Tumor Medulla Spinalis
Published on September 3, 2026
Risk Factors
Adults over 40 with known primary malignancy (lung, breast, prostate, renal, lymphoma); neurofibromatosis type 1 or 2; prior radiation exposure; von Hippel-Lindau disease
Etiology
Extradural: most commonly metastatic spread to vertebral body. Intradural-extramedullary: nerve sheath tumors (schwannoma, neurofibroma) or meningioma. Intramedullary: ependymoma (adults), astrocytoma (children)
Presentation
Progressive back pain that worsens at night or when supine, does not improve with rest, and is accompanied by gradually worsening neurological deficits (weakness, sensory changes, gait difficulty)
Classic Exam
Upper motor neuron signs below the lesion (hyperreflexia, spasticity, positive Babinski); sensory level on trunk exam; Brown-Sequard pattern (hemisection) for extramedullary tumors; cape-like dissociated sensory loss for intramedullary tumors; late bowel and bladder dysfunction
Diagnostics
MRI with gadolinium contrast showing an enhancing lesion; extradural masses cause vertebral body destruction and epidural compression; intradural-extramedullary tumors displace the cord; intramedullary tumors expand the cord from within
Management
Emergent high-dose dexamethasone for cord compression; surgical resection when feasible; radiation therapy for radiosensitive or unresectable tumors; chemotherapy is tumor-type dependent
KEYWORDS
"Pain worse at night," "progressive weakness," "sensory level," "back pain unresponsive to conservative measures," "known cancer with new neurological symptoms," "widened cord on MRI"
01Pathophysiology
Spinal cord neoplasms are broadly categorized by their anatomical relationship to the dura and the spinal cord itself, and this classification directly determines both the clinical presentation and the likely histology.
Extradural tumors are the most common spinal tumors overall and are almost always metastatic. Cancers of the lung, breast, prostate, kidney, and lymphoma reach the vertebral body through hematogenous spread via the Batson venous plexus, a valveless network of epidural veins that communicates with the systemic venous circulation. Once tumor seeds into the vertebral body, it can grow posteriorly into the epidural space and compress the spinal cord from outside the dura. This explains why the first symptom is typically localized back pain from periosteal stretching and vertebral destruction, followed later by myelopathic signs as the cord becomes compressed.
Intradural-extramedullary tumors arise within the dura but outside the cord parenchyma. The two classic examples are meningiomas (arising from arachnoid cap cells, most common in middle-aged women, typically thoracic) and schwannomas/neurofibromas (arising from Schwann cells of the dorsal nerve root). Because these tumors sit adjacent to the cord rather than within it, they compress one side of the cord first. This produces a Brown-Sequard pattern: ipsilateral upper motor neuron weakness and loss of proprioception/vibration below the lesion, with contralateral loss of pain and temperature sensation one to two levels below the lesion. This hemisection pattern is a high-yield exam clue that the lesion is extramedullary.
Intramedullary tumors grow within the cord substance itself. Ependymomas are the most common intramedullary tumor in adults and typically arise in the central canal region, while astrocytomas predominate in the pediatric population. Because these tumors begin centrally and expand outward, they first disrupt the anterior white commissure, where the spinothalamic fibers cross. This produces the classic cape-like (suspended) dissociated sensory loss: bilateral loss of pain and temperature in a dermatomal band at the level of the tumor, with preserved light touch and proprioception (carried in the posterior columns, which are affected later). As the tumor enlarges, it eventually compresses the corticospinal tracts and posterior columns, producing upper motor neuron weakness and loss of proprioception below the lesion.
The distinction between "pain worse at night or when lying down" and mechanical back pain is pathophysiologically important. Tumor-related pain worsens with recumbency because the epidural venous plexus engorges when supine, increasing pressure on already compressed neural structures. Mechanical pain, by contrast, worsens with activity and improves with rest. This single clinical detail is frequently the pivotal clue in a vignette.
02Classification and Clinical Manifestation
Extradural
COMMON TUMOR TYPES
Metastases (lung, breast, prostate, renal, lymphoma), primary vertebral tumors (chordoma, osteosarcoma)
TYPICAL PATIENT
Adult over 40 with known or occult malignancy
CLINICAL PATTERN
Back pain (earliest), followed by progressive myelopathy; bilateral symptoms common
DISTINGUISHING FEATURE
Vertebral body destruction on imaging; pain precedes neurological deficits by weeks to months
Intradural-extramedullary
COMMON TUMOR TYPES
Meningioma, schwannoma, neurofibroma
TYPICAL PATIENT
Meningioma: middle-aged women; Schwannoma: adults, associated with neurofibromatosis type 2
CLINICAL PATTERN
Radiculopathy at the level, then Brown-Sequard pattern below
DISTINGUISHING FEATURE
Well-circumscribed, enhancing mass that displaces cord to opposite side; dumbbell shape for schwannoma extending through neural foramen
Intramedullary
COMMON TUMOR TYPES
Ependymoma, astrocytoma, hemangioblastoma
TYPICAL PATIENT
Ependymoma: adults; Astrocytoma: children; Hemangioblastoma: von Hippel-Lindau disease
CLINICAL PATTERN
Central cord syndrome: cape-like dissociated sensory loss, then progressive weakness and long tract signs
DISTINGUISHING FEATURE
Cord expansion (widened cord) on MRI; syrinx commonly associated
COMPARTMENT | COMMON TUMOR TYPES | TYPICAL PATIENT | CLINICAL PATTERN | DISTINGUISHING FEATURE |
|---|---|---|---|---|
Extradural | Metastases (lung, breast, prostate, renal, lymphoma), primary vertebral tumors (chordoma, osteosarcoma) | Adult over 40 with known or occult malignancy | Back pain (earliest), followed by progressive myelopathy; bilateral symptoms common | Vertebral body destruction on imaging; pain precedes neurological deficits by weeks to months |
Intradural-extramedullary | Meningioma, schwannoma, neurofibroma | Meningioma: middle-aged women; Schwannoma: adults, associated with neurofibromatosis type 2 | Radiculopathy at the level, then Brown-Sequard pattern below | Well-circumscribed, enhancing mass that displaces cord to opposite side; dumbbell shape for schwannoma extending through neural foramen |
Intramedullary | Ependymoma, astrocytoma, hemangioblastoma | Ependymoma: adults; Astrocytoma: children; Hemangioblastoma: von Hippel-Lindau disease | Central cord syndrome: cape-like dissociated sensory loss, then progressive weakness and long tract signs | Cord expansion (widened cord) on MRI; syrinx commonly associated |
Pain
EXTRAMEDULLARY PATTERN
Radicular, well-localized early
INTRAMEDULLARY PATTERN
Diffuse, poorly localized, burning or dysesthetic
Motor deficit progression
EXTRAMEDULLARY PATTERN
Descending: starts at the level and moves downward
INTRAMEDULLARY PATTERN
Ascending: lower motor neuron signs at the level, upper motor neuron signs develop later
Sensory deficit
EXTRAMEDULLARY PATTERN
Brown-Sequard (hemisection); posterior column signs early if dorsal compression
INTRAMEDULLARY PATTERN
Dissociated (cape-like): loss of pain/temperature with preserved proprioception early; sacral sparing
Sacral function
EXTRAMEDULLARY PATTERN
Lost early (sacral fibers are outermost in spinothalamic and corticospinal tracts, compressed first from outside)
INTRAMEDULLARY PATTERN
Sacral sparing (sacral fibers are outermost, so an expanding central lesion reaches them last)
Sphincter dysfunction
EXTRAMEDULLARY PATTERN
Late
INTRAMEDULLARY PATTERN
Variable, can present earlier due to central gray involvement
CLINICAL FEATURE | EXTRAMEDULLARY PATTERN | INTRAMEDULLARY PATTERN |
|---|---|---|
Pain | Radicular, well-localized early | Diffuse, poorly localized, burning or dysesthetic |
Motor deficit progression | Descending: starts at the level and moves downward | Ascending: lower motor neuron signs at the level, upper motor neuron signs develop later |
Sensory deficit | Brown-Sequard (hemisection); posterior column signs early if dorsal compression | Dissociated (cape-like): loss of pain/temperature with preserved proprioception early; sacral sparing |
Sacral function | Lost early (sacral fibers are outermost in spinothalamic and corticospinal tracts, compressed first from outside) | Sacral sparing (sacral fibers are outermost, so an expanding central lesion reaches them last) |
Sphincter dysfunction | Late | Variable, can present earlier due to central gray involvement |
The concept of sacral sparing versus early sacral involvement is a commonly tested discriminator between intramedullary and extramedullary lesions. Because the spinothalamic tract is somatotopically organized with sacral fibers laminated most laterally (outermost), an external compression affects sacral fibers first (early sacral loss), while an internal expanding lesion affects sacral fibers last (sacral sparing).
03Diagnostic Workup
MRI of the entire spine with gadolinium
ROLE
Best initial test AND most accurate test
KEY FINDINGS
Demonstrates tumor location, extent, relationship to cord, presence of cord compression, enhancement pattern, and associated syrinx
Plain radiographs of the spine
ROLE
Low sensitivity screening; often the first abnormality seen in clinical practice
KEY FINDINGS
Vertebral body collapse, pedicle erosion ("winking owl sign"), pathologic fracture; normal in intradural tumors
CT myelography
ROLE
Alternative when MRI is contraindicated (pacemaker, severe claustrophobia)
KEY FINDINGS
Shows extradural block, intradural filling defects, or cord widening
CT of chest, abdomen, pelvis
ROLE
Staging and search for primary malignancy in suspected metastatic disease
KEY FINDINGS
Identifies lung mass, renal mass, hepatic metastases, lymphadenopathy
Bone scan (technetium-99m)
ROLE
Screening for multifocal skeletal metastases
KEY FINDINGS
Multiple areas of increased uptake; less anatomic detail than MRI
CSF analysis (via lumbar puncture)
ROLE
Adjunctive, not routinely first-line; risky if complete block is present
KEY FINDINGS
Elevated protein (Froin syndrome in complete block: xanthochromic, high protein, clotted CSF); cytology may show malignant cells in leptomeningeal disease
Tissue biopsy
ROLE
Definitive histological diagnosis when the primary is unknown and imaging is inconclusive
KEY FINDINGS
CT-guided percutaneous biopsy for extradural lesions; surgical biopsy for intradural tumors
TEST | ROLE | KEY FINDINGS |
|---|---|---|
MRI of the entire spine with gadolinium | Best initial test AND most accurate test | Demonstrates tumor location, extent, relationship to cord, presence of cord compression, enhancement pattern, and associated syrinx |
Plain radiographs of the spine | Low sensitivity screening; often the first abnormality seen in clinical practice | Vertebral body collapse, pedicle erosion ("winking owl sign"), pathologic fracture; normal in intradural tumors |
CT myelography | Alternative when MRI is contraindicated (pacemaker, severe claustrophobia) | Shows extradural block, intradural filling defects, or cord widening |
CT of chest, abdomen, pelvis | Staging and search for primary malignancy in suspected metastatic disease | Identifies lung mass, renal mass, hepatic metastases, lymphadenopathy |
Bone scan (technetium-99m) | Screening for multifocal skeletal metastases | Multiple areas of increased uptake; less anatomic detail than MRI |
CSF analysis (via lumbar puncture) | Adjunctive, not routinely first-line; risky if complete block is present | Elevated protein (Froin syndrome in complete block: xanthochromic, high protein, clotted CSF); cytology may show malignant cells in leptomeningeal disease |
Tissue biopsy | Definitive histological diagnosis when the primary is unknown and imaging is inconclusive | CT-guided percutaneous biopsy for extradural lesions; surgical biopsy for intradural tumors |
MRI with gadolinium is both the best initial test and the gold standard for spinal cord neoplasms. There is no separate "screening" and "confirmatory" test here; MRI accomplishes both. On the exam, the moment a vignette describes progressive neurological deficits with back pain, the next best step is always MRI of the spine. Ordering the scan of the entire spine is important because metastatic disease is frequently multifocal, and a single-level study may miss additional lesions that change management.
The imaging findings differ by compartment in characteristic ways. Extradural tumors show vertebral body destruction with an epidural soft tissue mass compressing the thecal sac. Intradural-extramedullary tumors appear as well-defined, homogeneously enhancing masses with a meniscus sign (CSF capping above and below the mass) and displacement of the cord to the opposite side. Intramedullary tumors show fusiform expansion of the cord itself, with variable enhancement and frequently an associated syrinx (fluid-filled cavity within the cord).
On plain films, the "winking owl" sign describes loss of a pedicle shadow on anteroposterior view, resulting from metastatic destruction. This is a classic radiographic finding but has low sensitivity compared to MRI.
If the clinical picture strongly suggests metastatic disease, the workup should also include CT of the chest, abdomen, and pelvis to find the primary tumor, along with relevant tumor markers (PSA for prostate, etc.). Lumbar puncture is generally avoided when there is a complete spinal block because of the risk of neurological deterioration from shifting pressure gradients.
04Management and Treatment
Acute cord compression from any cause
INTERVENTION
Dexamethasone
DETAILS
Loading dose of 10 mg IV, then 4 mg IV or PO every 6 hours; reduces vasogenic edema around the tumor and buys time before definitive treatment
Metastatic extradural tumor with cord compression
INTERVENTION
Radiation therapy (conventional external beam)
DETAILS
Standard first-line for most metastatic cord compression; typical regimen is 30 Gy in 10 fractions or 20 Gy in 5 fractions
Metastatic cord compression with high-grade block, bony instability, radioresistant tumor (renal cell, melanoma), or neurological deterioration during radiation
INTERVENTION
Surgical decompression and stabilization followed by radiation
DETAILS
Posterolateral decompressive laminectomy or anterior corpectomy with instrumented fusion, followed by adjuvant radiation
Intradural-extramedullary tumors (meningioma, schwannoma)
INTERVENTION
Surgical resection
DETAILS
Gross total resection is curative in most cases; meningiomas and schwannomas are well-encapsulated and amenable to complete removal
Intramedullary ependymoma
INTERVENTION
Surgical resection
DETAILS
Ependymomas have a clear cleavage plane, allowing gross total resection with good outcomes; adjuvant radiation if resection is subtotal
Intramedullary astrocytoma
INTERVENTION
Surgical debulking plus radiation
DETAILS
Astrocytomas are infiltrative without a clear cleavage plane, making complete resection difficult; postoperative radiation is typically given
Hemangioblastoma (especially with von Hippel-Lindau)
INTERVENTION
Surgical resection
DETAILS
Well-circumscribed vascular tumors; gross total resection is curative; screen for other VHL-associated lesions
Pain management
INTERVENTION
Corticosteroids, opioids, neuropathic agents (gabapentin, pregabalin)
DETAILS
Neuropathic pain is common; gabapentin starting at 300 mg daily titrated up, or pregabalin 75 mg twice daily
Long-term follow-up
INTERVENTION
Serial MRI surveillance
DETAILS
Frequency depends on tumor type and completeness of resection; typically every 3 to 6 months initially, then annually
CLINICAL SCENARIO | INTERVENTION | DETAILS |
|---|---|---|
Acute cord compression from any cause | Dexamethasone | Loading dose of 10 mg IV, then 4 mg IV or PO every 6 hours; reduces vasogenic edema around the tumor and buys time before definitive treatment |
Metastatic extradural tumor with cord compression | Radiation therapy (conventional external beam) | Standard first-line for most metastatic cord compression; typical regimen is 30 Gy in 10 fractions or 20 Gy in 5 fractions |
Metastatic cord compression with high-grade block, bony instability, radioresistant tumor (renal cell, melanoma), or neurological deterioration during radiation | Surgical decompression and stabilization followed by radiation | Posterolateral decompressive laminectomy or anterior corpectomy with instrumented fusion, followed by adjuvant radiation |
Intradural-extramedullary tumors (meningioma, schwannoma) | Surgical resection | Gross total resection is curative in most cases; meningiomas and schwannomas are well-encapsulated and amenable to complete removal |
Intramedullary ependymoma | Surgical resection | Ependymomas have a clear cleavage plane, allowing gross total resection with good outcomes; adjuvant radiation if resection is subtotal |
Intramedullary astrocytoma | Surgical debulking plus radiation | Astrocytomas are infiltrative without a clear cleavage plane, making complete resection difficult; postoperative radiation is typically given |
Hemangioblastoma (especially with von Hippel-Lindau) | Surgical resection | Well-circumscribed vascular tumors; gross total resection is curative; screen for other VHL-associated lesions |
Pain management | Corticosteroids, opioids, neuropathic agents (gabapentin, pregabalin) | Neuropathic pain is common; gabapentin starting at 300 mg daily titrated up, or pregabalin 75 mg twice daily |
Long-term follow-up | Serial MRI surveillance | Frequency depends on tumor type and completeness of resection; typically every 3 to 6 months initially, then annually |
Acute management of suspected spinal cord compression is time-sensitive. The single most important initial step is dexamethasone, which reduces peritumoral vasogenic edema and can temporarily halt or reverse neurological decline. This should be given immediately, even before imaging is completed, if clinical suspicion is high. Dexamethasone is the "next best step" answer whenever a vignette describes acute or subacute cord compression with neurological deficits.
For metastatic epidural cord compression, the landmark Patchell trial established that surgical decompression followed by radiation is superior to radiation alone in patients who are surgical candidates with a single area of compression, an expected survival of at least 3 months, and who are not completely paraplegic for more than 48 hours. However, radiation alone remains the standard approach for patients with radiosensitive tumors (lymphoma, myeloma, small cell lung cancer), those who are poor surgical candidates, or those with multilevel disease.
For primary spinal cord tumors, surgery is the mainstay. The key teaching point is the difference between ependymoma and astrocytoma: ependymomas are well-demarcated with a clear cleavage plane, making gross total resection feasible and often curative, while astrocytomas are infiltrative and rarely fully resectable, necessitating adjuvant radiation.
Contraindications and cautions: Prolonged high-dose corticosteroids carry risks of hyperglycemia, immunosuppression, gastric ulceration (prophylax with a proton pump inhibitor), and proximal myopathy. In patients with diabetes, blood glucose must be monitored closely. Radiation carries a risk of radiation myelopathy, which is a delayed (months to years) progressive myelopathy that can mimic tumor recurrence.
05Differential Diagnosis and Distractors
Transverse myelitis
WHY IT IS SIMILAR
Progressive bilateral weakness, sensory level, bowel/bladder dysfunction
KEY DISCRIMINATOR
Acute to subacute onset (hours to days, not weeks to months); often post-infectious or associated with autoimmune disease; MRI shows T2 hyperintensity over multiple segments without a discrete enhancing mass; no vertebral body destruction
Multiple sclerosis
WHY IT IS SIMILAR
Spinal cord lesion with upper motor neuron signs, sensory deficits
KEY DISCRIMINATOR
Relapsing-remitting course in a young woman; lesions are typically short-segment (fewer than 2 vertebral segments), peripheral within cord; brain MRI shows periventricular white matter lesions; oligoclonal bands in CSF
Epidural abscess
WHY IT IS SIMILAR
Back pain with progressive neurological deficits and cord compression
KEY DISCRIMINATOR
Fever, elevated ESR/CRP, leukocytosis; history of IV drug use, recent spinal procedure, or bacteremia; MRI shows rim-enhancing epidural collection, not a solid mass
Syringomyelia (without tumor)
WHY IT IS SIMILAR
Cape-like dissociated sensory loss, central cord pattern
KEY DISCRIMINATOR
Associated with Chiari malformation type 1; MRI shows a fluid-filled cavity (same signal as CSF) without an enhancing solid component; no cord expansion beyond the syrinx itself
Vitamin B12 deficiency (subacute combined degeneration)
WHY IT IS SIMILAR
Bilateral posterior column dysfunction (loss of proprioception, vibration) and corticospinal tract signs
KEY DISCRIMINATOR
No pain prominence; symmetrical findings; peripheral neuropathy also present; MRI may show T2 hyperintensity in posterior columns without mass; low serum B12 and elevated methylmalonic acid confirm
Guillain-Barre syndrome
WHY IT IS SIMILAR
Progressive ascending weakness with areflexia
KEY DISCRIMINATOR
Lower motor neuron pattern (areflexia, flaccidity), not upper motor neuron; sensory level is absent; CSF shows albuminocytologic dissociation (elevated protein, normal cell count); preceded by infection
Amyotrophic lateral sclerosis
WHY IT IS SIMILAR
Progressive weakness with upper and lower motor neuron signs
KEY DISCRIMINATOR
No sensory involvement; no pain; no bowel or bladder dysfunction until very late; fasciculations prominent; EMG/nerve conduction studies confirm widespread denervation
Vertebral compression fracture (osteoporotic)
WHY IT IS SIMILAR
Acute back pain, possible kyphotic deformity
KEY DISCRIMINATOR
Sudden onset after minimal trauma in elderly or osteoporotic patient; no neurological deficits unless retropulsed fragment; MRI shows marrow edema without enhancing soft tissue mass
DIFFERENTIAL | WHY IT IS SIMILAR | KEY DISCRIMINATOR |
|---|---|---|
Transverse myelitis | Progressive bilateral weakness, sensory level, bowel/bladder dysfunction | Acute to subacute onset (hours to days, not weeks to months); often post-infectious or associated with autoimmune disease; MRI shows T2 hyperintensity over multiple segments without a discrete enhancing mass; no vertebral body destruction |
Multiple sclerosis | Spinal cord lesion with upper motor neuron signs, sensory deficits | Relapsing-remitting course in a young woman; lesions are typically short-segment (fewer than 2 vertebral segments), peripheral within cord; brain MRI shows periventricular white matter lesions; oligoclonal bands in CSF |
Epidural abscess | Back pain with progressive neurological deficits and cord compression | Fever, elevated ESR/CRP, leukocytosis; history of IV drug use, recent spinal procedure, or bacteremia; MRI shows rim-enhancing epidural collection, not a solid mass |
Syringomyelia (without tumor) | Cape-like dissociated sensory loss, central cord pattern | Associated with Chiari malformation type 1; MRI shows a fluid-filled cavity (same signal as CSF) without an enhancing solid component; no cord expansion beyond the syrinx itself |
Vitamin B12 deficiency (subacute combined degeneration) | Bilateral posterior column dysfunction (loss of proprioception, vibration) and corticospinal tract signs | No pain prominence; symmetrical findings; peripheral neuropathy also present; MRI may show T2 hyperintensity in posterior columns without mass; low serum B12 and elevated methylmalonic acid confirm |
Guillain-Barre syndrome | Progressive ascending weakness with areflexia | Lower motor neuron pattern (areflexia, flaccidity), not upper motor neuron; sensory level is absent; CSF shows albuminocytologic dissociation (elevated protein, normal cell count); preceded by infection |
Amyotrophic lateral sclerosis | Progressive weakness with upper and lower motor neuron signs | No sensory involvement; no pain; no bowel or bladder dysfunction until very late; fasciculations prominent; EMG/nerve conduction studies confirm widespread denervation |
Vertebral compression fracture (osteoporotic) | Acute back pain, possible kyphotic deformity | Sudden onset after minimal trauma in elderly or osteoporotic patient; no neurological deficits unless retropulsed fragment; MRI shows marrow edema without enhancing soft tissue mass |
06Traps and High-Yield Pearls
The most common way students get questions on spinal cord neoplasms wrong is by failing to recognize the compartment-based logic that governs this topic. Exam questions are not simply asking "is there a spinal cord tumor?" They are testing whether you can determine where the tumor is based on the neurological examination pattern, and then match it to the correct tumor type.
The first trap involves confusing intramedullary and extramedullary presentations. If a vignette describes sacral sparing with a cape-like sensory deficit, the tumor is intramedullary. If the vignette describes early sacral loss with a Brown-Sequard pattern, it is extramedullary. Selecting the wrong compartment leads you to the wrong tumor type and wrong management.
The second trap is the "pain worse at night" clue. Students who have drilled mechanical back pain differentials may dismiss night pain as a red flag without connecting it to neoplasm. On the exam, back pain that is worse at night, unrelieved by rest, progressive over weeks, and accompanied by weight loss or a history of cancer should immediately trigger concern for metastatic cord compression, and the next step is always MRI, not conservative management or physical therapy.
A third trap is ordering the wrong imaging study. Plain radiographs and CT scans are insufficient to evaluate the spinal cord itself. A vignette may tempt you with a plain film showing a normal-appearing spine (intradural tumors cause no bony changes), leading you to falsely reassure the patient. The correct answer is always MRI with gadolinium when myelopathy is suspected.
Finally, students frequently forget that dexamethasone is the immediate first step in acute cord compression, even before arranging definitive imaging. The vignette may present an oncology patient with rapidly progressive leg weakness and a sensory level, and ask for the "next best step." The answer is dexamethasone, not MRI, not radiation, not surgery. Imaging follows immediately afterward, but the steroid is given first to halt ongoing cord injury from edema.
The core competency tested across all spinal cord neoplasm questions is the ability to localize the lesion based on clinical findings, select the appropriate imaging, and initiate time-sensitive treatment for cord compression.