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Flashcards in SPINE Deck (26)
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1
Q

SCOLIOSIS

Idiopathic (80%)

A
  1. Congenital—0–3 years, M>F. Left side convex. Usually regresses.
  2. Juvenile—4–9 years, females. Right side convex. Usually
    progresses.
  3. Adolescent—females. Right-sided thoracic convexity. Progressive if
    the Cobb angle at skeletal maturity is >30 degrees. If <30 degrees,
    the chance of progression is only 5%.
2
Q

SCOLIOSIS
Congenital anomalies (10%)
2

A

Progressive in 75% of patients.
1. Vertebral—failure of formation (wedge-shaped vertebrae, hemivertebrae, butterfly vertebrae),
Failure of segmentation (unilateral bar)
Mixed anomalies.

  1. Neurological—
    Chiari malformation, syringomyelia, tethered cord, diastematomyelia.
3
Q

SCOLIOSIS

Other causes 6

A
  1. Developmental dysplasias—diffusely involve multiple bones, e.g.
    achondroplasia, neurofibromatosis, osteogenesis imperfecta.
  2. Neuromuscular—cerebral palsy, spinocerebellar degeneration,
    poliomyelitis, muscular dystrophies (e.g. Duchenne).
  3. Tumour-related—osteoid osteoma, osteoblastoma, aggressive
    haemangioma, intraspinal tumours. Usually painful.
  4. Degenerative—acquired secondary to degenerative spondylosis.
    Most common in lumbar spine.
  5. Posttraumatic.
  6. Infection.
4
Q

SOLITARY COLLAPSED VERTEBRA
NB: vertebra plana = almost complete loss of anterior and
posterior vertebral body height.

A
  1. Osteoporosis—generalized osteopenia. Coarsened trabecular
    pattern in adjacent vertebrae due to resorption of secondary
    trabeculae.
  2. Neoplastic disease.
    (a) Metastasis—breast, lung, prostate, kidney and thyroid
    account for most patients with a solitary spinal metastasis. The
    disc spaces are preserved until late. The bone may be lytic,
    sclerotic or mixed ± pedicle destruction.
    (b) Multiple myeloma/plasmacytoma—a common site, especially
    for plasmacytoma. May mimic an osteolytic metastasis or be
    expansile and resemble an aneurysmal bone cyst.
    (c) Lymphoma—secondary > primary bone involvement.
  3. Trauma.
  4. Infection—with destruction of vertebral endplates and adjacent
    disc spaces. TB, in particular, can cause vertebra plana with relative
    preservation of the discs.
  5. Eosinophilic granuloma—commonest cause of solitary
    vertebra plana in childhood. The posterior elements are usually
    spared.
  6. Benign tumours—haemangioma, GCT and ABC.
  7. Paget’s disease—diagnosis is difficult when a solitary vertebra
    is involved. Neural arch is involved in most cases. Hallmarks
    are trabecular coarsening and bone expansion. If other
    noncollapsed vertebrae are affected, then diagnosis becomes
    much easier.
5
Q

MULTIPLE COLLAPSED VERTEBRAE

11

A
  1. Osteoporosis.
  2. Neoplastic disease—most commonly multiple myeloma,
    leukaemia and lymphoma. Disc spaces are usually preserved until
    late. Paravertebral soft-tissue mass is more common in myeloma
    than metastases.
  3. Trauma—unusual to involve >2–3 levels. Visible cortical
    discontinuity and angular deformity.
  4. Scheuermann’s disease/juvenile kyphosis—children and young adults; wedging of ≥3 adjacent vertebrae in the lower thoracic spine with irregular
    endplates, disc space narrowing and kyphosis.thoracic spine kyphosis >40° (normal 25-40°) or thoracolumbar spine kyphosis >30°
  5. Infection—destruction of endplates adjacent to a destroyed disc.
  6. Langerhans cell histiocytosis—children and adolescents. Disc spaces often enlarged.
  7. Sickle cell anaemia—characteristic step-like depression centrally
    in the endplates, resulting in H-shaped vertebrae. Small calcified spleen may be visible on plain film.
  8. Gaucher disease—also causes H-shaped vertebrae, but the spleen is typically enlarged. Also associated with other pathological fractures, AVN and Erlenmeyer flask deformity.
  9. Osteogenesis imperfecta—osteopenia with multilevel compression fractures.
  10. Osteomalacia—coarse trabeculae with “fuzzy” demineralization.
  11. Hyperparathyroidism—subperiosteal bone resorption and brown tumours
6
Q

EROSION, DESTRUCTION OR ABSENCE OF

A PEDICLE

A
  1. Metastasis—lumbar > thoracic > cervical, but neural compression
    is most common at thoracic level due to a smaller spinal canal.
  2. Multiple myeloma.
  3. Intraspinal tumours—e.g. ependymoma, nerve sheath tumours.
    Usually cause erosion or flattening of pedicles + widening of the
    interpedicular distance.
  4. TB* and other infections.
  5. Radiotherapy.
7
Q

SOLITARY DENSE PEDICLE

6 + other

A
  1. Osteoblastic metastasis—no change in size.
  2. Osteoid osteoma—some enlargement of the pedicle ± radiolucent
    nidus ± scoliosis.
  3. Bone island.
  4. Secondary to unilateral spondylolysis—stress-induced sclerosis of
    the contralateral pedicle.
  5. Congenitally absent/hypoplastic contralateral posterior elements.
  6. Osteoblastoma—lucent nidus is larger than osteoid osteoma
    (>2 cm), therefore usually presents as a lucency with a sclerotic
    margin rather than a purely sclerotic pedicle.
  7. Other sclerotic bone lesions—e.g. Paget’s disease, fibrous
    dysplasia, sarcoidosis, tuberous sclerosis.
8
Q

ENLARGED VERTEBRAL BODY

A

Generalized
1. Gigantism—occurs prior to growth plate fusion.
2. Acromegaly—particularly in AP dimension, with widened disc
spaces, osteopenia and posterior vertebral body scalloping.

Local (single or multiple)
1. Paget’s disease—trabecular coarsening and cortical thickening.
Can involve body or entire vertebra. ‘Picture frame’ appearance in
mixed phase, ivory vertebra in diffuse sclerotic phase.
2. Benign bone tumour.
(a) Aneurysmal bone cyst—typically purely lytic and expansile.
Involves both anterior and posterior elements more commonly
than one part alone. Rapid growth; fluid–fluid levels on MRI.
(b) Haemangioma—with a prominent vertical trabecular pattern.
(c) Giant cell tumour—involvement of the body alone is most
common. Expansion is minimal.
3. Fibrous dysplasia—commonly ground-glass matrix. Spine lesions
are more common in polyostotic disease. The neural arch is more
commonly involved than the vertebral body.
4. Hydatid—over 40% of cases of osseous hydatid disease occur in
vertebrae. Osteolytic expansile lesions, typically associated with
paraspinal cystic lesions extending into adjacent ribs.

9
Q

SQUARING OF ONE OR MORE VERTEBRAL BODIES

3

A
  1. Seronegative spondyloarthropathies—most commonly
    ankylosing spondylitis. ( Psoriatic, IBD As, Reactive, Undiff SpA)
  2. Paget’s disease.
  3. Rheumatoid arthritis
10
Q

BLOCK VERTEBRAE

7

A
  1. Klippel-Feil syndrome—C2/3 and C5/6 are most commonly
    affected. Narrowing of the vertebrae at the site of a fused/
    rudimentary disc space (‘wasp-waist’ sign). Fusion of posterior
    elements is also common. Often associated with other anomalies,
    e.g. other segmentation anomalies, scoliosis, dysraphism,
    spinal cord anomalies, Sprengel’s deformity of the scapula
    (± omovertebral bar), cervical ribs, genitourinary anomalies (e.g.
    unilateral renal agenesis), cardiac/aortic anomalies and deafness.
  2. Isolated congenital—failure of segmentation, frequently
    associated with hemivertebra and absent vertebra adjacent to
    block vertebra, ± posterior element fusion.
  3. Juvenile idiopathic arthritis—can mimic Klippel-Feil syndrome,
    but there may also be angulation at the fusion site (not a feature
    of congenital fusion), and typically the spinous processes do not
    fuse in juvenile idiopathic arthritis.
  4. Ankylosing spondylitis—squaring of anterior vertebral margins,
    syndesmophytes, calcification of intervertebral discs and adjacent
    ligaments. No wasp-waist sign.
  5. Infectious spondylodiscitis—fusion across the disc space occurs
    late in the course of the disease. Features suggesting TB include a
    calcified or thin-walled paravertebral abscess, gibbus deformity,
    subligamentous spread ≥3 vertebral levels and involvement of an
    entire vertebral body or multiple noncontiguous levels.
  6. Surgical fusion—no wasp-waist sign.
  7. Posttraumatic—no wasp-waist sign.
11
Q

IVORY VERTEBRAL BODY

7

A
  1. Metastasis—prostate and breast are the most common sources.
  2. Paget’s disease—vertebra is also mildly enlarged.
  3. Haemangioma.
  4. Low-grade infection—including TB.
  5. SAPHO syndrome.
  6. Lymphoma—more common in Hodgkin disease.
  7. Sarcoidosis.
12
Q

ATLANTOAXIAL SUBLUXATION

A

Trauma

  1. Osseous injury—C1/C2 fracture.
  2. Ligamentous injury—disruption of transverse ligaments.

Arthritides
1. Rheumatoid arthritis—in 20–25% of patients with severe disease.
Associated erosion of the odontoid ± pannus.
2. Psoriatic arthropathy—in 45% of patients with spondylitis.
3. Juvenile idiopathic arthritis—most commonly in seropositive
juvenile onset rheumatoid arthritis.
4. CPPD—calcified inflammatory tissue may surround the dens, and
can cause crowned dens syndrome in the acute setting.
5. Hydroxyapatite deposition disease (HADD)—can also cause
crowned dens syndrome with bone erosions, similar to CPPD.
6. Systemic lupus erythematosus—in 10%; reported association
with length of disease, Jaccoud’s arthropathy and hypermobility.
7. Ankylosing spondylitis—in 2% of cases. Usually a late feature.

13
Q

Congenital hypoplasia/absence of the dens

NB: in children <9 years it is normal for the tip of the odontoid
to fall well below the top of the anterior arch of the atlas.

A

Congenital hypoplasia can be isolated or occur as part of various
syndromes including Down’s (20%), Morquio, spondyloepiphyseal
dysplasia and achondroplasia.

Infection
1. C1/C2 infection—associated epidural phlegmon or abscess.

  1. Grisel syndrome—laxity of transverse/alar ligaments usually
    occurring in young children, caused by hyperaemia following a
    nearby infectious process, e.g. retropharyngeal abscess, otitis
    media, pharyngitis or upper respiratory tract infection
14
Q

INTERVERTEBRAL DISC CALCIFICATION

A

Most common

  1. Degenerative spondylosis—common, can involve any part of the disc.
  2. Following spinal fusion.
  3. Ankylosing spondylitis—peripheral annulus calcification + other characteristic features.

Less common

  1. DISH—anterior annulus calcification + flowing osteophytes.
  2. CPPD—calcification of annulus ± pulposus, ligaments and facet joints, but usually no ankylosis. Can cause acute calcific disc inflammation ± endplate erosion, which can mimic infection (disc calcification aids differentiation).
  3. HADD—can cause calcific disc inflammation similar to CPPD.

Rare

  1. Alkaptonuria/ochronosis—multilevel central disc calcification, disc space narrowing and severe osteopenia.
  2. Haemochromatosis—similar to CPPD.
  3. Gout—together with erosions and tophi.
  4. Poliomyelitis.
  5. Acromegaly.
  6. Hyperparathyroidism.
  7. Amyloidosis.
  8. Idiopathic—a transient painful phenomenon in the cervical spine of children.
  9. Juvenile chronic arthritides
15
Q

Osteophytes

A

Arise from endplate margins from Sharpey
fibres, usually horizontal or claw-like.
Represents degenerative disc disease. Very
common

16
Q

Syndesmophytes

Ossification of the annulus fibrosus. Thin, vertical and symmetrical. When severe, results in ‘bamboo spine.

A
  1. Ankylosing spondylitis—classic cause of syndesmophytes, usually as a later feature of the disease (after corner erosions, ‘shiny corners’ and squaring of the vertebral bodies). Other classic features include ossification of interspinous ligaments, ankylosis of facet joints and erosion/ankylosis of costovertebral joints.
  2. CPPD/haemochromatosis.
  3. Ochronosis—with internal disc calcification, disc space narrowing
    and osteopenia
17
Q

Nonmarginal osteophytes/paravertebral ossification

A
  1. Psoriatic arthropathy.
  2. Chronic reactive arthropathy—like psoriatic arthropathy, but less
    common.
  3. SAPHO—nonmarginal osteophytes ± erosions, bony bridging or
    ankylosis
18
Q

Undulating anterior or posterior ossification

A
  1. DISH—anterior ossification, most common in the
    thoracic spine with sparing of the left side due to
    aortic pulsations. Involves >3 contiguous vertebrae;
    disc height is usually preserved. Associated with
    enthesophytes elsewhere.
  2. Ossification of the posterior longitudinal ligament—usually
    involves the cervical spine; most common in East Asians
19
Q

POSTERIOR SCALLOPING OF VERTEBRAL BODIES

7

A
  1. Tumours in the spinal canal—ependymoma (especially
    myxopapillary type), dermoid, lipoma, nerve sheath tumour and,
    less commonly, meningioma. Chronic raised intraspinal pressure
    distal to a tumour producing spinal block also causes extensive
    vertebral scalloping.
  2. Neurofibromatosis—scalloping is due to mesodermal dysplasia
    and dural ectasia. Localized scalloping can also result from pressure
    resorption by a neurofibroma, ± enlargement of an intervertebral
    foramen and flattening of one pedicle (‘dumbbell tumour’).
    However, multiple wide thoracic intervertebral foramina are more
    likely because of lateral meningocoeles rather than tumours.
  3. Acromegaly—other spinal changes include increased axial
    diameters of the vertebral bodies giving a spurious impression of decreased vertebral height, osteoporosis, spur formation and calcified discs.
  4. Achondroplasia—with spinal stenosis (due to short pedicles) and
    anterior vertebral body beaks.
  5. Other congenital syndromes—e.g. Ehlers-Danlos/Marfan (both
    cause dural ectasia), mucopolysaccharidosis, osteogenesis imperfecta.
  6. Communicating hydrocephalus—if severe and untreated.
  7. Syringomyelia—especially if the onset is <30 years.
20
Q

ANTERIOR SCALLOPING OF

VERTEBRAL BODIES

A
  1. Aortic aneurysm—intervertebral discs remain intact. Well-defined
    anterior vertebral margin, ± calcification in aortic wall.
  2. Lymphadenopathy—e.g. mycobacterial infection, malignancy.
    Pressure resorption of bone results in a well-defined anterior
    vertebral body margin unless there is bony infiltration.
  3. Delayed motor development—e.g. Down’s syndrome
21
Q

WIDENED INTERPEDICULAR DISTANCE

A
  1. Myelomeningocoele—fusiform distribution of widened interpedicular distances with the greatest separation at the midpoint of the involved segment. Disc spaces are narrowed and bodies appear to be widened. Spinous processes and laminae are not identifiable. Facets may be fused into a continuous mass. Scoliosis in most cases ± kyphosis.
  2. Intraspinal mass—especially ependymoma.
  3. Diastematomyelia—50% occur between L1 and L3; 25% between
    T7 and T12. Widened interpedicular distances are common but
    not necessarily at the same level as the spur. The spur is visible in
    33% of cases and extends from the neural arch anteriorly.
    Intersegmental laminar fusion + a neural arch defect at the same
    or adjacent level is highly suggestive. A meningocoele, neurenteric
    cyst or dermoid may also be seen.
  4. Trauma—suggests a burst fracture.
22
Q

DIFFUSE LOW MARROW T1 SIGNAL

A
  1. Red marrow reconversion—due to chronic anaemia (e.g. anaemia
    of chronic disease, sickle cell, thalassaemia, spherocytosis) or
    increased oxygen demand (heavy smoking, endurance athletes), or
    in patients on marrow-stimulating therapy (GCSF).
  2. Diffuse malignant infiltration—e.g. metastases (most commonly
    from prostate or breast), myeloma, lymphoma, leukaemia. Marrow
    signal is often hyperintense to skeletal muscle on STIR/T2 fatsat
    (isointense in red marrow reconversion).
  3. Haemosiderosis—e.g. due to haemolytic anaemia or recurrent
    blood transfusions. Diffuse low T1 and T2 signal due to
    haemosiderin deposition in the marrow. Low signal is also present
    in the liver and spleen, confirming the diagnosis.
  4. Disorders causing diffuse bony sclerosis—e.g. myelofibrosis,
    mastocytosis, osteopetrosis.
  5. Gaucher disease—diffuse marrow infiltration by Gaucher cells.
    Bone infarcts may also be seen
23
Q

INTRASPINAL MASSES
Extradural mass
17

A
  1. Disc herniation, extrusion or sequestration—usually extradural
    space, but can occasionally penetrate dura, especially in
    the thoracic spine. Low/intermediate T2 signal ± rim
    enhancement. May calcify or be associated with posterior
    osteophytes.
  2. Metastases, myeloma and lymphoma—usually extending from
    the adjacent vertebral body. Primary bone tumours may also
    extend into the epidural space.
  3. Synovial cyst—related to facet joint arthrosis, located in
    the posterolateral epidural space. Unilocular cyst ± rim
    enhancement.
  4. Extradural meningeal cyst—e.g. perineural cyst (located along a
    spinal nerve, usually within the neural foramen) or extradural
    arachnoid cyst (located within the spinal canal, usually posterior).
    Perineural cysts are often multiple and bilateral and are common,
    especially in the sacrum (Tarlov cysts). Unilocular, no
    enhancement.
  5. Epidural phlegmon/abscess—lobulated tissue/collection typically
    associated with spondylodiscitis. Phlegmon enhances uniformly;
    abscess enhances only peripherally. Paravertebral abscess may
    also be present.
  6. Epidural fibrosis—postoperative scar/fibrosis in the surgical bed
    related to intervention, which demonstrates internal
    enhancement (unlike recurrent disc material).
  7. Neurofibroma—nodular or plexiform-enhancing mass related to
    nerve root ± dumbbell configuration due to transforaminal
    extension. T2 hyperintense, often with central hypointensity
    (target sign). May be multiple in NF1
  8. Schwannoma—more commonly intradural, but may also be
    transforaminal with a dumbbell appearance. Similar appearance
    to neurofibroma, but the target sign is less common, and internal
    cystic change, haemorrhage or fatty degeneration is more
    common. May be multiple in NF2.
  9. Epidural haematoma—typically extends over multiple vertebral
    segments; caused by trauma, intervention or coagulopathy.
    Signal characteristics relate to chronicity of blood products, but
    often T1 hyperintense.
  10. Epidural lipomatosis—diffuse proliferation of epidural fat, most
    common in the lower thoracic and lumbar spine, causing mass
    effect on the thecal sac. Most commonly due to steroids or
    obesity.
  11. Discal cyst—arises from the posterior disc margin via an annular
    fissure. Usually found in young Asian men.
  12. Other facet joint related lesions—e.g. tumoural calcinosis
    (lobulated densely calcified mass) or gouty tophi (erosive
    juxta articular soft tissue mass ± calcification).
  13. Extramedullary haematopoiesis—can be epidural and/or
    paravertebral in location, usually multifocal. Typically associated
    with widespread T1 hypointensity of bone marrow due to red
    marrow reconversion.
  14. Angiolipoma—can mimic epidural lipomatosis but contains
    nonfatty vascular components, which show intermediate T1
    signal + avid enhancement.
  15. Neuroblastoma and ganglioneuroma—tumours of childhood
    arising in adrenal or paravertebral sympathetic chain. Direct
    extension through the neural foramina into the spinal canal may
    occur.
  16. Hydatid cyst—usually epidural or intraosseous in location. Can
    be uni- or multilocular.
  17. Sarcoidosis—rare, usually related to vertebral involvement
24
Q

INTRASPINAL MASSES
Intradural extramedullary mass
14

A
  1. Schwannoma—most common tumour in this location. T2
    hyperintense + enhancement ± cystic change, etc.
  2. Meningioma—typically solitary with a dural tail. Usually T2
    isointense to cord (in contrast to nerve sheath tumours). Uniform
    enhancement, may be calcified. Can rarely be extradural. May be
    multiple in NF2.
  3. Neurofibroma—purely intradural location is less common.
  4. Arachnoid cyst—follows CSF signal on all sequences. No
    perceptible wall; its presence is usually inferred by focal deviation
    of the cord.
  5. Leptomeningeal metastases—may present as discrete
    enhancing nodules or diffuse leptomeningeal enhancement
    coating the cord and cauda equina. Can be haematogenous (e.g.
    from lung, breast, melanoma, lymphoma, leukaemia) or ‘drop’
    metastases from a CNS tumour (e.g. glioblastoma in adults,
    medulloblastoma in children).
  6. Other leptomeningeal processes—sarcoidosis can cause nodular
    leptomeningeal enhancement mimicking malignancy, although
    the presence of disease elsewhere helps make the diagnosis.
    Meningitis can cause smooth leptomeningeal enhancement.
  7. Dilated vessels—tortuous flow voids within CSF space. Most
    commonly due to a dural arteriovenous fistula (AVF); cord
    oedema is typically also present due to venous congestion. Other
    causes include AVM (intramedullary nidus/flow void also
    present—absent in AVF), hypervascular tumours with feeding
    vessels, and collateral vessels from IVC occlusion.
  8. Lipoma—fat signal, most common posteriorly in the thoracic region.
  9. Epidermoid cyst—either congenital (± dysraphism) or acquired
    secondary to lumbar puncture. Usually in the lumbosacral region,
    similar to arachnoid cyst on MRI but shows restricted diffusion.
  10. Dermoid cyst—young patients; usually in lumbosacral region
    (± dysraphism), often contains fat ± calcification.
  11. Neurenteric cyst—usually in the thoracic or cervical region
    anterior to the cord, ± vertebral anomalies. May contain T1
    hyperintense proteinaceous material.
  12. Malignant peripheral nerve sheath tumour—infiltrative
    heterogeneous enhancing mass ± bone destruction. Most are
    associated with NF1.
  13. Melanocytoma—rare benign tumour. Typically small, T1
    hyperintense, T2 hypointense, enhances. Mimics melanoma
    metastasis.
  14. Cysticercosis—rare, usually associated with cerebral disease.
    Well-defined cyst(s) + eccentric mural nodule (scolex). Can rarely
    be intramedullary or epidural.
25
Q

Intramedullary mass or swelling

7

A
  1. Tumours.
    (a) Ependymoma—most common intramedullary tumour in adults. Cervical > thoracic location. Well-defined, T2 hyperintense + avid enhancement + peritumoural oedema ±necrosis or haemorrhage (hypointense haemosiderin rim). Cysts are often seen internally or adjacent to the upper/lower
    poles of the tumour. Arises from ependymal cells within the
    central canal, so is located centrally within the cord ±associated syrinx.
    (b) Astrocytoma—most common intramedullary tumour in children and young adults. Thoracic > cervical location. Ill-defined, T2 hyperintense + patchy enhancement +peritumoural oedema. Can be eccentric, exophytic or involve the whole diameter of the cord. Often longer than ependymoma (>4 segments). Cystic change, haemorrhage and syrinx are less common compared to ependymoma.
    (c) Haemangioblastoma—small, well-defined, avidly enhancing
    mass + extensive cord oedema, cystic change/syrinx, tortuous feeding vessels (flow voids) in subarachnoid space ±haemorrhage. Usually in the posterior cord, eccentric or exophytic; multiple in vHL.
    (d) Metastases—small well-defined enhancing lesions +
    prominent cord oedema. Most commonly from lung or breast.
    (e) Lymphoma—non-Hodgkin lymphoma is more common. Poorly defined, variable homogenous enhancement.
    (f) Ganglioglioma—rare. Similar age group and imaging features
    to astrocytoma, but tumoural cysts are more common;
    adjacent cord oedema is less common, and cervical > thoracic location.
  2. Demyelination—cord inflammation (T2 hyperintense) ± swelling ±
    variable enhancement (reflects disease activity); can mimic
    astrocytoma.
    (a) Multiple sclerosis—cord lesions are variable but usually
    multifocal, small (<2 vertebral segments) and involve <1/2
    of the cross-sectional area of the cord. Most common in
    the cervical region, typically in the presence of brain
    involvement.
    (b) ADEM—acute monophasic postinfective autoimmune disorder,
    typically in children and adolescents. Multifocal or confluent
    cord lesions, nearly always in the presence of brain ±
    brainstem involvement.
    (c) Neuromyelitis optica—single very long cord lesion (>3
    vertebral segments) typically involving the whole
    cross-sectional area, with optic nerve involvement. The brain is
    usually spared.
    (d) Transverse myelitis—many causes (e.g. infective,
    autoimmune, paraneoplastic), but often idiopathic. Single long
    cord lesion (>2 vertebral segments) involving >2/3 of the
    cross-sectional area, usually in the thoracic region. No brain or
    optic nerve involvement.
    (e) Other myelopathies—e.g. vasculitis (often multifocal),
    radiation (limited to treatment field), vitamin B12 deficiency
    (involves dorsal columns only), schistosomiasis (usually involves
    conus, history of travel to endemic area).
  3. Acute cord infarction—often associated with aortic dissection or
    surgery. Central grey matter T2 hyperintensity (‘owl’s eye’
    appearance) and restricted diffusion extending >1 vertebral
    segment ± cord expansion, typically involving the thoracic cord.
    May also involve adjacent white matter (especially anterior spinal
    artery territory) or whole cord cross-section.
  4. Vascular malformations.
    (a) Cavernoma—well-defined T2 hyperintense lesion +
    hypointense foci (haemosiderin) giving a ‘popcorn’
    appearance. Minimal enhancement. If small, may be purely T2
    hypointense.
    (b) AVM—intramedullary nidus of vessels (flow voids) + multiple
    tortuous vessels in subarachnoid space + adjacent cord
    oedema ± haemorrhage. The vessels may enhance but there is
    no discrete enhancing mass.
  5. Spinal cord abscess—may be due to haematogenous spread of
    infection (adults) or direct infection via dysraphism (children).
    Small ring-enhancing mass with central T2 hyperintensity and
    restricted diffusion, with extensive surrounding cord oedema.
  6. Dermoid/epidermoid/neurenteric cysts—can be intramedullary.
  7. Sarcoidosis—enhancing nodules typically in the cervical or upper
    thoracic cord, usually located peripherally. Intracranial and systemic
    disease is usually also present.
26
Q

Lesions related to cauda equina

8

A
  1. Any intradural extramedullary mass—see earlier.
  2. Myxopapillary ependymoma (ME)—represents 90% of tumours
    arising from the filum terminale. Well-defined, T2 hyperintense +
    avid enhancement ± peripheral haemosiderin rim due to
    haemorrhage. Usually large, filling the spinal canal ± posterior
    vertebral scalloping because of slow growth.
  3. Paraganglioma—usually arises from filum terminale; much less
    common than ME and schwannoma. Similar appearance to ME,
    but tends to be smaller and typically has prominent flow voids
    inside and outside the mass.
  4. Filum terminale lipoma—fatty thickening of the filum ± cord
    tethering.
  5. Guillain-Barré syndrome (GBS)—smooth enhancement of cauda
    equina ± slight thickening. Acute clinical presentation with
    ascending paralysis.
  6. Chronic inflammatory demyelinating polyneuropathy (CIDP)—
    chronic equivalent of GBS. Similar MRI findings but nerve
    thickening is usually more pronounced and involves both intraand extradural portions of the spinal nerves.
  7. Hereditary polyneuropathies—e.g. Charcot-Marie-Tooth disease.
    Similar MRI findings to CIDP, but usually presents in younger
    patients.
  8. Other radiculopathies—e.g. viral (CMV if immunocompromised),
    chemo- or radiotherapy induced. Similar appearance to GBS