Ross Hauser, MD.

At Caring Medical, we see patients who have persistent neck or back pain together with symptoms affecting several other parts of the body. They may describe dizziness, a racing heart, bloating, abnormal sweating, temperature intolerance, fatigue, headaches, visual disturbances, urinary problems, or episodes of feeling faint. Some have seen several specialists without finding an explanation for the whole pattern.

These symptoms can involve the autonomic nervous system, which helps regulate functions that happen without conscious effort. Dysautonomia is an umbrella term for disturbances of that regulation. It is not one disease, and similar symptoms can arise from different causes.

Research published in 2026 reinforces the overlap between chronic musculoskeletal pain and autonomic symptoms. Other research examines this overlap in joint hypermobility and chronic lung disease. Our clinical interest is whether spinal instability contributes in a selected subgroup of patients. Understanding that possibility requires separating symptoms, structural findings, and a demonstrated autonomic disorder.

What does the autonomic nervous system control?

The autonomic nervous system influences heart rate, blood pressure, blood-vessel constriction and dilation, digestion, intestinal movement, sweating, temperature regulation, airway function, bladder function, pupil responses, and aspects of immune and inflammatory signaling.

Its two best-known divisions are the sympathetic and parasympathetic nervous systems. Sympathetic activity helps the body respond to demands, including exertion and stress. Parasympathetic activity supports functions such as digestion and recovery. Both operate continuously, with different effects in different organs. They do not function as a single switch between stress and relaxation.

Standing, moving, eating, breathing, and responding to temperature changes all require adjustments. For example, circulation must adapt when someone stands up so that sufficient blood continues to reach the brain. When regulation is impaired, a person may experience lightheadedness, palpitations, weakness, or difficulty tolerating activity.

The correct term is involuntary nervous system. Although breathing and some other functions can also be influenced consciously, most autonomic regulation happens automatically.

Symptoms that may warrant an autonomic evaluation

Possible symptoms include:

• Lightheadedness, near-fainting, or fainting after standing.
• An excessive or uncomfortable rise in heart rate, or blood-pressure fluctuations.
• Exercise intolerance, fatigue, weakness, or prolonged worsening after exertion.
• Abnormal sweating and difficulty tolerating heat or cold.
• Nausea, early fullness, bloating, constipation, or diarrhea.
• Urinary urgency, difficulty starting urination, or incomplete emptying.
• Blurred vision, difficulty adjusting to light, tremulousness, or brain fog.
• Symptoms that improve when lying down.

These symptoms are not specific to dysautonomia. Dehydration, anemia, medication effects, thyroid disease, diabetes, heart rhythm disorders, infection, vestibular disorders, migraine, anxiety, and sleep disorders can produce overlapping complaints. A symptom list cannot establish either dysautonomia or a cervical cause.

Sweating deserves consideration because it is an autonomic function, but excessive sweating also has other explanations. Our article on excessive sweating and cervical spine disorders explores that particular symptom.

Video: Dr. Ross Hauser explains spinal instability and autonomic symptoms

In this video, Dr. Hauser uses an anatomical illustration to explain why the relationship between the spine and nearby nerves deserves attention. He discusses ligament laxity, forward movement of vertebrae, and symptoms involving digestion, bladder function, concentration, vision, hearing, and swallowing. He also discusses posture, exercise, and Prolotherapy as ways of addressing a suspected mechanical problem.

The central clinical question is useful: Could a structural problem be contributing to symptoms in a patient who also has neck or back pain? The answer depends on the individual findings. The video presents our proposed spinal mechanism; it should not be interpreted as evidence that every listed symptom originates in the spine or that all autonomic disorders are reversible with spinal treatment.

What are autonomic ganglia, and where are they located?

Ganglia are collections of nerve-cell bodies outside the brain and spinal cord. They act as relay stations in nerve pathways. The sympathetic chains lie close to the vertebral column, while other sympathetic ganglia lie farther forward in the abdomen. Parasympathetic ganglia are generally located near or within the organs they supply. Both systems do not run as identical chains along the front of the entire spine.

The arrows in this illustration help show the close anatomical relationships between nerves and spinal structures. Dr. Hauser’s comparison with a communication system can help explain how an actual nerve injury or compression might disrupt signaling. However, anatomical proximity does not establish compression. The illustration cannot show whether a particular patient has nerve injury or identify the cause of that patient’s symptoms.

New 2026 research: Dysautonomia and chronic musculoskeletal pain

A systematic review and meta-analysis examined 17 studies involving 1,003 adults with chronic musculoskeletal pain and 417 healthy controls. Thirteen studies concerned fibromyalgia, three Ehlers-Danlos syndrome, and one rheumatoid arthritis. The pooled prevalence of dysautonomia was 64%, with considerable variation between studies. The pooled relative risk was 2.28 compared with healthy controls. (1)

This supports a clinically meaningful association. It does not mean that 64% of everyone with a sore neck, painful knee, or mechanical back problem has dysautonomia. The estimate comes from particular chronic-pain populations, and the diagnostic methods and definitions differed. The review also cannot determine whether pain preceded autonomic dysfunction or whether another process contributed to both.

A September 2026 study found a substantial symptom burden

A cross-sectional study compared 342 patients with clinician-confirmed chronic musculoskeletal pain with 57 healthy controls of similar age and sex distribution. Investigators used COMPASS-31, a questionnaire covering several autonomic symptom domains. A score of at least 17 met the study’s threshold for dysautonomia. Seventy-four percent of the pain group met that threshold, compared with 11% of controls. The adjusted relative risk was 7.4. Rates were high in both inflammatory and non-inflammatory conditions. (2)

Higher pain, anxiety, and depression scores were associated with greater autonomic symptom burden. These associations do not make the symptoms imaginary. They suggest that pain, mood, sleep, activity, and physiological regulation can interact.

The questionnaire is a screening measure, not a substitute for physiological testing or a diagnosis of POTS. The study measured associations at one point in time and did not evaluate cervical instability. It therefore supports asking chronic-pain patients about autonomic symptoms, but does not establish a neck disorder as their cause.

Dysautonomia is not the same as POTS

Postural orthostatic tachycardia syndrome, or POTS, is one form of dysautonomia. It involves chronic symptoms of orthostatic intolerance—difficulty tolerating an upright position—together with an excessive increase in heart rate after standing, without the blood-pressure fall that defines orthostatic hypotension. Diagnostic thresholds depend on age and clinical circumstances. Other causes of tachycardia must also be considered. (3)

A patient can have autonomic symptoms without meeting POTS criteria. Conversely, a POTS diagnosis does not explain why the condition developed.

Evaluation may include lying and standing heart rate and blood pressure, a standing test or tilt-table test, an electrocardiogram, rhythm monitoring, and selected laboratory investigations. Specialized testing may assess sweating, heart-rate responses to breathing, or blood-pressure responses to physiological challenges. Our article on POTS, the vagus nerve, and cervical spine instability discusses this diagnosis further.

Why chronic pain and autonomic symptoms may overlap

The relationship can operate in several directions. Persistent pain may disturb sleep, change breathing and stress responses, reduce activity, and contribute to deconditioning. Autonomic problems may limit standing and exercise, interfere with digestion, and worsen fatigue. Each can make the other harder to manage.

Inflammation, altered pain processing, small-fiber nerve dysfunction, medication effects, and connective-tissue disorders may also be relevant. Small nerve fibers include fibers involved in pain and temperature sensation as well as autonomic functions. This provides one possible explanation for overlapping symptoms in some patients, but it does not establish small-fiber neuropathy in everyone with chronic pain.

The 2026 studies support evaluating the whole symptom pattern rather than assuming that each complaint is unrelated. They do not identify a universal mechanism. (1) (2)

Joint hypermobility, hEDS, and autonomic symptoms

Hypermobile Ehlers-Danlos syndrome, or hEDS, and hypermobility spectrum disorders, or HSD, can involve joint symptoms together with orthostatic and other autonomic complaints. A retrospective cohort of 144 patients identified dysautonomia in 65% of female patients and 44% of male patients. Exercise intolerance was common, and activity often declined after the onset or worsening of the hypermobility-related condition. The predominantly female specialty cohort limits generalization. (4)

A clinical review also described associations between joint hypermobility syndromes and orthostatic tachycardia, anxiety, functional gastrointestinal disorders, and pelvic or bladder dysfunction. These associations help explain why someone with joint problems may also have digestive and urinary complaints. They do not establish ligament laxity as the cause of every symptom. (5)

A 2026 review strengthens the evidence for EDS and POTS overlap

A systematic review included 30 studies involving 8,421 patients with EDS and 12,983 patients with POTS. Reported proportions varied widely: POTS occurred in 17.5%–92.7% of EDS populations, and EDS occurred in 17.9%–50% of POTS populations. These are ranges across different study populations, not a single prevalence estimate for all patients. The authors concluded that the conditions frequently coexist and that management evidence remains incomplete. (6)

This makes the review relevant to patients with joint hypermobility, persistent pain, and orthostatic symptoms. It does not show that cervical instability explains the overlap. Further background is available in our article on dysautonomia, POTS, and hEDS.

Spinal ligament laxity and forward movement of vertebrae

Ligaments help restrain excessive movement between vertebrae. Injury, degeneration, or a connective-tissue disorder may reduce that restraint. Spinal stability also depends on discs, joints, muscles, and the coordinated function of these structures.

In this lumbar illustration, L3 is shown forward relative to L4, and L4 forward relative to L5. It helps readers visualize vertebral slippage. Such slippage can have several causes, including degenerative changes affecting discs and joints. Whether a segment is dynamically unstable requires assessment beyond a static illustration. Spondylolisthesis is the broader term for vertebral slippage; spondylolysis refers to a defect in part of a vertebra, and spondylosis describes degenerative spinal changes. These terms identify different findings and should not be treated as interchangeable.

Dr. Hauser discusses prolonged bending, sitting, and a forward-head or facedown posture as possible mechanical stresses. Sustained positions can increase musculoskeletal loading and provoke symptoms. A person’s posture alone does not establish pathological ligament laxity or show that nerves are being blocked.

Could cervical instability contribute to autonomic symptoms?

At Caring Medical, we consider a possible cervical contribution in selected patients, particularly when autonomic-type symptoms accompany significant neck pain, prior whiplash or head injury, joint hypermobility, abnormal cervical motion, or reproducible changes with head position.

The vagus nerves descend within the carotid sheaths beside the carotid arteries and internal jugular veins. They carry signals between the brain and organs in the chest and abdomen. Cervical sympathetic structures, the brainstem, spinal cord pathways, and sensory input from neck joints and muscles also relate to autonomic regulation.

Our published work proposes cervicovagopathy, a potential mechanism in which cervical dysstructure or instability could disturb vagus-nerve function. The paper includes retrospective measurements from a selected clinic population and a case example. This is a hypothesis supported by clinical observations, not a universally accepted diagnosis or proof that small ultrasound measurements mean nerve degeneration. (7)

Our earlier narrative and mechanistic paper discusses how altered cervical alignment might affect nearby neural and vascular structures. It provides a framework for investigation, but does not establish that forward-head posture causes systemic disease. (8)

What our 2026 cervical study adds

A retrospective cross-sectional study examined 227 young adults evaluated at our neck center for brain-based symptoms, including headaches, brain fog, concentration difficulty, anxiety, and related complaints. Reported findings included forward-head posture, reduced cervical lordosis, C1–C2 instability, reduced vagus-nerve and internal-jugular-vein cross-sectional measurements, and increased optic-nerve-sheath measurements. (9)

These findings describe a selected symptomatic cohort. There was no healthy comparison group, and the study did not test whether a treatment corrected dysautonomia. Ultrasound size measurements are not equivalent to direct measurement of nerve signaling. A structural finding must be interpreted with the history, examination, and appropriate diagnostic standards.

Digestive, urinary, sensory, and endocrine symptoms discussed in the video

The video’s symptom examples remain useful because patients often experience several complaints together. Bloating, nausea, bowel changes, and bladder dysfunction can occur in autonomic disorders. Brain fog, visual symptoms, light sensitivity, hearing complaints, and swallowing difficulty can also coexist with neck pain, although they have many possible neurological, eye, ear, gastrointestinal, and other causes.

Kidney function deserves a separate distinction. Changes in urination do not necessarily mean impaired kidney function. Kidney disease must not be inferred from a neck problem or assumed to improve with spinal treatment. Similarly, swallowing difficulty needs an appropriate evaluation; progressive difficulty swallowing or choking should not be attributed to cervical instability on the basis of this video.

Autonomic and endocrine systems interact, but thyroid and adrenal disorders are not simply failures of nerve input from the neck. A systematic review found no substantiation for “adrenal fatigue” as a medical condition. Genuine adrenal insufficiency is a different, recognized disorder requiring medical diagnosis and treatment. (10)

The video should therefore not be used to suggest that thyroid medication is unnecessary or that treating ligament laxity reverses thyroid or adrenal disease. The helpful question is whether a musculoskeletal problem coexists with the patient’s other condition and contributes to part of the symptom burden.

COPD and autonomic dysfunction: How chronic lung disease can affect nervous-system regulation.

Chronic obstructive pulmonary disease, or COPD, illustrates another relationship between chronic illness and autonomic regulation. COPD involves persistent airflow obstruction and can include chronic bronchitis, emphysema, or both. Breathlessness, cough, and reduced exercise tolerance may coexist with changes in cardiovascular and autonomic function.

A 2025 narrative review examined autonomic pathways in COPD, including airway narrowing, mucus production, inflammation, and cardiovascular effects. Vagal cholinergic pathways—using the chemical messenger acetylcholine—can influence contraction of airway smooth muscle and secretions. The review draws on experimental and clinical research; proposed mechanisms should not all be treated as established patient findings. (11)

What heart rate variability studies show

A systematic review and meta-analysis included 27 studies involving 839 people with COPD. Heart rate variability, or HRV, was generally reduced compared with controls, supporting an association with altered cardiac autonomic regulation. Differences in measurement methods and study populations limited clinical interpretation. (12)

HRV measures variation in the intervals between heartbeats. It does not directly measure lung function, identify the cause of breathlessness, or establish vagus-nerve compression. Our explanation of heart rate variability provides further background.

New 2026 research: Sympathetic activity can be increased

A systematic review and meta-analysis examined 11 studies involving 171 participants with COPD and 105 controls. Direct recordings of muscle sympathetic nerve activity showed higher resting activity in the COPD groups. Resting heart rate was also higher, although blood pressure did not significantly differ. (13)

This finding helps explain why autonomic imbalance is not adequately described as the whole system being too active or too weak. Cardiac regulation, airway cholinergic activity, and sympathetic signaling to blood vessels are different functions. Abnormalities can coexist without sharing one simple cause.

Nerve-directed treatments remain an evolving research area

AIRFLOW-3 was a randomized, double-blind, sham-controlled trial of targeted lung denervation, a bronchoscopic procedure intended to disrupt pulmonary parasympathetic nerves. It randomized 388 people with COPD, with both groups continuing medical treatment. The procedure did not meet its primary endpoint of delaying the first moderate or severe exacerbation over twelve months. Some breathlessness outcomes improved; suggested responder subgroups came from exploratory analyses requiring confirmation. (14)

Targeted lung denervation and vagus-nerve stimulation are different interventions. Their intended effects and evidence cannot be used interchangeably.

At Caring Medical, we consider these findings useful for understanding symptom overlap. They do not demonstrate that cervical instability causes COPD or that cervical Prolotherapy treats airflow obstruction, emphysema, or COPD exacerbations. Breathlessness still requires consideration of pulmonary, cardiac, and other causes. Our article on chronic cough and the vagus nerve discusses a related symptom without making cough equivalent to COPD.

How we evaluate patients at Caring Medical

Our evaluation considers the pattern and timing of symptoms: standing, exertion, meals, temperature, stress, neck position, and specific movements. Prior cardiac, neurological, rheumatological, gastrointestinal, and autonomic findings help place the symptoms in context.

Assessment may include orthostatic heart-rate and blood-pressure measurements, neurological and musculoskeletal examination, evaluation of joint hypermobility or ligament injury, and assessment of cervical alignment and motion. HRV, vagus-nerve assessment, and dynamic or vascular imaging may also be considered when clinically justified.

No single measurement establishes that the cervical spine is responsible for dysautonomia. HRV is influenced by breathing, age, physical conditioning, illness, medication, and recording conditions. Imaging and ultrasound findings also require interpretation rather than an automatic causal conclusion. Our discussion of determining the causes of dysautonomia, vagopathy, and autonomic imbalances explains the clinic’s structural perspective in greater detail.

Treatment: Addressing autonomic disorders and musculoskeletal problems

Treatment depends on the diagnosed condition. Options may include fluid and salt strategies when medically appropriate, compression garments, medication review, treatment of anemia or endocrine disease, sleep improvement, and individualized physical reconditioning. Fluid and salt advice needs particular care in people with kidney disease, heart failure, or hypertension. Exercise approaches also need modification when activity causes substantial delayed symptom worsening.

A review appearing in a 2026 issue evaluated 45 POTS treatment studies. It identified potential benefits from several non-drug and medication approaches but concluded that the evidence remains limited and larger trials are needed. This supports matching treatment to the patient’s autonomic disorder rather than assuming one intervention fits every symptom pattern. (15)

Cervical and lumbar stability, posture, and lordosis

Lordosis refers to the usual inward curve of the cervical or lumbar spine. Changes in alignment may coexist with pain and altered loading. A straightened cervical curve on an image does not by itself prove ligament injury, and a particular curve measurement does not demonstrate autonomic nerve compression.

This existing image supports the discussion of cervical alignment. It should be interpreted as an illustration of structure, not as evidence that correcting a curve cures dysautonomia. A static alignment image does not demonstrate how the vertebrae move during activity.

Posture changes and appropriately selected exercises may address mechanical strain and function. Their effects on a person’s autonomic symptoms depend on the underlying problem. The video’s description of complete reversibility should be understood as an optimistic clinical claim, not a guaranteed treatment result.

Research on cervical instability and Prolotherapy

Prolotherapy involves injections, commonly using dextrose, intended to stimulate a healing response in selected musculoskeletal tissues. Our earlier narrative review discussed capsular-ligament laxity, excessive joint movement, and chronic neck pain, proposing Prolotherapy as a treatment option for selected patients. A narrative review is not a controlled demonstration of efficacy. (16)

A 2026 case report described a 51-year-old woman with rheumatoid arthritis, chronic neck pain, migraines, vertigo, and autonomic dysfunction who improved after regenerative injections together with postural and chiropractic therapy. This is relevant to the proposed structural approach, but it involves one patient and several simultaneous interventions. It cannot isolate an injection effect, establish a response rate, or prove reversal of dysautonomia. (17)

Prolotherapy remains a musculoskeletal intervention rather than an established treatment for dysautonomia itself. Controlled evidence that it reliably corrects POTS, vagus-nerve dysfunction, or multisystem autonomic disease remains insufficient. Injection risks, including infection and injury to nearby structures, must also be considered, especially in the neck.

Research on lumbar instability and Prolotherapy

Our retrospective low-back-pain case series reported outcomes after dextrose Prolotherapy. Patients reported improvements in pain, stiffness, movement, and quality of life, with follow-up extending beyond their last treatment. These reports are useful preliminary observations, but the uncontrolled design and patient-reported outcomes limit what can be concluded about treatment effectiveness. The study did not establish treatment of autonomic dysfunction. (18)

Improvement in back pain does not establish that discs have returned to position or that lost disc height has regenerated. Those structural claims require their own evidence.

Readers can explore our related discussions of lumbar spinal stenosis, sacroiliac joint pain, and sciatica or lumbar radiculopathy. Our discussions of spinal fusion alternatives and bulging or herniated discs provide further context for mechanical back problems. These diagnoses should be distinguished from dysautonomia even when symptoms coexist.

Summary

Research supports important overlap between chronic musculoskeletal pain and autonomic symptoms. The 2026 chronic-pain studies support recognizing that symptom burden, while the EDS–POTS and COPD reviews show how autonomic abnormalities occur in different chronic conditions.

Dr. Hauser’s video explains our interest in the relationship between ligament laxity, spinal alignment, and nearby nerves. In selected patients, a cervical contribution may deserve investigation. Symptoms alone, altered posture, or an isolated imaging measurement cannot establish that connection.

A helpful evaluation distinguishes autonomic symptoms from a specific autonomic diagnosis, considers other medical causes, and determines whether a coexisting spinal problem is clinically meaningful. Treating a musculoskeletal problem and treating dysautonomia may be related in an individual case, but they should not be assumed to be the same treatment goal.

Medical disclaimer: This article provides patient education and does not replace diagnosis or treatment by a qualified healthcare professional. Autonomic symptoms can have serious cardiac, neurological, pulmonary, endocrine, renal, vascular, or medication-related causes. Treatment requires an appropriate individual evaluation.

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):rkag034. doi:10.1093/rap/rkag034. [Google Scholar]

2 Almutairi NA, Greenwood DC, Sivan M. Prevalence of dysautonomia in chronic musculoskeletal pain: a cross-sectional study. Rheumatology (Oxford). Published online September 16, 2026:keag511. doi:10.1093/rheumatology/keag511. [Google Scholar]

3 Sheldon RS, Grubb BP 2nd, Olshansky B, Shen WK, Calkins H, Brignole M, Raj SR, Krahn AD, Morillo CA, Stewart JM, Sutton R, Sandroni P, Friday KJ, Hachul DT, Cohen MI, Lau DH, Mayuga KA, Moak JP, Sandhu RK, Kanjwal K. 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):e41-63. doi:10.1016/j.hrthm.2015.03.029. [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. doi:10.1002/ajmg.a.62446. [Google Scholar]

5 Botrus G, Baker O, Borrego E, Ngamdu KS, Teleb M, Gonzales Martinez JL, Maldonado G 3rd, Hussein AM, McCallum R. Spectrum of Gastrointestinal Manifestations in Joint Hypermobility Syndromes. The American Journal of the Medical Sciences. 2018;355(6):573-580. doi:10.1016/j.amjms.2018.03.001. [Google Scholar]

6 Kwok CS, Hagger G, Gillespie D, Hall M, Nazari B, Chong D, Hinton J, Qureshi AI, Raj SR. The co-existence of Ehlers-Danlos syndrome and postural orthostatic tachycardia syndrome: A systematic review of the literature. Autonomic Neuroscience. 2026;267:103453. doi:10.1016/j.autneu.2026.103453. [Google Scholar]

7 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. doi:10.3389/fneur.2025.1572863. [Google Scholar]

8 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. doi:10.3389/fneur.2024.1430390. [Google Scholar]

9 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. doi:10.3389/fneur.2026.1749266. [Google Scholar]

10 Cadegiani FA, Kater CE. Adrenal fatigue does not exist: a systematic review. BMC Endocrine Disorders. 2016;16(1):48. doi:10.1186/s12902-016-0128-4. [Google Scholar]

11 Chen D, Zhou Z, Zhou Z, Zhao L, Chen Y. Autonomic nervous system dysfunction in chronic obstructive pulmonary disease: mechanistic insights and therapeutic implications. Annals of Medicine. 2025;57(1):2596426. doi:10.1080/07853890.2025.2596426. [Google Scholar]

12 Alqahtani JS, Aldhahir AM, Alghamdi SM, Al Ghamdi SS, AlDraiwiesh IA, Alsulayyim AS, Alqahtani AS, Alobaidi NY, Al Saikhan L, AlRabeeah SM, Alzahrani EM, Heubel AD, Mendes RG, Alqarni AA, Alanazi AM, Oyelade T. A systematic review and meta-analysis of heart rate variability in COPD. Frontiers in Cardiovascular Medicine. 2023;10:1070327. doi:10.3389/fcvm.2023.1070327. [Google Scholar]

13 Duiker B, Shirazi S, Sivak A, Stickland MK, Davenport MH, Steinback CD. Muscle sympathetic nerve activity in COPD: a systematic review and meta-analysis. European Respiratory Review. 2026;35(180):250267. doi:10.1183/16000617.0267-2025. [Google Scholar]

14 Shah PL, Slebos DJ, Sue R, Bhatt SP, Ghattas C, Strange C, Degano B, Valipour A, Eisenmann S, De Cardenas J, Marquette CH, Soto-Soto J, Sciurba FC, Conway F, Tonkin J, Tana A, Marchetti N, Hartman JE, Heluain V, Guibert N, Criner GJ. Randomized Sham-controlled Trial of Targeted Lung Denervation in Patients with Chronic Obstructive Pulmonary Disease (AIRFLOW-3). American Journal of Respiratory and Critical Care Medicine. 2025;211(12):2318-2329. doi:10.1164/rccm.202502-0404oc. [Google Scholar]

15 Schiweck N, Langer K, Maier A, Vilser D, Spiegler J. Systematic literature review: treatment of postural orthostatic tachycardia syndrome (POTS). Clinical Autonomic Research. 2026;36(1):3-16. doi:10.1007/s10286-025-01172-2. [Google Scholar]

16 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. doi:10.2174/1874325001408010326. [Google Scholar]

17 Jones HE, Ierulli JA, Williams C, Pitts J. The Treatment of Craniocervical Instability Using Regenerative Medicine Therapies: A Case Report. Cureus. 2026;18(7):e113501. doi:10.7759/cureus.113501. [Google Scholar]

18 Hauser RA, Hauser MA. Dextrose Prolotherapy for Unresolved Low Back Pain: A Retrospective Case Series Study. Journal of Prolotherapy. 2009;1(3):145-155. [Google Scholar]