Spontaneous Spinal Arachnoiditis Ossificans: A Case Report and Review of Diagnostic Pitfalls and Surgical Management

Spontaneous Spinal Arachnoiditis Ossificans: A Case Report and Review of Diagnostic Pitfalls and Surgical Management | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Spontaneous Spinal Arachnoiditis Ossificans: A Case Report and Review of Diagnostic Pitfalls and Surgical Management Louise Frances Steele Saukila, Emma Smedley, Mohamed Wael Mohamed, and 2 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8824283/v1 This work is licensed under a CC BY 4.0 License Status: Under Revision Version 1 posted 10 You are reading this latest preprint version Abstract Background Arachnoiditis ossificans (AO) is a rare neurological disorder marked by heterotopic ossification in the spinal arachnoid membrane, causing stenosis and neural compression. Spontaneous AO, lacking triggers like trauma or infection, is exceptionally rare (< 10 global cases), posing diagnostic challenges. Case Presentation A 36-year-old female presented with two years of progressive thoracic pain, lower limb weakness, and autonomic dysfunction, culminating in suspected acute cauda equina syndrome or rapidly progressive myelopathy. Initial MRI suggested arachnoid cysts, but contrast-enhanced imaging with CISS sequences defined multiloculated intradural cysts (T4–S2/3), with maximal prominence between T5-T7. Rapid neurological deterioration prompted emergency surgical decompression. Thoracic/lumbar laminectomies exposed calcified arachnoid plaques adherent to the dura; microsurgical debridement relieved neural compression and restored cerebrospinal fluid (CSF) flow. Histopathology confirmed benign ossified arachnoid cyst with lamellar bone. Postoperatively, interestingly, she achieved full neurological recovery, including migraine and bowel dysfunction resolution, highlighting the broad neural impact of AO, sustained at six months follow-up despite demonstration of residual cystic fluid on postoperative imaging. Conclusion This case highlights the diagnostic complexity of spontaneous AO: the limited specificity of MRI risks delays, while CT remains gold-standard for ossification detection. Early surgical decompression is critical, aligning with literature showing 60% neurological improvement. Conservative therapies offer limited benefit in advanced disease. Multidisciplinary care and lifelong surveillance are vital, given the progressive nature of AO and recurrence risks. Spontaneous AO should be suspected in unexplained myelopathy with systemic neurological decline, emphasizing timely intervention to mitigate irreversible damage. Spinal arachnoiditis ossificans idiopathic intradural ossification reversible myelopathy disrupted spinal CSF dynamics idiopathic progressive myelopathy Figures Figure 1 Figure 2 Figure 3 Introduction Arachnoiditis ossificans (AO) is a rare, progressive neurological disorder characterized by heterotopic ossification within the spinal arachnoid membrane, leading to spinal canal stenosis and compression of neural structures. 1 This condition typically arises as an end-stage complication of chronic adhesive arachnoiditis, where persistent inflammation triggers osseous metaplasia of arachnoidal cells, leading to the formation of calcified plaques. 2 AO is broadly categorized into two forms: primary (spontaneous) , with no identifiable inciting cause, and secondary , which accounts for most cases and is linked to prior spinal trauma, surgery, subarachnoid haemorrhage, infections, or intrathecal interventions. 3 Primary AO is exceptionally rare, with fewer than 10 cases reported globally, and its nonspecific presentation and idiopathic nature underscores the diagnostic challenges it poses. 2 4 Clinically, AO manifests with progressive myelopathy or cauda equina syndrome, including symptoms such as chronic back pain, sensory deficits, motor weakness, and bladder dysfunction. 5 Thoracic spine involvement, the most common site, often results in severe neurological compromise due to the narrow spinal canal, whereas lumbar lesions may present with milder, though debilitating, symptoms. 1 Distinguishing AO from benign meningeal calcifications is critical, as the former demands timely intervention to mitigate irreversible neurological damage. 2 We present a case of spontaneous AO to highlight diagnostic pitfalls, such as the limited specificity of magnetic resonance imaging (MRI), which may confuse ossifications with calcifications or hemosiderin deposits, and the necessity of computed tomography (CT) for definitive diagnosis. 5 Additionally, we consider conservative management versus surgical strategies to decompress the spinal cord and relieve neural compression, but which carry variable outcomes depending on lesion location and extent. Long-term outcomes remain unpredictable, with studies indicating surgical improvement in approximately 60% of cases, while conservative management is often reserved for non-progressive or minimally symptomatic disease. 6 By interrogating imaging findings, intraoperative insights, histopathological findings, and follow-up data, this case report should contribute valuable guidance for navigating this complex and underrecognized condition. Case Presentation Patient Information and Presentation A 36-year-old right-handed female physiotherapist presented with a two-year history of progressive, multisystem symptoms that acutely escalated over two months. Initial manifestations included chronic fatigue, exertional dyspnoea, dizziness, recurrent headaches, and localized pain involving the thoracic spine, upper lumbar region, chest, and abdomen. Over time, she developed bilateral L5 radiculopathy, worse on the left, with progressive lower extremity weakness and episodic collapses marked by sudden lower limb numbness and buckling. Her clinical course began insidiously with bowel habit alterations and generalized malaise, later expanding to exertional chest pain and transient neurological deficits. Her medical history included hypermobile joints, vestibular migraines refractory to medications and Botox therapy, recurrent vertigo, and a remote concussion without sequelae. There was no history of spinal trauma, infection, or prior surgery. Initial non-contrast spinal MRI identified a subdural collection spanning from T5 to the lumbar spine region, exhibiting loculations and solid components, radiologically suggestive of an arachnoid cyst. However, this finding inadequately explained her widespread symptomatology, prompting a request for contrast-enhanced MRI with CISS sequencing for detailed CSF space evaluation. Within 48 hours of initial imaging, she re-presented with acute neurological deterioration characterized by severe epigastric “band-like” pain, worsening left-leg sensorimotor deficits (including significant weakness), altered perineal sensation, and new-onset bladder/bowel dysfunction (urinary urgency, diminished rectal tone, and a single faecal incontinence episode). These features raised suspicion for cauda equina syndrome or compressive myelopathy, necessitating urgent neurosurgical re-assessment and repeat imaging to evaluate for evolving pathology. Examination Findings At first outpatient presentation, on examination she was independently mobile, with normal tone, power, deep tendon reflexes in upper and lower limbs, with equivocal plantars responses. During acute evaluation, her upper limbs had preserved power, and sensation, but brisker reflexes on the left side. The left lower limb demonstrated Medical Research council (MRC) 4/5 diffuse weakness (hip flexion to ankle dorsiflexion), reduced pinprick sensation across the L4-S1 dermatomes, and diminished perianal sensation. Hyperreflexia was noted in the left lower limb, though proprioception remained intact. Notably, she also had reduced sensation the left T5 dermatome. The right lower limb retained normal strength, sensation, and reflex activity. Within 24 hours, her condition deteriorated precipitously: left lower limb weakness progressed to 3/5 power, with persistent left-sided sensory deficits and hyperreflexia. These findings, coupled with evolving autonomic dysfunction, signalled urgent spinal cord compromise. Imaging Assessment Contrast-enhanced MRI whole spine with CISS sequence during acute presentation identified complex, multiloculated intradural arachnoid cysts posterior to the spinal cord, spanning from T4 to S2-S3 ( see Fig. 1 (c) ). These cysts exhibited well-defined rostral margins (T4-T7) but became less distinct caudally, inferred by ventral displacement of the cauda equina nerve roots and dural ectasia in the sacral canal. The spinal cord demonstrated normal signal intensity without compression, ventral herniation, or neural foraminal extension. Crowding of the cauda equina roots was observed, though CSF spaces remained moderately preserved, and no severe compression was evident. The cysts appeared stable compared to prior imaging, with maximal prominence between T5-T7 and T10-S2. Notably, vertebral alignment, bone marrow signal, and posterior fossa structures were unremarkable, and overall appearances were unchanged compared to the initial presentation MRI. On review of previous investigations, CT chest/abdomen/pelvis more than a decade earlier, performed to investigate night sweats, weight loss, and alcohol-induced flushing, this had been reported as normal. However, retrospective post-operative analysis of the thoracic spine revealed calcifications within the spinal canal, suggestive of early degenerative or inflammatory changes ( see Fig. 1 (a) and (b )). A CT Head to evaluate migrainous vertigo had been unremarkable. Surgical Intervention The patient underwent a one-stage thoracic and lumbar spinal decompression and arachnoid cyst fenestration. Following x-ray-guided level verification, a midline spinal incision was made and bilateral paravertebral muscle dissection for exposure of the thoracic spine (T7–T9). A laminoplasty was performed, with supplementary undercutting at T6 and T10 to ensure proximal and caudal extension of the decompression ( see Fig. 1 (c) ). Upon dural opening, CSF was released under high-pressure and calcified arachnoid cyst with ossified plaques identified, densely adherent to the dura and spinal cord ( see Fig. 2 ). The cyst walls exhibited a thickened, irregular "moth-eaten" morphology, which was meticulously dissected and removed to avoid spinal cord injury. Intrathecal lumbar catheters confirmed patency of the CSF pathways without residual tethering. Attention then shifted to the lumbar spine (L1 level), where a laminectomy exposed a tense dura. Dural release yielded CSF under high-pressure, revealing an arachnoid membrane compressing the cauda equina nerve roots. Fenestration of the membrane relieved nerve root bunching, with catheterization again verified unrestricted CSF flow. Haemostasis was achieved followed by watertight dural closure. A Valsalva manoeuvre confirmed no CSF leakage, and a non-suction drain was placed at the thoracic site prior to multi-layered closure. Postoperatively, the patient regained full consciousness with intact neurological function. Management included a tapered dosage of oral dexamethasone and 24 hours of bedrest prior to gradual mobilisation, with regular neurological assessment. Histopathology Microscopic analysis confirmed a benign ossified arachnoid cyst. The specimen consisted of fibrotic cyst wall fragments with macroscopic calcifications. Histology revealed a fibrocollagenous cyst wall lined by attenuated meningothelial cells, interspersed with mature lamellar bone (ossification) and focal meningothelial cell clusters. No malignant, inflammatory, or atypical features were identified. These findings correlated with intraoperative observations of calcified/ossified cyst walls. Microbiological results were unremarkable. Outcome and Follow-Up Short-Term The patient exhibited significant neurological recovery postoperatively, with complete resolution of left leg weakness (5/5 strength in all muscle groups), intact sensation, including awareness of catheter placement, and stable haemodynamic observations. Pain was well-controlled, and she remained alert and mobile. Postoperative MRI of the spine demonstrated reduced subdural fluid collections between T5–T12 and confirmed successful thoracic cyst fenestration. Septations within this region were less prominent, and thecal narrowing previously observed had resolved. No spinal cord signal abnormalities were identified. There was residual cauda equina displacement (L3–S1) suggesting persistent lumbar cystic fluid. Complementary CT imaging of the thoracic spine demonstrated air locules within fenestrated cavities (T5–T6) and faint dural calcifications. Calcified membranes adherent to the posterior dura were noted, with minimal residual calcification or collections at other thoracic levels. The patient had an uncomplicated hospital admission, with successful removal of the urinary catheter two days post-operatively and was discharged home on day 4. At six-week post-operative review, neurological examination revealed full lower limb strength (5/5), intact balance (negative Romberg, normal tandem gait), and independent ambulation. Mild left upper thigh hyperesthesia persisted but did not impair function. As a physiotherapist, a graded return to work was advised, avoiding heavy lifting until full recovery. Physiotherapy was initiated to optimize neuromuscular coordination. While residual thoracic air locules and lumbar cystic fluid warranted surveillance imaging, the patient’s recovery was highly favourable, with no functional deficits. Surgical intervention had achieved marked neurological restoration, with post-operative imaging underscoring successful thoracic decompression and residual lumbar findings requiring vigilance. The patient’s progress supported cautious optimism, emphasizing monitored recovery to safeguard long-term stability. Long Term Imaging and clinical evaluations at six months revealed sustained recovery with minimal residual pathology. MRI of the thoracic spine demonstrated complete resorption of postoperative gas near the laminoplasty site, though mild dorsal fluid reaccumulation at T6 to T12 caused subtle spinal cord distortion without compression or myelopathic signal changes. The fluid exhibited benign T2 hyperintensity, consistent with non-inflammatory serous collection. CT confirmed stable postoperative changes at T7–T9, including partial laminoplasty defects, well-fixed hardware, and a persistent calcified arachnoid cyst at T5. (See Fig. 3 (b) and (c)). Clinically, the patient reported resolution of all preoperative symptoms, including chronic migraines (discharged from Botox clinic after numerous prior treatments) and bowel dysfunction (discharged from gastroenterology). Neurological examination remained normal, with full motor strength, intact reflexes, and stable gait. A painless upper back lump, attributed to a prominent spinous process due to paraspinal muscle atrophy, was deemed non-pathological following review and imaging correlation. Surgical intervention achieved durable resolution of systemic symptoms (migraines, bowel dysfunction) linked to spinal cord compression. Residual benign fluid collections and calcified arachnoid pathology require ongoing surveillance but pose no immediate threat. This case illustrates the profound systemic impact of spinal pathology and the transformative potential of timely surgical decompression, with multidisciplinary follow-up ensuring holistic rehabilitation. Discussion AO is a rare and enigmatic disorder characterized by heterotopic ossification of the spinal arachnoid membrane. Spontaneous AO, defined by the absence of predisposing factors such as spinal trauma, surgery, infection or iatrogenic interventions, is exceptionally rare, with fewer than 10 cases reported in the literature. 7 8 Most documented cases involve secondary AO, triggered by chronic inflammation from spinal procedures (including extradural surgeries 9 , intrathecal pumps 10 , and nerve root or epidural injections 11 ), central nervous system infections (including syphilis and tuberculosis), trauma, or injection of intrathecal contrast media (for myelography). 1 12 13 The majority of patients with AO present with back pain and progressive myelopathy below the levels affected by this disease. 14 However, patients can also be asymptomatic, with the disease identified as an incidental finding or on autopsy. 15 The patient described here, presenting with progressive myelopathy, thoracic pain, bowel dysfunction, and B symptoms, exemplifies the diagnostic and therapeutic challenges of idiopathic AO, which lacks clear inciting factors. Pathogenesis of Spontaneous AO The pathogenesis of spontaneous AO remains poorly understood. It has a predominance in the thoracic spine (two-thirds of cases) which is thought to be due to the higher concentrations of arachnoid cells within this section of the spine. 16 Proposed mechanisms include metaplasia of arachnoid cells due to chronic CSF stasis or occult inflammatory processes that evade detection. Research highlights interleukin-6 (IL-6) and transforming growth factor-beta (TGF-β) as potential mediators of arachnoid cell metaplasia. 3 Unlike secondary AO, where ossification follows overt trauma or inflammation, spontaneous cases may arise from idiopathic dysregulated osteoblastic activity in meningothelial cells, potentially linked to altered CSF dynamics or genetic predisposition. 13 5 17 Hyperparathyroidism and calcium metabolism abnormalities may predispose to ossification, though evidence is inconclusive. 7 3 In contrast, secondary AO is driven by chronic inflammation from known insults, such as postoperative adhesions or intrathecal haemorrhage, which promote fibroblast proliferation, collagen deposition, and heterotopic ossification of the arachnoid layer. 5 11 10 17 Diagnostic Challenges The nonspecific symptomatology of AO often delays diagnosis, potentially having a devastating effect on patients’ outcomes and quality of life due to the progressive nature of the disease. 14 While MRI may reveal spinal cord compression or cystic lesions, it frequently fails to distinguish ossified plaques from tumours or calcifications, leading to misdiagnosis. Advanced MRI CISS sequences are improving localization of adhesions. 7 13 Non-contrast CT imaging is the gold standard, as it clearly delineates ossifications within the arachnoid layer. 5 11 14 For example, in one case, CT myelography initially missed ossified lesions due to contrast interference, underscoring the necessity of preoperative non-contrast CT to avoid diagnostic pitfalls. 5 Histopathology remains definitive, confirming lamellar bone within the arachnoid and excluding dural ossification or neoplastic processes. 7 Surgical Insights and Outcomes Early surgical decompression is critical to prevent irreversible spinal cord damage. Decompressive laminectomy with meticulous microsurgical dissection is the mainstay, though subtotal resection may be necessary if plaques adhere to critical neural structures. 7 Aggressive resection of adherent plaques risks worsening deficits, emphasising the need for judicious surgical planning. Intraoperative ultrasound has proven valuable in identifying hyperechoic ossified lesions and confirming relief of neural compression and restored CSF flow post-debridement. 5 Literature indicates that approximately 60% of patients experience neurological improvement postoperatively, though outcomes depend on preoperative symptom duration and lesion extent. 11 6 3 Patients with shorter preoperative symptom duration (< 6 months) and focal thoracic lesions tend to achieve better functional recovery, whereas those with longstanding compression or extensive lumbar involvement face higher risks of residual disability. 7 High-dose corticosteroid therapy may alleviate symptoms in early-stage AO by reducing inflammation. However, long-standing cases show limited efficacy, with studies reporting no improvement in 75% of patients treated with steroids alone. 6 7 Methotrexate and plasmapheresis have shown minimal benefit in chronic AO. Surgical decompression is ultimately superior for preventing irreversible cord damage, while conservative therapies should be reserved for stable or minimally symptomatic cases. Recovery is influenced by preoperative symptom severity, myelopathy duration, and surgical completeness. Recurrence rates are poorly quantified but appear linked to residual ossifications or persistent CSF flow obstruction. 5 The rarity of spontaneous AO complicates prognostic modelling, necessitating long-term surveillance with serial imaging. Most AO cases involve the lumbar spine following trauma or surgery, whereas idiopathic thoracic cases, as described here, are exceedingly rare. This patient’s presentation with systemic "B symptoms" (including weight loss and night sweats) further distinguishes her case, prompting broad differentials before AO was confirmed. Notably, her concurrent migraine resolution post-decompression suggests multifocal neural irritation from CSF dynamics disrupted by arachnoid pathology. 11 Conclusion Spontaneous AO is a rare and diagnostically elusive disorder characterized by idiopathic ossification of the spinal arachnoid membrane. Unlike secondary AO (linked to identifiable triggers such as spinal trauma, surgery, or infection), spontaneous AO arises without antecedent causes, complicating its recognition. This case report underscores the imperative to include AO in the differential diagnosis of unexplained progressive myelopathy, particularly when accompanied by nonspecific symptoms such as pain, autonomic dysfunction, or sensory deficits. While MRI is invaluable for assessing spinal cord compression, its inability to reliably distinguish ossified plaques from tumours or calcifications risks diagnostic delay. Non-contrast CT emerges as the gold standard, revealing pathognomonic linear or nodular hyperdensities along the spinal canal. Definitive diagnosis, however, hinges on histopathological confirmation, which demonstrates lamellar bone within the arachnoid layer and excludes mimics like dural ossification or neoplastic calcifications. Early surgical decompression is paramount to prevent irreversible spinal cord injury. Intraoperatively, ossified plaques adherent to neural or vascular structures required meticulous microsurgical dissection. Subtotal resection may be necessary to preserve neurological integrity, aided by intraoperative ultrasound to verify CSF flow restoration. Postoperatively, long-term surveillance with serial MRI/CT is critical to monitor for cyst reaccumulation or recurrent ossification, given the progressive potential of AO. Multidisciplinary collaboration optimizes management of systemic manifestations and guides rehabilitation, while ongoing research into AO pathogenesis and long-term outcomes is essential to refine therapeutic strategies. Spontaneous AO epitomizes the confluence of diagnostic vigilance, advanced imaging, and neurosurgical precision, where timely intervention can decisively alter a disease trajectory otherwise marked by relentless neurological decline. Key Points Suspect AO in idiopathic myelopathy, even without classic triggers. CT and histopathology are diagnostic cornerstones. Early surgery mitigates irreversible damage, balancing resection with neural preservation. Lifelong surveillance and multidisciplinary care counter AO insidious progression. Declarations Written informed consent for publication of their details was obtained from the patient for publication. As determined by the Health Research Authority decision tool, NHS REC review is not required for publication. Author Contribution LFSS designed the review and wrote the main manuscript text. ES performed the literature review.MWM prepared figure 2.PS contributed to the design of the review and critical analysis of the initial draft.DP contributed to the design of the review and critical analysis of the initial draft.All authors reviewed and approved the manuscript for submission References Steel CJ, Abrames EL, O’Brien WT (2015) Arachnoiditis Ossificans – A Rare Cause of Progressive Myelopathy. Open Neuroimaging J 9:13–20 Wachtel A Review of Arachnoiditis Ossificans with a Case Report [Internet]. Barrow Neurological Institute. [cited 2025 May 24]. Available from: https://www.barrowneuro.org/for-physicians-researchers/education/grand-rounds-publications-media/barrow-quarterly/volume-14-no-4-1998/review-arachnoiditis-ossificans-case-report/ Peng H, Conermann T Arachnoiditis. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 [cited 2025 May 24]. 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Clin Neurol Neurosurg 124:16–20 Dokponou YCH, Kacemi IE, Imoumby FN, Kouakou FL, Akroud SE, Gazzaz M (2021) Arachnoiditis Ossificans Mimicking Spinal Intradural Extramedullary Tumor: A Case Report and Review of the Literature. Open J Mod Neurosurg 11(3):157–163 Bagley JH, Owens TR, Grunch BH, Moreno JR, Bagley CA (2014) Arachnoiditis ossificans of the thoracic spine. J Clin Neurosci Off J Neurosurg Soc Australas 21(3):386–389 Ward M, Mammis A, Barry MT, Heary RF (2018) Novel Association Between Intrathecal Drug Administration and Arachnoiditis Ossificans. World Neurosurg 115:400–406 Bushaw MA, Ater MR Arachnoiditis Ossificans Following Repeat Epidural Steroid Injections: A Case Study. J Veterans Stud [Internet]. 2024 Dec 27 [cited 2025 May 24];10(3). 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Surg J 7(3):e174–e178 Krätzig T, Dreimann M, Mende KC, Königs I, Westphal M, Eicker SO (2018) Extensive Spinal Adhesive Arachnoiditis After Extradural Spinal Infection-Spinal Dura Mater Is No Barrier to Inflammation. World Neurosurg 116:e1194–e1203 Additional Declarations No competing interests reported. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8824283","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":604718903,"identity":"f327e6e3-feac-4a41-ab96-07dec73cf2e4","order_by":0,"name":"Louise Frances Steele Saukila","email":"data:image/png;base64,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","orcid":"","institution":"Leeds Centre for Neurosciences","correspondingAuthor":true,"prefix":"","firstName":"Louise","middleName":"Frances Steele","lastName":"Saukila","suffix":""},{"id":604718904,"identity":"3b10b2ec-d178-4766-9156-d7a73ac03aec","order_by":1,"name":"Emma Smedley","email":"","orcid":"","institution":"Leeds Centre for Neurosciences","correspondingAuthor":false,"prefix":"","firstName":"Emma","middleName":"","lastName":"Smedley","suffix":""},{"id":604718906,"identity":"c49041c8-fa74-43f3-a598-fda6cd9ffaa2","order_by":2,"name":"Mohamed Wael Mohamed","email":"","orcid":"","institution":"Leeds Centre for Neurosciences","correspondingAuthor":false,"prefix":"","firstName":"Mohamed","middleName":"Wael","lastName":"Mohamed","suffix":""},{"id":604718908,"identity":"b9ff26cc-c498-4a76-88ee-62ba5be50a63","order_by":3,"name":"Priyank Sinha","email":"","orcid":"","institution":"Leeds Centre for Neurosciences","correspondingAuthor":false,"prefix":"","firstName":"Priyank","middleName":"","lastName":"Sinha","suffix":""},{"id":604718915,"identity":"f9918392-5a12-4c4f-8e56-1e2c6007f113","order_by":4,"name":"Debasish Pal","email":"","orcid":"","institution":"Leeds Centre for Neurosciences","correspondingAuthor":false,"prefix":"","firstName":"Debasish","middleName":"","lastName":"Pal","suffix":""}],"badges":[],"createdAt":"2026-02-08 21:39:03","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8824283/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8824283/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":104582301,"identity":"d2394a2c-a5a7-4c03-b2b7-67b5c6d534a8","added_by":"auto","created_at":"2026-03-13 15:12:17","extension":"jpeg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":654286,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003ePre-operative imaging. \u003c/strong\u003e\u003cem\u003e\u003cstrong\u003e(a) and (b) Coronal and axial views, respectively, of a CT chest abdomen pelvis \u003c/strong\u003e\u003c/em\u003e\u003cem\u003efrom historical investigation of B symptoms, a decade prior to presentation. Although reported as normal, the green arrows indicate areas of calcification within the spinal canal. \u0026nbsp;\u003c/em\u003e\u003cem\u003e\u003cstrong\u003e(c) Sagittal and axial views of T2 MRI whole spine \u003c/strong\u003e\u003c/em\u003e\u003cem\u003edemonstrating multiloculated intradural arachnoid cysts posterior to the spinal cord, spanning from T4 to S2-S3. These cysts exhibited well-defined rostral margins (T4-T7) but became less distinct caudally, inferred by ventral displacement of the cauda equina nerve roots and dural ectasia in the sacral canal. The spinal cord demonstrated normal signal intensity without compression, ventral herniation, or neural foraminal extension. Crowding of the cauda equina roots was observed, though CSF spaces remained moderately preserved, and no severe compression was evident. The cysts appeared stable compared to prior imaging, with maximal prominence between T5-T7 and T10-S2. Markers indicate the levels of surgical decompression (T6-T10) and L1.\u003c/em\u003e\u003c/p\u003e","description":"","filename":"floatimage1.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-8824283/v1/b0d1e49074002c74cee2dd97.jpeg"},{"id":104582308,"identity":"d507ed99-ac2d-4239-970f-0a030ecabee1","added_by":"auto","created_at":"2026-03-13 15:12:20","extension":"jpeg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":556644,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cem\u003e\u003cstrong\u003eIntra-operative microscope imaging of arachnoid ossified plaques. \u003c/strong\u003e\u003c/em\u003e\u003cem\u003eFour snapshots taken intra-operatively after dural opening, demonstrating the thickened ossified arachnoid plaques, adherent to dura and underlying spinal cord, requiring meticulous sharp dissection for removal and restoration of pulsatile spinal cord movement.\u003c/em\u003e\u003c/p\u003e","description":"","filename":"floatimage2.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-8824283/v1/ad3f359ca5000f14c10a6b0f.jpeg"},{"id":104582431,"identity":"d7cf4b3d-d8ef-4b1c-af2d-b16a271c3acc","added_by":"auto","created_at":"2026-03-13 15:12:30","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":943146,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003ePost-operative imaging\u003c/strong\u003e\u003cem\u003e\u003cstrong\u003e. (a) Sagittal and axial views of non-contrast CT imaging immediately post-operatively\u003c/strong\u003e\u003c/em\u003e\u003cem\u003e. Overall improved appearances. Compressive change on the cord T5 and T6 from air pockets dorsally and anteriorly. \u0026nbsp;At T5 and T6 there is faint calcification within the anterior wall of the cyst (green arrow). The red markers indicate levels of surgical decompression. \u003c/em\u003e\u003cem\u003e\u003cstrong\u003e(b)\u003c/strong\u003e\u003c/em\u003e\u003cem\u003e \u003c/em\u003e\u003cem\u003e\u003cstrong\u003eSagittal and axial views of non-contrast CT imaging 6 months post-operatively. \u003c/strong\u003e\u003c/em\u003e\u003cem\u003eFrom T5 inferiorly, there is a complex dorsal calcified arachnoid cyst still present (green arrow). \u003c/em\u003e\u003cem\u003e\u003cstrong\u003e(c)\u003c/strong\u003e\u003c/em\u003e\u003cstrong\u003e \u003c/strong\u003e\u003cem\u003e\u003cstrong\u003eSagittal and axial views of T2 MRI at 6 months post-operatively\u003c/strong\u003e\u003c/em\u003e\u003cem\u003e.\u003c/em\u003e \u003cem\u003eResorption of the previously demonstrated postoperative gas subjacent to the laminoplasty. Slight reaccumulation of the dorsal collection, most apparent at T6 to T12 with slight cord distortion but no compression or myelopathic signal change.\u003c/em\u003e\u003c/p\u003e","description":"","filename":"floatimage3.png","url":"https://assets-eu.researchsquare.com/files/rs-8824283/v1/05da7911d882e0ad2178a9ca.png"},{"id":104582534,"identity":"334477ba-4da5-4c5a-8501-7c5211eac571","added_by":"auto","created_at":"2026-03-13 15:12:41","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":2888726,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8824283/v1/07fd9727-f9fa-4d13-bd85-70fbaf97b979.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Spontaneous Spinal Arachnoiditis Ossificans: A Case Report and Review of Diagnostic Pitfalls and Surgical Management","fulltext":[{"header":"Introduction","content":"\u003cp\u003eArachnoiditis ossificans (AO) is a rare, progressive neurological disorder characterized by heterotopic ossification within the spinal arachnoid membrane, leading to spinal canal stenosis and compression of neural structures.\u003csup\u003e\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e\u003c/sup\u003e This condition typically arises as an end-stage complication of chronic adhesive arachnoiditis, where persistent inflammation triggers osseous metaplasia of arachnoidal cells, leading to the formation of calcified plaques.\u003csup\u003e\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e AO is broadly categorized into two forms: \u003cem\u003eprimary (spontaneous)\u003c/em\u003e, with no identifiable inciting cause, and \u003cem\u003esecondary\u003c/em\u003e, which accounts for most cases and is linked to prior spinal trauma, surgery, subarachnoid haemorrhage, infections, or intrathecal interventions.\u003csup\u003e\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u003c/sup\u003e Primary AO is exceptionally rare, with fewer than 10 cases reported globally, and its nonspecific presentation and idiopathic nature underscores the diagnostic challenges it poses.\u003csup\u003e2 4\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eClinically, AO manifests with progressive myelopathy or cauda equina syndrome, including symptoms such as chronic back pain, sensory deficits, motor weakness, and bladder dysfunction.\u003csup\u003e\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u003c/sup\u003e Thoracic spine involvement, the most common site, often results in severe neurological compromise due to the narrow spinal canal, whereas lumbar lesions may present with milder, though debilitating, symptoms.\u003csup\u003e\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e\u003c/sup\u003e Distinguishing AO from benign meningeal calcifications is critical, as the former demands timely intervention to mitigate irreversible neurological damage.\u003csup\u003e\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eWe present a case of spontaneous AO to highlight diagnostic pitfalls, such as the limited specificity of magnetic resonance imaging (MRI), which may confuse ossifications with calcifications or hemosiderin deposits, and the necessity of computed tomography (CT) for definitive diagnosis. \u003csup\u003e5\u003c/sup\u003e Additionally, we consider conservative management versus surgical strategies to decompress the spinal cord and relieve neural compression, but which carry variable outcomes depending on lesion location and extent. Long-term outcomes remain unpredictable, with studies indicating surgical improvement in approximately 60% of cases, while conservative management is often reserved for non-progressive or minimally symptomatic disease.\u003csup\u003e\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e\u003c/sup\u003e By interrogating imaging findings, intraoperative insights, histopathological findings, and follow-up data, this case report should contribute valuable guidance for navigating this complex and underrecognized condition.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003ePatient Information and Presentation\u003c/p\u003e \u003cp\u003eA 36-year-old right-handed female physiotherapist presented with a two-year history of progressive, multisystem symptoms that acutely escalated over two months. Initial manifestations included chronic fatigue, exertional dyspnoea, dizziness, recurrent headaches, and localized pain involving the thoracic spine, upper lumbar region, chest, and abdomen. Over time, she developed bilateral L5 radiculopathy, worse on the left, with progressive lower extremity weakness and episodic collapses marked by sudden lower limb numbness and buckling. Her clinical course began insidiously with bowel habit alterations and generalized malaise, later expanding to exertional chest pain and transient neurological deficits.\u003c/p\u003e \u003cp\u003eHer medical history included hypermobile joints, vestibular migraines refractory to medications and Botox therapy, recurrent vertigo, and a remote concussion without sequelae. There was no history of spinal trauma, infection, or prior surgery.\u003c/p\u003e \u003cp\u003eInitial non-contrast spinal MRI identified a subdural collection spanning from T5 to the lumbar spine region, exhibiting loculations and solid components, radiologically suggestive of an arachnoid cyst. However, this finding inadequately explained her widespread symptomatology, prompting a request for contrast-enhanced MRI with CISS sequencing for detailed CSF space evaluation.\u003c/p\u003e \u003cp\u003eWithin 48 hours of initial imaging, she re-presented with acute neurological deterioration characterized by severe epigastric \u0026ldquo;band-like\u0026rdquo; pain, worsening left-leg sensorimotor deficits (including significant weakness), altered perineal sensation, and new-onset bladder/bowel dysfunction (urinary urgency, diminished rectal tone, and a single faecal incontinence episode). These features raised suspicion for cauda equina syndrome or compressive myelopathy, necessitating urgent neurosurgical re-assessment and repeat imaging to evaluate for evolving pathology.\u003c/p\u003e \u003cp\u003eExamination Findings\u003c/p\u003e \u003cp\u003eAt first outpatient presentation, on examination she was independently mobile, with normal tone, power, deep tendon reflexes in upper and lower limbs, with equivocal plantars responses.\u003c/p\u003e \u003cp\u003eDuring acute evaluation, her upper limbs had preserved power, and sensation, but brisker reflexes on the left side. The left lower limb demonstrated Medical Research council (MRC) 4/5 diffuse weakness (hip flexion to ankle dorsiflexion), reduced pinprick sensation across the L4-S1 dermatomes, and diminished perianal sensation. Hyperreflexia was noted in the left lower limb, though proprioception remained intact. Notably, she also had reduced sensation the left T5 dermatome. The right lower limb retained normal strength, sensation, and reflex activity. Within 24 hours, her condition deteriorated precipitously: left lower limb weakness progressed to 3/5 power, with persistent left-sided sensory deficits and hyperreflexia. These findings, coupled with evolving autonomic dysfunction, signalled urgent spinal cord compromise.\u003c/p\u003e \u003cp\u003eImaging Assessment\u003c/p\u003e \u003cp\u003eContrast-enhanced MRI whole spine with CISS sequence during acute presentation identified complex, multiloculated intradural arachnoid cysts posterior to the spinal cord, spanning from T4 to S2-S3 (\u003cem\u003esee\u003c/em\u003e Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e \u003cem\u003e(c)\u003c/em\u003e). These cysts exhibited well-defined rostral margins (T4-T7) but became less distinct caudally, inferred by ventral displacement of the cauda equina nerve roots and dural ectasia in the sacral canal. The spinal cord demonstrated normal signal intensity without compression, ventral herniation, or neural foraminal extension. Crowding of the cauda equina roots was observed, though CSF spaces remained moderately preserved, and no severe compression was evident. The cysts appeared stable compared to prior imaging, with maximal prominence between T5-T7 and T10-S2. Notably, vertebral alignment, bone marrow signal, and posterior fossa structures were unremarkable, and overall appearances were unchanged compared to the initial presentation MRI.\u003c/p\u003e \u003cp\u003eOn review of previous investigations, CT chest/abdomen/pelvis more than a decade earlier, performed to investigate night sweats, weight loss, and alcohol-induced flushing, this had been reported as normal. However, retrospective post-operative analysis of the thoracic spine revealed calcifications within the spinal canal, suggestive of early degenerative or inflammatory changes (\u003cem\u003esee\u003c/em\u003e Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e \u003cem\u003e(a) and (b\u003c/em\u003e)). A CT Head to evaluate migrainous vertigo had been unremarkable.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eSurgical Intervention\u003c/p\u003e \u003cp\u003eThe patient underwent a one-stage thoracic and lumbar spinal decompression and arachnoid cyst fenestration. Following x-ray-guided level verification, a midline spinal incision was made and bilateral paravertebral muscle dissection for exposure of the thoracic spine (T7\u0026ndash;T9). A laminoplasty was performed, with supplementary undercutting at T6 and T10 to ensure proximal and caudal extension of the decompression (\u003cem\u003esee\u003c/em\u003e Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e\u003cem\u003e(c)\u003c/em\u003e).\u003c/p\u003e \u003cp\u003eUpon dural opening, CSF was released under high-pressure and calcified arachnoid cyst with ossified plaques identified, densely adherent to the dura and spinal cord (\u003cem\u003esee\u003c/em\u003e Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). The cyst walls exhibited a thickened, irregular \"moth-eaten\" morphology, which was meticulously dissected and removed to avoid spinal cord injury. Intrathecal lumbar catheters confirmed patency of the CSF pathways without residual tethering.\u003c/p\u003e \u003cp\u003eAttention then shifted to the lumbar spine (L1 level), where a laminectomy exposed a tense dura. Dural release yielded CSF under high-pressure, revealing an arachnoid membrane compressing the cauda equina nerve roots. Fenestration of the membrane relieved nerve root bunching, with catheterization again verified unrestricted CSF flow. Haemostasis was achieved followed by watertight dural closure. A Valsalva manoeuvre confirmed no CSF leakage, and a non-suction drain was placed at the thoracic site prior to multi-layered closure.\u003c/p\u003e \u003cp\u003ePostoperatively, the patient regained full consciousness with intact neurological function. Management included a tapered dosage of oral dexamethasone and 24 hours of bedrest prior to gradual mobilisation, with regular neurological assessment.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eHistopathology\u003c/p\u003e \u003cp\u003eMicroscopic analysis confirmed a benign ossified arachnoid cyst. The specimen consisted of fibrotic cyst wall fragments with macroscopic calcifications. Histology revealed a fibrocollagenous cyst wall lined by attenuated meningothelial cells, interspersed with mature lamellar bone (ossification) and focal meningothelial cell clusters. No malignant, inflammatory, or atypical features were identified. These findings correlated with intraoperative observations of calcified/ossified cyst walls. Microbiological results were unremarkable.\u003c/p\u003e \u003cp\u003eOutcome and Follow-Up\u003c/p\u003e\n\u003ch3\u003eShort-Term\u003c/h3\u003e\n\u003cp\u003eThe patient exhibited significant neurological recovery postoperatively, with complete resolution of left leg weakness (5/5 strength in all muscle groups), intact sensation, including awareness of catheter placement, and stable haemodynamic observations. Pain was well-controlled, and she remained alert and mobile.\u003c/p\u003e \u003cp\u003ePostoperative MRI of the spine demonstrated reduced subdural fluid collections between T5\u0026ndash;T12 and confirmed successful thoracic cyst fenestration. Septations within this region were less prominent, and thecal narrowing previously observed had resolved. No spinal cord signal abnormalities were identified. There was residual cauda equina displacement (L3\u0026ndash;S1) suggesting persistent lumbar cystic fluid.\u003c/p\u003e \u003cp\u003eComplementary CT imaging of the thoracic spine demonstrated air locules within fenestrated cavities (T5\u0026ndash;T6) and faint dural calcifications. Calcified membranes adherent to the posterior dura were noted, with minimal residual calcification or collections at other thoracic levels.\u003c/p\u003e \u003cp\u003eThe patient had an uncomplicated hospital admission, with successful removal of the urinary catheter two days post-operatively and was discharged home on day 4.\u003c/p\u003e \u003cp\u003eAt six-week post-operative review, neurological examination revealed full lower limb strength (5/5), intact balance (negative Romberg, normal tandem gait), and independent ambulation. Mild left upper thigh hyperesthesia persisted but did not impair function. As a physiotherapist, a graded return to work was advised, avoiding heavy lifting until full recovery. Physiotherapy was initiated to optimize neuromuscular coordination.\u003c/p\u003e \u003cp\u003eWhile residual thoracic air locules and lumbar cystic fluid warranted surveillance imaging, the patient\u0026rsquo;s recovery was highly favourable, with no functional deficits. Surgical intervention had achieved marked neurological restoration, with post-operative imaging underscoring successful thoracic decompression and residual lumbar findings requiring vigilance. The patient\u0026rsquo;s progress supported cautious optimism, emphasizing monitored recovery to safeguard long-term stability.\u003c/p\u003e \u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eLong Term\u003c/h2\u003e \u003cp\u003eImaging and clinical evaluations at six months revealed sustained recovery with minimal residual pathology. MRI of the thoracic spine demonstrated complete resorption of postoperative gas near the laminoplasty site, though mild dorsal fluid reaccumulation at T6 to T12 caused subtle spinal cord distortion without compression or myelopathic signal changes. The fluid exhibited benign T2 hyperintensity, consistent with non-inflammatory serous collection. CT confirmed stable postoperative changes at T7\u0026ndash;T9, including partial laminoplasty defects, well-fixed hardware, and a persistent calcified arachnoid cyst at T5. \u003cem\u003e(See\u003c/em\u003e Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e \u003cem\u003e(b) and (c)).\u003c/em\u003e\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eClinically, the patient reported resolution of all preoperative symptoms, including chronic migraines (discharged from Botox clinic after numerous prior treatments) and bowel dysfunction (discharged from gastroenterology). Neurological examination remained normal, with full motor strength, intact reflexes, and stable gait. A painless upper back lump, attributed to a prominent spinous process due to paraspinal muscle atrophy, was deemed non-pathological following review and imaging correlation.\u003c/p\u003e \u003cp\u003eSurgical intervention achieved durable resolution of systemic symptoms (migraines, bowel dysfunction) linked to spinal cord compression. Residual benign fluid collections and calcified arachnoid pathology require ongoing surveillance but pose no immediate threat. This case illustrates the profound systemic impact of spinal pathology and the transformative potential of timely surgical decompression, with multidisciplinary follow-up ensuring holistic rehabilitation.\u003c/p\u003e \u003c/div\u003e"},{"header":"Discussion","content":"\u003cp\u003eAO is a rare and enigmatic disorder characterized by heterotopic ossification of the spinal arachnoid membrane. Spontaneous AO, defined by the absence of predisposing factors such as spinal trauma, surgery, infection or iatrogenic interventions, is exceptionally rare, with fewer than 10 cases reported in the literature.\u003csup\u003e7 8\u003c/sup\u003e Most documented cases involve secondary AO, triggered by chronic inflammation from spinal procedures (including extradural surgeries\u003csup\u003e\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e\u003c/sup\u003e, intrathecal pumps\u003csup\u003e\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e\u003c/sup\u003e, and nerve root or epidural injections\u003csup\u003e\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e\u003c/sup\u003e), central nervous system infections (including syphilis and tuberculosis), trauma, or injection of intrathecal contrast media (for myelography).\u003csup\u003e1 12 13\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eThe majority of patients with AO present with back pain and progressive myelopathy below the levels affected by this disease.\u003csup\u003e\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e\u003c/sup\u003e However, patients can also be asymptomatic, with the disease identified as an incidental finding or on autopsy.\u003csup\u003e\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e\u003c/sup\u003e The patient described here, presenting with progressive myelopathy, thoracic pain, bowel dysfunction, and B symptoms, exemplifies the diagnostic and therapeutic challenges of idiopathic AO, which lacks clear inciting factors.\u003c/p\u003e \u003cp\u003ePathogenesis of Spontaneous AO\u003c/p\u003e \u003cp\u003eThe pathogenesis of spontaneous AO remains poorly understood. It has a predominance in the thoracic spine (two-thirds of cases) which is thought to be due to the higher concentrations of arachnoid cells within this section of the spine.\u003csup\u003e\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e\u003c/sup\u003e Proposed mechanisms include metaplasia of arachnoid cells due to chronic CSF stasis or occult inflammatory processes that evade detection. Research highlights interleukin-6 (IL-6) and transforming growth factor-beta (TGF-β) as potential mediators of arachnoid cell metaplasia.\u003csup\u003e\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u003c/sup\u003e Unlike secondary AO, where ossification follows overt trauma or inflammation, spontaneous cases may arise from idiopathic dysregulated osteoblastic activity in meningothelial cells, potentially linked to altered CSF dynamics or genetic predisposition.\u003csup\u003e13 5 17\u003c/sup\u003e Hyperparathyroidism and calcium metabolism abnormalities may predispose to ossification, though evidence is inconclusive.\u003csup\u003e7 3\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eIn contrast, secondary AO is driven by chronic inflammation from known insults, such as postoperative adhesions or intrathecal haemorrhage, which promote fibroblast proliferation, collagen deposition, and heterotopic ossification of the arachnoid layer.\u003csup\u003e5 11 10 17\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eDiagnostic Challenges\u003c/p\u003e \u003cp\u003eThe nonspecific symptomatology of AO often delays diagnosis, potentially having a devastating effect on patients\u0026rsquo; outcomes and quality of life due to the progressive nature of the disease.\u003csup\u003e\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e\u003c/sup\u003e While MRI may reveal spinal cord compression or cystic lesions, it frequently fails to distinguish ossified plaques from tumours or calcifications, leading to misdiagnosis. Advanced MRI CISS sequences are improving localization of adhesions.\u003csup\u003e7 13\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eNon-contrast CT imaging is the gold standard, as it clearly delineates ossifications within the arachnoid layer.\u003csup\u003e5 11 14\u003c/sup\u003e For example, in one case, CT myelography initially missed ossified lesions due to contrast interference, underscoring the necessity of preoperative non-contrast CT to avoid diagnostic pitfalls.\u003csup\u003e\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u003c/sup\u003e Histopathology remains definitive, confirming lamellar bone within the arachnoid and excluding dural ossification or neoplastic processes.\u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eSurgical Insights and Outcomes\u003c/p\u003e \u003cp\u003eEarly surgical decompression is critical to prevent irreversible spinal cord damage. Decompressive laminectomy with meticulous microsurgical dissection is the mainstay, though subtotal resection may be necessary if plaques adhere to critical neural structures.\u003csup\u003e\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e\u003c/sup\u003e Aggressive resection of adherent plaques risks worsening deficits, emphasising the need for judicious surgical planning. Intraoperative ultrasound has proven valuable in identifying hyperechoic ossified lesions and confirming relief of neural compression and restored CSF flow post-debridement.\u003csup\u003e\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eLiterature indicates that approximately 60% of patients experience neurological improvement postoperatively, though outcomes depend on preoperative symptom duration and lesion extent.\u003csup\u003e11 6 3\u003c/sup\u003e Patients with shorter preoperative symptom duration (\u0026lt;\u0026thinsp;6 months) and focal thoracic lesions tend to achieve better functional recovery, whereas those with longstanding compression or extensive lumbar involvement face higher risks of residual disability. \u003csup\u003e7\u003c/sup\u003e\u003c/p\u003e \u003cp\u003eHigh-dose corticosteroid therapy may alleviate symptoms in early-stage AO by reducing inflammation. However, long-standing cases show limited efficacy, with studies reporting no improvement in 75% of patients treated with steroids alone.\u003csup\u003e6 7\u003c/sup\u003e Methotrexate and plasmapheresis have shown minimal benefit in chronic AO. Surgical decompression is ultimately superior for preventing irreversible cord damage, while conservative therapies should be reserved for stable or minimally symptomatic cases.\u003c/p\u003e \u003cp\u003eRecovery is influenced by preoperative symptom severity, myelopathy duration, and surgical completeness. Recurrence rates are poorly quantified but appear linked to residual ossifications or persistent CSF flow obstruction.\u003csup\u003e\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e\u003c/sup\u003e The rarity of spontaneous AO complicates prognostic modelling, necessitating long-term surveillance with serial imaging.\u003c/p\u003e \u003cp\u003eMost AO cases involve the lumbar spine following trauma or surgery, whereas idiopathic thoracic cases, as described here, are exceedingly rare. This patient\u0026rsquo;s presentation with systemic \"B symptoms\" (including weight loss and night sweats) further distinguishes her case, prompting broad differentials before AO was confirmed. Notably, her concurrent migraine resolution post-decompression suggests multifocal neural irritation from CSF dynamics disrupted by arachnoid pathology. \u003csup\u003e11\u003c/sup\u003e\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eSpontaneous AO is a rare and diagnostically elusive disorder characterized by idiopathic ossification of the spinal arachnoid membrane. Unlike secondary AO (linked to identifiable triggers such as spinal trauma, surgery, or infection), spontaneous AO arises without antecedent causes, complicating its recognition. This case report underscores the imperative to include AO in the differential diagnosis of unexplained progressive myelopathy, particularly when accompanied by nonspecific symptoms such as pain, autonomic dysfunction, or sensory deficits.\u003c/p\u003e \u003cp\u003eWhile MRI is invaluable for assessing spinal cord compression, its inability to reliably distinguish ossified plaques from tumours or calcifications risks diagnostic delay. Non-contrast CT emerges as the gold standard, revealing pathognomonic linear or nodular hyperdensities along the spinal canal. Definitive diagnosis, however, hinges on histopathological confirmation, which demonstrates lamellar bone within the arachnoid layer and excludes mimics like dural ossification or neoplastic calcifications.\u003c/p\u003e \u003cp\u003eEarly surgical decompression is paramount to prevent irreversible spinal cord injury. Intraoperatively, ossified plaques adherent to neural or vascular structures required meticulous microsurgical dissection. Subtotal resection may be necessary to preserve neurological integrity, aided by intraoperative ultrasound to verify CSF flow restoration. Postoperatively, long-term surveillance with serial MRI/CT is critical to monitor for cyst reaccumulation or recurrent ossification, given the progressive potential of AO.\u003c/p\u003e \u003cp\u003eMultidisciplinary collaboration optimizes management of systemic manifestations and guides rehabilitation, while ongoing research into AO pathogenesis and long-term outcomes is essential to refine therapeutic strategies. Spontaneous AO epitomizes the confluence of diagnostic vigilance, advanced imaging, and neurosurgical precision, where timely intervention can decisively alter a disease trajectory otherwise marked by relentless neurological decline.\u003c/p\u003e"},{"header":"Key Points","content":"\u003cp\u003e \u003cb\u003eSuspect AO\u003c/b\u003e in idiopathic myelopathy, even without classic triggers.\u003c/p\u003e \u003cp\u003e \u003cb\u003eCT and histopathology\u003c/b\u003e are diagnostic cornerstones.\u003c/p\u003e \u003cp\u003e \u003cb\u003eEarly surgery\u003c/b\u003e mitigates irreversible damage, balancing resection with neural preservation.\u003c/p\u003e \u003cp\u003e \u003cb\u003eLifelong surveillance\u003c/b\u003e and multidisciplinary care counter AO insidious progression.\u003c/p\u003e"},{"header":"Declarations","content":" \u003cp\u003eWritten informed consent for publication of their details was obtained from the patient for publication. As determined by the Health Research Authority decision tool, NHS REC review is not required for publication.\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eLFSS designed the review and wrote the main manuscript text. ES performed the literature review.MWM prepared figure 2.PS contributed to the design of the review and critical analysis of the initial draft.DP contributed to the design of the review and critical analysis of the initial draft.All authors reviewed and approved the manuscript for submission\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eSteel CJ, Abrames EL, O\u0026rsquo;Brien WT (2015) Arachnoiditis Ossificans \u0026ndash; A Rare Cause of Progressive Myelopathy. Open Neuroimaging J 9:13\u0026ndash;20\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWachtel A Review of Arachnoiditis Ossificans with a Case Report [Internet]. Barrow Neurological Institute. [cited 2025 May 24]. 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NMC Case Rep J 9:295\u0026ndash;299\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHackert J, Ma\u0026szlig;mann L, Sure U, Forsting M, Kleinschnitz C, Pul R et al (2021) Immunotherapies in chronic adhesive arachnoiditis - A case series and literature review. eNeurologicalSci 24:100350\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMaulucci CM, Ghobrial GM, Oppenlander ME, Flanders AE, Vaccaro AR, Harrop JS (2014) Arachnoiditis ossificans: clinical series and review of the literature. Clin Neurol Neurosurg 124:16\u0026ndash;20\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDokponou YCH, Kacemi IE, Imoumby FN, Kouakou FL, Akroud SE, Gazzaz M (2021) Arachnoiditis Ossificans Mimicking Spinal Intradural Extramedullary Tumor: A Case Report and Review of the Literature. Open J Mod Neurosurg 11(3):157\u0026ndash;163\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBagley JH, Owens TR, Grunch BH, Moreno JR, Bagley CA (2014) Arachnoiditis ossificans of the thoracic spine. J Clin Neurosci Off J Neurosurg Soc Australas 21(3):386\u0026ndash;389\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWard M, Mammis A, Barry MT, Heary RF (2018) Novel Association Between Intrathecal Drug Administration and Arachnoiditis Ossificans. World Neurosurg 115:400\u0026ndash;406\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBushaw MA, Ater MR Arachnoiditis Ossificans Following Repeat Epidural Steroid Injections: A Case Study. J Veterans Stud [Internet]. 2024 Dec 27 [cited 2025 May 24];10(3). 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World Neurosurg 126:189\u0026ndash;193\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDonalisio M, Egea M, Dunet V, Omoumi P, Mourad C (2024) Arachnoiditis ossificans. Skeletal Radiol 53(5):1019\u0026ndash;1021\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eDomenicucci M, Ramieri A, Passacantilli E, Russo N, Trasimeni G, Delfini R (2004) Spinal arachnoiditis ossificans: report of three cases. Neurosurgery 55(4):985\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBrunner A, Leoni M, Eustacchio S, Kurschel-Lackner S (2021) Spinal Arachnoiditis Ossificans: A Case-Based Update. Surg J 7(3):e174\u0026ndash;e178\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKr\u0026auml;tzig T, Dreimann M, Mende KC, K\u0026ouml;nigs I, Westphal M, Eicker SO (2018) Extensive Spinal Adhesive Arachnoiditis After Extradural Spinal Infection-Spinal Dura Mater Is No Barrier to Inflammation. World Neurosurg 116:e1194\u0026ndash;e1203\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"european-spine-journal","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"esjo","sideBox":"Learn more about [European Spine Journal](http://link.springer.com/journal/586)","snPcode":"586","submissionUrl":"https://submission.springernature.com/new-submission/586/3","title":"European Spine Journal","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Hybrid","inReviewEnabled":true,"inReviewRevisionsEnabled":false},"keywords":"Spinal arachnoiditis ossificans, idiopathic intradural ossification, reversible myelopathy, disrupted spinal CSF dynamics, idiopathic progressive myelopathy","lastPublishedDoi":"10.21203/rs.3.rs-8824283/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8824283/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eBackground Arachnoiditis ossificans (AO) is a rare neurological disorder marked by heterotopic ossification in the spinal arachnoid membrane, causing stenosis and neural compression. Spontaneous AO, lacking triggers like trauma or infection, is exceptionally rare (\u0026lt;\u0026thinsp;10 global cases), posing diagnostic challenges.\u003c/p\u003e \u003cp\u003eCase Presentation A 36-year-old female presented with two years of progressive thoracic pain, lower limb weakness, and autonomic dysfunction, culminating in suspected acute cauda equina syndrome or rapidly progressive myelopathy. Initial MRI suggested arachnoid cysts, but contrast-enhanced imaging with CISS sequences defined multiloculated intradural cysts (T4\u0026ndash;S2/3), with maximal prominence between T5-T7. Rapid neurological deterioration prompted emergency surgical decompression. Thoracic/lumbar laminectomies exposed calcified arachnoid plaques adherent to the dura; microsurgical debridement relieved neural compression and restored cerebrospinal fluid (CSF) flow. Histopathology confirmed benign ossified arachnoid cyst with lamellar bone. Postoperatively, interestingly, she achieved full neurological recovery, including migraine and bowel dysfunction resolution, highlighting the broad neural impact of AO, sustained at six months follow-up despite demonstration of residual cystic fluid on postoperative imaging.\u003c/p\u003e \u003cp\u003eConclusion This case highlights the diagnostic complexity of spontaneous AO: the limited specificity of MRI risks delays, while CT remains gold-standard for ossification detection. Early surgical decompression is critical, aligning with literature showing 60% neurological improvement. Conservative therapies offer limited benefit in advanced disease. Multidisciplinary care and lifelong surveillance are vital, given the progressive nature of AO and recurrence risks. Spontaneous AO should be suspected in unexplained myelopathy with systemic neurological decline, emphasizing timely intervention to mitigate irreversible damage.\u003c/p\u003e","manuscriptTitle":"Spontaneous Spinal Arachnoiditis Ossificans: A Case Report and Review of Diagnostic Pitfalls and Surgical Management","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-03-13 15:12:08","doi":"10.21203/rs.3.rs-8824283/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-05-15T18:28:40+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-04-14T08:37:56+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-04-11T02:28:00+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"328788753921447228455037472443918203692","date":"2026-03-18T15:07:05+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"68002921797491478225683205014631304912","date":"2026-03-11T23:54:19+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"225893204603463764866435814636668078504","date":"2026-03-11T21:37:15+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-03-09T21:34:34+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-02-11T04:16:07+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-02-11T04:15:27+00:00","index":"","fulltext":""},{"type":"submitted","content":"European Spine Journal","date":"2026-02-08T21:33:13+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"european-spine-journal","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"esjo","sideBox":"Learn more about [European Spine Journal](http://link.springer.com/journal/586)","snPcode":"586","submissionUrl":"https://submission.springernature.com/new-submission/586/3","title":"European Spine Journal","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Hybrid","inReviewEnabled":true,"inReviewRevisionsEnabled":false}}],"origin":"","ownerIdentity":"6c9aae1c-f8da-4a14-9a13-8702eedb5d01","owner":[],"postedDate":"March 13th, 2026","published":true,"recentEditorialEvents":[{"type":"decision","content":"Revision requested","date":"2026-05-15T18:28:40+00:00","index":"","fulltext":""}],"rejectedJournal":[],"revision":"","amendment":"","status":"in-revision","subjectAreas":[],"tags":[],"updatedAt":"2026-05-15T18:39:37+00:00","versionOfRecord":[],"versionCreatedAt":"2026-03-13 15:12:08","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8824283","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8824283","identity":"rs-8824283","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}