Spinal Cord Injury Flashcards by Rai Christiana

Descending motor function:

Lateral corticospinal (pyramidal) tract

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Joint sensation, position, vibration, discriminative touch

Posterior column

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Pain and temperature

Lateral spinothalamic tract

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Somatic motor

Anterior horn cells

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Autonomic sympathetic

Intermediolateral cell column

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Motor Signs of Spinal Cord Disorders

• Autonomic neuron signs

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• Autonomic neuron signs

• Intermediolateral cell column (T1-L2)
• Sacral autonomic (PSY) neurons (S2-S4)

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Intermediolateral cell column (T1-L2)

Horner’s syndrome:
IPSILATERAL

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Intermediolateral cell column location

T1-L2

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Horner’s syndrome:

• Miosis
• Ptosis
• Anhydrosis
• Enophthalmos

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Sacral autonomic (PSY) neurons location

S2-S4

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Sacral autonomic (PSY) neurons (S2-S4)

Urinary and bowel incontinence

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• Loss of vibration sense
• Loss of position sense
• Loss of 2 point discrimination
• Loss of deep touch
• IPSILATERAL to affected side in dermatomes below or at the level of spinal cord lesion
TRACTS
SEGMENTS

• Posterior column

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• Loss of pain sensation
• Loss of temperature sensation
• CONTRALATERAL to affected tract in dermatomes
beginning one or 2 segments below the level of the lesion

• Lateral spinothalamic tract

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Pattern of lamination of the spinothalamic tract

• Sacral Sparing

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• Lesion affecting the dorsal root will cause diminution or loss of all sensory modalities
• IPSILATERAL and in dermatomes supplied by the involved dorsal root

Dorsal root signs

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Bilateral diminution or loss of pain and temperature sensations in dermatomes supplied by the involved spinal cord segments

Anterior white commissure signs

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Hyperextension injuries, syringomyelia, intramedullary tumors

Central cord

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Often cervical
Dissociated sensory deficits (loss of pain and temperature with preserved
proprioception affecting dermatomes at level of lesion)

As lesion enlarges, weakness, muscle wasting, absent DTRs in arms, and spastic paraparesis occur

Central cord

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Anterior spinal artery territory ischemia (aortic dissection, aortic aneurysm surgery, atherosclerosis, vasculitis)

Anterior cord

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Sudden loss of pain and temperature below level of lesion, paraparesis and urinary incontinence, but preserved proprioception

Anterior cord

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Multiple sclerosis or demyelination, cervial spondylitic. myelopathy, spinal cord tumors, atlantoaxial subluxation, Friedreich ataxia, subacute combined degeneration

Posterior cord

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Sensory ataxia (proprioceptive loss), paresthesia, weakness, extensor plantar responses, urinary incontinence, and hermitte phenomenon

Posterior cord

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Trauma, multiple sclerosis or demyelination, cord compression

Lateral cord
(Brown-Séquard)

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Weakness paresthesia, and proprioceptive loss ipsilateral to lesion Loss of pain and temperature contralateral to lesion

Lateral cord (Brown-Séquard)

Trauma, cord compression

Complete cord

Loss of sensory, motor, and autonomic function below level of lesion

Complete cord

Amyotrophic lateral sclerosis, primary lateral sclerosis, progressive muscular atrophy, poliomyelitis, HTLV-1 infection, hereditary spastic paraparesis

Pure motor

Spastic paraparesis or tetraparesis with hyperactive DTRs (UMN) Weakness (monoparesis, paraparesis, tetraparesis), atrophy, fasciculations (LMN)

Pure motor

Intramedullary tumors, dermoid tumors, lipomas, metastatic tumors

Conus

Rectal and urinary incontinence, loss of anal reflexes, impotence, saddle anesthesia (S3-5 dermatomes), little or no weakness

Conus

Intervertebral disk herniation, tumors, infections, arachnoiditis

Caudal equina

Areflexic and flaccid paraparesis with back pain that radiates down posterior aspect of both legs, sensory loss in distribution of involved roots, urinary and fecal incontinence

Cauda equina

Brown sequard syndrome UMN at and below the level of the lesion • Paralysis, spasticity, hyperreflexia, Babinski, clonus

Ipsilat corticospinal tract sign

Brown sequard syndrome • Decreased vibration, position, 2-point discrimination and deep touch at and below the level of the lesion

Ipsilat posterior column sign

Brown sequard syndrome LMN in muscles supplied by affected cord segment • Paralysis and atrophy, loss of myotatic reflexes, fibrillations, fasciculation, hypotonia

Ipsilat Ventral horn sign

Loss of pain and temperature beginning one or 2 segments below the level of lesion Brown-sequard syndrome

Contralat spinothalamic tract signs

Brown sequard syndrome Segmental loss of thermal sense in dermatomes one or two segments below the level of the hemisection due to the interruption of the spinothalamic fibers crossing in anterior commissure

Bilateral

• Degenerative disease of AHC and LCST bilaterally • UMN+LMN • Progressive • Involves brainstem motor nuclei • Spared eye movement and sacral neurons for sphincter control

Anterior horn and Lateral Corticospinal Tract Syndrome (Motor Neuron Disease or ALS)

• Lesion in central canal will encroach on the anterior white commissure (crossing fibers of pain and temperature sensations • Segmental and bilateral loss of pain and temperature in such dermatomes

Central Cord Syndrome (Syringomyelia)

Bilateral but selective degeneration of some of the posterior and lateral column tracts with loss of kinesthesia and discriminative touch, UMN signs • Vitamin B12 deficiency (pernicious anemia), Friedreich's ataxia

Combined system degeneration syndrome

• Abrupt onset • Flaccid LMN paralysis (spinal shock) occurs within minutes or hours below the level of the lesion and impaired bowel and bladder function • Dissociated sensory loss characterized by loss of pain and temperature with preservation of posterior column function • With time, UMN signs predominate • Development of painful dysesthesia after 6-8 months

Anterior Spinal Artery Syndrome

Motor spinal shock

• Flaccid bilateral paralysis of all muscles innervated by segments of the spinal cord affected and myotomes below • Sudden withdrawal of a predominantly facilitating or excitatory influence from supraspinal centers • Shift into UMN in later stages • Release of segmental reflexes below the level of the lesion from supraspinal inhibitory influences

Sensory spinal shock

All sensations are lost bilaterally at and below the lesion • Hyperpathic zone at the border of the lesion and for one or 2 segments above it

Bladder function spinal shock

• Urinary retention for 8 days to 8 weeks • Subsequently, a state of automatic bladder emptying occurs • Sensory receptors in the bladder wall evoke reflex contraction of detrusor muscles

Bowel function spinal shock

• Paralysis and fecal retention • Subsequently, intermittent automatic reflex defecation muscles

• Early sphincter dysfunction, urinary incontinence, loss of voluntary emptying of bladder, increased residual urine volume and absent sensation of urge to urinate • Constipation, impaired sexual function • Symmetric loss of S2-S4 sensations (saddle anesthesia) • Loss of ankle jerk

Conus medullaris syndrome

Conus medillaris syndrome • Symmetric loss of

S2-S4 sensations (saddle anesthesia)

Conus Medullaris Syndrome Reflex

Loss of ankle jerk

• Early occurrence of radicular pain in dermatomes supplied by the affected roots • LMN in muscles supplied by affected nerves

Cauda equina syndrome

Leading cause of disability especially among younger people, with high impact on years lived with disability

Traumatic spinal cord injury

Most common cause of traumatic spinal cord injury

MVA

Leading cause of disability especially among younger people, with high impact on years lived with disability

Laceration from missile injury, sharp bone fragments dislocation, or severe distraction, with or without transection Distraction resulting in forcible stretching of the spinal column in the axial plane with shearing of the spinal cord or its blood supply Impact with persistent compression in burst fractures Impact with only transient compression after hyperextension injuries

Traumatic spinal cord injury MOI Primary mechanism

• Initial mechanical injury due to local deformation and energy transformation • Impact of bone and ligament against the SC • Subsequent compression, stretching, crushing of the spinal cord

Traumatic spinal cord injury MOI Secondary mechanism

• Cascade of biochemical and cellular processes that are initiated by primary mechanisms • Damage neural structures on cellular level • Microvascular changes, excitatory amino acids, membrane destabilization, free radicals, inflammatory mediators and neuroglial apoptosis

4 group TSCI Pathobiology

Solid cord injury Contusion/cavity Laceration Massive compression

grossly appears normal without evidence of softening, discoloration or cavity formation; damage can be seen on histologic examination

Solid cord injury

no breach or disruption in surface anatomy, no dural adhesions

Contusion/cavity

clear cut disruption of surface anatomy

Laceration

macerated or pulpified; with severe vertebral body fracture or dislocation

Massive compression

4 phases histopathology

1. Immediate 2. Acute 3. Intermediate 4. Late

• Actual mechanical disruption of tissues that occur at the time of injury • Tears, compression, distortions • Vasodilation, congestion (hyperemia) and petechial hemorrhages • Some with no changes • Pathology of SCI is also due to secondary mechanisms

Immediate phase (first 2 hours)

• Vascular changes, edema, hemorrhage, inflammation, neuronal and myelin changes • Edema: vasogenic vs cytotoxic • Pressure-induced ischemia, alter astroglial functions • Seen from 3 hrs to 3 days after injury • Vascular injury • Occur primarily in gray matter following contusion injury • Hemorrhages due to rupture of postcapillary venules or sulcal arterioles, either from mechanical disruption by trauma or from intravascular coagulation leading to venous stasis and distention • Inflammatory • Neutrophil influx peak at 2 days, disappear by 3 days • Neuronal injury • Necrosis and apoptosis • Axonal swelling (retraction balls) • Myelin breakdown - swelling of myelin sheaths and its fragmentation and phagocytosis by macrophages • Oligodendrocyte death

Acute phase (hours to 1-2 days)

swelling of myelin sheaths and its fragmentation and phagocytosis by macrophages

Myelin breakdown

• Prominent glial responses with elimination of necrotic debris, beginning of astroglial scarring, resolution of edema, tissue revascularization and BBB restoration

Intermediate phase (days to weeks)

• Wallerian degeneration, astroglial and mesenchymal scar formation, development of cysts and syrinx and schwannosis • SC replaced by fibrous connective tissue and collagen - act as barriers for axonal migration • Cysts and syrinx - surrounded by astrogliotic wall and represent the final healing phase of necrosis; filled with ECF, residual macrophages, small bands of connective tissue and blood vessels; not clinical problem but do not provide a good substrate for regeneration • Schwannosis - aberrant intra- and extramedullary proliferation of Schwann cells with associated axons; barrier to healing; aberrant axons can cause pain, spasticity and other chronic responses

Late phase (weeks to months/years)

act as barriers for axonal migration

SC replaced by fibrous connective tissue and collagen

surrounded by astrogliotic wall and represent the final healing phase of necrosis; filled with ECF, residual macrophages, small bands of connective tissue and blood vessels; not clinical problem but do not provide a good substrate for regeneration

Cysts and syrinx

aberrant intra- and extramedullary proliferation of Schwann cells with associated axons; barrier to healing; aberrant axons can cause pain, spasticity and other chronic responses

Schwannosis

-identify an unstable fracture

X-ray

• Lateral cervical radiograph -identify an unstable fracture • Lateral, anteroposterior, odontoid view • Up to 60% of fractures are missed on radiographs • Conscious patient - dynamic flexion-extension radiographs to assess unstable ligamentous or osteoligamentous injuries

X-ray

Ct scan limitation

• Limitation: relative inability to detect changes in soft tissue including the spinal cord and ligaments

• Minimum neuroimaging required for symptomatic and unconscious patient • Negative predictive value of 99-100%

X-ray + CT

• Best technique for imaging the spinal cord • Indications: • FND with normal x-rays • Noncorrelation between neurologic deficit and x-ray findings • Deterioration after treatment • Failed attempts at closed reduction

MRI

Traumatic Spinal Cord Injury Neurologic Assessment and Classification

ASIA (American Spinal Injury Association) Impairment Scale

Traumatic Spinal Cord Injury Neurologic Assessment and Classification Motor level

most caudal key muscle group that is grades 3/5 or greater, with segments cephalad to that level graded 5/5

Traumatic Spinal Cord Injury Neurologic Assessment and Classification Sensory level

most caudal dermatome to have normal light touch AND pinprick sensations on BOTH sides

Traumatic Spinal Cord Injury Neurologic Assessment and Classification Neurologic level of injury

most caudal level at which BOTH motor and sensory modalities are intact

Brown-Sequard Syndrome % of traumatic SCI

1-5

Brown-Sequard Syndrome % Best prognosis for ambulation of the SCl syndromes

75-90%

Disproportionately more motor impairment of UE > LE • Bladder dysfunction • Varying degrees of sensory loss below the level of lesion

Central cord syndrome

Causes of central cord syndrome

• Most common in elderlies with preexisting cervical spondylosis with superimposed hyperextension injury of cervical spine • Cord compression occurs between osteophyte-disk complexes anteriorly and in-folded ligamentum flavum posteriorly • Falls • MVA

Central cord syndrome % most common sci syndrome

Central cord syndrome Favorable prognosis for functional recovery

• Younger patients with good hand function • Early motor recovery • Absence of lower extremity impairment

• Affects the anterior 2/3 of spinal cord with preservation of the posterior columns • Complete paralysis • Loss of pain and temperature sensation below the lesion • Preservation of touch and proprioception

Anterior cord syndrome

Anterior cord syndrome % of traumatic SCI

Causes of anterior cord syndrome

Flexion injuries, direct damage from bony fragments or disc compression, or ASA occlusion • Poor prognosis for functional improvement

Posterior cord syndrome %

Lesion of posterior column with loss of touch and proprioception below level of injury • Preservation of pain and temperature • Preservation of motor strength

Posterior cord syndrome

Posterior cord syndrome causes

• Hyperextension • PSA occlusion • Nontraumatic injuries (tumor or Vit B12 deficiency)

• Injury of the caudal spinal cord and associated sacral nerve roots within the spinal canal • Conus: between L1-L2 vertebra • Combination of UMN+LMN signs

Conus medullaris syndrome

Conus location

L1 - L2

Conus medullaris syndrome findings

• Saddle anesthesia • Areflexic bladder and bowel • Variable LE weakness and sensory loss

Skin is intact with non blanchable erythema

Stage I

Partial thickness skin loss involving the epidermis and dermis

Stage II

Full thickness skin loss extending to subcutaneous tissue but does not cross the fascia beneath it. Slough or eschar may be visible; may be foul-smelling

Stage III

Full thickness skin loss extends through the fascia with considerable tissue loss; there may be muscle, bone, tendon or joint involvement

Stage IV

Depth unknown because slough or eschar obscures the extent of tissue damage

Unstageable

Occurs with prolonged pressure and shear forces at bone-muscle interface Intact or non-intact skin w/ persistent, non-blanched, deep red, maroon or purple discoloration

Deep tissue injury

spreads to deeper tissue and bone, blood

Infection

severe fluid and protein loss

Wounds are catabolic

• Injuries above T6 • Loss of coordinated autonomic responses to physiologic stimuli • Uninhibited or exaggerated SY response to noxious stimuli can lead to extreme HPN through vasoconstriction • Stimuli: bladder dysfunction, bowel impaction, pressure sores, bone fractures or occult visceral disturbances • Manifestations: hypertension, bradycardia, headache, sweating • Severity of attacks correlate with severity of SCl

Autonomic dysreflexia

Autonomic dysreflexia manifestation

hypertension, bradycardia, headache, sweating

Orthostatic hypotension • Gradual position changes • Compression stockings • Abdominal binders • Medical therapy (a-adrenergic agonist midodrine, mineralocorticoid fludrocortisone

Autonomic dysreflexia

• Upper and midcervical spine (C3-5, output to phrenic nerve) • Severity of respiratory failure and need for assisted ventilation is directly related to the level of severity of SCI • Impaired cough strength and difficulty mobilizing lung secretions - increased risk for pneumonia • Chest physiotherapy • Vaccination • DVT and pulmonary embolism

Pulmonary disease

• Neurogenic bladder • Infections • Vesicoureteral reflux • Renal failure • Calculi • Impaired sensation of bladder fullness, motor control of bladder and sphincter function • Clean intermittent catheterization • Sexual dysfunction

Genitourinary complications

• Structured bowel regimen employing regular diet, 2-3L/day, 30g fiber • Chemical and mechanical stimulation

Gastrointestinal dysfunction

Gastrointestinal dysfunction • Structured bowel regimen employing regular diet,

2-3 L/day, 30 g fiber

deposition of bone within soft tissue around peripheral joints; pain and inflammation in affected joints

Heterotropic ossification

• Osteoporosis secondary to disuse - prone to fractures • Heterotropic ossification - deposition of bone within soft tissue around peripheral joints; pain and inflammation in affected joints • Tx: passive ROM, bisphosphonates, NSAIDs

Abnormal bone metabolism

Disruption of the descending inhibitory pathways, with increase in excitability of spinal reflexes and resting muscle tone • Pain, decreased mobility, muscle spasms, contractures

Spasticity

Spasticity prevention

• Proper positioning, passive ROM exercises, appropriate splinting, oral mediations (baclofen, tizanidine, diazepam)

• Depression • Suicidality • Drug addiction

• Psychiatric complications

Inflammatory processes of the spinal cord, both infectious and noninfectious

Myelitis

involves white matter

Leukomyelitis

involves the gray matter; Polio virus

Poliomyelitis

involves cross sectional area of the cord

Transverse myelitis

additional involvement of the meninges

Meningomyelitis

Myelitis diagnostic studies

• Spine MRI with contrast • CSF analysis • Infectious agents • Demyelination

Myelitis treatment

• Supportive • Disease specific

Occur from direct spread (vertebral osteomyelitis, local surgical or anesthetic procedure) or hematogenous spread from distant infection • Some with no source found • Risk factor: IV drug use, immunosuppression • Clinical findings: • Back pain, fever • Radicular pain followed by rapidly evolving motor and sensory deficits below level of lesion, sphincter disturbances

Spinal Epidural Abscess

Spine epidural abscess Laboratory finding

• Peripheral leukocytosis • Elevated ESR • Blood cultures • CSF analysis in unruptured abscess: increased WBC, increased protein, normal glucose

Spinal Epidural Abscess Imaging

MRI

Spinal Epidural Abscess Treatment

Drainage • Stabilization of spine • Systemic antibiotics

Development of fluid-filled gliosis-lined cavity within the spinal cord (intramedullary) =

Syrinx

• Cavity is irregular and disrupts the anterior horns of gray matter and gray matter ventral to central canal

Syringomyelia

Syringomyelia common loc

C2 and T9-11

• Can extend to brainstem =

Syringobulbia

Cape like distribution of decreased pain and temperature sensation in the back, arms and hands, in which occurs due to disruption of the crossing spinothalamic tracts • Varying degrees of weakness in arms (LMN type, involvement of cervical AHC) and legs (UMN, involvement of the lateral corticospinal tract) • +/ - Horner's syndrome - intermediolateral columns • Preserved bowel and bladder function unless syrinx extend to sacral cord

Syringomyelia

Syringomyelia Imaging

MRI

- direct communication between arteries and veins without interposition of pathologic network

Arteriovenous fistulas

vascular network interposed between feeding arteries and draining veins

Arteriovenous malformation -

• Radicular pain, sensory disturbance, leg weakness, bladder dysfunction • Slowly progressive in most - due to compression • 10% sudden onset - due to hemorrhage or infarction • Weakness and numbness may increase after ambulation • Pathognomonic bruit over the spinal cord in 25% for patients with intradural AVM • Often affects lower thoracic and conus medullaris

Spinal Cord Arteriovenous Shunts

Spinal Cord Arteriovenous Shunts Imaging

Angiography

Spinal Cord Arteriovenous Shunts • Treatment

• Complete closure of shunt • Embolization • Ligation of feeding vessel and excise the abnormality

• Rare • 1-2% of vascular neurologic illnesses • 5-8% of all acute myelopathies • Sudden onset of symptoms • Moderate-severe back pain at side of cord infarction (most often in thoracic region) followed by paraplegia within minutes • Usually associated with paraparesis and loss of pain sensation below the level of infarction bilaterally with intact proprioception and vibration sense • Loss of bladder control • Causes: severe hypotension, aortic dissection, aortic surgery, cardioembolism, vasculitis, atherosclerosis

Spinal Cord Infarction

single; anterior 2/3

Anterior spinal artery -

- dorsal 1/3; greater anastomosis

• Paired posterior spinal arteries

is discontinuous and require multiple feeders

Anterior spinal artery is

least amount of anastomosis; at highest risk

T4-T8

painless paraparesis or quadriparesis that may be sporadic or occur with postural changes but with no loss of consciousness or intracranial localizing features

Spinal TIAs

• Sudden onset paraplegia, loss of pain sensation, loss of bladder control, pain at infarction site • Initial absence or hypoactivity of DTRs then becomes hyperreflexia • Spinal TIAs - painless paraparesis or quadriparesis that may be sporadic or occur with postural changes but with no loss of consciousness or intracranial localizing features • Occur in patients with foraminal stenosis during cervical or lumbar extension

Spinal Cord Infarction

Spinal Cord Infarction Treatment

Direct to predisposing condition • Aspirin

• Sudden onset of pain at the site of hemorrhage (most often the upper thoracic) • Paresthesia and weakness occurring hours or days later below the level of spinal pain • Urinary retention

Spinal Epidural and Subdural Hematomas

Spinal Epidural and Subdural Hematomas Diagnostics

• CT - Spinal EDH - high density, oblong mass that sometimes impinges on the lateral aspect of the cord • MRI

Spinal Epidural and Subdural Hematomas Prognosis

Dependent on degree of neurologic deficit, timing of decompression (<12hrs)

Motor or sensory loss segmentally or below the level of lesion • Loss of bladder or bowel control • Back pain • Progressive course • Abnormal CT or MRI

Spinal cord tumors

Intramedullary

Ependymoma Astrocytoma Hemangioblastoma

Intradural, extramedullary

Meningioma Schwannoma Neurofibroma

Extradural

Metastatic cancer Primary bony lesions, including multiple myeloma

Spinal Cord Tumors Most common metastatic tumors are found in

vertebral body and epidural space • Source: lung, breast, prostate, Gl

Spinal Cord Tumors • Diagnostics:

• Contrast enhanced MRI • Biopsy and surgical excision

• Travel hematologically through arterial system or retrogradely through Batson venous plexus • Leptomeningeal metastasis from extension from nearby bone or spread through CSF

Metastatic Cord Compression

Clinical features: • Weakness, sensory loss, urogenital dysfunction • PAIN • Slowly progressive in compressive tumor growth vs acute in vertebral fracture due to tumor • Red flags: • Age >60 • Associated weight loss • Worse at night • Thoracic rather than lumbar pain • tenderness

Metastatic Cord Compression

Metastatic Cord Compression Imaging

Imaging of choice: MRI with contrast • Visualization of cord, soft tissue involvement and edema

detect bony metastasis

CT scan

Metastatic Cord Compression Outcome

poor • Average life expectancy of 4-15 months