Research review September 2026

Adhesive arachnoiditis and hypermobile Ehlers–Danlos syndrome

A source-cited synthesis of what is well established, what is clinical observation, and where the evidence gaps still are — for a disease that is often missed, and a connection that is still being characterized.

First AA treatment case series
2025–26
Tennant cohort with AA
80%
Prior spinal procedures
402
Median time to diagnosis
12 mo

Updated September 2026 to reflect the 2025–26 publication of the first successful AA treatment case series and the death of Dr. Forest Tennant on August 13, 2026.

01

Executive summary

Adhesive arachnoiditis (AA) is a persistent inflammatory and fibrotic disease of the arachnoid layer of the spinal meninges. Scar tissue clumps the cauda equina nerve roots, obstructs cerebrospinal fluid flow, and produces severe, often intractable, neuropathic pain and neurological deficits. There is no definitive cure; management is aimed at controlling inflammation, preserving function, and preventing progression.12

The connection between AA and hypermobile Ehlers–Danlos syndrome (hEDS) is a working clinical hypothesis with substantial supporting observation but limited high-quality controlled evidence. In July 2026, a small open-label study of a successful AA treatment (Tennant, Porcelli & Sands, n=20; 20/20 with symptomatic pain relief) appeared in a journal that describes itself as peer-reviewed but is not indexed in PubMed and whose publisher appears on Beall's list of potentially predatory open-access publishers — an important caveat noted below.10 A related 2025 clinical review by Porcelli & Tennant appeared in the indexed Medical Journal of Southern California Clinicians.12 The connection itself remains supported mainly by clinical observation. Three lines of evidence anchor the case:

  1. Tennant Foundation 2024 clinic study. Of 45 people with diagnosed hEDS and intractable pain, 80% (36/45) had MRI-documented adhesive arachnoiditis. That AA subgroup had collectively undergone 124 surgeries and 278 epidural injections. 3
  2. Tennant Foundation MRI series. In their broader review of MRI-documented AA cases, essentially 100% had EBV autoimmunity and ~70% showed EBV reactivation. About half of the AA patients they saw did not know they had hEDS/HSD.4
  3. Peer-reviewed neurosurgical reviews. hEDS is independently associated with dural ectasia, Tarlov cysts, spontaneous CSF leaks, tethered cord, Chiari I, and craniocervical instability — with increased dural fragility as the shared proposed mechanism. These reviews, however, do not name adhesive arachnoiditis as an established hEDS complication.56

Two caveats. The strongest quantitative claims about the hEDS ↔ AA relationship come from one clinician-researcher's clinic-based series (Forest Tennant, MD, DrPH, MPH) and the associated Tennant Foundation bulletins — small, self-selected, and not peer-reviewed. And mainstream neurology, neurosurgery, and EDS guidelines do not yet name adhesive arachnoiditis as an established hEDS complication.6 Both facts should be kept in view when applying this literature clinically.

02

What adhesive arachnoiditis is

Definition and architecture

Arachnoiditis is a chronic inflammation of the arachnoid mater and subarachnoid space, most often in the spinal cord. Its severe fibrotic form — adhesive arachnoiditis — is characterized by leptomeningeal thickening, dural adhesions, scar-tissue formation, and clumping of the cauda equina nerve roots. Scar tissue encapsulates the nerve roots, impedes CSF flow, and can progress to chronic adhesive arachnoiditis, arachnoiditis ossificans (ossification of the arachnoid, a rare end-stage form), and secondary syringomyelia.1

A 2024 scoping review of 176 studies and 510 patients — which proposes renaming the broader entity spinal adhesive arachnoidopathy (SAA) — found that AA is the dominant pathological form (80.8% of SAA cases) and the form most likely to produce secondary syringomyelia (39.3%).2

Pathophysiology in six steps

  1. 1 An inflammatory insult reaches the subarachnoid space.
  2. 2 Collagen deposition and fibroblast proliferation begin.
  3. 3 Fibrosis and intradural scarring develop.
  4. 4 Nerve roots adhere to each other and to the arachnoid–dural wall.
  5. 5 CSF flow is obstructed; nutrient delivery and waste clearance are impaired.
  6. 6 Nerve-root atrophy, cyst formation, calcification, or ossification follow.

Causes and risk factors

The etiology is heterogeneous. In the 510-patient pooled review, the frequency distribution was:

Etiology of spinal adhesive arachnoidopathy across 510 patients2
Etiology Share Distribution
Trauma22.7%
Infection (mostly bacterial meningitis, esp. tuberculous)17.7%
Surgery (67.7% of these were spinal surgery)15.4%
Hemorrhage (91% subarachnoid)13.5%
Chiari I malformation5.7%
Anesthesia (epidural > spinal > paravertebral)5.4%
Myelography (older oil-based agents)4.5%
Spinal stenosis / herniated disc3.6%
Spinal injections (intrathecal chemo, ESI)3.1%
Idiopathic2.8%
Familial2.4%
Autoimmune disease1.2%

StatPearls groups risk factors into chemical (oil-based contrast, preservatives, direct local-anesthetic toxicity, intrathecal chemotherapy, epidural steroid injections), mechanical (trauma, spinal surgery, disc herniation), inflammatory (ankylosing spondylitis, Guillain–Barré, autoimmune vasculitis), and infectious (TB, syphilis, HIV, fungal).1

"Surgery and epidural corticoid injections are often cited as the cause of AA, but they are actually co-factors, as the person who receives surgery and/or epidural injections has some underlying spinal disorder that medically indicates the need... clinical data collected by the authors suggests that spine surgeries and epidural injections done on some individual patients may be excessive and even causative of adhesive arachnoiditis."

— MedCentral clinical overview, 80-case series7

Epidemiology

  • < 1,000 case reports since Horsley described the entity in 1909 — widely regarded as underdiagnosed1
  • 1.75 – 7 M adult Americans estimated to have AA based on back-pain epidemiology2
  • 44 yr mean age in pooled series; 12-month median time to diagnosis (IQR 3–36)2
  • 44.4% develop progressive neurological deterioration2

Symptoms and diagnosis

The most common features in the 510-patient cohort were abnormal motor function (78.8%), abnormal nerve sensations (39.6%), and pain (37.5%). Late urinary involvement — urgency, frequency, incontinence — occurs in about 23%.12

AA is a clinical diagnosis supported by imaging. Laboratory tests, EMG, and nerve-conduction studies are unreliable. MRI is the imaging modality of choice; noncontrast CT is more sensitive for arachnoiditis ossificans. Contrast MRI is the definitive tool for detecting active dural involvement and CSF seepage. Characteristic MRI findings include:

  • Nerve-root clumping in the thecal sac — the classic sign
  • Loculated arachnoid cysts
  • Increased T2 signal in the cord
  • Cord swelling, displacement, or atrophy
  • Arachnoid septations and syrinx formation

Two diagnostic pitfalls. Radiologic severity does not always match clinical severity. And MRI signs may take up to 6 months to appear after an inciting event such as a spinal tap or epidural injection.17

Treatment (non-EDS-specific)

No definitive cure. Management is multimodal and supportive: neuropathic pain agents (gabapentin, pregabalin, duloxetine), NSAIDs, opioids as needed, muscle relaxants; physical therapy, CBT, neuromodulation; surgery in narrowly selected cases (shunting, cyst fenestration, adhesiolysis) but with an explicitly poor long-term prognosis and risk of worsening. Intrathecal steroids are generally not recommended and can worsen the disease.1

A specialized outpatient protocol from the Tennant Foundation adds acetazolamide for high spinal-canal pressure (125 mg × 2 days, escalating to 250 mg once or twice daily), tissue-restoration hormones (HCG, nandrolone, DHEA, testosterone), and daily "spinal fluid flow exercises" including rocking-chair therapy.8

New — July 18, 2026

First successful AA treatment reported in the literature

Tennant, Porcelli & Sands published Low Dose Methylprednisolone and Ketorolac Treatment for Adhesive Arachnoiditis in the International Journal of Emergency Medicine & Pain Management. In 20 patients with chronic AA given low-dose methylprednisolone 4 mg plus oral ketorolac 10 mg (or injectable ketorolac 15–30 mg) 1–3 days/week for 30–180 days:

  • 20 / 20 achieved symptomatic pain relief
  • 17 / 20 reported improved pain control
  • 13 / 20 reported improved physical activity
  • 9 / 20 reported fewer bed-bound days

The authors describe this as the first successful published treatment for AA in the 153 years since the condition was defined in medical dictionaries in 1873. It is a small, single-center, open-label study — not a randomized controlled trial — and, importantly, the publishing journal is a Medwin Publishers title that is not indexed in PubMed/MEDLINE. Medwin appears on Jeffrey Beall's list of potentially predatory open-access publishers, so the "peer-reviewed" framing should be treated with caution. The findings are consistent with the same authors' work in the indexed Medical Journal of Southern California Clinicians (Porcelli & Tennant, March 2025).1012

A neurosteroid alternative — Arachnoiditis Hope, 2026

Arachnoiditis Hope has since published a corticosteroid-free alternative built on three neurosteroids (natural hormones made in the CNS that suppress inflammation, help regenerate nerve tissue, and reduce pain), used together for greater effect:

  • Pregnenolone — 200 mg twice a day
  • DHEA (dehydroepiandrosterone) — 200 mg twice a day
  • Palmitoylethanolamide (PEA) — 600–1200 mg twice a day, 1–2 month trial; can be added to an existing pain-relief program

The organization notes that these neurosteroids carry fewer complications than corticosteroids (DHEA may cause hair loss or bleeding irregularities in premenopausal women), and that a 2025 Nutrition Reviews meta-analysis found PEA meaningfully reduces pain within 4–6 weeks. Methylene blue is additionally mentioned as an emerging non-opioid adjunct (contraindicated with antidepressants).11

03

What hEDS does to the spine and meninges

Before evaluating the AA link, it helps to review what hEDS by itself is known to do to the spine and dura, independent of AA. Two peer-reviewed sources anchor this section: the Henderson et al. 2017 review in Seminars in Medical Genetics,5 and the 2022 Journal of Neurosurgery: Spine scoping review.6

Dural ectasia

Weakening and outward bulging of the dura around the spinal cord, especially lumbosacral. Low back pain, headache, weakness, numbness — often improved when supine.

Peer-reviewed

Tarlov (perineurial) cysts

CSF-filled sacs on nerve roots, most often sacral. "The belief that all Tarlov cysts are asymptomatic has no support in the literature." Inflammatory cells found in walls of symptomatic cysts.

Peer-reviewed

Spontaneous spinal CSF leaks

Orthostatic headache with imaging-confirmed leak. Increased dural fragility is the proposed mechanism. Association with hEDS and cEDS documented, exact incidence unclear.

Peer-reviewed

Tethered cord syndrome

Present in 6.75% of 2,149 hEDS patients (Petrucci et al., Mayo Clinic Proceedings IQO, 2024).

Peer-reviewed

Chiari malformation type I

Present in 7.91% of 2,149 hEDS patients. Strongly correlates with hereditary connective-tissue disease.

Peer-reviewed

Craniocervical / atlantoaxial instability

Present in 31.6% of 2,149 hEDS patients; 37.2% in a smaller CTD cohort. Can alter CSF flow and intracranial pressure.

Peer-reviewed

Early degenerative disc disease

Discopathy, segmental instability, kyphosis widely reported in hEDS. Leads to mechanical pain and myelopathy.

Peer-reviewed

IIH with CTD phenotype

75.6% IIH prevalence in an 86-patient CTD cohort. Unusual demographic: non-obese young women, symptoms at lower opening pressures.

Peer-reviewed

The mechanistic thread through all of these is collagen-related dural and connective-tissue fragility. hEDS involves defects in collagen production and extracellular-matrix composition that weaken the dura, arachnoid, ligaments, and vessel walls, and impair CSF containment.

Procedural risks in EDS — the honest picture

The peer-reviewed literature here is thinner than patients often need. Documented risks include CSF-leak complications after tethered-cord release, technically more difficult craniocervical fusion (altered anatomy, high-riding vertebral arteries, poor bone quality), and wound-healing complications. But epidural anesthesia, spinal anesthesia, and lumbar puncture in EDS are essentially not discussed in the major reviews — both Henderson (2017) and the JNS Spine scoping review (2022) call this an unstudied evidence gap. This is exactly the space the Tennant Foundation work attempts to fill.56

04

Pelvic floor, low-back pain, and dyspareunia in hEDS

Alongside the spinal and meningeal picture, hEDS drives a related pattern in the lumbopelvic system — low back "weakness," deep-core fatigue, lower-abdominal pain, and painful intercourse. In clinic these are often treated as separate problems. They are usually one story: hypertonic pelvic-floor dysfunction driven by connective-tissue laxity above and below.

How common this is

  • 43% dyspareunia in 386 women with hEDS (Hugon-Rodin et al., Orphanet J Rare Dis, 2016), with high rates of dysmenorrhea and menorrhagia alongside13
  • 105 studies pooled in the 2020 scoping review; elevated urinary incontinence, pelvic organ prolapse, dyspareunia, and fecal incontinence across EDS subtypes14
  • 63.6% of 612 chronic-pelvic-pain patients met a data-driven diagnostic threshold for high-tone pelvic-floor dysfunction (Till et al., AJOG, 2025); the broader literature reports 58–79%15
  • 63.7% / 50% of 1,146 women with EDS or HSD reported dyspareunia; 50% screened positive for vulvodynia — roughly six times the general-population rate (Glayzer et al., Am J Med Genet C, 2021)17

The pattern: hypertonic, not weak

The subjective experience is "my low back and core feel weak" — but on gynecologic exam, the pelvic-floor muscles (levator ani, obturator internus, coccygeus) are tender to palpation. That is the classic finding for hypertonic (high-tone) pelvic-floor dysfunction, also called pelvic-floor myalgia or levator ani syndrome. The muscles are chronically over-contracted, unable to fully relax, and tender when touched — which is why they feel exhausted (they are) but also why conventional strengthening ("just do Kegels") often makes them worse.

  1. 1 Lax ligaments and joint capsules provide less passive stability for the lumbar spine and pelvis in hEDS.
  2. 2 The nervous system recruits muscles to compensate — pelvic floor, deep abdominals, paraspinals, and diaphragm all pulled into constant bracing.
  3. 3 Muscles fatigue and become chronically hypertonic. Guarding becomes the default; the ability to switch smoothly between contraction and relaxation is lost.
  4. 4 Referred pain radiates to the low back, hips, lower abdomen, and thighs. Penetration stretches muscles that are already stuck short and tender → dyspareunia.

Hypertonic vs. hypotonic — they look similar, they need opposite treatment

Two very different pelvic-floor patterns that share symptoms16
Feature Hypertonic Hypotonic
Muscle stateOveractive, guarded, increased resting toneGenuinely underactive and weak
Cannot relaxYes — stuck shortNot the primary problem
Typical mechanism in hEDSProtective bracing for lax jointsPostpartum, aging, or severe CT compromise
DyspareuniaCommonLess specific
ConstipationCommon (muscles won't release for defecation)Possible
Urinary urgency, frequency, incomplete emptyingCommonMore often frank incontinence
Referred pain to low back, hips, abdomenCommonLess common
Kegels as first stepOften worsens symptomsMay be appropriate after assessment

Both patterns can produce incontinence and prolapse sensations, so an internal exam by a pelvic-floor physical therapist — not a symptom questionnaire alone — is what distinguishes them.

Contributors beyond muscle tone

Multiple hEDS-related factors can amplify pelvic and lower-abdominal pain in parallel with the pelvic-floor pattern:16

  • Sacroiliac and pubic-symphysis instability — lumbopelvic pain, sometimes worse with weight-bearing on one leg
  • Connective-tissue fragility of vaginal tissue — dryness, tearing, postcoital bleeding
  • Vulvodynia and vestibulodynia — nerve-driven vulvar or vestibular pain, often with mast-cell involvement; 50% of women with EDS/HSD screen positive for vulvodynia in the Glayzer survey17
  • Mast cell activation — histamine in pelvic tissue worsens vaginitis and dyspareunia
  • Central sensitization and nociplastic pain — amplifies signals from the whole region
  • Endometriosis and pelvic congestion — disproportionately common in hEDS
  • Referred pain from hip, lumbar spine, or abdominal wall

First-line management

Pelvic-floor physical therapy is consistently described as "the cornerstone of conservative management." For hEDS specifically, the sequencing matters:16

  1. Internal exam by a trained pelvic-floor PT first. External + internal palpation is the gold standard for distinguishing hypertonic from hypotonic. Ask about pelvic-health credentials (PRPC, WCS, or Herman & Wallace training) and ideally hEDS familiarity.
  2. Down-training before strengthening. If the exam shows hypertonicity, the first phase is learning to lengthen and release — not contract. Diaphragmatic breathing (rib and belly expansion), postural retraining, hands-on trigger-point release.
  3. Biofeedback is especially useful in hEDS because proprioception is impaired — many patients cannot tell whether their pelvic floor is contracting or relaxing. Real-time feedback is the fix.
  4. Address the bowel side. Constipation and straining perpetuate guarding. Adequate hydration, ~25–30 g fiber daily, a footstool at the toilet (better puborectalis angle), no straining.
  5. Only after resting tone normalizes: gentle, coordinated strengthening of the deep- core system as a unit — pelvic floor, transverse abdominis, multifidus, diaphragm — timed with breath. Isometric first, progressed slowly.
  6. Adjuncts as needed: vaginal dilator or wand work for internal release; positioning changes during intercourse that reduce depth and let the patient control pacing; topical estrogen for tissue tolerance; pessary consultation if prolapse is present.

Neurologic red flags — when this stops being a pelvic-floor problem. Given the hEDS + Tarlov-cyst + spinal-canal-vulnerability context, a few features warrant urgent evaluation rather than PT referral: new saddle numbness (perineum, inner thighs, buttocks), new urinary retention or fecal incontinence, sudden bilateral leg weakness or new foot-drop, pain that wakes you from sleep or is dramatically worse lying flat, or fever with the pelvic pain. These are cauda-equina and infection red flags — not the usual hEDS pelvic-floor pattern.

05

The proposed hEDS ↔ AA connection

The clinical observation

Forest Tennant, MD, DrPH, MPH — a retired intractable-pain clinician now running the Tennant Foundation and Arachnoiditis Hope — was the first to publish widely on this specific link. His clinic's core observation: when patients with hEDS present with severe, unremitting spinal pain, MRI often shows AA. The reverse is also true — when patients present with AA, a substantial proportion have unrecognized hEDS or HSD.34

Tennant Foundation, March 2024 — cohort snapshot

45 people with diagnosed hEDS and intractable pain. Small, self-selected, clinic-based, not peer-reviewed. The author is explicit: "cannot be assumed... universal applicability."3

80%had MRI-confirmed AA (36/45)
94%female (34/36 in AA subgroup)
124total surgeries in AA subgroup
278total epidural injections in AA subgroup
12.9 yrmean age at first pain episode
48.7 yrmean age hEDS was finally diagnosed
36%bed-bound most hours
50%had Tarlov cysts
41.7%had spinal fluid leaks
75%had migraine

The proposed mechanism — a two-hit model

  1. Hit 1

    Collagen-poor spinal tissues

    Every collagen-containing structure in the spine — vertebrae, intervertebral discs, ligaments, dural sac, arachnoid, cauda equina epineurium — is weakened in hEDS/HSD. This is said to predispose to early degenerative disc disease, herniation, Tarlov cysts, tethered cord, Chiari, spontaneous CSF leaks, and scoliosis. The peer-reviewed hEDS literature independently confirms these conditions at meaningfully increased prevalence.4

  2. Hit 2

    Repeated invasive procedures generate the inflammatory insult

    Because the underlying spinal disease is progressive and painful, hEDS patients are often offered many epidural steroid injections and eventually spinal surgery. Tennant's clinical statement is unambiguous:

    "We've had no one who developed arachnoiditis who had not had spinal procedures. All of them had invasive procedures, whether it was epidural injections and/or surgery." — Forest Tennant, MD3

    He is careful that the procedures "don't cause it, but accelerate the problem." The MedCentral 80-case series makes the same point: 86.3% had received one or more epidural injections; 53.8% had at least one spinal surgery.7

  3. Hit 3?

    Latent-virus reactivation and autoimmunity

    In MRI-documented AA cohorts from the Tennant clinic, essentially 100% showed EBV autoimmunity and about 70% showed EBV reactivation. The proposed chain is that collagen deficiency permits deeper tissue invasion by viruses (EBV, CMV, HHV-6, Lyme borreliosis), and reactivated EBV in spinal tissue drives autoimmune inflammation of the arachnoid. This part of the model is supported only by the Tennant Foundation's own case series and is not independently confirmed.4

The dural erosion / CSF seepage bridge

A related mechanism, based on Byron Stookey's 1927 dural-adhesion observations and confirmed on contrast MRI by the Tennant group: AA itself can extend through the arachnoid–dural covering, making it porous and permeable and causing chronic spinal-fluid seepage into paraspinal muscle. Because CSF is acidic and toxic to soft tissue, this seepage causes secondary inflammation and worsens both AA and hEDS-associated musculoskeletal symptoms. In a review of > 600 AA MRIs, at least half showed some form of spinal-fluid seepage or leakage. That helps explain why Tarlov cysts and CSF leaks co-cluster with AA in hEDS patients — both directions of causation are plausible.8

The state of the evidence, honestly

Strong

Peer-reviewed literature clearly establishes hEDS-associated dural ectasia, spontaneous CSF leaks, Tarlov cysts, tethered cord, Chiari, and CCI.569

Moderate

The general framing that AA disproportionately affects people with genetic collagen disorders of the EDS type is echoed in non-EDS-specialized clinical review.7

Emerging

Specific quantitative connection claims — 80% AA in hEDS-plus-intractable-pain, ~100% EBV autoimmunity, procedural triggering — come from Tennant Foundation clinic series and bulletins and have not been independently replicated. The associated treatment protocol has now appeared in two journal outlets: a March 2025 clinical review in the indexed Medical Journal of Southern California Clinicians (Porcelli & Tennant), and a July 2026 n=20 open-label series in an International Journal of Emergency Medicine & Pain Management (Medwin Publishers), a journal not indexed in PubMed whose publisher appears on Beall's list. Neither is a randomized controlled trial, and neither by itself validates the etiologic claims about the hEDS ↔ AA connection.341012

Gap

The 2022 JNS Spine scoping review does not name AA as an established hEDS complication and explicitly calls for evidence-based prevention protocols for "epidural anesthesia, spinal anesthesia, dural puncture, post-dural-puncture CSF leak, adhesive arachnoiditis, and surgical wound-healing complications" in EDS.6

06

Practical implications

What follows reflects what the cited sources recommend. It is educational, not medical advice. Decisions should be made with a clinician who has direct knowledge of the patient.

Screening

Bidirectional

hEDS + > 90 days of severe spinal pain → screen for AA with contrast MRI, and consider EBV activity testing.

AA diagnosis → screen for EDS, especially with childhood hypermobility, widespread pain, or multiple failed procedures.47

Procedural caution

Avoid invasive spinal procedures when possible

Given the Tennant clinic observation that every AA case in their series had undergone spinal procedures, treat precursors (carpal tunnel, dysautonomia) aggressively without invasive procedures if feasible.3

Time-sensitive

60-day post-procedural window

Symptoms within 60 days of an epidural or spinal tap — increased back pain, dizziness, leg weakness, burning skin, urinary changes — should be treated urgently. MRI signs can take up to 6 months to appear.7

If confirmed

Multimodal, avoid intrathecal steroids

Anti-inflammatory therapy, neuropathic pain agents, PT, neuromodulation. Surgery has a poor long-term track record and should be reserved for specific indications (progressive syrinx, CSF-flow obstruction, ossified plaque).1

Adjunct — single-source

Tennant protocol additions

Acetazolamide for high spinal pressure; tissue-restoration hormones for CSF leak; daily spinal-fluid-flow exercises (rocking-chair therapy). Worth discussing with a pain specialist, but not peer-reviewed standard-of-care.8

Prevention while young

Early hEDS diagnosis matters

Hypermobile children should be identified early and not pushed toward joint-destructive activities (gymnastics, football). Nutrition, protein and collagen intake are discussed as commonly used practices, not validated protocols.3

Pelvic floor

Refer to a pelvic-floor PT before strengthening

For low-back "weakness," lower-abdominal pain, or dyspareunia in hEDS, first-line is an internal pelvic-floor exam by a PT with pelvic-health credentials (PRPC, WCS, or Herman & Wallace). Down-training and biofeedback come before Kegels.16

07

Manual, power-assist, or power?

The base you choose decides two things that matter most with AA and hEDS: how much work your shoulders and wrists do, and which seat functions you can have.

Three main wheelchair types compared
Manual (ultralight) Power-assist manual Power wheelchair
How it moves You push the handrims Motors in the wheel hubs or an add-on unit boost each push Joystick or alternative control; no pushing
Load on shoulders and wrists Highest. Ultralights (under 30 lb) need less force, but overuse injuries such as impingement and rotator cuff tendinopathy are common Lower; "decreased upper limb strength is required" Minimal for driving
Heart-rate and blood-pressure demand Arm propulsion "can increase diastolic blood pressure response and cardiac afterload" — worth weighing with POTS Reduced, since the motor does part of the work Low
Tilt, recline, leg rests, standing Manual tilt-in-space chairs exist, but knee-pivot tilt typically offers 15–20°, below the roughly 30° linked to meaningful pressure relief Same as the manual chair it's added to Full range of power tilt, recline, elevating leg rests, seat elevation, and standing, operable on your own
Weight and transport Lightest; easiest to transport without special equipment Battery adds weight and "can make transportation more difficult" Heaviest; usually doesn't break down for storage, so transport is harder
Maintenance Least Adds battery and motor upkeep More than a manual chair
Best fit Part-time use during flares or for long distances, with good upper-body function and stamina People who can use a manual chair "but cannot consistently propel it due to upper extremity pain or overuse" Pain or instability with any propulsion, severe fatigue, frequent falls, orthostatic intolerance, or need for power seat functions

Sources: AAPM&R20; RESNA 202519; RESNA service guide21; EDS Society18; hEDS Info23.

What this means with AA and hEDS together

  • Sitting intolerance points toward power. The seat functions that relieve lumbosacral loading — deep tilt, recline paired with leg rests, and standing — are mainly available on power bases, and power operation lets you reposition without help.1922
  • Unstable shoulders point away from full-time manual propulsion. The EDS Society notes that many people with EDS or HSD "find self-propelling wheelchairs challenging," and that power assist or a power chair "may be more appropriate."18
  • A manual chair can still have a role as a lighter second chair for travel or short outings, used intermittently.23
  • Scooters are a fourth option — lighter and less costly than power chairs — but they need good trunk control and intact arm function to steer, and their larger turning radius makes indoor use challenging.20

Try all three before deciding

RESNA's service guide describes a user with shoulder pain and carpal tunnel symptoms who trialed an optimized ultralight manual chair, a pushrim-activated power-assist chair, and power chairs in clinic. "Due to pain with propulsion even with the 'assist' products, he ruled out every option except the power wheelchair."21 A hands-on trial of each type, ideally on the surfaces you actually use, is the most reliable way to decide.

Use is not all-or-nothing. The EDS Society notes wheelchairs "can be used part-time, full-time, or situationally," and that each type "comes with its own unique challenges, including transportation and cost."18

08

Wheelchair and seating setup

No wheelchair guideline has been written specifically for adhesive arachnoiditis or hEDS. The setup below combines general seating guidance (RESNA, AAPM&R) with what the AA and EDS sources say about sitting tolerance and joint protection. It is a starting point for a seating evaluation, not a prescription.

Why sitting is the problem

In AA, the inflammatory-adhesive mass most often sits near L5–S1, "the joint that must endure the most pressure when we sit," so many people "cannot sit very long without causing themselves great pain." In an 80-case MRI-documented series, 87.5% reported pain relief on standing, and the authors' severity scale uses the ability to sit or stand in one position for 10 minutes as a dividing line between moderate and severe disease.22 StatPearls notes that people who have difficulty sitting because of pain "may benefit significantly from motorized assistive devices like standing wheelchairs."1

hEDS adds a second constraint: the arms and shoulders that would push a manual chair are themselves unstable. The EDS Society states there is "no one 'best' wheelchair for people with EDS or HSD," that frequent users need a chair "customized to help them move around without injuring other parts of their body," and that many "find self-propelling wheelchairs challenging," in which case "a power assist device or power wheelchair may be more appropriate."18

The core principle: change position often

RESNA's 2025 position paper recommends "a dynamic sitting posture — periodically changing their position using seat functions — … rather than maintaining a static posture for extended periods," and notes that 25% of users in one study used their wheelchair to treat pain by changing position.19 For someone whose pain comes from sustained lumbosacral loading, the seat functions that let you shift weight off L5–S1 and the sacrum matter more than the frame.

Suggested setup to discuss at a seating evaluation
Component Suggested option Why
Base Power chair, or a manual chair with power assist Protects unstable shoulders and wrists. Power assist suits people who can use a manual chair but "cannot consistently propel it due to upper extremity pain or overuse."20
If manual Adjustable ultralight (under 30 lb), rigid frame, axle forward, ergonomic handrims Ultralights "require less force to propel, therefore reducing risk of repetitive strain shoulder injuries."2021
Tilt-in-space Power tilt, ideally to 30° or more Shifts load off the buttocks and sacrum without changing hip angle. In one cited study, tilt under 20° did not reduce peak sit-bone or sacral pressure, while 30° tilt with 100° recline cut peak sit-bone pressure by 20% and sacral pressure by 10%.19
Recline Power recline, used with tilt Opens the hip angle and supports rest. Commonly used comfort range is 95–110°. With 30° of recline, every tested tilt angle lowered coccyx pressure; with 10° of recline, none did.19
Elevating leg rests Power leg rests, always paired with recline Helps orthostasis and swelling (relevant to POTS). Raising the legs without recline can increase pressure under the coccyx and sacrum.1920
Standing function Consider a standing power chair Directly addresses sitting intolerance. StatPearls advises testing "standing acceptance and vibration endurance" first; AAPM&R notes it won't work with contractures or reduced bone density.120
Seat elevator Power seat elevation Assists transfers and reaching; in a RESNA case example it was prescribed "to reduce upper extremity strain with transfers … and reaching activities."2021
Back support Solid or contoured back, with pelvic support as needed AAPM&R lists sling, solid, and custom backs and warns that inadequate trunk support can lead to "pain, pressure ulcers, or further deformity." The RESNA case examples used contoured backs with pelvic support to bring the pelvis toward neutral.2021
Cushion Pressure-redistributing cushion chosen with pressure mapping Options include foam, gel, air cell, and custom-molded. RESNA supports pairing pressure-relieving cushions with tilt for people who can't do their own weight shifts.1920

How to use the seat functions

  1. Tilt on a schedule, not only when it hurts. One study cited by RESNA recommended tilting every 30 minutes for at least 1–2 minutes.19
  2. Go deep enough. In the cited studies, 15° of tilt did not lower sit-bone pressure or raise blood flow; 30° or more did, and 40° tilt with 100° recline cut peak sacral and sit-bone pressure by about 40%.19
  3. Pair leg elevation with recline to avoid adding coccyx and sacral pressure and pulling the pelvis backward.19
  4. Return to upright in order: recline first, then leg rests, then tilt. This keeps the pelvis in place without friction or shear.19
  5. Keep moving out of the chair. The EDS Society warns that "deconditioning occurs quickly," can worsen joint instability and POTS, and recommends continuing joint-friendly exercise alongside wheelchair use.18

Keeping the pelvis positioned correctly

No chair sets your pelvis automatically. Pelvic position is decided during the evaluation, held by specific parts of the seating system, protected by how you use the seat functions, and rechecked over time.

  1. It's measured first, on a mat. The clinician examines you lying down and sitting to see your pelvic tilt, obliquity (one side lower), and rotation, and whether each is flexible or fixed. A "comprehensive pelvis and hip posture exam" is standard before prescription.2021
  2. The seat holds the base. Correct seat depth (about 2 inches short of the back of the knee), seat slope or "dump," and a cushion with contours or build-ups where needed. In one RESNA case, a cushion build-up under the side of a subluxing hip brought the pelvis back toward neutral.2021
  3. The back and pelvic supports hold the angle. A contoured back with "support at the posterior pelvis to decrease the posterior tilt," plus an anterior pelvic support or pelvic belt "for stability," keeps you from rolling back onto your tailbone.2021
  4. Footrest angle protects it. Tight hamstrings pull the pelvis into posterior tilt. In one case, setting the knees at 95° with an angle-adjustable footplate let the pelvis sit neutral; AAPM&R warns against footrests mounted so far forward they add hamstring tension.2021
  5. Seat functions can undo it if used out of order. Raise leg rests only with recline, to avoid posterior pelvic tilt ("sacral sitting"), and return upright in the order recline → leg rests → tilt so the pelvis stays put without shear.19
  6. It's verified and rechecked. Pressure mapping shows whether weight is spread evenly; RESNA's case examples included a one-month follow-up, and refitting should happen after weight change, disease progression, or a new condition.21

Self-check: if you find yourself sliding forward, sitting on your tailbone, or leaning to one side by the end of the day, the position isn't holding. That's a reason to call the seating team, not something to push through.

Fitting basics

  • Aim for roughly 90° at hips, knees, and elbows as a starting guideline, adjusted for comfort20
  • Seat depth: buttocks-to-back-of-knee minus about 2 inches, so the seat edge doesn't press behind the knee20
  • Seat width: widest point of hips or thighs plus 1–2 inches total20
  • Armrests set to allow about 30° shoulder flexion and 60° elbow flexion20

Getting it prescribed

AAPM&R recommends evaluation by a multidisciplinary seating and wheelchair clinic (physiatrist, OT, PT, and supplier).20 RESNA recommends that a licensed clinician be involved in every evaluation and that the supplier hold a RESNA ATP or Seating and Mobility Specialist (SMS) credential.19 RESNA's service guide adds that "a product trial should be arranged" before final selection.21 For power mobility in the U.S., the prescriber must document a face-to-face mobility exam; the order goes to the supplier within 45 days and the device must be delivered within 120 days.20

Printable evaluation checklist. A one-page-per-topic checklist covers what to record before the appointment, what to ask the team to assess, which features to trial, measurements, and follow-up.

Open printable checklist →

09

Reading & sources

Peer-reviewed

  1. Arachnoiditis (StatPearls). NCBI Bookshelf, updated 2023. Standard clinical reference. Read →
  2. Spinal Adhesive Arachnoidopathy, the Disorder More Than Simply Adhesive Arachnoiditis, 2024. Largest recent pooled analysis of AA epidemiology and mechanisms (176 studies, 510 patients). Read →
  3. Henderson FC et al. Neurological and Spinal Manifestations of the Ehlers-Danlos Syndromes. Am J Med Genet C Semin Med Genet. 2017; 175(1):195–211. The single most-cited review of EDS neurological complications. Read →
  4. Spinal Manifestations of Ehlers-Danlos Syndrome: A Scoping Review. J Neurosurg Spine. 2022. Authoritative neurosurgical consensus and evidence-gap map. Read →
  5. Hypermobile Ehlers–Danlos Syndrome and Spontaneous CSF Leaks: The Connective Tissue Conundrum, 2024. Detailed mechanism review for dural fragility. Read →
  6. Spinal adhesive arachnoiditis: three case reports and review, 2021. Read →
  7. Petrucci et al. Neurologic and Neurosurgical Manifestations in Hypermobile Ehlers-Danlos Syndrome. Mayo Clin Proc Innov Qual Outcomes, 2024. Source of the 2,149-patient prevalence data.

Pelvic floor & women's health in hEDS

  1. Hugon-Rodin J, Lebègue G, Becourt S, Hamonet C, Gompel A. Gynecologic symptoms and the influence on reproductive life in 386 women with hypermobility type Ehlers-Danlos syndrome: a cohort study. Orphanet Journal of Rare Diseases. 2016;11(1):124. DOI: 10.1186/s13023-016-0511-2. Source of the 43% dyspareunia figure; also reports 76% menorrhagia and 72% dysmenorrhea. Among sexually active participants, 61% reported severe dyspareunia. PubMed →
  2. Gilliam E, Hoffman JD, Yeh G. Urogenital and pelvic complications in the Ehlers-Danlos syndromes and associated hypermobility spectrum disorders: a scoping review. Clinical Genetics. 2020;97(1):168–178. DOI: 10.1111/cge.13624. Scoping review of 105 studies; urinary complications 41%, gynecological 36%, obstetrical 25%. PubMed →
  3. Till SR, Schrepf A, Arewasikporn A, Kratz AL, Missmer SA, As-Sanie S. Data-driven diagnosis and clinical presentation of high-tone pelvic floor dysfunction. American Journal of Obstetrics and Gynecology. Epub 2025 Dec 17; DOI: 10.1016/j.ajog.2025.12.036. Cross-sectional study of 612 chronic-pelvic-pain patients; validates a summative tenderness score ≥ 12/60 on palpation of six pelvic-floor muscle groups (bilateral pubococcygeus, iliococcygeus, obturator internus) as a diagnostic threshold (sensitivity 82.3%, specificity 79.1%). Identifies dyspareunia and impaired sexual function as hallmark symptoms of HTPFD. PubMed →
  4. Foster A. Hypermobility, Ehlers-Danlos Syndrome, and Your Pelvic Floor: A Comprehensive Guide. The Fibro Guy, 2026. Non–peer-reviewed clinical synthesis of the peer-reviewed literature above; used here for the hypertonic-vs-hypotonic comparison framing and PT sequencing. Read →
  5. Glayzer JE, McFarlin BL, Castori M, Suarez ML, Meinel MC, Kobak WH, Steffen AD, Schlaeger JM. High rate of dyspareunia and probable vulvodynia in Ehlers-Danlos syndromes and hypermobility spectrum disorders: an online survey. American Journal of Medical Genetics Part C: Seminars in Medical Genetics. 2021;187(4):599–608. DOI: 10.1002/ajmg.c.31939. Online survey of 1,146 women with EDS/HSD: 63.7% dyspareunia, 50% positive vulvodynia screen (≈6× general-population rate); high rates of TMJ dysfunction (56.4%), fibromyalgia (40.0%), endometriosis (26.5%), and MCAS (10.2%). PubMed →

Wheelchair & seating

  1. The Ehlers-Danlos Society. Braces, Splints & Mobility Aids. Undated web page. Guidance on wheelchair use, customization, power assist, and deconditioning in EDS/HSD. Read →
  2. Kenderish J, James T, Russell R, Cianciolo H, Bernstein J, Denfeld G. RESNA Position on the Application of Tilt, Recline, and Elevating Leg Rests for Wheelchairs: Literature Update 2023. RESNA, approved by the Board of Directors February 26, 2025. Source for tilt/recline angles, pressure findings, and repositioning sequence. PDF →
  3. Doan T, Delaney K, Manguinao M. Wheelchair and Power Mobility for Adults. AAPM&R PM&R KnowledgeNow; last updated January 9, 2025. Wheelchair categories, seat functions, measurements, and prescription requirements. Read →
  4. Arledge S, Armstrong W, Babinec M, Dicianno BE, et al. RESNA Wheelchair Service Provision Guide. RESNA, approved January 26, 2011. Assessment, trials, and case examples including ultralight configuration and seat elevation for upper-limb preservation. PDF →
  5. Tennant F, Porcelli MJ, Guess KS. Adhesive Arachnoiditis: A Clinical Update. May/June 2020; hosted by Arachnoiditis Hope. Source for the L5–S1 sitting-pressure explanation, the 80-case profile (87.5% pain relief on standing), and the 10-minute sit/stand severity criteria. PDF →
  6. hEDS Info. Assistive Devices. Patient-education site; not peer reviewed. Used for how manual and power mobility are typically used in hEDS. Read →

Clinician-observation & practice literature (Tennant Foundation and affiliated)

  1. Tennant F. The Ehlers-Danlos Syndrome (EDS) and Intractable Pain Connection. Tennant Foundation, March 2024. Read →
  2. Tennant F, Porcelli MJ, Sands J. Low Dose Methylprednisolone and Ketorolac Treatment for Adhesive Arachnoiditis. International Journal of Emergency Medicine & Pain Management, 2026 — published by Medwin Publishers. Integrity note: the journal is not indexed in PubMed/MEDLINE and the publisher appears on Beall's list of potentially predatory open-access publishers, so its "peer-reviewed" claim should be treated with caution. Primary reporting via Dr. Tennant's own column at Pain News Network, July 18, 2026. Read →
  3. Viña I, López-Moreno M. Meta-Analysis of Palmitoylethanolamide in Pain Management: Addressing Literature Gaps and Enhancing Understanding. Nutrition Reviews. 2025 Jul 1;83(7):e1604–e1618. 18 RCTs, 1,196 patients; significant pain reduction at 4–6 weeks. DOI: 10.1093/nutrit/nuae203. PubMed →
  4. Porcelli MJ, Tennant FS. Adhesive Arachnoiditis: An Old Disease Re-Emerges. Medical Journal of Southern California Clinicians. 2025;17(1):37–46. Indexed peer-reviewed clinical review of the same treatment framework, in a legitimate venue. DOI: 10.38206/1070105. PDF →
  5. Arachnoiditis Hope Bulletin ED-38 — Association of EDS and AA, 2025. Read →
  6. ACMCRN. Spinal Fluid Complications, Tarlov Cysts, and EDS in Adhesive Arachnoiditis. Best single lay-clinical synthesis of the hEDS ↔ AA ↔ CSF-leak triangle. Read →
  7. Tennant F et al. Adhesive Arachnoiditis: No Longer a Rare Disease. MedCentral. Read →
  8. Tennant F. The Link Between Collagen Deficiency and Arachnoiditis. Pain News Network, Aug 2024. Read →
  9. Anson P. The Tragic Connection Between Ehlers-Danlos and Arachnoiditis. Pain News Network, June 2024. Read →
  10. Anson P. The Lifesaving Legacy of Dr. Forest Tennant. Pain News Network, August 14, 2026. Legacy overview. Read →
  11. Forest Tennant obituary (Jan 23, 1941 – Aug 13, 2026). Forest Lawn Covina Hills. Primary source for death date. Read →
In memoriam

Forest Tennant, MD, DrPH, MPH — January 23, 1941 – August 13, 2026. Much of the clinical-observation literature on the hEDS ↔ AA connection reviewed here is Dr. Tennant's. He continued research, writing, and correspondence with patients until his final days, and lived to see the first successful AA treatment study of his career reach the journal literature just weeks before his death.