Spinal Cord Compression

Mechanical Compression and Direct Tissue Injury

• Direct compression narrows the spinal canal, disrupting the organized architecture of white matter tracts and gray matter nuclei
• Loss of cerebrospinal fluid (CSF) circulation around the spinal cord impairs normal buffering and waste clearance
• Stretching and distortion of nerve fibers disrupts saltatory conduction along myelinated axons
• Progressive demyelination occurs with chronic compression due to oligodendrocyte dysfunction

Vascular Compromise and Ischemic Cascade

• Compression occludes the anterior spinal artery and radicular arteries supplying the spinal cord, leading to hypoperfusion
• Venous congestion develops as outflow is obstructed, elevating intracranial cord pressure and worsening ischemia
• The watershed zones (mid-thoracic region T2-T4, lower lumbar region) are particularly vulnerable to ischemic injury due to tenuous vascular supply
• Ischemia triggers glutamate excitotoxicity, calcium influx, mitochondrial dysfunction, and programmed cell death (apoptosis)
• Duration of ischemia is the critical determinant of reversibility—irreversible neuronal loss begins within 6-8 hours of complete ischemia

Inflammatory and Edema-Mediated Mechanisms

• Compression triggers release of inflammatory mediators (TNF-α, IL-6, IL-8) from resident microglia and infiltrating immune cells
• Spinal cord edema develops (both vasogenic and cytotoxic components), perpetuating secondary injury
• Breakdown of the blood-spinal cord barrier increases vascular permeability and leukocyte infiltration
• Free radical generation and lipid peroxidation damage myelin and axonal membranes
• Astrocyte activation and glial scar formation contribute to chronic neurological deficits even after decompression

Degenerative/Spondylotic Causes (Most Common in Adults)

• Cervical spondylotic myelopathy (CSM): Osteophytic ridges, disk bulging, hypertrophic ligamentum flavum narrowing the cervical spinal canal; accounts for ~50% of myelopathy in developed nations
• Lumbar stenosis: Central canal stenosis, lateral recess stenosis, or foraminal stenosis from hypertrophic facet joints and ligamentum flavum; presents with neurogenic claudication
• Thoracic stenosis: Less common; often idiopathic or from ossified posterior longitudinal ligament (OPLL)
• Risk factors: advanced age, male gender, prior cervical trauma, congenital canal stenosis

Neoplastic Causes (20-30% of Acute Compression)

• Epidural metastases (most common spinal malignancy): Breast, lung, renal cell carcinoma, lymphoma spread to vertebral bodies or epidural space
• Intradural tumors: Meningiomas, nerve sheath tumors (schwannomas, neurofibromatosis type 2), ependymomas
• Intramedullary tumors: Syrinx, hemangioblastoma, ependymoma, astrocytoma causing cord expansion
• Risk factor: active malignancy or cancer history

Traumatic Causes

• Acute disk herniation: Large central or paracentral herniation following cervical extension injury or heavy lifting
• Fracture-dislocation: Vertebral body fractures, burst fractures with retropulsion, facet dislocation
• Epidural hematoma: Spinal epidural hematoma (SEH) from trauma, anticoagulation, coagulopathy, vascular malformation
• Acute central cord syndrome: Hyperextension injury with anterior cord ischemia

Inflammatory/Infectious Causes

• Epidural abscess: Bacterial infection (Staphylococcus aureus most common) from hematogenous seeding, vertebral osteomyelitis, or direct inoculation
• Tuberculosis: Pott's disease with vertebral body destruction, granulation tissue, and kyphotic deformity
• Viral myelitis: HSV-2, VZV, enterovirus causing cord inflammation and swelling
• Spondylodiscitis: Vertebral body infection with epidural extension

Vascular Causes

• Spinal arteriovenous fistula (dAVF): Abnormal shunt causing chronic venous hypertension and myelopathy
• Spinal cord infarction: Anterior spinal artery occlusion from atherosclerosis, dissection, or aortic pathology
• Subarachnoid hemorrhage: SAH causing mass effect and inflammation

Other Causes

• Ossified posterior longitudinal ligament (OPLL): Common in East Asian populations; congenital or acquired
• Tethered spinal cord: Filum terminale tethering or intramedullary mass causing progressive myelopathy
• Atlantoaxial subluxation: Rheumatoid arthritis, Down syndrome, connective tissue disorders, odontoid fracture
• Intraspinal hemorrhage: Epidural, subdural, or subarachnoid bleeding from trauma, anticoagulation, bleeding disorders
• Arachnoiditis: Scarring of arachnoid from prior surgery, infection, or tethering causing cord compression

Cardinal Symptoms

• Myelopathic pain: Deep axial neck or back pain (often absent in acute compression), radiating arm or leg pain if nerve root involvement
• Lower extremity weakness: Insidious onset in cervical myelopathy; progressive difficulty walking, climbing stairs, or rising from chair; upper extremity weakness if cervical level
• Gait disturbance: Shuffling gait, spasticity, loss of balance; "myelopathic gait" with wide base, hyperreflexia, and spasticity
• Sensory loss: Paresthesias in hands or feet (glove-and-stocking distribution if generalized); loss of proprioception and vibration sense; patchy sensory level if focal compression
• Bladder/bowel dysfunction: Urinary hesitancy, urgency, or incontinence; fecal incontinence (red flag suggesting cauda equina or conus syndrome)
• Sexual dysfunction: Erectile dysfunction, loss of genital sensation (red flag for cauda equina syndrome)

Acute vs. Chronic Presentation

• Acute compression (trauma, epidural hematoma, acute disk herniation): Sudden onset paraplegia/tetraplegia, complete sensory loss, areflexia initially (spinal shock) progressing to hyperreflexia
• Subacute compression (infection, malignancy): Progressive symptoms over days to weeks; mixed upper and lower motor neuron signs
• Chronic compression (cervical spondylosis, OPLL): Slowly progressive myelopathy over months to years; hyperreflexia, spasticity, minimal acute pain

Physical Examination Findings

• Spasticity: Increased muscle tone with velocity-dependent resistance (clasp-knife phenomenon)
• Hyperreflexia: Brisk deep tendon reflexes; exaggerated jaw jerk (if cervical involvement); clonus (sustained rhythmic contraction after sudden stretch)
• Weakness: Pyramidal weakness (antigravity muscles more affected than others); increased strength in finger flexors vs. extensors (C8-T1 patterns)
• Pathological reflexes: Babinski sign (extensor plantar response), Hoffmann sign (finger flexion with middle finger percussion), Clonus, Oppenheim sign, jaw jerk

• Segmental weakness: Atrophy at the level of compression
• Fasciculations: Visible muscle twitching at compression level
• Areflexia: Absent or diminished reflexes at the level of compression with brisk reflexes below

• Sensory level: Abrupt demarcation of sensory loss corresponding to spinal cord segment (though often imprecise)
• Proprioceptive loss: Romberg sign positivity, pseudoathetosis, sensory ataxia
• Vibration sense loss: Greater impairment than pin-prick sensation in dorsal column compression
• Suspended sensory level: Loss of pain/temperature sensation with preserved vibration/proprioception (central cord syndrome with syrinx)

• Spastic gait: Stiff, shuffling, narrow-based
• Ataxic gait: Wide-based, unsteady (dorsal column involvement)
• Romberg sign: Positive (loss of proprioception)
• Tandem walk: Impaired balance

• Acute urinary retention with post-void residual >100 mL
• Bilateral leg pain with radiation to buttocks and perineum
• Bilateral leg weakness or asymmetric weakness
• Perianal anesthesia (loss of sensation in saddle distribution)
• Anal sphincter tone loss (decreased anal wink reflex)
• Recent onset erectile dysfunction with urinary symptoms

Clinical Assessment and History

• Timeline of symptom onset (acute vs. gradual progression dictates urgency)
• Constitutional symptoms (fever, night sweats, weight loss suggesting infection or malignancy)
• Cancer history, immunosuppression (suggesting metastatic disease or infection)
• Anticoagulation use (suggesting epidural hematoma)
• Recent spinal procedures or trauma
• Bowel/bladder symptoms (red flag for surgical emergency)
• Progressive vs. stable symptoms (progression indicates ongoing compression)

Laboratory Tests

• Complete blood count: Elevated WBC with left shift suggests infection/abscess; leukocytosis in malignancy
• Blood cultures: Obtained before antibiotics if epidural abscess suspected (positive in ~50% of cases)
• Inflammatory markers: Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) elevated in infection (ESR >40 mm/h highly suggestive); malignancy; rheumatologic disease
• Cerebrospinal fluid (CSF) analysis: Performed only after imaging to rule out mass; lymphocytic pleocytosis with elevated protein in inflammatory/infectious myelitis; malignant cells in neoplastic compression
• Coagulation studies: PT, PTT, platelet count if anticoagulated or bleeding disorder suspected
• Tumor markers: PSA, carcinoembryonic antigen (CEA) in suspected malignancy

Imaging Studies

• Indications: All suspected spinal cord compression; prerequisite for surgical planning
• Sequences: T1-weighted (anatomic detail), T2-weighted (edema/cord signal change), STIR (fluid-sensitive), gradient echo (hemorrhage detection)
• Compression findings:
• Loss of CSF signal (CSF obliteration) around cord
• Cord atrophy or expansion
• T2 hyperintensity within cord indicating edema or ischemic change (associated with worse prognosis if extensive)
• T1 hypointensity suggesting myelomalacia
• Etiology-specific findings:
• Degenerative: Osteophytes, disk bulging, facet hypertrophy, ligamentum flavum thickening
• Neoplastic: Heterogeneous mass enhancement, bone destruction, paraspinal extension
• Infectious: Vertebral body T2 hyperintensity, diskitis, paraspinal abscess enhancement
• Vascular: Serpiginous flow voids (dAVF); cord infarction with territory-appropriate T2 hyperintensity
• Traumatic: Fracture, dislocation, epidural hematoma (T1 hyperintense acute blood), cord contusion
• Timing: Urgent (within 24 hours) for acute compression with neurological deficit; within 48 hours for progressive symptoms

• Indications: When MRI contraindicated or unavailable; better for bony anatomy and acute hemorrhage
• Findings:
• Canal diameter narrowing
• Fracture fragments, dislocation
• Epidural hematoma (hyperdense acute blood)
• Calcified lesions (OPLL, old tuberculosis)
• CT myelography: Rarely used; intrathecal contrast demonstrates cord atrophy and compression
• Limitations: Poor soft tissue differentiation; radiation exposure

• Limited utility; may show gross fractures, kyphosis, or canal narrowing
• Inadequate for definitive evaluation of cord compression

Neurophysiologic Testing

• Somatosensory evoked potentials (SSEPs): Measure posterior column function; prolonged latencies or reduced amplitudes indicate dorsal column involvement; prognostically useful
• Motor evoked potentials (MEPs): Assess corticospinal tract integrity; abnormalities predict poor recovery
• Electromyography (EMG): Denervation patterns localize lesion; distinguish upper vs. lower motor neuron involvement
• Needle examination: Fibrillations and positive sharp waves indicate acute denervation at compression level
• Utility: Prognostic value; minimal diagnostic role given MRI superiority

Diagnostic Criteria for Myelopathy

• Clinical criteria: Progressive or acute bilateral lower extremity weakness/sensory loss with hyperreflexia/spasticity and imaging evidence of cord compression
• Severity grading (Japanese Orthopedic Association scale): Assesses motor, sensory, and bladder function; useful for prognosis
• Mild: Minimal functional impairment; JOA 15-17/18
• Moderate: Significant functional limitation; JOA 12-14/18
• Severe: Severe disability with gait dysfunction; JOA <12/18

Differential Diagnosis Considerations

• Multiple sclerosis: Inflammatory demyelinating disease; older age and acute onset favors compression; brain MRI lesions suggest MS
• Transverse myelitis: Acute bilateral weakness with sensory level; normal CSF protein/glucose; inflammatory changes on MRI
• Guillain-Barré syndrome: Ascending paralysis with areflexia; albuminocytologic dissociation (elevated CSF protein with normal WBC)
• Amyotrophic lateral sclerosis (ALS): Progressive weakness but no sensory loss; denervation on EMG; normal MRI

Medical Management (Non-Surgical)

• Indications: Acute spinal cord injury from trauma (within 8 hours of injury); inflammatory myelitis (MS, transverse myelitis); some infectious causes (TB with severe neurological deficit)
• Mechanism: Anti-inflammatory; stabilizes blood-spinal cord barrier; reduces lipid peroxidation and free radical formation
• Regimen:
• Acute traumatic injury: Methylprednisolone 30 mg/kg IV bolus followed by 5.4 mg/kg/h infusion for 24-48 hours (per NASCIS III trial)
• Inflammatory myelitis: Methylprednisolone 1 g IV daily × 3-5 days, then oral taper
• Limitations: No evidence for benefit in degenerative myelopathy or malignant compression; modest effects in traumatic injury; complications with prolonged use
• Monitoring: Hyperglycemia, infection risk, gastric ulceration (use PPI prophylaxis)

Neurologic complications (mechanism → signal)

• Irreversible paraplegia/tetraplegia: prolonged ischemia and axonal loss below the lesion; heralded by loss of ambulation — pre-treatment ambulatory status is the single strongest predictor of post-treatment ambulation, so any new weakness is an emergency.
• Respiratory failure: lesions at or above C5 denervate the phrenic outflow (C3–C5); rising PaCO₂, falling vital capacity, paradoxical abdominal breathing. Emergency — secure the airway before imaging.
• Neurogenic shock: loss of descending sympathetic tone in cervical/high-thoracic lesions gives hypotension with bradycardia (unlike hemorrhagic shock). Emergency. Distinguish from spinal shock, the transient flaccid areflexia that later converts to spasticity.
• Autonomic dysreflexia: lesions at or above T6; a noxious stimulus below the lesion (bladder distension, fecal impaction) triggers unopposed sympathetic surge — paroxysmal severe hypertension, pounding headache, flushing/sweating above the level, pallor below, reflex bradycardia. Emergency (risk of hypertensive hemorrhage). Per Consortium for Spinal Cord Medicine guidance: sit the patient upright, loosen constriction, relieve the trigger, then a short-acting antihypertensive.
• Neurogenic bladder: retention with overflow, recurrent UTI, and hydronephrosis; venous thromboembolism from immobility; pressure ulcers; late spasticity, neuropathic pain, and post-traumatic syringomyelia (progressive ascending deficit years later).
• Pathologic fracture / spinal instability: tumor-eroded vertebral body; mechanical pain worse with movement and better at rest — signals a need for stabilization rather than radiation alone.

Treatment-related complications

• Corticosteroids: hyperglycemia, GI ulceration (PPI cover), immunosuppression, insomnia/psychosis, proximal myopathy, avascular necrosis — worse with high dose and prolonged courses; taper once definitive therapy begins.
• Surgical: postoperative epidural hematoma — new deficit after an initially stable exam is an emergency requiring immediate re-imaging and evacuation; dural tear with CSF leak (positional headache); wound breakdown, especially in a previously irradiated field; C5 palsy with deltoid/biceps weakness days after cervical decompression; hardware failure.
• Radiotherapy: pain flare, esophagitis, myelosuppression, and delayed radiation myelopathy months to years later with progressive myelopathy and cord T2 signal change.

• New or progressive back pain in a patient with known cancer is malignant epidural compression until proven otherwise. Pain that is worse when recumbent or at night, or that wakes the patient, is the classic stem detail — it precedes weakness by weeks and is the window in which outcome can still be changed.
• **Single best next step: start dexamethasone and get urgent MRI of the entire spine with and without contrast.** Do not delay steroids for imaging when deficits are present, and do not image only the symptomatic level — synchronous metastatic deposits at other levels are common and change the radiation field. NCCN Central Nervous System Cancers guidance frames this whole-spine approach.
• The association examiners test: breast, lung, and prostate are the top solid tumors seeding the epidural space, spread is hematogenous to the vertebral body with posterior extension, and the thoracic spine is the most common site.
• Definitive therapy is not steroids. Based on the Patchell trial, direct decompressive surgery followed by radiotherapy outperforms radiotherapy alone in selected patients with a single site of compression and reasonable functional status; radiosensitive tumors (lymphoma, myeloma, germ cell) respond well to radiation.
• Ambulatory status at presentation predicts ambulatory status afterward — this is the prognostic fact stems hinge on, and the reason compression is treated as an emergency rather than an urgency.
• Cauda equina versus conus medullaris: cauda equina is asymmetric, flaccid, areflexic, with radicular pain and later saddle anesthesia/retention; conus lesions are symmetric, cause early bowel/bladder dysfunction, and mix upper and lower motor neuron signs.
• Common distractors to avoid: plain radiographs and bone scan (insensitive and too slow), and lumbar puncture before imaging in a suspected compressive lesion. Reserve CT myelography for patients who truly cannot have MRI.
• ***Hoffmann sign*, Lhermitte phenomenon, and hyperreflexia with a sensory level localize the lesion above the conus; absent sensory loss** with pure motor findings should redirect you toward ALS rather than compression.