2e:I[856015,["/_next/static/immutable/chunks/1xzisbplk9czp.js","/_next/static/immutable/chunks/3j2i1faptc_-9.js","/_next/static/immutable/chunks/0gcbsntq5_9qd.js","/_next/static/immutable/chunks/08tq8rmv423j5.js","/_next/static/immutable/chunks/3o-s-fbpanizg.js","/_next/static/immutable/chunks/0-t9leoxnnuho.js","/_next/static/immutable/chunks/311zvdjfxff-f.js","/_next/static/immutable/chunks/1a_hqhrsle_n_.js"],"default"] 2f:T64dc,

FEATURE	DETAIL
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)
PATIENT 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 PHYSICAL 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
KEY DIAGNOSTIC RESULTS	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"

1. Pathophysiology

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.

2. Classification and Clinical Manifestation

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

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).

3. Diagnostic Workup

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.

4. Management and Treatment

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.

5. Differential Diagnosis and Distractors

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

6. Traps 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.

1f:["$","$L2e",null,{"article":{"id":"fa8b4c3b-9457-447b-a8b8-3a1b07ed8c10","title":"Tumor Medulla Spinalis","content":"$2f","category":"Neurologi","created_at":"2026-09-03T16:28:18.023407+00:00","status":"published","subcategory":null},"questionCount":0,"sections":[{"id":"section-pathophysiology","num":"01","title":"Pathophysiology"},{"id":"section-classification-and-clinical-manifestation","num":"02","title":"Classification and Clinical Manifestation"},{"id":"section-diagnostic-workup","num":"03","title":"Diagnostic Workup"},{"id":"section-management-and-treatment","num":"04","title":"Management and Treatment"},{"id":"section-differential-diagnosis-and-distractors","num":"05","title":"Differential Diagnosis and Distractors"},{"id":"section-traps-and-high-yield-pearls","num":"06","title":"Traps and High-Yield Pearls"}],"hasSummaryTable":true}]