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Arachnoiditis
Arachnoiditis
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Arachnoiditis
Myelogram showing arachnoiditis in the lumbar spine
Illustration of Arachnoiditis
SpecialtyNeurosurgery

Arachnoiditis is an inflammatory condition of the arachnoid mater or 'arachnoid', one of the membranes known as meninges that surround and protect the central nervous system. The outermost layer of the meninges is the dura mater (Latin for hard) and adheres to inner surface of the skull and vertebrae.[1] The arachnoid is under or "deep" to the dura and is a thin membrane that adheres directly to the surface of the brain and spinal cord.[1]

Signs and symptoms

[edit]

Arachnoid inflammation can lead to many painful and debilitating symptoms which can vary greatly in each case, and not all people experience all symptoms.[2][3][4] Chronic pain is common, including neuralgia, while numbness and tingling of the extremities can occur with spinal cord involvement, and bowel, bladder, and sexual functioning can be affected if the lower part of the spinal cord is involved.[2][3][4] While arachnoiditis has no consistent pattern of symptoms, it frequently affects the nerves that supply the legs and lower back.[2][3][4] Many patients experience difficulty sitting for long (or even short) periods of time due to discomfort or pain.[4][2]

Etiology

[edit]

Arachnoiditis has been described as having many different etiologies. As an infectious source, tuberculosis,[5][6] syphilis,[5][6] candida,[6] mycosis,[6] and HIV.[2] As a mechanical source, spinal and cranial surgery,[7] trauma,[8] and disc herniation.[8] Prior disease including ankylosing spondylitis,[5][9] autoimmune vasculitis,[2] and Guillain–Barré syndrome[2] have been known to cause arachnoiditis. Chemical causes include morphine,[10] myelograms with oil-based radiographic contrast agents,[10] phenolic solutions,[11] chlorhexidine,[12] epidural injection of steroids and antibiotics,[5] blood in subarachnoid hemorrhage,[13] epidural blood patches and anesthetics.[14][15]

Oftentimes, the precise cause of arachnoiditis is not known due to the variable latency from cause to symptom onset. With growing incidence of spine surgery, a common cause of arachnoiditis is lumbar spine procedures.[16]

Pathogenesis

[edit]

The above etiologies can cause inflammation of the arachnoid, leading to arachnoiditis. This inflammation is enough to cause pain and even potentially neurological deficits - symptoms caused by nerves not communicating properly with the body's mechanisms for sensation and movement.[3][17] The inflammation can lead to the formation of scar tissue and adhesion that can make the spinal nerves "stick" together, a condition where such tissue develops in and between the leptomeninges - between dura and arachnoid or pia and arachnoid.[17] This condition can be very painful, especially when progressing to adhesive arachnoiditis. Adhesive arachnoiditis occurs when inflammation leads to recruitment of cells to the area and fibrous exudate, and ensuing deposition of collagen forms bands that could cause ischemia or even atrophy of the spinal cord or nerve roots.[17][18] Chronic inflammation could lead to arachnoiditis ossificans, in which the inflamed arachnoid becomes ossified, or turns to bone, and is thought to be a late-stage complication of the adhesive form of arachnoiditis.[19] More serious complications can occur, including spinal cord swelling, myelomalacia, cauda equina syndrome, and hydrocephalus.[18][20]

Diagnosis

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Diagnosis is based on a combination of clinical findings, patient examination, and imaging evaluation.[21] The most common affected area is the lumbar region of the back, and includes the classic symptomatic triad of back pain, neurological deficits, and MRI with notable adhesions.[22] For the ossificans form of the condition, unenhanced CT may better show the presence and extent of arachnoid ossifications, and is complementary to MRI, as MRI can be less specific and findings can be confused with regions of calcification or hemosiderin.[23][24]

Treatment

[edit]

Arachnoiditis can be difficult to treat and treatment is generally limited to alleviation of pain and other symptoms.[25] While arachnoiditis may not yet be curable with the potential to be life-altering, management including medication, physical therapy, and if appropriate, psychotherapy, can help patients cope with the difficulties it presents.[25]

Medications that have been used to treat arachnoiditis include nonsteroidal anti-inflammatory drugs,[26] pulse steroid therapy with methylprednisolone,[26][2][27] and multi-modal pain regimens.[2] Surgical intervention generally has a poor outcome and may only provide temporary relief,[25] but some cases of surgical success have been reported.[28] Epidural steroid injections to treat sciatic pain have been linked as a cause of the disease by the U.S. Food and Drug Administration as well as in other research, and are therefore discouraged as a treatment for arachnoiditis as they will most likely worsen the condition.[29][30][31]

Prognosis

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Arachnoiditis is a chronic disorder with no known cure,[25] and prognosis may be difficult to determine because of an unclear correlation between the beginning of the disease or source and the appearance of symptoms. For many, arachnoiditis is a disabling disease that causes chronic pain and neurological deficits,[23] and may also lead to other spinal cord conditions, such as syringomyelia.[32][33]

References

[edit]

Further reading

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[edit]
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Arachnoiditis

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from Grokipedia
Arachnoiditis is a rare, chronic inflammatory disorder of the , one of the three protective membranes () surrounding the and , which can lead to debilitating , neurological dysfunction, and potential . This condition arises when causes the arachnoid to become irritated and scarred, often resulting in adhesions that clump roots together and disrupt flow. Primarily affecting the lumbosacral spine, arachnoiditis is progressive and incurable, with symptoms varying by severity and location but commonly including severe stinging or burning , numbness, tingling, and . The most common causes of arachnoiditis include complications from spinal surgeries or procedures, such as or epidural injections, accounting for up to 90% of cases in some reports; direct spinal trauma; infections like or ; and exposure to chemical irritants such as oil-based contrast dyes. Less frequently, it may stem from chronic compression of spinal nerves or autoimmune processes, though idiopathic cases occur. In its adhesive form—the most severe variant—fibrous scar tissue binds nerve roots, resembling "the bark of a " on , which exacerbates neurological impairment and can involve the brain in rare instances, leading to . Symptoms typically manifest as chronic lower radiating to the legs, with additional effects on , bowel, and ; in cervical or thoracic involvement, patients may experience arm or leg weakness, sensory loss, and even or . relies on a combination of clinical history, physical examination, and advanced imaging, particularly contrast-enhanced MRI to detect clumping, loculated cysts, or empty theca syndrome, supplemented by CT if needed. (EMG) or lumbar may aid in ruling out other conditions but are not definitive. Treatment focuses on symptom management rather than reversal, incorporating multidisciplinary approaches such as to maintain mobility, pharmacological interventions including nonsteroidal anti-inflammatory drugs (NSAIDs), gabapentinoids, or antidepressants for , and psychological support to address the profound impact on . stimulation or intrathecal pumps may provide relief in cases, while early inflammatory stages might respond to corticosteroids like intravenous ; however, surgery is generally discouraged as it can worsen adhesions, and opiates are avoided due to dependency risks. remains guarded, with many patients facing permanent , underscoring the importance of prevention through careful spinal interventions.

Background

Definition and Anatomy

Arachnoiditis is defined as a chronic inflammatory condition affecting the , one of the three protective that envelop the and . This inflammation primarily targets the arachnoid layer in the spinal region, leading to progressive scarring and adhesion formation within the subarachnoid space. The occupies a central position between the tough, outermost and the delicate, innermost , forming a web-like, avascular barrier that separates the subdural and subarachnoid spaces. It plays a crucial role in enclosing the subarachnoid space, where (CSF) circulates to provide mechanical cushioning, buoyancy, and nutrient transport to the . The arachnoid's vascular interface occurs primarily through arachnoid granulations—small, finger-like projections that extend into the —enabling the bulk absorption of CSF into the bloodstream to maintain balance. While arachnoiditis can theoretically involve the cranial , it predominantly manifests in the , with lumbar and thoracic segments affected most frequently and lumbosacral involvement following closely as a common site of disease progression. Cranial cases are exceedingly rare compared to spinal presentations. The nomenclature "arachnoiditis" originates from the Greek term "," denoting , a reference to the filmy, web-like adhesions that characterize the inflamed upon postmortem histological examination. These adhesions arise from sustained , which briefly disrupts the normal architecture of the arachnoid without altering its fundamental anatomical role.

Epidemiology

Arachnoiditis is a rare , with the true prevalence and incidence difficult to ascertain due to underdiagnosis, nonspecific symptoms, and historical underreporting. The exact annual incidence is unknown due to underdiagnosis and diagnostic challenges, though it is considered rare. Reports indicate approximately 25,000 new cases annually, primarily in regions with higher rates of spinal procedures such as North and , , and , though comprehensive registries like those from the National Institute of Neurological Disorders and Stroke (NINDS) do not provide updated 2025 prevalence data beyond acknowledging its rarity. As of 2025, the condition has seen increased recognition, potentially due to rising spinal procedures and advanced imaging, with some recent studies reporting a higher female predominance (65-81%) in documented cases. Demographically, arachnoiditis predominantly affects adults, with a mean age at diagnosis around 44 to 61 years, most commonly in the 40- to 60-year-old range. Demographic studies show varying gender distribution, with some cohorts reporting approximately 45-55% . The condition is underreported across all demographics due to reliance on advanced imaging like MRI for confirmation, which may not be routinely performed in ambiguous presentations. Cases occur worldwide but are more frequently documented in , , , and , where access to spinal procedures is greater. Temporal trends show increased recognition since the , coinciding with the rise in epidural steroid injections and spinal surgeries for management, contributing to higher iatrogenic incidence rates post-procedure—estimated at 1-2% in some surgical cohorts. Historically, a peak occurred in the to from using oil-based contrasts like Pantopaque, which was associated with a notable number of cases of chronic inflammation before water-soluble alternatives were adopted. Associated conditions include prior spinal surgeries (in over 50% of reported cases) and historical , with NINDS noting ongoing challenges in tracking these trends amid evolving procedural practices.

Causes

Etiology

Arachnoiditis arises from a variety of initiating factors that irritate or inflame the , leading to its pathological changes. These etiological agents are broadly classified into mechanical, chemical, infectious, and other categories, with historical shifts reflecting changes in medical practices. Mechanical causes involve direct physical disruption or irritation of the arachnoid membrane. , such as or other procedures involving meningeal manipulation, is a prominent trigger, accounting for approximately 15% of cases in systematic reviews. Trauma, including spinal fractures or injuries, contributes to about 23% of instances, often through formation or direct tissue damage. Spinal taps, or punctures, can also induce irritation via needle trauma, particularly if multiple procedures are performed. Disk herniation represents another mechanical etiology, where extruded material contacts the arachnoid. Chemical causes primarily stem from the introduction of irritant substances into the subarachnoid space. Historically, oil-based contrast dyes like Pantopaque (iophendylate) used in were a leading culprit, responsible for many cases in the mid-20th century until their decline after the with the adoption of safer water-soluble agents. More recently, epidural steroid injections, local anesthetics, and other intrathecal agents have emerged as significant triggers, with case reports indicating a rise in such incidents since the amid increased procedural volumes. Accidental injection of neurotoxic preservatives or blood from also falls into this category. Infectious etiologies involve pathogens that invade the , prompting an inflammatory response. Bacterial infections, such as those from or , are common, comprising over 17% of documented cases and often linked to prior episodes. Viral agents like and varicella-zoster virus, as well as fungal pathogens including and Candida, contribute similarly through meningeal spread. Parasitic infections, such as , represent rarer infectious triggers. Other causes include subarachnoid hemorrhage from non-infectious sources, which irritates the arachnoid via blood products and accounts for about 13% of cases. Tumors or space-occupying lesions compressing the arachnoid can initiate the condition mechanically or through secondary effects. Idiopathic arachnoiditis, where no clear trigger is identified, is uncommon, occurring in less than 10% of cases. The etiological landscape has evolved: contrast dye-related incidents decreased post-1980s, while mechanical and injection-related causes have become more prevalent with advances in spinal interventions.

Risk Factors

Arachnoiditis susceptibility is influenced by both non-modifiable and modifiable risk factors, with prior spinal interventions representing a primary non-modifiable contributor. A history of spinal surgery, such as or , significantly elevates the risk, with postoperative adhesive arachnoiditis occurring in 6% to 16% of surgery cases due to mechanical irritation or chemical exposure during the procedure. Trauma to the spine, including , also predisposes individuals without altering the underlying event. Genetic predispositions, such as variations in or fibrinolytic pathways, have been suggested but remain uncertain based on limited evidence from recent reviews. Modifiable factors primarily involve iatrogenic exposures that can be mitigated through procedural precautions. Repeated epidural injections for management increase the risk of chemical arachnoiditis, particularly when particulate steroids are used, though the incidence remains rare at approximately 1 in 50,000 injections. Exposure to certain spinal anesthetics or contrast agents during can trigger inflammatory responses, emphasizing the importance of selecting non-neurotoxic alternatives. Untreated spinal infections, such as those from bacterial or , further heighten vulnerability if not addressed promptly with antibiotics or antivirals. Comorbid conditions that impair immune function or increase procedural complications contribute to overall susceptibility. Autoimmune diseases like promote chronic inflammation that may exacerbate arachnoid responses to triggers.

Pathophysiology

Pathogenesis

Arachnoiditis begins with an initial inflammatory response in the and subarachnoid space, triggered by various insults that irritate the delicate membrane. This phase involves the release of pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α), which promote arachnoid irritation, , and hyperemia of nerve roots. These cytokines contribute to the breakdown of the blood-cerebrospinal fluid (CSF) barrier, allowing inflammatory mediators and potentially harmful substances to enter the subarachnoid space, exacerbating local tissue damage and impairing nutrient delivery due to the arachnoid's avascular nature. The inflammatory process progresses to adhesion and formation, where fibrinous exudates organize into bands that bind nerve roots together, leading to clumping and encapsulation. deposition by activated fibroblasts follows, resulting in that contracts and distorts the subarachnoid space, often manifesting as an "empty " on due to the apparent absence of free-floating nerve roots. This disrupts normal CSF circulation, creating loculations and further promoting chronic . The disease typically advances through distinct stages of progression. In the acute stage, nerve root swelling and predominate, driven by initial vascular leakage and inflammatory cell infiltration. The subacute stage features the development of adhesions and early as fibrinous material matures into collagenous scars. In chronic cases, severe progression may involve , with metaplastic formation within the arachnoid, leading to rigid encasement of neural structures. Neurogenic mechanisms arise from these structural changes, including nerve root ischemia caused by compressive adhesions that restrict vascular supply, resulting in hypoxia and subsequent demyelination of affected axons. Obstruction of CSF flow by fibrotic bands compounds this by causing gradients and stasis, which impair waste clearance and nutrient transport to neural tissues. At the molecular level, involves activation within the arachnoid, which drives excessive (ECM) remodeling through upregulated synthesis of collagens and other fibrous proteins. Recent single-nucleus studies highlight how fibroblasts differentiate into pro-fibrotic subtypes during the phase, perpetuating ECM deposition and tissue stiffening, while microglial activation amplifies the inflammatory milieu.

Classification

Arachnoiditis is primarily classified by its anatomical location, with spinal involvement being the most common form, predominantly affecting the lumbosacral region followed by the cervical spine, while cerebral cases are rare and often linked to prior infectious . Mixed presentations involving both spinal and cranial regions can occur in advanced or multifocal disease. Morphologically, arachnoiditis manifests in distinct subtypes based on the pattern of inflammation and scarring: adhesive arachnoiditis, characterized by clumping and adherence of nerve roots; cystic arachnoiditis, featuring localized arachnoid cysts or fluid collections within the subarachnoid space; and arachnoiditis ossificans, a rare variant involving or of adhesions, typically as an end-stage progression. Severity is assessed radiologically using systems such as the Delamarter classification, which includes (central clumping of nerve roots), Group 2 (peripheral adherence to the , often with the "empty thecal sac" sign), and Group 3 (mass-like replacement of the by or ); this provides high diagnostic accuracy via MRI, though recent reviews note challenges in consensus and for staging. Historically, early descriptions from the emphasized gross pathological findings like adhesions and without standardized staging, contrasting with modern MRI-based systems. Recent updates from 2025 case series have incorporated the optochiasmatic variant into cranial classifications, highlighting its role in tuberculous meningitis-related arachnoiditis with basal meningeal enhancement and visual pathway involvement.

Clinical Presentation

Signs and Symptoms

Arachnoiditis primarily manifests as in the lower back that often radiates to the legs, presenting as with a burning or stinging quality, exacerbated by movement or activity. This pain is frequently neuropathic, arising from and adhesions that compress roots in the . Sensory disturbances are common, including numbness, tingling (paresthesias), or in affected dermatomes, with —pain from non-painful stimuli—emerging in advanced stages due to ongoing irritation. Motor symptoms may involve , spasms, or , leading to gait imbalances; in severe cases, can occur, though it is rare. Autonomic dysfunction often includes bladder and bowel issues, such as urgency, , or incontinence (reported in approximately 23% of cases), alongside sexual impairment from involvement. Symptoms typically progress variably over years, potentially stabilizing with persistent or worsening with further adhesions; in cranial arachnoiditis, headaches are a prominent feature. These manifestations significantly impair , with patient surveys indicating high rates of chronic and reduced functionality among affected individuals.

Complications

Arachnoiditis, particularly in its advanced stages, can give rise to several neurological complications due to chronic inflammation and adhesions disrupting (CSF) dynamics and neural function. One prominent is , where formation develops within the as a result of obstructed CSF flow, leading to progressive and further neurological deficits. This complication has been documented in numerous cases, with 771 instances reported across 77 studies involving 1,679 patients with diseases of the leptomeninges, including arachnoiditis. may also occur, especially in cases involving cranial arachnoiditis, where adhesions block CSF pathways, resulting in increased and associated symptoms. Systemic effects of arachnoiditis extend beyond the , frequently involving psychological and pharmacological dependencies. Chronic use for carries a high of dependency, as patients often require escalating doses to control intractable symptoms, mirroring broader patterns in syndromes where long-term therapy leads to tolerance and . Additionally, depression and anxiety are prevalent, affecting approximately 40% of individuals with conditions like arachnoiditis, driven by the unrelenting nature of symptoms and reduced ; long-term studies have noted severe psychological impacts, including in up to 4% of cases. Rare complications include arachnoiditis ossificans, a condition characterized by of the arachnoid membrane, which can cause and progressive neurological compression through mechanical narrowing of the . This entity, reported in fewer than 100 cases historically, typically follows prior trauma or and may necessitate decompressive . Immobility from advanced also heightens the risk of secondary infections, such as urinary tract infections or ulcers, due to reduced mobility and compromised immune responses in chronic illness. Early intervention, particularly in acute or subacute phases—such as prompt treatment of underlying infections or administration of high-dose corticosteroids—can mitigate progression and reduce the incidence of these complications by interrupting formation and . For instance, addressing epidural infections surgically in the initial stages prevents arachnoiditis development altogether in some scenarios, while timely therapy has shown potential to limit formation and other sequelae.

Diagnosis

Diagnostic Methods

Diagnosis of arachnoiditis relies primarily on imaging techniques, with magnetic resonance imaging (MRI) serving as the gold standard for visualization of characteristic features such as nerve root clumping and the empty thecal sac sign. On T1- and T2-weighted sequences, clumped nerve roots appear distorted and aggregated, often resembling a "grape cluster," while the empty thecal sac indicates adherence of roots to the thecal margins, displacing cerebrospinal fluid (CSF). These findings are most evident in the lumbar spine, where the condition predominantly affects the cauda equina. In cases where MRI is contraindicated, such as in patients with pacemakers or metallic implants, computed tomography (CT) myelography provides an alternative by injecting contrast into the to highlight adhesions and root abnormalities. This modality offers detailed assessment of the subarachnoid space but involves invasive and . Imaging findings vary by classification: in the mild adhesive type, peripheral clumping of nerve roots is observed centrally within the , whereas the cystic variant presents with intrathecal masses or loculated CSF collections that may cause cord compression. Laboratory evaluation includes CSF analysis via to identify potential infectious or inflammatory etiologies, often revealing elevated protein levels and mild pleocytosis even in non-infectious cases. Blood tests for inflammatory markers, such as (ESR) and (CRP), help rule out systemic inflammation, though elevations may occur in active disease. Electromyography (EMG) aids clinical correlation by confirming through detection of patterns in affected muscle groups, supporting the when imaging shows root involvement. Recent applications of diffusion tensor imaging (DTI), an advanced MRI method, enable early detection of microstructural changes in the not apparent on standard sequences, as shown in 2024 studies on arachnoiditis ossificans.

Differential Diagnosis

Arachnoiditis must be differentiated from other spinal and neurological conditions that present with similar symptoms such as , , and sensory disturbances. Key spinal disorders include herniated disc and . Herniated disc typically causes focal, acute due to mechanical compression of a specific , whereas arachnoiditis produces more diffuse, from widespread adhesions and . is characterized by bony narrowing of the leading to compressive symptoms, distinguished on MRI by ligamentum flavum hypertrophy or changes rather than the adhesions and clumping seen in arachnoiditis. Inflammatory conditions like (MS) and Guillain-Barré syndrome also enter the differential. MS often features relapsing-remitting symptoms with multifocal involvement, including in (CSF) analysis, which are typically absent in arachnoiditis. Guillain-Barré syndrome presents with acute ascending weakness and areflexia following an infection, showing elevated CSF protein without pleocytosis, in contrast to the chronic, progressive course of arachnoiditis. Infectious etiologies, such as tuberculous spondylitis and , require exclusion through targeted testing. Tuberculous spondylitis may mimic arachnoiditis with spinal inflammation but is identified by positive tuberculin skin tests, interferon-gamma release assays, or cultures from spinal tissue, often accompanied by systemic symptoms like fever and . , caused by , presents with radiculoneuritis and is confirmed via serologic testing (e.g., followed by ), distinguishing it from the noninfectious adhesions in arachnoiditis. Neoplastic processes, including and spinal , can imitate arachnoiditis through or meningeal involvement. appears as a well-defined, dural-based with homogeneous contrast enhancement on MRI, unlike the irregular, non-enhancing clumping in arachnoiditis; may be needed if imaging is equivocal. Metastases often show nodular leptomeningeal enhancement and systemic malignancy history, differing from the diffuse inflammatory pattern without discrete in arachnoiditis. Distinguishing arachnoiditis relies on a history of predisposing factors like prior spinal procedures or injections, which strongly favor it over mimics. Recent literature emphasizes multimodal assessment, integrating clinical , advanced imaging such as MRI (reported sensitivity of 92% for diagnosing adhesive arachnoiditis), and laboratory tests for definitive differentiation.

Management

Treatment Options

Treatment of arachnoiditis focuses on symptom relief and supportive care, as no cure exists. Pharmacological interventions primarily target neuropathic pain and inflammation. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, are commonly prescribed to alleviate inflammation and mild pain. In early inflammatory stages, high-dose corticosteroids such as intravenous methylprednisolone may be used to reduce inflammation. Gabapentinoids, including pregabalin and gabapentin, are effective for managing chronic neuropathic pain associated with the condition. Short-term use of opioids may be considered for severe acute pain flares, while tricyclic antidepressants like amitriptyline provide additional relief for persistent neuropathic symptoms. Non-pharmacological strategies emphasize improving function and reducing without medication. , particularly aquatic exercises in warm water, helps maintain mobility, strengthen supporting muscles, and minimize spinal stress. (TENS) delivers low-level electrical currents to disrupt pain signals and offer temporary relief. Lifestyle modifications, including through balanced diet and gentle activity, reduce mechanical load on the spine and support overall symptom control. Interventional procedures provide targeted for refractory cases. Spinal cord stimulation involves implanting a device to deliver electrical impulses to the , providing significant pain relief and functional improvement in many patients with chronic arachnoiditis-related pain. Intrathecal pumps can administer analgesics directly into the spinal fluid for localized effect, though their use requires careful monitoring to avoid exacerbating . Repeat spinal injections are generally avoided due to the risk of worsening arachnoid adhesions. Surgical interventions, such as adhesiolysis to release adhesions, are rarely performed owing to high complication rates and limited , with success in only about 60% of selected cases; they are typically reserved for focal compressive lesions causing severe neurological deficits. Emerging approaches post-2020 include multidisciplinary clinics that integrate pharmacological, physical, and psychological therapies to optimize outcomes, alongside ongoing into and regenerative strategies.

Prognosis

Arachnoiditis is a chronic inflammatory condition of the that typically follows an unpredictable course, ranging from stable with fluctuating symptoms to progressive in advanced stages. In a long-term study of 50 patients followed for 10 to 21 years, symptoms such as and neurological impairment remained largely stable after , without natural progression of the disease itself, though severity fluctuated over time. The condition is incurable, but early supportive can help stabilize function and prevent worsening, particularly if the underlying cause is addressed promptly. Factors influencing include the extent of spinal involvement, the type of arachnoiditis (e.g., forms tend to cause more severe adhesions and poorer outcomes), and the timeliness of intervention. and thoracic regions are most commonly affected, leading to greater motor and sensory deficits when multiple levels are involved. Surgical interventions often yield short-term relief but carry a risk of exacerbating adhesions, resulting in a poor long-term . Early through and conservative care may preserve mobility in a subset of patients, though specific functional maintenance rates vary widely due to limited large-scale data. Patients with arachnoiditis generally have a normal lifespan, though one reported an average reduction of 12 years, attributed partly to comorbidities and treatment complications rather than the disease directly. develops in many cases, with permanent motor weakness, , and autonomic dysfunction; late-onset urinary symptoms occurred in 23% of followed patients. The majority in long-term observations were unable to return to full-time employment, reflecting significant functional limitations. Quality of life is profoundly impacted, with leading to reliance on narcotics, , and psychological distress, including a noted risk of in severe cases. Advanced disease correlates with high levels of and reduced daily functioning. Recent 2024 analyses emphasize multidisciplinary approaches, including techniques like spinal cord stimulation, which can provide relief in select refractory cases, improving overall outcomes.

References

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