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Myelitis

Myelitis is inflammation of the spinal cord, a critical component of the central nervous system that transmits signals between the brain and the body, potentially disrupting motor, sensory, and autonomic functions. The annual incidence of transverse myelitis, one of the most common forms, is estimated at 1 to 8 new cases per million people worldwide.^[1]^[2] This condition, a form of myelopathy, arises from diverse etiologies and can manifest acutely or chronically, often damaging the myelin sheath and underlying nerve fibers, leading to symptoms such as weakness, sensory loss, and bladder dysfunction.^[3] Myelitis encompasses several subtypes, with transverse myelitis being one of the most common, characterized by inflammation spanning a segment of the spinal cord across multiple levels, often bilaterally.^[4] Other notable forms include acute flaccid myelitis (AFM), which primarily affects the gray matter and causes sudden limb weakness, particularly in children, and is frequently linked to viral infections; longitudinally extensive transverse myelitis, seen in conditions like neuromyelitis optica spectrum disorder (NMOSD); and infectious or radiation-induced variants.^[5]^[2] Idiopathic cases account for 15-30% of instances, while secondary myelitis occurs in the context of multiple sclerosis, acute disseminated encephalomyelitis (ADEM), or systemic autoimmune diseases like systemic lupus erythematosus (SLE).^[2] Common causes include infectious agents such as viruses (e.g., enteroviruses, herpesviruses), bacteria (e.g., in neurosyphilis), or parasites, as well as autoimmune mechanisms where the immune system mistakenly attacks spinal cord tissues.^[3]^[2] Symptoms typically develop rapidly over hours to days and may involve back or neck pain, bilateral limb weakness or paralysis below the lesion level, paresthesias, loss of bowel or bladder control, and in severe cases, respiratory compromise if the cervical cord is affected.^[6] Diagnosis relies on clinical presentation, MRI showing cord lesions, cerebrospinal fluid analysis for inflammation markers, and exclusion of compressive causes.^[2] Treatment focuses on addressing the underlying cause, reducing inflammation, and managing symptoms, with high-dose intravenous corticosteroids (e.g., methylprednisolone 1 g/day for 3-5 days) as first-line therapy to limit damage.^[4] For refractory cases, plasma exchange or intravenous immunoglobulin may be employed, alongside immunosuppressive agents for autoimmune-related myelitis; supportive care includes pain management, physical therapy, and rehabilitation to improve outcomes.^[2] Prognosis varies, with partial recovery common in mild cases but permanent disability possible in up to one-third of patients, emphasizing early intervention.^[7]

Overview

Definition

Myelitis is an inflammatory condition of the spinal cord that can target the white matter, gray matter, or both, damaging the myelin sheaths insulating nerve fibers where involved and may extend to axons and oligodendrocytes, resulting in demyelination, axonal injury, and perivascular infiltration.^[8] This inflammation disrupts the transmission of neural signals between the brain and the body, potentially leading to motor, sensory, and autonomic dysfunction depending on the affected spinal cord segment.^[4] The involvement can be focal, affecting a specific segment, or diffuse, spanning multiple levels of the cord.^[8] Myelitis is distinct from related conditions such as radiculitis, which involves inflammation of the spinal nerve roots rather than the cord itself, and meningomyelitis, which encompasses both spinal cord inflammation and involvement of the surrounding meninges.^[8] These differentiations are crucial for accurate diagnosis, as radiculitis typically presents with root-level pain and weakness, while meningomyelitis may include meningeal signs like nuchal rigidity.^[8] While transverse myelitis represents the prototypical acute form of this condition, characterized by bilateral inflammation across a spinal cord segment, the term myelitis serves as a broader descriptor encompassing various inflammatory etiologies, including infectious, autoimmune, and idiopathic processes.^[8] This broader scope highlights myelitis as a heterogeneous group of disorders rather than a singular entity.^[8] The first medical descriptions of acute myelitis appeared in the literature in 1882, initially attributed to vascular lesions or acute inflammatory events in the spinal cord, often in infectious contexts.^[7]

Epidemiology

Myelitis is a rare neurological condition, with the global incidence of acute myelitis estimated at 1 to 8 cases per million population per year. Transverse myelitis, a specific subtype, has a reported incidence of 1 to 4 cases per million annually, though rates can vary based on diagnostic criteria and regional factors. In endemic regions for human T-lymphotropic virus type 1 (HTLV-1), such as Japan and the Caribbean, seroprevalence reaches 1-5% in adults, with HTLV-1-associated myelopathy/tropical spastic paraparesis developing in approximately 0.25% of carriers in Japan and up to 2-4% in Caribbean populations. These elevated rates highlight the role of infectious agents in amplifying myelitis burden in specific locales.^[1]^[9] Demographic patterns show a bimodal age distribution, with peaks among children and young adults (10-19 years) and middle-aged individuals (30-39 years), though cases occur across all ages. Autoimmune forms of myelitis exhibit a slight female predominance (approximately 1.5:1 female-to-male ratio), potentially linked to hormonal and immunological factors. Incidence is notably higher in immunocompromised populations, such as those with HIV, where myelopathies including myelitis affect 5-10% of patients with advanced disease, correlating with immune suppression levels. No strong racial or familial predispositions are evident in idiopathic cases.^[1]^[10]^[11] Geographic variations reflect etiological differences, with infectious myelitis more prevalent in developing countries due to higher exposure to viral and bacterial pathogens, such as in Latin America and French Guiana where rates reach 1-6 cases per million. In contrast, idiopathic and autoimmune subtypes predominate in developed nations, comprising up to 30-40% of cases in regions like North America and Europe. Overall incidence remains stable, but recognition of autoimmune subtypes has increased since 2010, driven by improved diagnostics like aquaporin-4 antibody testing, which identifies neuromyelitis optica spectrum disorders in up to 70-80% of suspected cases.^[12]^[13]^[14]

Types

Transverse myelitis

Transverse myelitis (TM) is an inflammatory disorder of the spinal cord characterized by acute or subacute development of motor, sensory, and autonomic dysfunction referable to the spinal cord, with bilateral signs (although not necessarily symmetric), a clearly defined sensory level, and progression to nadir over 4 hours to 21 days, accompanied by evidence of inflammation.^[15] It involves rapid-onset neurological deficits due to immune-mediated damage to the myelin and potentially axons in the spinal cord, distinguishing it from compressive or vascular myelopathies.^[8] Subtypes of TM are classified based on lesion extent and etiology. Idiopathic TM accounts for 15-30% of cases, occurring without an identifiable underlying cause after comprehensive evaluation, and is presumed to result from an aberrant immune response targeting the spinal cord.^[7] Partial TM features shorter lesions, typically involving one to two vertebral segments and often asymmetric involvement, and is commonly associated with multiple sclerosis (MS) as an initial manifestation.^[7] In contrast, longitudinally extensive TM (LETM) involves lesions spanning three or more vertebral segments, representing a hallmark of neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), with symmetric clinical features and a higher risk of recurrence in antibody-positive cases.^[16]^[7] Clinically, TM is marked by rapid progression to nadir over hours to days, with bilateral weakness, sensory loss, and autonomic dysfunction below a distinct sensory level, most frequently affecting the thoracic cord.^[8] Diagnosis requires exclusion of compressive, vascular, or neoplastic causes through imaging and clinical assessment. The 2002 Transverse Myelitis Consortium Working Group criteria for acute TM include: sensory, motor, or autonomic dysfunction attributable to the spinal cord; bilateral signs (not necessarily symmetric); a clearly defined sensory level; progression to nadir within 4 hours to 21 days; and evidence of inflammation on cerebrospinal fluid analysis (pleocytosis or elevated IgG index) or magnetic resonance imaging (gadolinium enhancement or T2 hyperintensity).^[15] For idiopathic cases, there must be no history of prior demyelinating events.^[15] MRI typically reveals intramedullary T2 hyperintense lesions, confirming the transverse extent.^[8]

Acute flaccid myelitis

Acute flaccid myelitis (AFM) is a rare but serious subtype of myelitis characterized by sudden onset of weakness or paralysis, primarily in the arms or legs, often in children following a respiratory or gastrointestinal viral illness. It predominantly affects the anterior horn cells in the gray matter of the spinal cord, leading to a polio-like syndrome. AFM has been associated with enteroviruses, particularly enterovirus D68, with increased cases reported since 2014. Diagnosis involves clinical features, MRI showing gray matter lesions, and cerebrospinal fluid analysis. Unlike classic TM, AFM typically spares sensory functions and has a poorer prognosis for motor recovery.^[5]

Myelitis in systemic diseases

Myelitis in multiple sclerosis (MS) typically presents with partial, asymmetric lesions confined to fewer than two vertebral segments, distinguishing it from more extensive forms seen in other conditions; these lesions are common in relapsing-remitting MS and contribute to sensorimotor deficits.^[17] Approximately 20-30% of initial demyelinating events in MS involve the spinal cord, often as a presenting feature with good recovery following acute attacks due to the inflammatory nature of the pathology. In neuromyelitis optica spectrum disorder (NMOSD), myelitis manifests as longitudinally extensive transverse myelitis (LETM) spanning three or more vertebral segments, frequently accompanied by optic neuritis, leading to severe and often relapsing neurological impairment.^[18] Aquaporin-4 immunoglobulin G (AQP4-IgG) antibodies are positive in 70-80% of NMOSD cases, targeting astrocytes and driving the inflammatory cascade that underlies these spinal cord attacks.^[19] Other systemic diseases associated with myelitis include myelin oligodendrocyte glycoprotein antibody disease (MOGAD), which is pediatric-predominant and often follows a monophasic course with optic neuritis or myelitis as key features, though relapses occur in about 50% of cases.^[20] Acute disseminated encephalomyelitis (ADEM) involves post-infectious multifocal demyelination affecting the brain and spinal cord, resulting in myelitis alongside encephalopathy in a typically monophasic episode.^[21] Sarcoidosis leads to myelitis through granulomatous inflammation in the spinal cord, causing compressive or infiltrative damage that may mimic neoplastic processes.^[22] Within systemic lupus erythematosus (SLE), myelitis occurs in approximately 1-2% of patients, often as an early manifestation with longitudinally extensive lesions and a risk of poor prognosis if untreated.^[23] Paraneoplastic myelitis is rare, affecting about 1% of cancer patients, particularly those with small-cell lung cancer and anti-Hu antibodies, where immune-mediated spinal cord inflammation precedes or accompanies tumor detection.^[24]

Symptoms

Neurological symptoms

Neurological symptoms in myelitis primarily manifest as deficits in motor and sensory function due to inflammation affecting the spinal cord, often presenting below the level of the lesion. Motor symptoms typically begin with acute weakness or flaccid paralysis, predominantly affecting the lower extremities more than the upper ones, and can progress rapidly to paraparesis or complete paraplegia in up to 50% of cases at peak deficit.^[8] This initial flaccid phase may evolve into spasticity with upper motor neuron signs such as hyperreflexia, particularly in thoracic or cervical lesions.^[8] Upper cervical involvement (C1-C5) can extend weakness to all four limbs, while thoracic lesions, which account for about 70% of cases, primarily impact the legs.^[8] Sensory symptoms include paresthesia, dysesthesia, or complete sensory loss below the level of the lesion, often at a thoracic or cervical dermatome, with common sensations of burning, tingling, numbness, or a band-like tightness across the trunk.^[4]^[6] In demyelinating forms of myelitis, Lhermitte's sign—an electric shock-like sensation radiating down the spine upon neck flexion—may occur due to irritation of posterior column fibers in the cervical cord.^[25] These sensory disturbances can also involve heightened sensitivity to touch, heat, or cold at the lesion site.^[6] Progression of symptoms is usually acute to subacute, reaching nadir within 4 hours to 21 days, with bilateral involvement typical in transverse myelitis (affecting both sides of the body below the lesion), though asymmetric patterns may occur in multiple sclerosis-related cases.^[8]^[6] Cranial nerves are generally spared in isolated myelitis, distinguishing it from encephalomyelitis, unless specific infectious etiologies like varicella-zoster virus are involved.^[26] Autonomic symptoms such as bladder dysfunction may overlap but are addressed separately.^[4]

Autonomic and systemic symptoms

Autonomic dysfunction is a prominent feature of myelitis, often manifesting as disruptions in bladder, bowel, and sexual function due to involvement of spinal pathways regulating these systems. Urinary symptoms, including retention and incontinence, affect nearly all patients during the acute phase, frequently requiring catheterization to manage retention and prevent complications.^[8] Bowel dysfunction occurs in about 50% of cases, typically presenting as constipation from slowed transit and increased sphincter tone or, less commonly, incontinence due to loss of rectal sensation.^[27] Sexual dysfunction, such as erectile difficulties in men or reduced sensation and orgasmic challenges in women, is also common, stemming from impaired neural control of pelvic organs.^[6] In lesions at or above the high thoracic level (T6), orthostatic hypotension may arise from disrupted sympathetic outflow, leading to blood pressure instability upon postural changes.^[28] Systemic symptoms accompany autonomic issues and reflect the inflammatory process or secondary effects. Back pain at the level of the lesion, often radicular in nature, is reported in many patients as an initial or concurrent feature, exacerbated by spinal cord irritation.^[29] Fever may occur particularly in infectious forms of myelitis, signaling an underlying systemic response to pathogens. Fatigue is a frequent systemic complaint, contributing to overall debility during the acute illness. In cervical myelitis affecting the upper cord (C3-C5), respiratory compromise can develop due to phrenic nerve involvement and diaphragmatic weakness, potentially requiring mechanical ventilation in severe cases.^[8] Complications from autonomic and systemic involvement often stem from immobility and organ dysfunction. Secondary urinary tract infections (UTIs) are a common complication in patients with bladder retention, necessitating vigilant monitoring and antimicrobial therapy. Deep vein thrombosis (DVT) is a risk due to prolonged immobility and venous stasis, highlighting the need for prophylactic anticoagulation in affected individuals.^[30] Temporally, autonomic symptoms typically peak within 1-2 weeks of onset, aligning with the progression to nadir deficit over 4 hours to 21 days, but they may persist longer than motor deficits in some cases, contributing to chronic disability.^[8]

Causes

Infectious causes

Infectious myelitis arises from direct invasion of the spinal cord by pathogens or through immune-mediated responses triggered by infection, often presenting as acute inflammation with potential for longitudinal extensive involvement. Pathogens reach the spinal cord via hematogenous spread, direct extension from adjacent structures, or axonal transport, leading to neuronal damage, demyelination, or vascular complications.^[31] Common agents include viruses, bacteria, parasites, and fungi, with incidence varying by geographic region, host immunity, and exposure risk; in immunocompetent individuals, viral etiologies predominate, while opportunistic infections surge in those with HIV/AIDS or immunosuppression.^[8] Viral causes encompass a range of neurotropic agents that directly infect neural tissue or provoke parainfectious inflammation. Enteroviruses, particularly enterovirus D68 (EV-D68), are implicated in pediatric acute flaccid myelitis, a poliomyelitis-like syndrome, with outbreaks linked to respiratory infections in children under 18 years, accounting for the majority of cases during peak seasons like 2014, 2016, 2018, 2022, and 2024, with cases continuing into 2025.^[32] Herpesviruses such as varicella-zoster virus (VZV), herpes simplex virus (HSV), and cytomegalovirus (CMV) cause myelitis predominantly in immunocompromised hosts, manifesting as necrotizing or hemorrhagic spinal cord lesions; VZV often follows dermatomal zoster reactivation, while CMV targets the lower thoracic cord in advanced HIV.^[33] West Nile virus, transmitted by mosquitoes, leads to neuroinvasive disease in less than 1% of infections, with 10-20% of those cases involving myelitis or acute flaccid paralysis, often with anterior horn cell involvement and epidemic peaks in summer months.^[34] Bacterial causes typically involve spirochetes or atypical pathogens that disseminate systemically before targeting the spinal cord. Lyme disease, caused by Borrelia burgdorferi transmitted via tick bites, presents with myelitis overlapping radiculoneuritis in 3-15% of neuroborreliosis cases, featuring painful sensory deficits and thoracic cord enhancement on MRI, particularly in endemic areas like the northeastern United States.^[35] Syphilis, due to Treponema pallidum, can result in tabes dorsalis-like myelopathy in tertiary neurosyphilis, with degeneration of the dorsal columns leading to ataxia, lightning pains, and Argyll Robertson pupils, though rare in the antibiotic era.^[36] Mycoplasma pneumoniae induces post-infectious myelitis, often 2-4 weeks after respiratory illness, through molecular mimicry triggering immune-mediated transverse cord inflammation, more common in children and young adults.^[37] Parasitic and fungal causes are less frequent but significant in endemic regions or immunocompromised states. Schistosomiasis, primarily from Schistosoma mansoni or S. haematobium, causes cervical or conus medullaris myelitis in travelers exposed to contaminated freshwater, with egg deposition provoking granulomatous inflammation and lower limb paresis; outbreaks have been reported in groups returning from sub-Saharan Africa.^[38] In AIDS patients, toxoplasmosis (Toxoplasma gondii) rarely involves the spinal cord, presenting as intramedullary mass lesions or longitudinally extensive myelitis with ring-enhancing foci on MRI, usually as part of disseminated disease in CD4 counts below 100 cells/μL.^[39] Parainfectious mechanisms occur without ongoing viral replication, driven by aberrant immune responses following resolved infection. Post-varicella myelitis emerges days to weeks after VZV rash, involving T-cell mediated inflammation of the spinal cord without detectable virus in cerebrospinal fluid. Similarly, Epstein-Barr virus (EBV) triggers immune-mediated myelitis, often in immunocompetent hosts, with oligoclonal bands indicating intrathecal antibody production against viral antigens.^[40]^[41]

Non-infectious causes

Non-infectious causes of myelitis encompass a range of immune-mediated, idiopathic, and non-microbial etiologies that lead to spinal cord inflammation without direct pathogen involvement. Idiopathic transverse myelitis, a subset of myelitis where no specific cause is identified despite thorough evaluation, represents approximately 15-30% of transverse myelitis cases.^[42] In many of these idiopathic instances, up to 50% of patients report a preceding respiratory or gastrointestinal illness, though no active pathogen is detectable, suggesting a possible post-infectious immune dysregulation.^[43] Autoimmune mechanisms play a central role in non-infectious myelitis, often linked to central nervous system disorders such as multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD), where spinal cord inflammation arises from aberrant immune responses against myelin or other neural components. Genetic factors, including associations with HLA-DRB1*15:01 alleles, increase susceptibility to MS-related myelitis by influencing T-cell mediated autoimmunity.^[44] Environmental modifiers, such as vitamin B12 deficiency, can also mimic myelitis through subacute combined degeneration of the spinal cord, characterized by demyelination due to impaired myelin synthesis.^[8] Rare immune triggers include post-vaccination reactions, with case reports documenting transverse myelitis following human papillomavirus (HPV) vaccination, though large-scale studies indicate no causal association and an incidence far below 1 per million doses.^[45] Drug-induced myelitis is another uncommon etiology, particularly with immune checkpoint inhibitors used in cancer therapy, where neurologic immune-related adverse events, including myelitis, occur in about 1% of patients.^[46] Other non-infectious causes involve vascular, neoplastic, and traumatic processes. Ischemic myelitis, resulting from spinal cord infarction due to arterial occlusion or embolism, accounts for roughly 5% of acute myelopathy cases presenting with inflammatory features.^[8] Neoplastic causes include intramedullary tumors such as ependymomas or astrocytomas, which can induce secondary inflammation and mimic idiopathic myelitis. Traumatic myelitis may develop post-spinal injury, where initial mechanical damage triggers a delayed inflammatory response in the cord parenchyma.^[8] Links to systemic autoimmune diseases, such as systemic lupus erythematosus, are noted but often classified separately.^[8]

Pathophysiology

Inflammatory mechanisms

In myelitis, immune activation plays a central role in the pathogenesis, particularly in autoimmune forms where T-cell infiltration into the spinal cord parenchyma initiates and amplifies inflammation. Activated T cells, including CD4+ and CD8+ subsets, cross the blood-spinal cord barrier and release proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), which recruit additional immune cells like macrophages and microglia, perpetuating a cascade of local inflammation. This process is evident in conditions like neuromyelitis optica spectrum disorder (NMOSD), where aberrant T-cell responses contribute to tissue damage.^[47]^[48]^[49] Breakdown of the blood-spinal cord barrier (BSCB) is a critical early event that facilitates immune cell entry and exacerbates inflammation in myelitis. Endothelial dysfunction, often triggered by cytokines or autoantibodies, increases vascular permeability, allowing serum proteins and inflammatory mediators to leak into the spinal cord extracellular space, leading to vasogenic edema and further immune activation. In autoimmune myelitis, this barrier disruption is mediated by matrix metalloproteinases (MMPs) secreted by activated astrocytes and microglia, which degrade tight junction proteins in the BSCB.^[8]^[50] Demyelination in myelitis arises through antibody-mediated mechanisms or complement activation, resulting in the loss of oligodendrocytes and myelin sheaths. In AQP4-IgG-positive NMOSD, aquaporin-4 autoantibodies bind to astrocytes, activating the complement system and causing primary astrocyte necrosis, which secondarily leads to oligodendrocyte injury and demyelination via inflammation and phagocytosis by macrophages, distinct from the T-cell-dominated processes in multiple sclerosis.^[18]^[17]^[51]^[52] In infectious myelitis, viral entry contributes to inflammation through direct neuronal tropism or endothelial infection leading to vasculitis. For instance, poliovirus binds to the CD155 receptor on motor neurons, facilitating viral replication and subsequent immune-mediated inflammation in the anterior horn of the spinal cord. Alternatively, viruses targeting endothelial cells, such as certain enteroviruses, induce vasculitis, which disrupts the BSCB and promotes cytokine release, bridging infection to broader inflammatory responses.^[53]^[54] The inflammatory process in myelitis unfolds in distinct stages, beginning with acute edema and necrosis within the first 24-48 hours, driven by rapid influx of fluid and immune cells causing cytotoxic swelling of the spinal cord. This phase transitions to subacute inflammation with ongoing cytokine-mediated damage, followed by a chronic stage characterized by gliosis, where reactive astrocytes and microglia form scar tissue that limits further inflammation but may impede repair. These stages highlight the temporal progression from immune activation to structural remodeling in the spinal cord.^[8]^[55]^[56]

Neurological damage processes

In myelitis, the inflammatory process primarily targets the myelin sheaths surrounding spinal cord axons, leading to demyelination that impairs saltatory conduction and neural signaling efficiency. Concurrently, direct axonal injury occurs through immune-mediated attack by monocytes, lymphocytes, and activated microglia, resulting in axonal transection and fragmentation within the lesion epicenter. Distal to the lesion, Wallerian degeneration ensues, characterized by progressive breakdown of axons and their myelin sheaths due to loss of trophic support from the neuronal cell body, often visible on follow-up MRI as cord atrophy. This degeneration contributes to irreversible functional deficits, as seen in conditions like neuromyelitis optica spectrum disorder (NMOSD) where longitudinally extensive transverse myelitis (LETM) lesions span multiple segments.^[8]^[57]^[58] Damage in myelitis extends beyond white matter tracts to encompass gray matter structures, with heterogeneous involvement depending on the etiology and lesion location. In poliomyelitis-like syndromes, such as acute flaccid myelitis (AFM), inflammation preferentially affects anterior horn cells, causing motor neuron destruction and flaccid paralysis akin to historical poliomyelitis cases. White matter pathology predominates in classic transverse myelitis, but gray matter incursion can amplify motor deficits; conversely, posterior column involvement disrupts ascending sensory pathways, leading to loss of proprioception, vibration sense, and fine touch discrimination below the lesion level. This dual compartment damage underscores the mixed inflammatory nature of myelitis, distinguishing it from pure demyelinating disorders like multiple sclerosis.^[59]^[60]^[29] Endogenous repair mechanisms in myelitis are constrained, with oligodendrocytes attempting remyelination of spared axons through differentiation from precursor cells, though efficacy remains limited due to persistent inflammation and incomplete restoration of functional myelin sheaths. Glial scar formation, driven by reactive astrocytes and microglia, further impedes regeneration by depositing inhibitory extracellular matrix components like chondroitin sulfate proteoglycans, which physically block axonal sprouting and chemically suppress growth cone advancement. In chronic phases, this fibrotic barrier stabilizes the lesion but perpetuates disconnection of neural circuits.^[61]^[62]^[63] Secondary pathophysiological effects compound primary inflammatory damage, including ischemia from associated vasculitis that narrows spinal vasculature and reduces perfusion, or compressive effects from vasogenic edema that elevates intramedullary pressure and exacerbates tissue hypoxia. These mechanisms, observed in autoimmune or infectious myelitis variants, can lead to additional necrosis and amplify the extent of axonal and neuronal loss beyond the initial inflammatory zone.^[64]^[8]^[29]

Diagnosis

Clinical evaluation

The clinical evaluation of myelitis begins with a detailed history taking to characterize the onset and progression of symptoms, which typically occur acutely or subacutely over hours to days, reaching a nadir within 4 hours to 21 days in most cases.^[8] Clinicians inquire about preceding events, such as recent infections (e.g., viral or bacterial), vaccinations, or autoimmune conditions, which precede approximately 50% of cases and help identify potential parainfectious or immune-mediated etiologies.^[29] Systemic symptoms like fever, back pain, or early urinary retention are elicited, alongside identification of a sensory level, often marked by a band-like dysesthesia or paresthesia corresponding to the spinal lesion site or one level above/below it.^[4] This history also assesses for autonomic involvement, such as bowel or bladder dysfunction, to localize the inflammatory process within the spinal cord.^[8] Physical examination focuses on neurological assessment to confirm spinal cord involvement and guide localization. Motor function is evaluated using the Medical Research Council (MRC) scale for grading power, revealing flaccid paraparesis or quadriparesis that may progress to complete paralysis in up to 50% of patients at peak severity, initially due to spinal shock.^[8] Sensory mapping involves testing for loss of pinprick, vibration, or temperature sensation below the lesion level, often with a sharply demarcated sensory level and associated dysesthesias like burning or tingling.^[29] Reflexes are typically diminished or absent in the acute phase (hyporeflexia from lower motor neuron effects), transitioning to hyperreflexia and spasticity later, with pathological signs such as a positive Babinski sign indicating upper motor neuron involvement above the lesion.^[4] Additional findings may include autonomic instability, such as urinary retention, underscoring the need for prompt bedside evaluation to differentiate myelitis from mimics.^[8] Differential diagnosis requires distinguishing myelitis from conditions with overlapping features, such as Guillain-Barré syndrome, which presents with ascending paralysis and areflexia without a clear sensory level.^[29] Spinal cord compression from trauma, neoplasm, or abscess must be excluded, particularly in cases with insidious or apoplectic onset and radicular pain, while vitamin B12 deficiency causes a slower, progressive subacute combined degeneration with symmetric sensory ataxia and proprioceptive loss.^[8] Red flags prompting urgent assessment include rapid progression to nadir within hours, suggesting vascular or compressive causes, or fever indicating infectious myelitis; after thorough evaluation, 15-30% of cases remain idiopathic as a diagnosis of exclusion.^[29]

Laboratory and imaging tests

Magnetic resonance imaging (MRI) of the spine is the cornerstone for diagnosing myelitis, typically revealing T2 hyperintensities indicative of inflammation and edema within the spinal cord, present in over 90% of acute cases.^[8] In acute phases, gadolinium enhancement is often observed, highlighting active inflammation and blood-spinal cord barrier disruption, while T1-weighted images may show cord swelling.^[29] Whole-spine imaging is recommended to evaluate the full extent of involvement, as lesions can span multiple segments, particularly in longitudinally extensive transverse myelitis associated with conditions like neuromyelitis optica spectrum disorder (NMOSD).^[65] Cerebrospinal fluid (CSF) analysis via lumbar puncture is essential to confirm inflammation and identify potential infectious or autoimmune etiologies. Pleocytosis is common, with lymphocytic predominance in viral myelitis (e.g., due to enteroviruses or herpesviruses) and neutrophilic predominance in bacterial cases (e.g., from Lyme disease or pyogenic infections).^[66] Elevated protein levels are frequently noted, reflecting barrier dysfunction, while oligoclonal bands appear in approximately 85-95% of multiple sclerosis (MS)-associated myelitis cases but are less common (15-30%) in NMOSD.^[47] Polymerase chain reaction (PCR) testing of CSF for pathogens, such as varicella-zoster virus or Mycobacterium tuberculosis, aids in pinpointing infectious causes.^[25] Blood tests support etiological classification by detecting systemic inflammation or specific antibodies. Autoantibody panels include testing for aquaporin-4 (AQP4-IgG) in NMOSD and myelin oligodendrocyte glycoprotein (MOG-IgG) in MOG-associated disease, which guide targeted therapies.^[2] Antinuclear antibodies (ANA) screen for connective tissue disorders like systemic lupus erythematosus, while serologies for HIV, Lyme disease (Borrelia burgdorferi), and human T-lymphotropic virus type 1 (HTLV-1) identify infectious triggers.^[67] Inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are elevated in non-infectious inflammatory myelitis.^[68] Advanced electrophysiological studies, including somatosensory evoked potentials (SSEPs), can detect subclinical conduction delays in cases with normal MRI, confirming myelopathy through prolonged latencies.^[67] Spinal cord biopsy is rarely performed due to risks but may be indicated in atypical cases, such as suspected neurosarcoidosis, where it can reveal non-caseating granulomas.^[69]

Treatment

Acute therapies

The primary goal of acute therapies for myelitis is to rapidly reduce spinal cord inflammation, mitigate neurological damage, and stabilize the patient during the initial phase of the condition. These interventions are typically initiated upon suspicion of myelitis, often in hospital settings, and are tailored based on whether the etiology is infectious or immune-mediated. High-dose corticosteroids form the cornerstone of treatment for non-infectious cases, while specific antivirals are employed for confirmed viral causes. If initial therapy fails, adjunctive immunomodulatory procedures like plasma exchange or intravenous immunoglobulin (IVIG) may be considered to expedite recovery. Corticosteroids are the first-line treatment for acute myelitis in most immune-mediated cases, administered as high-dose intravenous methylprednisolone at 1 g per day for 3-5 days to suppress inflammation and reduce spinal cord edema. This regimen has been shown to lead to clinical improvement in 50-70% of adult patients with post-infectious immune-mediated transverse myelitis, with faster recovery compared to lower doses or oral steroids.^[70] Oral prednisone taper may follow to prevent rebound inflammation, though intravenous administration is preferred for its superior bioavailability in acute settings.^[4] For patients who do not respond to corticosteroids within 5-7 days, plasma exchange (PLEX) is recommended, involving 5-7 sessions over 10-14 days to remove circulating inflammatory antibodies and proteins from the blood. In neuromyelitis optica spectrum disorder (NMOSD)-associated myelitis, a subtype of inflammatory myelitis, PLEX initiated within 2 weeks of symptom onset achieves significant functional improvement in approximately 50-65% of cases, with reductions in disability scores observed post-treatment.^[71] This procedure is particularly beneficial when performed early, as delayed initiation correlates with poorer outcomes. Intravenous immunoglobulin (IVIG) serves as an alternative or adjunctive therapy, especially in pediatric or steroid-refractory immune-mediated myelitis, dosed at 0.4 g/kg per day for 5 days (total 2 g/kg) to modulate the immune response by neutralizing autoantibodies.^[72] In children with acute transverse myelitis, IVIG has demonstrated efficacy in promoting recovery when combined with steroids, with clinical improvement noted in case series of immune-mediated presentations.^[73] It is generally reserved for cases unresponsive to initial therapies due to its cost and potential side effects like headache or aseptic meningitis. In instances of infectious myelitis, such as those caused by herpes simplex virus (HSV), targeted antivirals like acyclovir are administered intravenously at 10 mg/kg every 8 hours for 14-21 days to inhibit viral replication and limit cord damage.^[74] This approach is critical for viral etiologies, where empirical antiviral therapy may be started pending confirmation, particularly in immunocompromised patients or those with rash suggestive of herpes zoster.^[75] Supportive care is integral to acute management, focusing on symptom relief and complication prevention. Pain control involves multimodal analgesia, including gabapentin for neuropathic pain or short-term opioids for severe dysesthetic symptoms, to improve patient comfort and facilitate early mobilization.^[4] Additionally, deep vein thrombosis (DVT) prophylaxis with low-molecular-weight heparin (LMWH), such as enoxaparin at 40 mg subcutaneously daily, is standard in immobilized patients to reduce thromboembolic risk, which is elevated due to spinal cord immobility.^[76] These measures, alongside bladder and bowel management, help prevent secondary complications during the inflammatory phase.

Long-term management

Long-term management of myelitis, particularly in recurrent forms such as those associated with neuromyelitis optica spectrum disorder (NMOSD) or multiple sclerosis (MS), emphasizes relapse prevention through immunosuppression, alongside rehabilitation to address residual deficits and symptom control to improve quality of life.^[4]^[77] For patients with AQP4-IgG positive NMOSD-related myelitis, targeted monoclonal antibody therapies approved by the FDA are now first-line for relapse prevention, including eculizumab and ravulizumab (complement C5 inhibitors, approved 2019 and 2024, respectively, reducing annualized relapse rates by approximately 90% in trials), inebilizumab (anti-CD19 monoclonal antibody, approved 2020, with 77% relapse risk reduction), and satralizumab (IL-6 receptor inhibitor, approved 2020, reducing relapses by 74% in AQP4-positive patients).^[78]^[79] Off-label immunosuppressive therapies like rituximab or azathioprine remain options, particularly where approved agents are inaccessible. Rituximab, a monoclonal antibody targeting CD20-positive B cells, has been shown to decrease the annualized relapse rate by up to 88% in NMOSD patients, with approximately two-thirds achieving complete remission.^[80] Azathioprine, an oral purine analog, reduces relapse rates by about 72% in NMOSD when used with concurrent prednisone, though it carries a higher treatment failure rate of 53%.^[80] These agents require regular monitoring for infections due to their impact on immune function, including screening for opportunistic pathogens and adjusting doses based on clinical response.^[81] Rehabilitation forms a cornerstone of long-term care, tailored to mitigate neurological residuals. Physical therapy focuses on strengthening exercises, gait training, and coordination to preserve muscle function and prevent contractures, while occupational therapy assists in adapting daily activities such as self-care and mobility.^[4]^[82] Bladder management often involves intermittent catheterization or medications to control dysfunction, reducing risks like urinary tract infections.^[83] Symptom management targets common residuals to enhance functionality and well-being. Spasticity is addressed with baclofen, a GABA-B receptor agonist that reduces muscle tone through intrathecal or oral administration.^[84] Neuropathic pain, prevalent in up to 83% of NMOSD cases, responds to amitriptyline, a tricyclic antidepressant that modulates pain pathways at low doses.^[85]^[86] Psychological support, including psychotherapy, is essential for addressing depression and anxiety arising from disability, with talk therapy helping patients cope with emotional and behavioral challenges.^[82]^[87] Ongoing monitoring is critical to detect subclinical progression and guide therapy adjustments. Serial MRI scans of the spinal cord and brain help identify new lesions indicative of relapse in NMOSD.^[88] Aquaporin-4 antibody titers may be periodically assessed, though they do not reliably predict relapses and are more useful for confirming diagnosis.^[89] In recurrent forms, live vaccines should be avoided to minimize relapse risk, with inactivated vaccines administered cautiously under medical supervision.^[90]^[91]

Prognosis

Recovery outcomes

Recovery from myelitis varies significantly by subtype, with transverse myelitis (TM) being the most studied. For TM, recovery typically follows distinct phases, beginning with acute deterioration that peaks around 2 weeks after symptom onset, as 80% of patients reach maximal deficit within 10 days.^[92] This is followed by a partial recovery phase lasting 3-6 months, during which most neurological improvements occur, and a plateau phase from 6-12 months onward, after which further gains are limited.^[8] Overall for TM, approximately one-third of patients achieve full recovery with minimal lasting deficits, one-third experience moderate disability such as gait disturbances or bowel dysfunction, and one-third face severe disability including paraplegia.^[87] In acute flaccid myelitis (AFM), a subtype primarily affecting children, prognosis is generally poorer, with fewer than 10% achieving complete recovery and most experiencing persistent limb weakness and motor deficits despite rehabilitation.^[93] For infectious myelitis, outcomes depend on the pathogen and timeliness of treatment; viral causes often allow partial recovery similar to TM if addressed early, while untreated bacterial or parasitic infections can lead to higher rates of permanent disability or mortality.^[59] In transverse myelitis specifically, about two-thirds of patients regain ambulatory status by 2 years post-onset.^[94] Outcomes are notably better in cases of partial transverse myelitis compared to longitudinally extensive transverse myelitis (LETM), with good functional recovery rates of around 80% versus 40%, respectively.^[95] Long-term sequelae affect many survivors, including chronic pain reported in approximately 40-67% of cases and fatigue in about 50%.^[96] In-hospital mortality for TM remains low at less than 2%, primarily due to complications like respiratory failure in severe cervical involvement, though overall long-term mortality can reach 10% in some inflammatory myelopathy cohorts.^[97] Recent 2025 studies highlight improved recovery with early plasma exchange (PLEX), showing clinically significant EDSS improvements of 1-2 points in responsive patients, particularly in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).^[98]

Influencing factors

Lesion characteristics significantly influence the prognosis of myelitis. Shorter spinal cord lesions spanning fewer than three vertebral segments are associated with better functional recovery compared to longitudinally extensive transverse myelitis (LETM), which involves three or more segments and correlates with poorer outcomes (odds ratio [OR] 12.34 for Rankin score ≥2).^[95] Dorsally located lesions, which predominantly affect the posterior columns, are linked to worse sensory recovery due to disruption of ascending sensory pathways, whereas ventral or lateral lesions may spare some sensory function while impacting motor outcomes more severely.^[8] The underlying etiology plays a critical role in recovery rates. Idiopathic or viral-associated myelitis generally yields higher full recovery rates, around 60%, owing to monophasic courses and effective immune modulation, in contrast to neuromyelitis optica spectrum disorder (NMOSD), where only about 19-30% achieve complete recovery due to recurrent inflammation and axonal damage.^[99] Age greater than 40 years halves the odds of a good outcome across etiologies, with older patients facing increased risks of persistent disability (OR approximately 0.5 for favorable recovery; adjusted OR 4.26 for poor outcome if >50 years).^[100] Therapeutic timing and patient comorbidities further modify prognosis. Initiating high-dose corticosteroids or plasma exchange within 24 hours of symptom onset improves ambulation recovery rates to approximately 70%, compared to 40% with delayed intervention, by limiting secondary axonal injury.^[101] Comorbidities such as diabetes exacerbate outcomes by impairing vascular integrity and immune response, leading to higher disability scores and reduced treatment efficacy.^[102] Biomarkers provide additional prognostic insights. Cerebrospinal fluid (CSF) pleocytosis below 50 cells/μL indicates a favorable course, with lower cell counts correlating to reduced inflammation and better neurological recovery (elevated polymorphonuclear cells confer OR 6.09 for poor outcome).^[100] Persistent gadolinium enhancement on MRI at 3 months post-onset signals ongoing active inflammation and predicts poor medium-term recovery (OR 5.473 for incomplete recovery).^[103]

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Sep 9, 2025 · The median age was 39 years, and there was a bimodal age distribution with peaks around the age of 30 years and 45 years for both men and women ...
[99]
Prognostic factors for relapse and outcome in pediatric acute ...
Acute transverse myelitis (ATM) is an inflammatory syndrome of the spinal cord, affecting both children and adults. In children the estimated incidence is 1.7–2 ...
[100]
Frequency of diabetes and other comorbidities in chronic ... - PubMed
Aug 31, 2020 · Patients with diabetes had higher disability scores, worse quality of life and a less frequent treatment response compared with patients ...Missing: myelitis | Show results with:myelitis
[101]
Persistently Gadolinium-Enhancing Lesion Is a Predictor of Poor ...
Jan 19, 2021 · Our study found that persistently gadolinium-enhancing lesion is a poor prognosis predictor after NMOSD attack.