SPINE

Question 1

SCOLIOSIS

Idiopathic (80%)

Answer 1

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%.

Question 2

SCOLIOSIS
Congenital anomalies (10%)
2

Answer 2

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

2. Neurological—
   Chiari malformation, syringomyelia, tethered cord, diastematomyelia.

Question 3

SCOLIOSIS

Other causes 6

Answer 3

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.

Question 4

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

Answer 4

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.

Question 5

MULTIPLE COLLAPSED VERTEBRAE

11

Answer 5

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

Question 6

EROSION, DESTRUCTION OR ABSENCE OF

A PEDICLE

Answer 6

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.

Question 7

SOLITARY DENSE PEDICLE

6 + other

Answer 7

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.

Question 8

ENLARGED VERTEBRAL BODY

Answer 8

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.

Question 9

SQUARING OF ONE OR MORE VERTEBRAL BODIES

3

Answer 9

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

Question 10

BLOCK VERTEBRAE

7

Answer 10

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.

Question 11

IVORY VERTEBRAL BODY

7

Answer 11

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.

Question 12

ATLANTOAXIAL SUBLUXATION

Answer 12

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.

Question 13

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.

Answer 13

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.

2. 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

Question 14

INTERVERTEBRAL DISC CALCIFICATION

Answer 14

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

4. DISH—anterior annulus calcification + flowing osteophytes.
5. 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).
6. HADD—can cause calcific disc inflammation similar to CPPD.

Rare

7. Alkaptonuria/ochronosis—multilevel central disc calcification, disc space narrowing and severe osteopenia.
8. Haemochromatosis—similar to CPPD.
9. Gout—together with erosions and tophi.
10. Poliomyelitis.
11. Acromegaly.
12. Hyperparathyroidism.
13. Amyloidosis.
14. Idiopathic—a transient painful phenomenon in the cervical spine of children.
15. Juvenile chronic arthritides

Question 15

Osteophytes

Answer 15

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

Question 16

Syndesmophytes

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

Answer 16

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

Question 17

Nonmarginal osteophytes/paravertebral ossification

Answer 17

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

Question 18

Undulating anterior or posterior ossification

Answer 18

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

Question 19

POSTERIOR SCALLOPING OF VERTEBRAL BODIES

7

Answer 19

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.

Question 20

ANTERIOR SCALLOPING OF

VERTEBRAL BODIES

Answer 20

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

Question 21

WIDENED INTERPEDICULAR DISTANCE

Answer 21

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.

Question 22

DIFFUSE LOW MARROW T1 SIGNAL

Answer 22

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

Question 23

INTRASPINAL MASSES
Extradural mass
17

Answer 23

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

Question 24

INTRASPINAL MASSES
Intradural extramedullary mass
14

Answer 24

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.

Question 25

Intramedullary mass or swelling

7

Answer 25

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.

Question 26

Lesions related to cauda equina

8

Answer 26

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