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Spinal cord compression

Spinal cord compression is a medical emergency involving excessive pressure on the spinal cord from surrounding tissues, such as vertebral bones, intervertebral discs, tumors, abscesses, or hematomas, which can disrupt neural function and lead to potentially irreversible neurological deficits if not addressed promptly.^[1] This condition arises from various etiologies and requires urgent evaluation to prevent permanent damage to motor, sensory, and autonomic pathways.^[1] The primary causes of spinal cord compression include degenerative conditions like spondylosis, which narrows the spinal canal through age-related changes such as disc herniation or ligament thickening, particularly in the cervical spine among adults over 55.^[1] Neoplastic processes, such as metastatic spinal cord compression (MSCC) from cancers like breast, lung, or prostate, account for 2.5% to 5% of cancer-related deaths and often affect the thoracic spine due to vertebral body metastasis.^[1] Infectious etiologies, including spinal epidural abscess (SEA) with an incidence of 5.1 cases per 10,000 hospital admissions, typically result from bacterial spread leading to pus accumulation in the epidural space.^[1] Less commonly, spontaneous spinal epidural hematoma (SSEH), occurring at a rate of 0.1 per 100,000 people, can cause acute compression due to vascular rupture.^[1] Symptoms of spinal cord compression often begin with localized back or neck pain, progressing to radicular pain, motor weakness, sensory disturbances like numbness or paresthesia, gait instability, and in severe cases, bowel or bladder dysfunction.^[2] In MSCC, pain is the initial symptom in 80% to 95% of cases, while SEA may present with fever in 30% to 75% of patients.^[1] Diagnosis relies on clinical examination revealing hyperreflexia, clonus, or positive Babinski sign, supported by magnetic resonance imaging (MRI) with gadolinium contrast as the gold standard, offering 93% sensitivity and 97% specificity for detecting compression.^[1] Treatment prioritizes rapid decompression to preserve function, with high-dose corticosteroids like dexamethasone (10 mg IV bolus followed by 4 mg every 6 hours) used initially for MSCC to reduce edema.^[1] Surgical interventions, such as laminectomy or tumor resection, are indicated for progressive deficits or when conservative measures fail, while antibiotics are essential for SEA and evacuation for SSEH within 48 hours.^[1] For degenerative causes like cervical myelopathy, which affects 15,000 to 20,000 U.S. patients annually and is more prevalent in males over 40, nonsurgical options including physical therapy may suffice for mild cases, but surgery is often required to halt progression and alleviate symptoms.^[3] Early intervention is critical, as prolonged compression can result in ischemia, demyelination, and permanent paralysis.^[1]

Background

Definition and Epidemiology

Spinal cord compression refers to the application of external pressure on the spinal cord by adjacent structures, including tumors, abscesses, hematomas, or degenerative elements such as herniated discs or osteophytes, which disrupts normal cord function within the epidural space and meninges.^[1] This pressure impairs spinal cord perfusion, leading to ischemia through vascular compression and venous congestion, followed by edema formation and subsequent neurological dysfunction manifesting as myelopathy.^[1] Unlike radiculopathy, which involves isolated compression of spinal nerve roots and typically produces dermatomal pain, sensory changes, or motor deficits without cord-level involvement, spinal cord compression directly affects the cord parenchyma, resulting in broader deficits such as bilateral weakness and sensory loss below the lesion level.^[1] Metastatic spinal cord compression (MSCC), a predominant etiology in adults with cancer, occurs in 2.5% to 5% of patients who succumb to cancer, with the highest incidences associated with primary tumors of the lung (24.9%), prostate (16.2%), breast, and multiple myeloma (11.1%).^[1] Recent trends show an increasing incidence of MSCC inpatient admissions, with an annual percent change of 4.78% from 2009 to 2019, alongside decreasing in-hospital mortality.^[4] In patients with solid tumors, the clinical incidence of spinal metastases is approximately 15.67%, of which 9.56% progress to MSCC.^[5] The overall annual incidence of MSCC in the general population is estimated at 8.1 cases per 100,000 inhabitants, though this varies by region and underreporting may occur due to diagnostic challenges.^[5] Non-metastatic forms, such as those from degenerative spondylosis, affect 5% to 10% of adults over age 55, while rarer causes like spinal epidural abscesses have an incidence of 5.1 cases per 10,000 hospital admissions, and spontaneous epidural hematomas occur at 0.1 per 100,000.^[1] Neoplastic compression predominantly affects individuals aged 50 to 70 years, reflecting the epidemiology of underlying malignancies, whereas traumatic or degenerative causes show bimodal peaks, with younger adults (under 40) more prone to trauma-related cases and older populations to chronic degeneration.^[1] A slight male predominance is observed, particularly in metastatic cases (approximately 60% male), attributed to higher cancer incidence in men for relevant primaries like lung and prostate.^[6] Key risk factors include a history of malignancy, osteoporosis (predisposing to pathologic fractures), exposure to trauma, and degenerative spine diseases such as spondylosis or disc herniation.^[1]

Clinical Significance

Spinal cord compression is classified as a medical emergency due to its potential to cause rapid and irreversible neurological damage if not addressed promptly. Untreated compression can lead to permanent paralysis, loss of bowel and bladder control, and increased mortality risk, particularly in cases arising from metastatic disease. The time-sensitive nature of intervention is critical, with optimal outcomes associated with treatment initiation within 24 to 48 hours of symptom onset to preserve ambulation and minimize deficits.^[1]^[7] The condition carries substantial clinical impact, resulting in significant disability in a majority of affected individuals, with up to 75% experiencing motor deficits at diagnosis and many facing long-term impairment such as paraplegia or incontinence. Metastatic spinal cord compression, which accounts for a substantial proportion of acute cases, is associated with higher morbidity and poorer prognosis compared to benign causes, often complicating advanced cancer and contributing to overall disease mortality in 2.5% to 5% of patients dying from malignancy. This is particularly prevalent in cancers like lung, prostate, and breast, where it affects patient quality of life and functional independence.^[1]^[8] Beyond individual outcomes, spinal cord compression imposes a heavy public health burden, driving extensive healthcare utilization through emergency admissions, surgical interventions, and extended rehabilitation. The economic costs are amplified by high readmission rates—1-year readmission rates of 37.8% to 47.2%—and lifelong care needs for survivors with disabilities, mirroring the broader societal impact of spinal cord injuries estimated at millions per patient over a lifetime.^[9]^[10]^[11] Historically, its recognition as an oncologic emergency traces back to the early 20th century, with formalized management protocols emerging in the 1970s amid rising cancer survival rates and improved diagnostic capabilities.^[1]^[10]^[11]

Pathophysiology

Relevant Spinal Anatomy

The spinal cord is a cylindrical structure of nervous tissue that extends from the foramen magnum, where it is continuous with the medulla oblongata of the brainstem, to the level of the L1-L2 vertebrae in adults, terminating as the conus medullaris.^[12] It is divided into 31 segments: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal, with each segment corresponding to paired spinal nerves that emerge via dorsal and ventral roots.^[12] In cross-section, the spinal cord consists of an inner core of gray matter surrounded by white matter; the gray matter forms a butterfly-shaped region with dorsal (posterior) horns containing sensory neuron cell bodies, ventral (anterior) horns housing motor neuron cell bodies, and lateral horns in the thoracic and upper lumbar regions for autonomic functions.^[13] The surrounding white matter is organized into ascending and descending tracts, such as the corticospinal tracts for voluntary motor control and the spinothalamic tracts for pain and temperature sensation, which facilitate communication between the brain and periphery.^[14] The spinal cord is protected within the vertebral column, a flexible bony structure composed of 33 vertebrae (7 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 4 coccygeal) that forms the spinal canal.^[12] It is enveloped by three meninges: the outermost dura mater, the middle arachnoid mater, and the innermost pia mater, with cerebrospinal fluid circulating in the subarachnoid space between the arachnoid and pia to provide cushioning.^[15] Between the dura and the vertebral canal lies the epidural space, containing fat, connective tissue, and venous plexuses; adjacent structures include intervertebral discs, which act as shock absorbers between vertebral bodies, and the ligamentum flavum, a yellow elastic ligament connecting adjacent laminae that forms the posterior boundary of the spinal canal.^[16] The spinal canal is narrowest in the mid-cervical region at C3-C7, where the anteroposterior diameter averages 13-15 mm, and at the thoracolumbar junction, predisposing these areas to compression effects on the cord.^[17] The spinal cord's vascular supply is primarily from the anterior spinal artery, which arises from the vertebral arteries and runs along the anterior median fissure to supply the anterior two-thirds of the cord, including the corticospinal and spinothalamic tracts, making this region particularly vulnerable to ischemia due to its end-artery nature and limited collaterals in the thoracolumbar area.^[18] Two posterior spinal arteries, branches of the vertebral or posterior inferior cerebellar arteries, supply the dorsal columns; radicular arteries, including the artery of Adamkiewicz (typically at T9-L2), provide segmental reinforcement.^[19] Venous drainage occurs via an anterior median vein and a posterior spinal vein, forming a valveless plexus that empties into the azygos and lumbar veins, with potential for congestion in pathological states.^[20]

Mechanisms of Compression and Injury

Spinal cord compression initiates a primary injury through direct mechanical pressure that deforms neural tissue, disrupts axonal integrity, and causes immediate neuronal damage. This mechanical deformation reduces the cross-sectional area of the spinal cord, leading to local tissue strain and potential hemorrhage at the site of compression.^[21] Concurrently, vascular compromise arises as compression impinges on spinal vasculature, particularly the vulnerable anterior spinal artery, resulting in ischemia and potential infarction of gray and white matter.^[1] Secondary processes exacerbate the initial insult, including vasogenic edema from increased vascular permeability and inflammatory responses that further elevate intramedullary pressure.^[22] The injury cascade unfolds in phases, beginning with excitotoxicity where excessive glutamate release from damaged neurons triggers calcium influx and mitochondrial dysfunction in surrounding cells.^[21] This progresses to apoptosis, involving caspase activation and programmed cell death in neurons and oligodendrocytes, peaking within hours to days post-compression.^[21] Demyelination follows as oligodendrocytes undergo apoptosis under hypoxic conditions, impairing axonal conduction and contributing to Wallerian degeneration.^[21] Central to this cascade is disruption of the blood-spinal cord barrier (BSCB), mediated by matrix metalloproteinases (MMPs) that degrade tight junctions, allowing influx of inflammatory mediators and exacerbating edema and secondary ischemia.^[22] Mechanisms differ between acute and chronic compression. In acute scenarios, vascular-dominant injury predominates, with rapid onset of hemorrhage, vasospasm, and thrombosis leading to profound ischemia within minutes to hours.^[21] Chronic compression, often degenerative, involves sustained low-grade ischemia, progressive vascular rarefaction, and persistent microglial activation, fostering a degenerative milieu with gradual axonal loss over weeks to months.^[22] Site-specific effects vary by spinal level due to the cord's somatotopic organization. Cervical compression primarily impacts upper and lower limb motor pathways as well as respiratory centers via phrenic nerve involvement, while thoracic compression affects descending tracts to bowel and bladder control through autonomic dysregulation.^[21] Severity levels, particularly in metastatic cases, are often assessed using the Bilsky grading system, which categorizes epidural spinal cord compression from grade 0 (bone-only disease) to grade 3 (complete cord effacement without cerebrospinal fluid visualization), guiding prognostic and therapeutic decisions.^[23]

Causes

Neoplastic Causes

Neoplastic causes of spinal cord compression primarily arise from tumors originating within the spine or metastasizing from distant sites, with metastatic lesions accounting for approximately 85% of cases.^[24] These conditions often result in epidural compression through direct tumor growth, vertebral body destruction, or extension into the spinal canal, leading to neurological deficits.^[25] Metastatic tumors represent the most common etiology, occurring in 5-10% of patients with advanced cancer and predominantly affecting the thoracic spine.^[7] The primary sources include cancers of the lung (approximately 25% of cases), prostate (16%), and breast (13%), with spread frequently occurring via the valveless Batson's vertebral venous plexus, facilitating hematogenous dissemination to the vertebral bodies.^[26]^[27] This epidural involvement often leads to rapid symptom onset due to mass effect and associated vasogenic edema from tumor-induced vascular permeability.^[28] In contrast, primary spinal tumors are rare, comprising about 15% of neoplastic compressions, and typically exhibit slower progression compared to metastases.^[24] Common examples include extradural or intradural extramedullary tumors such as meningiomas (25-30% of intradural tumors) and schwannomas (about 25% of primary intradural spinal tumors), which arise from arachnoid cap cells or Schwann cells, respectively, and may compress the cord through gradual expansion.^[29]^[30] Pathologically, neoplastic compression often involves osteolytic bone destruction by metastatic deposits, forming epidural masses that encroach on the spinal cord, with multiple vertebral levels affected in up to 30% of cases.^[31] This multifocal involvement heightens the risk of instability and ischemia, exacerbating cord injury.^[32]

Non-Neoplastic Causes

Non-neoplastic causes of spinal cord compression arise from benign, non-cancerous processes that can lead to mechanical impingement on the spinal cord, often presenting with varying degrees of acuity depending on the underlying etiology. These include traumatic injuries, infectious or inflammatory conditions, degenerative disorders, and other factors such as hematomas or vascular anomalies. Unlike neoplastic compression, these causes frequently allow for potential recovery with timely diagnosis and treatment, though outcomes depend on the duration and severity of compression.^[1] Traumatic spinal cord compression typically results from fractures or dislocations of the vertebrae, most commonly due to high-impact events such as motor vehicle accidents (MVAs) or falls from height. These injuries cause acute onset of symptoms through direct mechanical disruption or secondary instability, with cervical spine involvement being particularly prevalent. Epidemiological data indicate that traumatic spinal cord injuries occur at an incidence of 12-57 cases per million population annually in high-income countries, and approximately 10-15% of spinal fractures are associated with neurological compromise including cord compression. Ischemic mechanisms, such as vascular occlusion from displaced bone fragments, may exacerbate the injury in the acute phase.^[33]^[34]^[35] Infectious and inflammatory causes often manifest subacutely with systemic signs like fever and back pain, stemming from collections of pus or granulomatous tissue in the epidural space. Spinal epidural abscess, the most common infectious etiology, is frequently caused by Staphylococcus aureus hematogenous spread from distant sites such as skin infections or endocarditis, leading to cord compression via mass effect. Tuberculosis can produce granulomas or pott's disease with vertebral involvement, particularly in endemic regions, compressing the cord through abscess formation or bone destruction. These conditions require urgent antimicrobial therapy to prevent irreversible deficits.^[36]^[37]^[38] Degenerative causes predominate in older adults and develop chronically through age-related spinal changes that narrow the canal and impinge on the cord. Cervical spondylotic myelopathy (CSM), resulting from spinal stenosis, disc herniation, or ossification of the posterior longitudinal ligament (OPLL), is the leading non-traumatic cause of spinal cord dysfunction in individuals over 55 years, affecting up to 95% with some degenerative changes by age 60, though symptomatic compression occurs in a subset.^[39]^[1]^[40] These progressive conditions highlight the role of cumulative wear in non-acute compression. Other non-neoplastic etiologies include spontaneous hematomas, frequently linked to anticoagulant therapy such as warfarin or direct oral anticoagulants, which disrupt hemostasis and allow bleeding into the epidural or subdural space, causing rapid compression. Vascular malformations, like arteriovenous malformations (AVMs), can lead to compression through hemorrhage or mass effect from dilated vessels, though they are rarer and often congenital. These diverse causes underscore the need for tailored evaluation in non-traumatic presentations.^[41]^[42]^[1]

Clinical Presentation

Signs and Symptoms

Spinal cord compression presents with a spectrum of neurological deficits arising from impaired spinal cord function, often beginning insidiously and worsening over time. The hallmark initial symptom is localized back or neck pain, which is the most common presenting symptom overall. In metastatic cases, it affects 80 to 95% of patients and is characterized as constant, aching, exacerbated by movement, coughing, or at night.^[1] This pain may radiate along dermatomes (radicular pain) and is frequently accompanied by point tenderness over the spinous process at the compression site.^[43] In infectious cases, such as spinal epidural abscess, patients may present with fever (in 30% to 75% of cases) or other systemic signs of infection.^[1] Sensory disturbances are prominent and include numbness, paresthesia (tingling or "pins and needles"), and altered sensation such as reduced sensitivity to pain, temperature, or touch, often delineating a distinct sensory level below the lesion where deficits abruptly change.^[1] These symptoms reflect disruption of ascending sensory pathways and may initially be unilateral before becoming bilateral.^[43] Motor impairments manifest as progressive weakness (myelopathy) in the limbs below the compression, evolving from mild fatigue to spastic paresis or paralysis, with upper motor neuron signs including hyperreflexia, clonus, spasticity, and a positive Babinski sign.^[1] Gait instability or ataxia is common due to proprioceptive loss and muscle weakness, contributing to falls. In metastatic cases, motor deficits are evident in 35 to 75% of patients at diagnosis.^[1]^[43] Autonomic dysfunction involves bowel and bladder disturbances, such as urinary retention, hesitancy, overflow incontinence, or fecal incontinence, arising from detrusor-sphincter dyssynergia and loss of reflex control.^[1] Sexual dysfunction, including erectile failure in men and reduced lubrication in women, is also frequent, alongside potential orthostatic hypotension from sympathetic pathway involvement.^[43] The specific manifestations depend on the spinal level affected. Cervical compression often leads to quadriparesis, involving weakness in both upper and lower extremities, with possible respiratory compromise if high cervical.^[1] Thoracic involvement typically produces paraparesis confined to the lower limbs, a midline sensory level on the trunk, and early autonomic features.^[43] Lumbosacral compression resembles cauda equina syndrome, featuring flaccid lower extremity weakness, hyporeflexia (lower motor neuron pattern), saddle anesthesia, and severe bowel/bladder dysfunction.^[1]

Progression and Staging

Spinal cord compression manifests in distinct temporal patterns based on the underlying etiology and speed of symptom onset. Acute compression typically develops within minutes to 48 hours and may be associated with atraumatic causes such as disc herniations, expanding hematomas, or acute infectious processes.^[44] Subacute compression evolves over days to weeks, commonly due to infectious processes like epidural abscesses or expanding hematomas, allowing for a more gradual but still urgent progression of deficits.^[44] Chronic compression unfolds over weeks to months, frequently resulting from degenerative conditions such as spinal stenosis or slow-growing tumors, where symptoms may insidiously worsen over time.^[44] Neurological impairment from spinal cord compression is assessed using standardized scales to quantify deficits and guide therapeutic urgency. The Frankel scale classifies motor function from grade A (complete paralysis with no sensory or motor function below the injury level) to grade E (normal function), providing a simple framework for evaluating functional deficits in compressive injuries.^[45] The American Spinal Injury Association (ASIA) Impairment Scale expands on this with grades A through E, incorporating detailed sensory and motor testing to determine completeness of injury; for instance, grade C indicates incomplete motor function where most key muscles score below 3/5 strength.^[46] In cases of metastatic epidural spinal cord compression, the extent of compression is evaluated radiologically using the Bilsky grading system on a 0-3 scale: grade 0 denotes bone-only disease without soft tissue involvement, grade 1 indicates epidural extension without cord compression, grade 2 shows cord compression with visible cerebrospinal fluid space, and grade 3 reflects complete effacement of the cerebrospinal fluid around the cord.^[47] The pace of progression carries significant prognostic implications, with rapid symptom evolution correlating to poorer neurological recovery and higher rates of permanent disability.^[48] Ambulatory status at the time of diagnosis serves as a critical predictor of functional outcome, where pre-treatment ability to walk independently is associated with improved post-intervention mobility and survival in metastatic cases.^[49]

Diagnosis

Clinical Assessment

Clinical assessment of spinal cord compression relies on a thorough history and targeted physical examination to suspect the condition and localize the level of involvement. During history-taking, clinicians inquire about the onset of symptoms, which may be acute in cases of trauma or epidural hematoma but more insidious and progressive in neoplastic or degenerative etiologies. Back pain is a hallmark feature, reported in 80-95% of patients with metastatic spinal cord compression, often characterized as constant, localized, and exacerbated at night or with Valsalva maneuvers such as coughing or straining. A prior history of malignancy, particularly breast, lung, or prostate cancer, serves as a critical red flag, as it increases the likelihood of metastatic disease causing compression. Details of any recent trauma, including the mechanism and timing, are essential to differentiate traumatic from non-traumatic causes. Red flags such as new-onset urinary or fecal incontinence, saddle anesthesia (numbness in the perianal region), or gait instability warrant immediate concern for cauda equina syndrome or advanced cord involvement. The physical examination emphasizes a comprehensive neurological evaluation to detect deficits and establish the compression level. Motor strength is systematically assessed using the Medical Research Council scale (0-5), where 0 indicates no contraction and 5 denotes normal power, testing key myotomes such as elbow flexors (C5), wrist extensors (C6), and ankle dorsiflexion (L4-L5) to identify the most caudal level with at least grade 3 strength. Sensory examination involves testing dermatomes for light touch and pinprick sensation on a 0-2 scale (0 for absent, 2 for normal), aiming to delineate a sensory level corresponding to the site of compression. Deep tendon reflexes are evaluated bilaterally, with hyperreflexia and a positive Babinski sign suggesting upper motor neuron involvement above the lesion, while hyporeflexia may indicate lower motor neuron or root pathology. The straight-leg raise test is performed to differentiate radiculopathy from cord compression, as it typically reproduces radicular leg pain at 30-70 degrees of hip flexion in lumbar root irritation but is less provocative in pure cord syndromes. Vital signs, including blood pressure and heart rate, are monitored for autonomic instability, such as orthostatic hypotension or bradycardia, which may signal cervical or high thoracic involvement disrupting sympathetic pathways. In patients with suspected neoplastic compression, the Spinal Instability Neoplastic Score (SINS) is a validated screening tool to evaluate spinal stability and guide surgical candidacy, scoring factors like pain, lesion location, and radiographic alignment to classify spines as stable (0-6 points), potentially unstable (7-12 points), or unstable (13-18 points) with high interobserver reliability. Symptom progression is typically gradual in neoplastic cases, allowing time for intervention if recognized early.

Imaging and Laboratory Tests

Magnetic resonance imaging (MRI) serves as the gold standard for diagnosing spinal cord compression, offering high sensitivity and specificity for detecting cord involvement, reported at 93% and 97%, respectively.^[50]^[1] T1-weighted sequences with gadolinium contrast enhancement are particularly useful for delineating tumors and epidural masses, while T2-weighted imaging highlights spinal cord edema and signal changes indicative of compression or ischemia.^[51] Whole-spine MRI is recommended to identify multifocal lesions, especially in neoplastic cases, as it visualizes the entire neuraxis without radiation exposure.^[52] Computed tomography (CT) complements MRI by providing superior bony detail, such as vertebral fractures or osteolytic changes, which may contribute to compression in traumatic or degenerative etiologies.^[53] It is particularly valuable when MRI is contraindicated, such as in patients with pacemakers or severe claustrophobia. CT myelography, involving intrathecal contrast, can be employed as an alternative to assess thecal sac compression if MRI is unavailable, though it carries risks of contrast-related complications.^[50] Emerging modalities like positron emission tomography-computed tomography (PET-CT) aid in staging metastatic disease by identifying primary tumors and distant spread, with fluorodeoxyglucose (FDG) uptake helping differentiate malignant from benign lesions.^[54] Laboratory tests support imaging by identifying underlying causes but are not diagnostic for compression itself. A complete blood count (CBC) with differential evaluates for infection or anemia, while erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) assess inflammation, often elevated in infectious or neoplastic processes.^[55]^[56] Tumor markers, such as prostate-specific antigen (PSA) for prostate cancer or carcinoembryonic antigen (CEA) for colorectal metastases, guide etiology when malignancy is suspected.^[57] Cerebrospinal fluid (CSF) analysis is rarely performed due to the risk of herniation from lumbar puncture in the setting of compression.^[58]

Treatment

Initial Medical Management

The initial medical management of spinal cord compression focuses on rapid pharmacological and supportive interventions to reduce cord edema, alleviate pain, and prevent secondary complications, particularly in cases of metastatic etiology common in cancer patients. High-dose corticosteroids, such as dexamethasone, are administered immediately upon suspicion of compression to stabilize the patient before definitive therapy. The standard regimen involves an intravenous bolus of 10 mg followed by 4 mg every 6 hours, or a total daily dose of 16 mg divided into 2-4 administrations, with tapering over 10-14 days to minimize risks.^[1]^[59]^[60] These agents reduce perilesional edema and inflammation, thereby improving neurologic function and analgesia in affected individuals.^[1] Potential side effects include psychosis, gastric ulceration requiring proton pump inhibitor prophylaxis, and hyperglycemia, necessitating close monitoring.^[1]^[59] For infectious causes like spinal epidural abscess, immediate broad-spectrum antibiotics are essential, guided by culture results. For spontaneous spinal epidural hematoma, urgent surgical evacuation is required.^[1] Pain management is a cornerstone of initial care, employing a stepwise approach tailored to symptom severity. Non-opioid analgesics like nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen are used for mild pain, while opioids such as morphine or oxycodone are indicated for moderate to severe cases; adjuncts like gabapentin or pregabalin address neuropathic components.^[59] Immobilization techniques, including bed rest and a cervical collar for thoracic or cervical lesions, further support pain relief by limiting spinal movement and reducing further irritation.^[60]^[59] Supportive measures address autonomic and thrombotic risks associated with immobility. For neurogenic bladder dysfunction, intermittent catheterization or urology consultation is initiated as needed to prevent urinary retention or infection.^[60] Deep vein thrombosis prophylaxis, starting with mechanical methods like compression devices, is recommended to mitigate thromboembolic events.^[60] All interventions should commence within 1 hour of clinical suspicion to optimize outcomes, involving multidisciplinary input from palliative care and neurology.^[59]^[1]

Surgical and Interventional Options

Surgical intervention is indicated for spinal cord compression when there is spinal instability, an unknown etiology requiring urgent decompression, or failure of conservative medical therapy to halt neurological deterioration. In such cases, prompt surgery within 24 to 48 hours of symptom onset has been shown to significantly improve neurological outcomes, particularly in preserving or restoring ambulatory function. Preoperative administration of high-dose corticosteroids, such as dexamethasone, may be used briefly to reduce edema and stabilize the patient prior to surgery.^[1] Common surgical procedures for decompression include laminectomy, which involves removing part or all of the vertebral lamina to relieve pressure on the spinal cord, often combined with tumor resection in neoplastic cases to excise compressive lesions.^[1] For compression due to vertebral fractures, minimally invasive options such as vertebroplasty or kyphoplasty are employed, where bone cement is injected into the fractured vertebra to stabilize it and indirectly decompress the cord. Spinal stabilization is frequently integrated into these procedures through fusion techniques or instrumentation, such as pedicle screws and rods, to prevent further deformity and maintain alignment. Postoperative outcomes vary based on preoperative status, with studies reporting neurological improvement in 50% to 70% of patients who were ambulatory prior to surgery, including gains in motor strength and sensory function. Complications occur in a minority of cases, with infection rates around 5% and hardware failure in approximately 2% to 10%, depending on the complexity of the instrumentation used.

Radiation and Systemic Therapies

Radiation therapy plays a central role in managing spinal cord compression, particularly when caused by metastatic tumors, by targeting the compressive lesion to alleviate symptoms and prevent further neurological deterioration. External beam radiotherapy is the standard approach for most cases of metastatic spinal cord compression, typically delivered in a fractionated regimen of 30 Gy over 10 fractions to balance efficacy with spinal cord tolerance. This modality effectively controls tumor growth and provides pain relief in approximately 80% of patients, with improvements often observed within 1-2 weeks of treatment. Alternative fractionation schedules, such as 20 Gy in 5 fractions or a single 8 Gy dose, may be used for patients with limited life expectancy to minimize treatment burden while maintaining palliative benefits.^[61]^[62]^[63] For isolated or oligometastatic lesions, stereotactic radiosurgery (SRS) or stereotactic body radiotherapy (SBRT) offers a precise, high-dose alternative to conventional external beam therapy, delivering ablative radiation (typically 16-24 Gy in 1-3 fractions) while sparing surrounding tissues. SRS is particularly suitable for radioresistant tumors or cases without significant cord impingement, achieving local control rates exceeding 80% at one year and comparable pain relief to fractionated regimens. This technique is often reserved for patients with favorable performance status and limited disease burden, as it requires advanced imaging and immobilization to mitigate risks like radiation myelopathy.^[64]^[65] Systemic therapies complement radiation by addressing the underlying malignancy, with selection guided by the primary tumor histology. Chemotherapy regimens are tailored to the tumor type; for primary spinal gliomas causing compression, temozolomide is commonly administered concurrently with or following radiation, demonstrating improved progression-free survival in responsive cases. In metastatic settings, agents such as platinum-based compounds or taxanes are used based on the primary cancer (e.g., lung or breast), though their role is often adjunctive due to limited penetration into epidural spaces. Hormone therapy is indicated for hormone receptor-positive tumors, such as breast cancer metastases, where tamoxifen inhibits estrogen-driven growth, reducing lesion size and associated compression in up to 30% of responsive patients.^[66]^[67] Bone-modifying agents like bisphosphonates (e.g., zoledronic acid) or denosumab are integral for preventing skeletal-related events in bone-dominant metastases, including spinal cord compression. These agents inhibit osteoclast activity, delaying pathologic fractures and retropulsion that exacerbate compression; denosumab, in particular, reduces the incidence of such events by 17% compared to zoledronic acid in solid tumor metastases. Administration is typically monthly via intravenous or subcutaneous routes, with monitoring for hypocalcemia.^[68]^[69] In combined approaches, radiation is frequently integrated post-operatively following surgical decompression to enhance local control, with regimens like 30 Gy in 10 fractions initiated within 1-2 weeks of surgery to optimize neurological recovery. For advanced disease, these therapies shift toward palliation, prioritizing symptom relief over aggressive tumor eradication, often in multidisciplinary regimens that include corticosteroids for edema reduction.^[70]

Emerging and Supportive Approaches

Recent advancements in the management of metastatic spinal cord compression (MSCC) have focused on immunotherapy and targeted therapies to address underlying tumor biology, particularly in patients with specific molecular profiles. Checkpoint inhibitors, such as pembrolizumab and nivolumab, have shown promise in treating spinal metastases from primaries like non-small cell lung cancer (NSCLC), renal cell carcinoma (RCC), and melanoma, with systematic reviews indicating high rates of tumor control (up to 80%) when used as adjuvant therapy alongside local treatments. In responders, these agents can extend overall survival by 6-12 months compared to historical controls, as evidenced by improved progression-free survival in phase III trials for PD-L1-positive tumors. For instance, in NSCLC with high PD-L1 expression, first-line pembrolizumab achieves a 5-year overall survival rate of 31.9% versus 16.3% with chemotherapy (KEYNOTE-024 trial).^[71]^[72] Targeted therapies, including tyrosine kinase inhibitors (TKIs) for EGFR-mutant lung cancer, have demonstrated durable responses in MSCC cases, with osimertinib extending progression-free survival to 10.1 months versus 4.2 months in patients with T790M-positive NSCLC after progression on prior EGFR TKI therapy (AURA3 trial). In frontline settings, it achieves 18.9 months PFS compared to 10.2 months with first-generation TKIs (FLAURA trial). Recent FLAURA2 trial (2023, updated 2025) demonstrated that adding chemotherapy to osimertinib in frontline EGFR-mutant NSCLC extends median overall survival to 47.5 months from 37.6 months. These agents are particularly effective when genetic profiling identifies actionable mutations, allowing for personalized intervention that stabilizes spinal lesions and delays neurological deterioration. Minimally invasive ablation techniques, such as radiofrequency ablation (RFA), provide targeted tumor destruction and pain relief in spinal metastases, with systematic reviews reporting significant pain reduction in 70-90% of cases and low complication rates (under 5%), often combined with vertebral augmentation for structural support.^[72]^[73]^[74]^[75]^[76] Supportive care emphasizes multidisciplinary rehabilitation to optimize recovery and quality of life, with physical therapy (PT) and occupational therapy (OT) initiated as early as day 1 post-stabilization to prevent contractures, maintain muscle strength, and promote functional independence. Evidence-based guidelines recommend integrated PT/OT programs starting immediately after acute management, leading to improved ambulation rates (up to 60% in ambulatory patients) and reduced hospital stays. Pain management follows structured algorithms prioritizing multimodal approaches, including opioids, anticonvulsants like gabapentin, and interventional procedures, which achieve adequate control in over 80% of MSCC patients while minimizing side effects. Psychological support is integral, addressing adjustment disorders and depression through cognitive-behavioral interventions and peer groups, which enhance coping and reduce emotional distress in 50-70% of individuals with spinal cord involvement.^[77]^[78]^[79] Advances in neuroprotection, such as riluzole—a glutamate antagonist—have been explored in trials for acute spinal cord injury, including compression scenarios, but demonstrate limited efficacy in MSCC, with phase II/III studies showing modest improvements in neurological scores (e.g., 5-10 point gains on ASIA scale) without consistent survival benefits or broad adoption due to variable outcomes and safety concerns in oncology settings. These supportive strategies collectively bridge gaps in conventional care, extending functional survival and addressing holistic needs in MSCC patients.^[80]^[81]

Prognosis and Complications

Prognostic Factors

Prognostic factors for spinal cord compression, particularly in the context of metastatic disease, encompass patient characteristics, tumor features, and clinical presentation at diagnosis, which collectively influence survival and functional recovery such as ambulation.^[82] For example, in a cohort of patients with metastatic spinal cord compression (MSCC) secondary to lung cancer, favorable predictors included early diagnosis within 24 hours of symptom onset (univariate hazard ratio [HR] 0.37, 95% confidence interval [CI] 0.20–0.66), preservation of ambulatory status prior to intervention (adjusted HR 0.36, 95% CI 0.14–0.92 compared to non-ambulatory), and single-level or limited vertebral involvement (1–2 levels; adjusted HR 0.36, 95% CI 0.15–0.87).^[82] Tumors with high radiosensitivity, such as lymphoma, contribute to more favorable results, with treatment achieving complete remission in 75% of cases and 5-year overall survival reaching 72.9%.^[83] In contrast, several unfavorable factors portend poorer outcomes. Pre-existing paralysis lasting more than 48 hours significantly impairs recovery, as shorter symptom duration (<48 hours) is tied to higher rates of ambulation restoration (8–9% regain with timely intervention).^[49] Compression involving multiple vertebral levels worsens prognosis, with vertebral fractures noted as a negative predictor in multiple studies.^[49] Poor performance status, such as Eastern Cooperative Oncology Group (ECOG) score greater than 2, is associated with reduced survival (adjusted HR 0.29 for ECOG 1–2 vs. ≥3, 95% CI 0.11–0.80 in lung cancer MSCC).^[82] The presence of extraspinal metastases similarly detracts from survival, as incorporated in predictive models evaluating metastatic burden.^[84] Scoring systems aid in stratifying prognosis, with the Tokuhashi score being widely used for metastatic spinal cord compression to forecast survival based on a 0–15 scale incorporating general condition, number of extraspinal and vertebral metastases, major organ involvement, primary tumor site, and palsy severity.^[84] Scores of 0–8 predict survival less than 6 months, 9–11 predict 6–12 months, and 12–15 predict over 1 year, with overall predictive accuracy around 66%.^[84] One-year survival rates in metastatic cases vary by primary tumor, ranging approximately 10–50%, influenced by factors like tumor histology and extent of disease.^[8]

Long-Term Outcomes and Rehabilitation

Long-term outcomes for spinal cord compression vary significantly depending on whether the underlying cause is malignant or benign, as well as the timeliness of intervention. In cases of metastatic spinal cord compression, median overall survival varies but is often in the range of 3 to 12 months following diagnosis; one study of patients with lung cancer metastases reported a median of 5.5 months.^[82] Prompt surgical decompression combined with radiation can enable 30-50% of nonambulatory patients to regain ambulation, as evidenced by systematic reviews showing 64% neurological improvement from nonambulatory to ambulatory status in surgically treated groups compared to 29% with radiation alone. For benign causes, such as cervical spondylotic myelopathy, outcomes are more favorable, with 50-80% of patients experiencing symptom improvement after surgical intervention, and up to 80% achieving full or near-full recovery when decompression occurs early.^[82]^[85]^[1] Survivors of spinal cord compression often face persistent complications that impact quality of life. Chronic pain affects up to 80% of individuals with resulting spinal cord injury, manifesting as neuropathic or musculoskeletal types that require multimodal management. Spasticity occurs in approximately 70% of cases, leading to muscle hypertonus and involuntary spasms that can hinder mobility. Other common issues include pressure ulcers, particularly at sites like the sacrum and ischium, which arise from immobility and affect up to 30% of patients; depression, which exacerbates functional limitations; and secondary infections such as urinary tract infections from catheterization.^[86]^[86]^[86] Rehabilitation for spinal cord compression follows a multiphase approach to optimize recovery and independence. The acute phase (first 6-12 weeks) emphasizes passive range-of-motion exercises, positioning to prevent contractures, and respiratory support to maintain lung function. In the subacute phase, active strengthening, tilt-table training for orthostatic tolerance, and balance exercises facilitate wheelchair transfers and early mobility. The community reintegration phase focuses on home adaptations, occupational therapy for daily activities, and psychological support to address depression, which affects about 33% of patients in the initial months. Assistive devices, such as manual or powered wheelchairs, ankle-foot orthoses, and functional electrical stimulation systems, are integral to enhancing ambulation and upper extremity function. Bowel and bladder programs, including intermittent catheterization and scheduled evacuations, promote autonomy, particularly for injuries at thoracic or lumbar levels.^[77]^[77]^[77] Emerging therapies, including stem cell trials, offer experimental promise for long-term recovery. A 2024 phase I/II study of intrathecal mesenchymal stromal cells from bone marrow or umbilical cord sources in chronic spinal cord injury patients demonstrated safety and modest efficacy, with significant improvements in American Spinal Injury Association (ASIA) scores and motor function observed over 22 months of follow-up, though larger trials are needed to confirm benefits.^[87]

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