates varied substantially between studies. People with chronic musculoskeletal pain were more than twice as likely as healthy controls to demonstrate dysautonomia. (1)

The large variation among the studies is important. Different patient populations and different subjective and objective testing methods were combined. The review supports an association between chronic musculoskeletal pain and autonomic dysfunction, but it cannot identify one cause or establish that the relationship operates in the same way for every pain condition.

A new cross-sectional study found a substantial autonomic symptom burden

A September 2026 cross-sectional study published in Rheumatology compared 342 patients with clinician-confirmed chronic musculoskeletal pain with 57 approximately age- and sex-matched healthy controls. The investigators used the Composite Autonomic Symptom Score-31, or COMPASS-31. A score of 17 or higher was considered indicative of dysautonomia for the study. (2)

Seventy-four percent of the chronic-pain group met this symptom-score threshold, compared with 11% of the controls. After adjustment, patients with chronic musculoskeletal pain were 7.4 times as likely to meet the threshold. Rates were similarly high in inflammatory and non-inflammatory musculoskeletal conditions. Greater pain, anxiety, and depression scores were associated with a greater autonomic symptom burden.

This study supports routinely asking patients with persistent musculoskeletal pain about dizziness, orthostatic symptoms, palpitations, gastrointestinal complaints, sweating abnormalities, and temperature intolerance. These symptoms should not automatically be dismissed as unrelated to the patient’s pain condition.

At the same time, the study must be interpreted carefully:

  • COMPASS-31 is a validated symptom questionnaire, but it is not equivalent to a tilt-table test or a diagnosis of POTS, orthostatic hypotension, or another specific autonomic disorder.
  • The study was cross-sectional. It cannot determine whether pain contributes to autonomic symptoms, autonomic dysfunction amplifies pain, or shared biological and psychological factors affect both.
  • Associations with anxiety and depression do not mean the symptoms are imaginary. They do mean that pain, mood, sleep, activity, and autonomic regulation may interact in complex ways.
  • The study did not evaluate cervical instability and does not demonstrate that a neck disorder caused the autonomic symptoms.

Dysautonomia is not the same as POTS

Postural orthostatic tachycardia syndrome, or POTS, is one form of dysautonomia. It is characterized by chronic orthostatic symptoms accompanied by an excessive increase in heart rate after standing, without the blood-pressure fall required for a diagnosis of orthostatic hypotension. Formal criteria depend on age and clinical context. A symptom questionnaire by itself cannot diagnose POTS. (3)

Evaluation may include lying and standing heart rate and blood-pressure measurements, a ten-minute stand or lean test, tilt-table testing, an electrocardiogram, rhythm monitoring, and laboratory testing chosen for the patient’s presentation. More specialized autonomic testing may examine sweating, heart-rate responses to breathing, or blood-pressure responses to physiological challenges.

Our related article on POTS, the vagus nerve, and cervical spine instability discusses this diagnosis in greater detail.

Why chronic pain and autonomic symptoms may overlap

The relationship is probably bidirectional and multifactorial rather than a single pathway.

Persistent pain can alter sleep, physical activity, breathing, stress responses, and cardiovascular conditioning. Reduced activity may contribute to deconditioning and worsen orthostatic intolerance. Conversely, impaired blood-pressure regulation, poor exercise tolerance, disrupted sleep, gastrointestinal dysfunction, and heightened physiological arousal may increase fatigue and make pain harder to manage.

Inflammation, altered pain processing, small-fiber nerve dysfunction, medication effects, and connective-tissue disorders may also contribute in selected patients. The 2026 studies identify an important clinical overlap, but they do not establish one universal mechanism.

Joint hypermobility, hEDS, and autonomic symptoms

Dysautonomia is frequently reported in people with hypermobile Ehlers-Danlos syndrome (hEDS) and hypermobility spectrum disorders (HSD). In a retrospective cohort of 144 patients with hEDS or HSD, dysautonomia was identified in 65% of female patients and 44% of male patients. Exercise intolerance was common, and many patients reported a major reduction in physical activity following the onset or worsening of their hypermobility-related condition. (4)

Hypermobility disorders may also involve functional gastrointestinal, pelvic, bladder, and orthostatic complaints. A clinical review found particularly strong associations between joint hypermobility syndromes and orthostatic tachycardia, anxiety disorders, functional gastrointestinal disorders, and pelvic or bladder dysfunction. (5)

These are associations, not proof that one condition always causes the others. Readers seeking more information can review our discussion of EDS and hypermobility disorders and our article on dysautonomia, POTS, and hEDS.

What are we seeing in this image?

Here we have the lumbar spine. Lumbar spinal stability is seen as the vertebrae lined up in their proper position.

  • In this image look at the L3 vertebrae. See how it is riding forward of L4? This is spinal instability caused by stretched-out ligaments at L3/L4. The L3 has slid forward on the L4.
  • Now, look at the L4 vertebrae. See how it has slid forward of the L5 vertebrae? This is spinal instability caused by stretched-out ligaments at L4/L5.

Could cervical instability contribute to autonomic symptoms?

For most people with dysautonomia, cervical instability will not be the only—or necessarily the primary—explanation. At Caring Medical, we consider a possible cervical contribution in a selected subgroup, particularly when autonomic-type symptoms occur with significant neck pain, prior whiplash or head injury, joint hypermobility, abnormal cervical motion, or symptoms that reproducibly change with head or neck position.

The vagus nerves descend through the carotid sheaths on either side of the neck, near the internal jugular veins and carotid arteries. The upper cervical spinal cord, brainstem, cervical sympathetic structures, and sensory input from cervical joints and muscles also participate in cardiovascular and autonomic regulation. We have proposed the term cervicovagopathy for a potential disorder in which cervical dysstructure or instability may stretch, compress, or otherwise disturb vagus-nerve function. This remains a proposed mechanism rather than a universally accepted diagnosis. (6)

Our 2024 narrative review described proposed pathways by which ligamentous cervical instability and loss of normal cervical alignment could affect neural and vascular structures in the neck. Because this was a narrative and mechanistic paper, it should be treated as a framework for investigation, not proof that forward-head posture or cervical instability causes systemic dysautonomia. (7)

A 2026 retrospective cross-sectional study from our center examined 227 patients, ages 20 to 50, who presented with chronic brain-based symptoms. The cohort had high rates of neck pain, altered cervical alignment, C1-C2 instability, reduced internal jugular vein and vagus-nerve cross-sectional measurements, and elevated optic-nerve-sheath measurements. Because all patients were evaluated at a specialty neck center, there was no healthy control group, and the design was cross-sectional, the results demonstrate patterns within a selected population—not causation or prevalence in the general public. (8)

The practical message is that a cervical contribution may deserve investigation when the history, examination, and imaging point in that direction. Autonomic symptoms alone are not sufficient evidence of cervical instability.

How we evaluate patients at Caring Medical

Our evaluation begins with the pattern and timing of symptoms. We ask whether symptoms are related to standing, exertion, meals, temperature, stress, neck position, or specific movements. We review prior cardiac, neurological, rheumatological, gastrointestinal, and autonomic testing rather than assuming every symptom begins in the neck.

When appropriate, assessment may include:

  • orthostatic heart-rate and blood-pressure measurements;
  • neurological and musculoskeletal examination;
  • evaluation of joint hypermobility and ligament injury;
  • assessment of cervical alignment and motion;
  • heart-rate variability testing as one measure of autonomic regulation;
  • vagus-nerve assessment; and
  • dynamic imaging or vascular assessment when clinically justified.

No single test proves that the cervical spine is responsible for dysautonomia. Findings must be interpreted together and correlated with the patient’s symptoms. Our longer discussion of this process is available in Determining the Causes of Dysautonomia, Vagopathy, and Autonomic Nervous System Imbalances.

Treatment 

Dysautonomia treatment should be individualized and may involve hydration and salt strategies when medically appropriate, compression garments, medication review, treatment of anemia or endocrine disorders, sleep improvement, physical reconditioning, and medications directed by a clinician familiar with the specific autonomic diagnosis.

If examination identifies painful ligament laxity or mechanical instability, treatment may also address the musculoskeletal problem. Our earlier narrative review discussed capsular-ligament laxity as a potential contributor to chronic neck pain and proposed prolotherapy as one treatment option for selected patients. (9)

However, prolotherapy is not an established treatment for dysautonomia itself. Evidence that improving cervical stability will reliably correct POTS, vagus-nerve dysfunction, or multisystem autonomic symptoms remains limited. At Caring Medical, any discussion of injection treatment should be based on evidence of a treatable ligament or joint problem—not simply the presence of dizziness, fatigue, anxiety, digestive symptoms, or an elevated questionnaire score.

When symptoms require urgent medical care

Seek urgent evaluation for chest pain, new or severe shortness of breath, fainting during exertion, sustained or irregular rapid heart rhythms, new weakness or numbness, difficulty speaking, sudden severe headache, loss of bladder or bowel control, rapidly progressive walking difficulty, or signs of gastrointestinal bleeding. These symptoms should not be attributed to dysautonomia or cervical instability without appropriate medical assessment.

Summary

The emerging research supports a clinically important association between chronic musculoskeletal pain and autonomic symptoms. The strongest responsible conclusion is that clinicians should ask about dysautonomia symptoms and evaluate them when appropriate.

For selected patients, especially those with significant neck pain, trauma, hypermobility, or position-dependent symptoms, cervical instability may be one contributor worth investigating. Current evidence does not establish it as a universal cause. A careful evaluation should distinguish a validated autonomic disorder from symptom screening, consider alternative diagnoses, and determine whether any cervical finding is clinically meaningful.

References
1 Almutairi NA, Greenwood DC, Sivan M. The prevalence of dysautonomia in chronic musculoskeletal pain: a systematic review and meta-analysis. Rheumatology Advances in Practice. 2026;10(2). [Google Scholar]
2 Almutairi NA, Greenwood DC, Sivan M. Prevalence of dysautonomia in chronic musculoskeletal pain: a cross-sectional study. Rheumatology (Oxford). 2026 Sep 16. doi:10.1093/rheumatology/keag511. [Google Scholar]
3 Sheldon RS, Grubb BP 2nd, Olshansky B, et al. 2015 Heart Rhythm Society expert consensus statement on the diagnosis and treatment of postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope. Heart Rhythm. 2015;12(6). [Google Scholar]
4 Ruiz Maya T, Fettig V, Mehta L, Gelb BD, Kontorovich AR. Dysautonomia in hypermobile Ehlers-Danlos syndrome and hypermobility spectrum disorders is associated with exercise intolerance and cardiac atrophy. American Journal of Medical Genetics Part A. 2021;185(12):3754-3761. [Google Scholar]
5 Botrus G, Baker O, Borrego E, et al. Spectrum of gastrointestinal manifestations in joint hypermobility syndromes. American Journal of the Medical Sciences. 2018;355(6):573-580. [Google Scholar]
6 Hauser RA, Matias D, Rawlings BR. Cervicovagopathy: ligamentous cervical instability and dysstructure as a potential etiology for vagus nerve dysfunction in the cause of human symptoms and diseases. Frontiers in Neurology. 2025;16:1572863. [Google Scholar]
7 Hauser RA, Matias D, Rawlings B. The ligamentous cervical instability etiology of human disease from the forward head-facedown lifestyle: emphasis on obstruction of fluid flow into and out of the brain. Frontiers in Neurology. 2024;15:1430390. [Google Scholar]
8 Hauser RA, Griffiths M, Watterson A, Matias D, Steilen C, Rawlings BR. Brain-based symptoms reported in young adults evaluated for cervical spine etiology: a retrospective, cross-sectional clinical study with preliminary data on over 200 patients. Frontiers in Neurology. 2026;17:1749266. [Google Scholar]
9 Steilen D, Hauser R, Woldin B, Sawyer S. Chronic neck pain: making the connection between capsular ligament laxity and cervical instability. The Open Orthopaedics Journal. 2014;8:326-345. [Google Scholar]

Medical disclaimer: This article is for educational purposes and is not a substitute for diagnosis or treatment by a qualified healthcare professional. Dysautonomia symptoms can have many causes, including serious cardiac, neurological, endocrine, vascular, or medication-related conditions. Treatment recommendations must be individualized after an appropriate medical evaluation.

 

The problem of bad messaging is a problem of cervical and spinal ligament laxity.

For some people, when there are neurological problems that do not seem to have an answer, an answer may be found in cervical and spinal ligament laxity. This is the situation where the ligaments, the connective tissue that holds the vertebrae in the proper place have become weakened through degenerative disease or injury. For most, this problem occurs with degenerative wear and tear. The ligaments basically become stretched out.

 

Hurting the function of the autonomic nervous system.

Above we asked: What are we seeing in this image? For some, it may be the cause of many of your neurological symptoms. What you see here in the lumbar spine can occur equally in the cervical spine. This image could be the visualization of your digestive problems, urinary problems, concentration problems, heart rate, and blood pressure problems, all the symptoms and diagnoses mentioned above caused by spinal instability.

Are your problems related to Autonomic Nervous System Imbalances? How do we know?

We offer dynamic Autonomic Nervous System testing to try to understand and solve the challenges you may be facing because your nervous system is not working properly. While our main focus is an understanding of structural breakdown in the spine and its repair through Prolotherapy injections, explained below, we also help assess emotional or stressful problems. The testing is explained at length in our article: Determining the Cause(s) of Dysautonomia, Vagopathy, and Autonomic Nervous System Imbalances.

Non-surgical treatment – Cervical and Lumbar Spine Stability and Restoring Lordosis -Making a case for regeneration and repair of the spinal ligaments

Above we demonstrated these problems with images of the lumbar spine. In this section, we will use the cervical spine.

What are we seeing in this image?

When the natural curve of the spine is distorted, we can understand that ligament laxity is occurring. Again, the spinal ligaments are no longer strong enough to hold the vertebrae in their proper alignment.

Cervical instability on DMX

Research on spinal instability and Prolotherapy

Caring Medical has published dozens of papers on Prolotherapy injections as a treatment in difficult to treat musculoskeletal disorders. Prolotherapy is an injection technique utilizing simple sugar or dextrose.

Published research papers and articles from our doctors at Caring Medical on low back pain

Prolotherapy works to stabilize the ligaments of the spine allowing discs to get back into position and can even create space for a person who has lost space due to one or more degenerated discs. In Prolotherapy research from the doctors at Caring Medical, patients with more than four years of unresolved low back pain were shown to have had their pain improved, stiffness, range of motion, and quality of life improved, even 12 months subsequent to their last Prolotherapy session.

These articles will offer a more extensive explanation of the treatment:

Research on cervical instability and Prolotherapy

We propose that in many cases of chronic neck pain, the cause may be underlying joint instability due to capsular ligament laxity. Currently, curative treatment options for this type of cervical instability are inconclusive and inadequate. Based on clinical studies and experience with patients who have visited our chronic pain clinic with complaints of chronic neck pain, we contend that prolotherapy offers a potentially curative treatment option for chronic neck pain related to capsular ligament laxity and underlying cervical instability.”

References

1 Botrus G, Baker O, Borrego E, Ngamdu KS, Teleb M, Martinez JL, Maldonado III G, Hussein AM, McCallum R. Spectrum of gastrointestinal manifestations in joint hypermobility syndromes. The American journal of the medical sciences. 2018 Jun 1;355(6):573-80. [Google Scholar]

 

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