Myelopathy is compromise of the spinal cord; from compression, intrinsic lesions or inflammation (myelitis). Causes bladder and bowel incontinence, spasticity, weakness and ataxia. With compression, a clinical motor/sensory spinal level may be evident, but could be several vertebral bodies higher (esp thoracic). Limited healing and plasticity (ability for other neurons to take on tasks of damaged areas), less than the brain, causing permanent damage (after ~24hrs of acute cord compression).
Low back pain in younger patients is usually discogenic, in older patients is usually due to facet joint synovitis. Radiculopathy is from impingement of spinal nerves (within spinal canal, lateral recess, neural foramen or extraforaminal course), usually from compression. Specific dermatomal sensory/motor deficits. Causes include disc herniation, spinal stenosis, uncovertebral joint spurring, less commonly malignant or infectious processes. In patients tends to be due to discs, older patients fixed stenotic lesions. Peripheral nervous system able to withstand injury and regenerate.
Plain radiographs useful for trauma or evaluating degenerative processes, but not sensitive or cost effective for nondegenerative disease (neoplasm, infection).
Myelography usually used with CT, when MR is contraindicated. Ionic contrast contraindicated, as it may cause severe inflammation, seizures, arachnoiditis or death. Higher concentration used in cervical/thoracic region (smaller subarachnoid space). Midline prone LP usually L2-3 with injection after CSF backflow seen. C1-2 punctures.
MRI – Surface coils and motion-suppresion techniques (anterior saturation band, gradient moment nulling, cardiac/respiratory gating) needed. FSE for spine. FS T2 for marrow, STIR best for marrow oedema. GRE degraded because of susceptibility from bony trabeculae, only useful for blood breakdown products, overestimates size of calcium. Bony narrowing of spinal canal and foramina is exaggerated due to motion. Gadolinium for infection or intrathecal metastases, but may obscure vertebral metastases (making them isointense with marrow fat), solved with FS or comparison with precontrast T1. DWI helps distinguish metastases (restriction) from fractures.
When any diffuse spinal process is seen (intramedullary or leptomeningeal), the brain should be imaged for a similar process.
Vertebral low T1 is very sensitive, but may be from radiation, infection, tumour, anaemia of chronic disease (increased marrow iron).
Expansion of the cord:
- Demyelinating disease – ADEM, MS, transverse myelitis.
- Infection – Extramedullary eg meningitis with vascular compromise, AIDS.
- Inflammation – Sarcoid, SLE.
- Tumour – Metastases, primary.
- Subacute necrotizing myelopathy – Progressive myelopathy with necrosis of the cord. From ADEM, Devic syndrome, infection (HSV, SLE, EBV, MS, mumps, toxoplasmosis, TB), SDAVM, venous HTN (Foix-Alajouanine syndrome), vacuolar myelopathy in AIDS.
- Vascular – Acute infarction, AVM, cavernous angioma, haemorrhage, venous HTN.
Increased cord signal DDx:
- Anterior horn cells (‘snake/owl eyes’ – chronic ischaemia, compression, viruses
- Dorsal column – subacute combined degneration
- Dorsolateral – MS, demyelination
- Central – wide differential
Vertebra plana from osteoporosis, steroids, tumours (leukemia, myeloma), LCH, fracture, osteogenesis imperfecta, mucopolysaccharidoses.
From variety of causes. Ill-defined high T2, commonly central. Can have ill-defined peripheral enhancement at site of maximal compression. In chronic phase ‘owls/snake eyes’ T2 hyperintensity with loss of volume (myelomalacia).
Congenital and Developmental Disorders
Tumours cause focal/diffuse cord expansion, high T2, almost always enhance. Location of lesions must be confimed on 2 views, as large intradural lesions may simulate extradural mass, bilateral extradural disease may flatten the cord simulating expansion and thus intramedullary.
- Intramedullary (intradural) lesions – Confined to spinal cord itself, may be exophytic, cord widened on all views. CSF space thinned on all sides in all views. Widening of interpedicular distance from slow expansion in <10%. Includes ependymoma, astrocytoma, haemangioblastoma, lipoma, epidermoid/dermoid, myelitis, infection, ADEM, syringohydromyelia, intramedullary AVM; rarely metastases, abscess, teratoma.
- Intradural extramedullary (IDEM) lesions – Outside the cord, with CSF forming acute angles with the mass (which may have dural attachment = ‘marble on the carpet’). Widened CSF on ipsilateral side of cord, effaced contralaterally. Includes meningioma, schwannoma, neurofibroma, haemangiopericytoma, lipoma, epidermoid/dermoid, arachnoid cyst/adhesion, drop/leptomeningeal met, veins, extramedullary AVM.
- Extradural – CSF has obtuse angles with the mass (marble under the carpet), CSF effaced on both sides of cord, cord may be widened in one plane from mass effect. Includes degenerative (herniated disc , synovial cyst, osteophyte, rheumatoid pannus) or nondegenerative (metastases, abscess, haematoma, tumour expansion/invasion, epidural lipomatosis).
Nontumoral/reactive cysts are cranial or caudal to the tumour, from dilatation of the central canal (?fluid produced by the tumour), they don’t enhance, hypoechoic, no septations, disappear after solid tumour resection. Tumoral cysts occur within the tumour (esp astrocytoma), may have peripheral enhancement.
Localised tumours (eg ependymoma) can be excised, whereas diffuse tumours (eg astrocytoma) cannot be completely excised (may have biopsy/debulking). Potentially differentiated using diffusion tensor imaging (DTI) where a tumour is thought unresectable if it contains fibres passing through >50% of the tumour.
Most common spinal cord tumour in adults lower cord. Cellular (intramedullary) or myxopapillary (filum terminale) types. Genetically and epidemiologically different from intracranial ependymomas. Peak 30s, M>F, increased risk with NF2. Slow growing from ependymal lining of central canal or cell rests along filum. Usually benign, may have metastases to extraspinal retroperitoneum and LN. Most sacral or spinal cord. Well-defined, expansile, low T1, high T2, variable enhancement. Generally more focal than astrocytomas (average length 3-4 vertebral bodies). Some adjacent oedema. Common cysts (nontumoral), syrinx and haemorrhage with hypointense rim (‘cap sign’), may cause SAH. Displaces descending white matter tracts/fibres. Complete curative excision may be impossible, except myxopapillary type (esp if well encapsulated).
- Myxopapillary ependymoma in filum terminale – May extend into conus, through neural foramina or into subcutanoeous sacrococcygeal region. Multilobulated, encapsulated, mucin-containing, haemorrhage, calcify. Iso T1, high T2, enhance.
Most common spinal cord tumour in children, peak 20s, M>F, increased risk with NF1. 75% in upper/midthoracic cord. Most are low grade pilocytic (WHO I) or fibrillary (WHO II)., rarely grade IV/GBM Fusiform cord expansion, may be exophytic (appearing extramedullary), low T1, high T2, variable enhancement. Ill-defined, may involve entire cord diameter, longer cord segments (average 7 vertebral bodies) than ependymoma. Tends to disrupt traversing neural tracts. DTI cab be used to predict resectability, poaaibly grade (but not useful for differentiating from ependymoma). Cystic ccomponent in 60% (usually tumoral cysts). Haemorrhage uncommon (cf ependymoma). Syrinx common in pilocytic astrocytomas. Disrupts descending white matter tracts/fibres.
Uncommon, occur in spine and posterior fossa. Seen on 1/3 of those with vHL; 1/3 of those with spinal HB have vHL. Cervical and thoracic spine, may be intramedullary or eccentric appearing extramedullary, predominantly dorsal cord, may be on nerve roots. Cystic and solid which has dense vascular blush, diffuse cord expansion (cf AVM), extensive oedema. Intratumoral flow voids when large. Completely solid in 25%. 40% associated with cysts. 20% multiple. On angiography there is a dilated feeding artery, tumour stain and draining vein. DDx drop metastasis from cerebellar haemangioblastoma.
Galgliogliomas and gangliocytomas have similar appearance, behaviour and treatment. Rare, most commonly children and young adults (2nd most common after astrocytoma in children). Large mature neurons or ganglion cells ± glial cells. Slow-growing, low grade. Most cervical, long segment. Mixed T1, high T2, prominent tumoral cysts, patchy enhancement extending to pial surface. No oedema or haemosiderin. May calcify.
Filum terminale and cauda equina. Avid enhancement, cystic components, haemosiderin, varaible flow voids.
Rare, from growth along perivascular spaces from CSF spread, or haematogenous. Cord expansion, marked oedema, enhancement. Most thoracic and cervical. Usually solitary involving 2-3 segments. Predominantly lung and breast cancer.
May be incidental, ‘congenital’, may be associated with bifid spinal canal. Usually thoracic, also commonly filum terminale, M>F. Intradural or extradural. May be extensive compressing the spinal cord. High T1, low T2, supresses with FS, chemical shift artifact in frequency-encoding direction. Suspect teratoma if cysts, haemorrhage or debris seen. May have dorsal dermal sinus tract.
Most common intradural tumour, from the denticulate ligament. F>M, mean age 45yo. If multiple consider NF2. 80% thoracic. Usually IDEM, but may have extradural component (more likely malignant). May have dense calcification. Low T1, iso T2, dense homogeneous enhancement, broad dural tail. May expand the neural foramina, but to less extent than schwannomas. Tend to be posterolateral (cf anterior nerve sheath tumours). DDx schwannoma (less vascular, may undergo cystic necrosis), neurofibroma (usually extends through neural foramen and lacks broad dural base).
(Neurinoma, neurilemmoma, neuroma). From Schwann cells, ecapsulated and extrinsic to the nerve, usually from dorsal sensory nerve roots. NF2 associated with meningiomas, schwannomas and mixed nerve sheath tumuors. Most common intraspinal mass. Most solitary (3x more common than neurofibroma), sporadic, peak 40s. Extension into neural foramen (esp cervical, thoracic; lumbar tend to remain within dural sac), may give classic ‘dumbbell’ appearances (part intraspinal, part extraspinal). May have cystic degeneration (from Antoni B tissue), internal haemorrhage, fatty degeneration (cf neurofibroma). Enhance.
Collagen and myxoid tissue infiltrating the nerve without encapsulation, malignant potential. Associated with NF1 (with kyphoscoliosis, ribbon ribs, scalloped posterior vertebral bodies, dural ectasia, cafe-au-lait spots); not associated with NF2. Often multiple. Plexiform neurofibromas are diffuse multinodular, may extend through multiple adjacent neural foramina. Heterogeneous enhancement with areas of low signal (cf schwanoma), target sign (low central T2 surrounded by high T2).
Malignant Nerve Sheath Tumours
From schwannoma or plexiform neurofibroma. Painful, aggressive.
Rare primary melanoma in spinal cord or nerve roots. From melanocytes of Schwann cells. If melanotic is high T1, low T2.
(Drop metastases). Subarachnoid seeding from posterior fossa medulloblastomas, ependymomas, pineal region tumours, glioblastoma, haemangioblastoma, leukaemia, lymphoma, lung, breast, melanoma, colorectal, renal, gastric. Implant on pia and grow into small intradural nodules. CSF high T1 with reduced CSF-cord differentiation (‘dirty CSF’). Irregular cord margin wih enhancement, may deposit on nerve roots or cauda equina (Christmas balls). ‘Carcinomatous meningitis’ – leptomeningeal metastases with inflammation and pachymeningeal thickening (DDx infection, Guillain-Barre, post-op arachnoiditis). ‘Sugar coating’/’cake frosting’ – thin smooth sheets of cells on cord and roots without disc rete mass.
Metastases include breast, lung, prostate, renal, Ewing sarcoma, neuroblastoma, melanoma, lymphoma, leukemia, myeloma, sarcoma. Haematogenous metastases usually implant in the posterior vertebral body, extending into pedicle and posterior elements. Pelvic tumours (eg prostate) may ascend via Batson venous plexus. Direct extension may be from retroperitoneum or mediastinal tumours, primitive paraspinous neural remnants (neuroblastoma, ganglioneuroma, ganglioneuroblastoma). Osteblastic tumours include prostate, breast, carcinoid, ovarian, TCC and lymphoma. Replacement of marrow causing low T1/high T2 (higher water content), apart from sclerosis being dark. Best seen on STIR, T2 FS. Irregular, diffuse vertebral body involvement, marked in pedicles. Intense enhancement, may obscure the lesion within fat unless FS used. Diffusion restriction from ‘marrow packing’. Epidural spread can occur when cortex breached, but usually limited to level of vertebral involvement (except lymphoma). Disks usually spared, except prostate CA.
NOMS framework assesses NOMS to determine treatment (eg radiotherapy, radiosurgery, chemotherapy, surgery):
- Neurologic – neural compression
- Oncologic – sensitivity to radiation. Typically radiosensitive primaries: breast, prostate, ovarian, neuroendocrine (usually sclerotic). Typically radioresistant primaries: RCC, thyroid, HCC, colon, NSCLC, sarcoma, melanoma (usually lytic).
- Mechanical stability
- Systemic status – metastatic load
- <10yo – EG
- 10-20yo – osteoid osteoma, ABC
- 20-50yo – GCT
- 40-60yo – plasmacytoma, chordoma, haemangioma
- >60yo – metastases, myeloma
- Haemangioma – Common (12%), benign, usually incidental. Fully developed blood vessels. F>M, most lower thoracic and lumbar spine. May have pain with growth (esp pregnancy) or compression fracture. Round, may replace entire vertebral body extending into pedicles, arches and spinous process; cortical margins usually preserved except occasionally fracture or epidural extension. Vertical striations (vascular channels with thickened trabeculae), high T1 and T2 (fat and water). May produce venous hypertension with spinal cord expansion (Foix-Alajouanine syndrome). Occasionally compresses spinal cord.
- Aggressive haemangioma – Increased vascular stroma, less fat. Low T1, high T2. May have extra-osseous extension, may be painful. Maintains stippled appearance with thickened vertical trabeculae.
- Chordoma – Locally invasive, slow growing from remnants of notochord. 50% sacral, 15% spine (esp cervical). Lytic, occasionally sclerotic rim, high T2. May involve disc space, multiple vertebral bodies. May appear similar to herniated disks, schwannoma, ependymoma.
- Chondrosarcoma – Bony destruction, chondroid calcification.
- ABC – Circmscribed, multiloculated, occasional haemorrhage with fluid levels. Esp posterior elements, lamina.
- GCT – Lytic, sacrum and vertebral bodies.
- Osteoblastoma (‘giant osteoid osteoma’) – >15-20mm, posterior elements or transverse process, lytic/calcific nidus with sclerotic rim. Hypervascular nidus.
- Osteoid osteoma – <15mm, posterior elements or transverse process, lytic/calcific nidus with sclerotic rim. Nocturnal pain relieved by aspirin. Hypervascular nidus.
- EG – Children, rapidly growing in vertebral body with bone loss and collapse (vertebra plana). Most C-spine. Heterogeneous T1.
- Osteochondroma – From posterior elements esp thoracic/lumbar.
- Ewing sarcoma – Most lumbosacral. May cross disc spaces, cause fever, anaemia.
- Paget disease – Enlargement of all vertebral elements, thickened cortex, sclerosis. Malignant transformation to osteosarcoma in 10%.
- Leukaemia causes diffuse even replacement of marrow with tumour. Solid leukaemic infliltrates (chloromas) may involve epidural space. Parameningeal chloromas may grow through foramina similar to lymphoma.
- Multiple myeloma – Patterns of marrow involvement include: type 1 normal (<20% plasma cell infiltration); 2 circumscribed low T1; 3 diffuse low T1 high T2 and enhancement (>50% plasma cell infiltration); 4 diffuse and focal leisons; 5 heterogeneous and patchy (early mild infiltration on background of fatty and normal marrow). Compression fractures in 50-70%. Unusual to involve the pedicles. Solitary plasmacytomas may cause vertebra plana (DDx LCH, leukaemia, severe osteoporosis). Often indolent metabolically, hence cold on bone scan.
- Myelofibrosis – Very dark marrow T1 and T2 (replacement with fibrous tissue).
- Extramedullary haematopoiesis – Patients with haemoglobinopathies (eg sickle cell disease) is usually paraspinous, may infiltrate into spinal canal. Bone marrow repopulation (eg transplantation) has haematopoietic dark T1 predominantly adjacent to endplates (richer blood supply).
- Lymphoma – Most B-cell NHL. Extradural > intradural > intramedullary. Epidural and paraspinous masses usually more extensive than other metastases, may mimic infection. May invade spinal canal via neural foramina, causing cord compression.
Siderosis from recurrent haemorrhage in spinal vascular malformation, tumour (ependymoma, haemangioblastoma).
Spinal Vascular Malformations
- Spinal dural arteriovenous fistula (SDAVF, SDAVM, type I AVM) – 70% of spinal malformations. Insidious weakness/sensory changes with late presentation, M>F, 40s-50s. Increased CSF protein. Nidus in dura esp nerve root sleeve where radiculomeningeal artery enters a radicular vein under the pedicle, most drain into spinal pial vein(s), may be uni- or bi-lateral. Esp dorsal lower thoracic cord or conus. Foix-Alajouanine syndrome (angiodysgenetic necrotizing myelopathy) when associated with ischaemic myelopathy, overlying meningitis, slowly progressive neurologic symptoms. Increased venous plexus pressure (valveless) with congestion and oedema ± infarction of cord (high T2, enlarged conus ± enhancement) with peripheral low T2 (typical of venous HTN ?deoxyhaemoglobin in pial vessels). Dilated plexus esp posterior to spinal cord (any ‘bumps’ are abnormal) may be seen as serpiginous filling defects on myelography. Haemorrhage very rare.
- Spinal cord AVM (SCAVM, type II AVM) – 20s, M=F, acute symptoms. Intramedullary AVMs fed by anterior and posterior spinal arteries, drain into spinal veins. Most cause intramedullary haemorrhage (acute Sx), may cause ischaemia from steal. High flow lesions have visible signal voids.
- Juvenile AVMs (type III AVM) – Rare, potentially extensive intramedullary, extramedulalry and extraspinal components, young patients, poor prognosis.
- Spinal cord AVF (type IV AVM) – IDEM single communicating fistula without intervening capillary network, on pial surface. Usually ventral or lateral involving anterior and posterior spinal aa. Haemorrahge (SAH) in 30% when there is venous HTN, may be intracranial if venous drainage extends there. May cause venous aneurysm. Type IVa-IVc correlates with larger fistula size.
DDx normal flow voids that may be seen with CSF pulsation, maximal lateral to the cord, improved with cardiac gating and do not enhance. Tx embolisation and/or surgery, depending on blood supply. Need to image intercostal, vertebral, costovervical, thyrocervical and subclavian arteries to identify all feeding vessels; may even feed from iliac aa, hypogastric or sacral aa.
Spinal Cord Infarction
Usually post-op, esp upper thoracic or thoracolumbar regions. Rapid onset <4hrs. Acute bladder and bowel dysfunction, loss of perineal sensation, sensory and motor deficits. Pain common Conus ischaemia may occur after occlusion of the artery of Adamkiewicz. From AAA, atheroma, aortic surgery, dissection, verebral occlusion, arteritis (esp posterior spinal aa), vascular malformations, pregnancy, hypotension/arrest, sickle cell, miningitis/arachnoiditis, diabetes, degenerative disease of the spine, disc herniation injuring spinal a. Enlarged cord esp conus. Bright T2 and DWI in corresponding vascular territory. Anterior horn cells (‘snake eyes’) in more chronic phase. variable enhancement (grey > white) then myelomalacia. Associated high signal in a vertebraV(bone infarct).
(Cavernoma). Uncommon, 30-50yo, F>M, may be inherited. Intramedullary, usually cervical or thoracic. Similar to cerebral lesions with round, heterogeneous high T1 and T2 (metHb) surrounded by low T2 (haemosiderin). Minimal mass effect or oedema (unless recent haemorrahge). May enhance, calcify. Usually progressive with Brown-Sequard syndrome (ipsilateral hemiplegia, loss of proprioception, hyperasthesia; contralateral loss of pain and temperature).
Within the posterior epidural space. May be infiltrative. Vascular, but no flow voids. May contain muscle components (angiomyolipoma).
(Myelitis). May be focal or diffuse. Transverse myelitis – Inflammation of the spinal cord with corresponding rapidly progressive neurological dysfunction. Can be short segment or longitudinally extensive (>3 vertebra segments, LETM). MRI changes can lag behind clinical symptom worsening/improvement. Includes:
- ADEM – usually longer segment, mimics IATM
- MS – usually short, typically posterolateral
- NMO – usually long
- Connective tissue diseases (SLE, RA, Sjogren)
- Vascular malformation
- Infections, post-infections
- Idiopathic = IATM (idiopathic acute transvere myelitis).
Myelitis onset occurs from 4hrs to 21 days to peak symptoms (compared to ischaemic <4hrs). Idiopathic (?small vessel vasculopathy) occurs over days-weeks with demyelination, perivascular lymphocytes, necrosis over multiple segments, involves entire cross-section of the cord with high T2, variable enhancement (nodular, meningeal).
Multiple Sclerosis (MS)
Most common, multiple deficits/lesions separated anatomically and temporally. When spinal MS predominates, it tends to be progressive (cf relapsing/remitting). Isolated spinal cord disease in <20%. 2/3 in cervical region. Best seen on T2 or STIR as high signal, may be low T1. Usually no change in cord diameter, but occasional expansion in acute phase from oedema. Myelomalacia (atrophy) from ‘burnt out’ plaques. Tend to be peripheral in cord (white matter) and posterior, doesn’t respect grey-white interface, oedema and enhancement may extend centrally (perivenular inflammation). Usually <2 vertebral segments in length, <1/2 area of cord. Devic syndrome usually monophasic, longer-segment, associated with optic neuritis, older patients and worse prognosis than MS.
Neuromyelitis Optica (NMO)
Typically longer segment T2 hyperintensity in the cord, central, often expansion and lower T1 signal than MS. Variable ill-defined enhancement.
SLE related vacuolar degeneration from necrotising arteritis causing cord ischaemia and injury, or antibodies damaging tissue directly. Diffuse high T2 with cord swelling, less well-defined margins than MS, may involve 4-5 vertebral body segments. Dramatic MR improvement with corticosteroids (cf MS).
Subacute Combined Degeneration
From vitamin B12 (cobalamin) deficiency. Cervical and upper thoracic myelopathy, may also involve optic tracts, brain, peripheral nerves. Parasthesia in hands/feeet, loss of proprioception and vibration, sensory ataxia, spasticity, lower limb weakness. From pernicious anaemia (most), terminal ileum diease. Demyelination and axonal los in posterior and lateral spinal cord. May have associated low T1 and T2 in marrow from haematopoietic hyperplasia. DDx folate deficiency, NO toxicity, copper deficiency.
Rheumatoid Arthritis (RA)
Focal inflammation (pannus) destroys the transverse ligament of C1 (atlantoaxial isntability), allowing odontoid to sublux posteriorly and compress the cord esp in flexion. Intermittent cord compression caUses myelomalacia. Frank atlantoaxial instability in 5% of RA patients. Most have involvement elsewhere (eg hands). DDx fibrous pseudotumour, chronic instability after trauma.
Similar to brain. Peak 6-18/12 with high T2, variable enhancement, later atrophy. May cause paralysis. Normal erythropoietic marrow is destroyed and replaced by fat, causing it to be homogeneously bright on T1; in children this may later repopulate with cells. Stunted growth may occur from epiphyseal injury.
Amyotrophic Lateral Sclerosis (AML)
Anterior horn cell atrophy ± abnormal cord signal. May be associated with corticospinal tract abnormal. Reduced fractional anisotropy increasing mean diffusivity. Progressive spinal muscular atrophy if isolated to lower motor neurons.
Guillain-Barre Syndrome (acute inflammatory polyradiculoneuropathy) – Progressive ascending motor weaknes affecting >1 limb, involving peripheral nerves. May occur after vaccinations, evolving over max 4/52. Spinal nerves esp lumbar may enhance, meningeal enhancement.
Hereditary motor and sensory neuropathies (HMSN) – Concentric proliferation of Schwann cells interspersed with collagen after multiple episodes of demyelination and remyelination, giving and onion bulb appearance to the nerve. Nerve root enlargement and occasionally enhancement.
- Charcot-Marie-Tooth disease (HMSN 1) – AD, slowly progressive distal atrophy (esp peroneal muscles) with pes cavus, scoliosis. Involves posterior columns, optic nerve, acoustic nerve.
- Dejerine-Sottas disease (HMSN 3) – AR, slowly rogressive motor and sensory loss and ataxia, pes cavus, scoliosis. Enlarged peripheral and cranial nerves with hypomyelination, variable enhancement.
Chronic inflammatory demyelinating polyradiculoneuropathy (CIPD) – Acquired gradual onset of proximal weakness, paresthesia, numbness. Enlarged cranial ane peripheral nerves, may enhance. May have cranial lesions similar to MS.
Diffuse leptomeningeal granulomatous nodules, usually enhancing. May cause intramedullary (infiltration of perivascular spaces) or vertebral body granulomatous changes, most C-spine. DDx carcinomatous and mycobacterial meningitis.
Leptomeningeal inflammation. Normal free-layering lumbar roots of cauda equina (should be able to see ventral and dorsal rootlets) may become adherent to each other (‘pseudofilum’) or to the peripheral wall of thecal sac (’empty sac’). May or may not enhance. May cause adhesions, arachnoid cysts. Causes include:
- Pantopaque (iodophenylundecyclic acid) – Previously used in myelography. Pearly white beads of residual Pantopaque on plain film, high T1 (high lipid content).
- Infection (TB or pyogenic meningitis) – In TB there is leptomeningeal enhancement, enhancing nodules of spinal cord and roots (DDx sarcoid, mets).
- Subarachnoid haemorrhage – Iatrogenic (surgery, spinal/epidural anaesthesia), trauma, AVM/aneurysm.
- Inflammatory diseases
Most from arterial seeding (bacteraemia from skin, GIT, lungs), spinal dysraphism, surgery. Cord infection usually viral; extramedullary usually pyogenic. Enhancement is often the earliest sign.
Claw sign – obliquely orientated DWI around the disk (‘>’ shaped), suggesting type 1 Modic change.
(Pyogenic spondylodiscitis). Primary infection of discitis is rare in adults (poor blood supply), aa penetrate growing disc in children; hence in adults most infections direct spread from vertebrae esp anterosuperior endplates (richest blood supply) caused by haematogenous seeding (esp lung or UTI). Most S.aureus (produces enzyme rapidly ‘digesting’ discs), Streptococcus, Peptostretococcus, others include gram negative Escherichia coli, Proteus, Pseudomonas, Klebsiella, Salmonella (associated with sickle cell disease). Severe back pain unrelieved by any position, fever, WCC, ESR (masked with ABs). Discitis would inevitably spread to adjacent vertebrae via subligamentous spread, may spread several levels under anterior/posterior longitudinal ligmaents (unusual for tumour) esp TB. Osteomyelitis – loss of marrow T1, high T2, normal DWI, destruction worse at the endplates with loss of definition. Discitis – destruction of disc space, low T1 high T2, enhancement. Osteomyelitis/discitis complex pattern is classic for infection, disc very rarely involved in neoplasm. May have epidural or paravertebral abscess. XR will only show if there is bony destruction, which may be up to 4-8/52 later. Endplates may become sclerotic late in course from healing, may cause fusion across obliterated disc space. Bone scans sensitive, but not specific, indium-labelled white cell and gallium scans more specific, but relatively insensitive. DDx discogenic vertebral sclerosis (low T1), but doesn’t enhance, renal spondyloarthropathy (amyloid deposition esp C-spine in dialysis with destruction of disc and endplates, low T2). Disc aspirates low yield after ABs. Vacuum phenomenon (gas in disc) means infection is very unlikely.
Brucella causes osteoblastic and osteoclastic activity, may have ‘parrot beak’ (like anterior osteophyte) and Schmorl’s nodes.
Nonpyogenic infections are usually indolent (no pain or WCC). Increased risk with immunosuppresion eg chemotherapy and AIDS which are also at risk or metastases and lymphoma respectively.
- Tuberculosis of the spine (Pott disease, tuberculous spondylitis) – Slow collapse of one/more vertebral bodies, spreading under longitudinal ligaments, may have skip areas. Esp lower T-spine. May cause acute kypotic/gibbus deformity, cord compression (with epidural abscess, bone fragments). Discs usually preserved. Often associated with epidural, paravertebral, subligamentous (involving multiple levels) or psoas abscess. Late-stage large paraspinal abscesses without severe pain or frank pus (‘cold abscess’). May infect meninges causing pachymeningitis with dramatic enhancement. >50% have pulmonary disease. DDx sarcoidosis, fungus, brucellosis.
- Fungal infections – Candida and Aspergillus (oncology patients), coccidioidomycosis (endemic areas, spares the discs), blastomycosis (endemic areas, can destroy disks and ribs), cryptococcus (associated with meningitis, vetebral destruction), cystecercosis, intramedullary toxoplasmosis (in AIDS), echinococcus.
Paraspinous disease (eg psoas infection) may be from osteomyelitis or epidural abscess.
From direct extension (osteomyelitis/discitis) or haematogenous. S.aureus (most common), G-neg, anaerobes, mycobacteria, fungi. Dura acts as effective barrier with craniocaudal spread up to 3-4 spaces (unusual for neoplasm). May cause cord compression. Most posterior (ventral dura closely approximated to PLL), lower thoracic/lumbar. Variable appearace, may be rounded rim-enhancing (frank pus) or oblong thickened granulation tissue/phlegmon (most). MR without fat sat may obscure pathology due to normal bright fat (even with Gad). May cause thrombophlebitis with cord oedema/infarction, meningitis (high T1 in CSF with enhancement of CSF and nerve roots).
Rare, most associated with surgery or violation of dura. Can rapidly spread to subarachnoid space causing meningitis. May see dark surrounding dura.
- Infection – Usually from haematogenous seeding, unless there is congenital/acquired disruption of the leptomeninges. Leptomeningeal enhancement relatively late, may not be present. LP required to exclude.
Anterior horn cell injury with polio, flavivirus, enterovirus; may have associated rhombecephalitis. Herpes zoster causes cord swelling and enhancement with shingles. Measles causes autoimmune damage (subacute sclerosing panencephalitis), ADEM. Many viruses have poorly understood mechananism. Sudden high fever (?virus) then within 4/52 rapid onset motor/sensory/autonomic dysfunction at a certain level (transverse myelitis). Focal high T2 variable enhancement, may have expansion.
Spinal Cord Abscess
Rare, usually from direct seeding in overwhelming sepsis. High T2 with rim enhancement. Large amount of surrounding oedema.
Intramedullary lesions include:
- Viral infection – CMV, HSV, HZV
- Vacuolar myelopathy (AIDS-associated myelopathy) – Common, ?from HIV effects, secondary infection, nutritional deficiency or drugs. Vacuolation in spinal white matter with lipid-laden macrophages esp dorsal columns and lateral corticospinal tracts. Usually long segment high T2, may have necrosis.
- Subacute necrotizing myelopathy
Degeneration and Arthritides
Degenerative Disc Disease
Degenerative disc disease is not truely OA as they are not synovial joints. Reduced disc height may increase facet OA, neural implingement, impaction of spinous processes with OA-like changes (Baastrup’s disease). Sharply demarcated endplate signal (cf infection), vacuum disc phenomenon, bulges and protrusions common. Endplate/traction spurs (spinal/claw osteophytes) start close to endplate and extend horizontally, but may curve around bulging disc and fuse. Spondylosis deformans – advanced disease with prominent spurs and subluxations. Modic endplate changes:
- Type 1 – Fibrovascular infiltration with low T1, high T2.
- Type 2 – Fibrofatty infiltration with high T1 and T2. Marrow conversion from red to yellow.
- Type 3 – Reactive/discogenic sclerosis with low T1 and T2, may be triangular shaped in anterior superior endplate.
With degeneration there is dessication of the nucleus pulposus (loss of T2), reduced tissue resilience and redued disc height. With aging the nucleus pulposis is replaced by fibrocartilage, becoming less defined from the annulus fibrosis. Fissures have negative pressure so gas (nitrogen) comes out of solution and deposits in the disc close to the subchondral bone (vacuum/cleft phenomenon). Gas implies mobility, shouldn’t be seen at fused levels. Calcification common. Disc changes cause abnormal motion (esp C-spine) with vertebral body displacement, subluxation of facet joints, uncovertebral ostephytic spurs (causing foraminal narrowing), endplate osteophytes (bars, posterior will narrow spinal canal). Calcified disc and bony osteophytes have similar appearances. Degeneration increases the risk of herniation.
Spondylosis deformans is endplate osteophyes with significant spinal degenerative disease, may lead to fatigue fractures with concave depression of endplates. Anterolateral disc protrusions cause traction on Sharpey’s fibres and anterior osteophytes several mm from the discovertebral junction which extend horizontally then vertically. There is preservation of disc height, peripheral vacuum phenomenon, absent subchondral eburnation. Facet joint arthropathy is worse in L-spine. Loss of vertebral height causes loss of normal cervical lordosis then kyphosis. Lumbar facet hypertrophy and ostephytes may compress the lateral recess and neural foramen, worse in the more anterior superior facets (lie closer to the nerve).
Disc herniation imaging should generally wait for 4-6 weeks as radicular symptoms tend to improve with rest and NSAIDS. Internal disc disruption (IDD) – endplate fatigue fractures increases stress of disc ligaments (esp posteriorly), causing radial fissure then circumferential fissure then herniation. Signs of IDD include Modic endplate changes and high intensity zones (HIZ).Gas in the spinal canal implies a disc herniation. In L-spine the roots exit in the upper neural foramen just under the pedicle (hence disc herniations compress the lower exiting nerve), whereas in the C-spine they exit in the lower neural foramen. Thoracic herniations are insidius, usually T6-9 levels. The herniated disc may be calcified.
- Annular fissure (previously tear) – Separation of annular fibres, avulsion from vertebral body insertion or break through fibres. Traumatic or degenerative. Usually posterior, rarely anterior. High intensity zone (HIZ) in posterior annulus ≠ fissure, but may predict a fissure. Fissures usually annular then circumferential, weakening the disc prone to herniation. May cause back pain. Globular or linear high T2, may enhance.
- Herniation – Localised (<90 deg) displacement of disc material (nucleus, cartilage, fragmented apophyseal bone and or annulus) beyond limits of normal disc space. Contained if covered by outer annulus, uncontained if not. Location is central, paracentral (subarticular at level of disc, lateral recess at level of vertebra), foraminal (lateral), or extraforaminal (far lateral). May rupture through PLL, rarely through dural into intradural space. Normal midline septum from PLL to vertebral body prevents subligamentous herniations to pass to contralateral side. May have surrounding enhancing granulation tissue.
- Protrusion – Greatest distance (any direction) of herniation from the disc is less than the edges at the base in every plane.
- Extrusion – Distance of herniation is greater than base, when there is no continuity with donor disk, disc material extends above or below the disc space. It is migrated if it is displaced from the extrusion.
- Sequestration (noncommunicating/free fragment) – No continuity with parent disk. May migrate superiorly or inferiorly. Major cause of failed surgery, contraindicates chymopapain, percutaneous discectomy and microdiscectomy. Requires exploration to remove.
- Disc bulge – Broad based (25-100%) displacement of disc material (usually annulus fibrosis). May cause symptoms if impresses on the thecal sac. 50% of asymptomatic patients have a bulge/protrusion, treatment is on clinical grounds.
Much of the pain is usually due to inflammation, rather than mechanical compression of a nerve. Granulation tissue may be much larger than disc tissue, which is best seen with contrast administration. Structure changes alone do to cause pain.
Spontaneous reduction occurs up to 6-12 months later (esp >6mm) improving symptoms, ?from continued disc dehydration and shrinkage, fragmentation and phagocytosis. Acute epidural enhacement is associated with acute herniations, proceding inwards with time. Peridiscal enhancement is a good sign ?neovascularity contributing to resorption of the disc material. Annulus tear will fill with vascularised granulation tissue and may heal.
DDx conjoined nerve root (V5%) esp L5-S1 where 2 nerve roots traverse in same dural pouch, exiting through same or different foramina. Occasionalyl enlarge the neural foramen.
(Intravertebral herniation). May be asymptomatic or associated with infection, trauma, malignancy, osteopenia, intervertebral osteochondrosis. Similar intensity to parent disc, well-defined, rim enhancement and sclerosis (low T2). Occasional bone marrow oedema (?recent irritation). Chronic Schmorl’s nodes may be associated with fatty endplate changes. Limbus vertebra – disc herniation into ring apophysis in children with back pain; similar appearane to a small corner fracture.
Discogenic vertebral sclerosis – Variant of a Schmorl node. Usually focal sclerosis adjacent to endplate, associated disc space narrowing, osteophytosis. Can be lytic or mixed lytic-sclerotic. Typically middle-aged women with chronic low back pain.
Juvenile kyphosis is >40deg kyphosis of T3-T12; from scoliosis, idiopathic (including postural kyphosis) or Scheuermann disease. Unknown aetiology (?microtrauma of congenitally weak endplates, ?osteochondrosis). M>F, begins at puberty, most lower thoracic spine, pain, rigid lower thoracic kyphosis. Thoracic vertebral body wedging (at least 3 contiguous vertebra >5degrees), disc space narrowing, endplate irregularity.
Normal ~12mm diameter, stenosis if <10mm. Mild stenosis <1/3 diameter reduction; Moderate 1/3-2/3, Severe >2/3 narrowing.
Encroachment of bony or soft tissue structures onto one/more neural elements causing symptoms, generally doesn’t apply if solely from disc bulge. Congenital or acquired, but congenital doesn’t usually cause Sx (even if severe) unless associated with some acquired stenosis. Central stenosis (compression of the thecal sac from normal round shape, usually AP direction), lateral (subarticular recess – bony canal where the nerve rests before entering the neural foramen) or neuroforaminal stenosis. Subjectively mild, moderate or severe. Measurements currently not useful due to variations in shape. From bony hypertrophy/osteophytes/overgrowth (DJD, Pagets, achondroplasia, posttraumatic), spondylolisthesis, superior facet hypertrophy in DJD, ligamentum flavum hypertrophy (>5mm), disc bulge/protrusion/extrusion/sequestration, post-op scar, other soft tissue mass, and/or congenital variants (eg short pedicles). In lumbar spine stenosis causes T/trefoil shape from narrow canal and facet hypertrophy, usually degenerative. MRI tends to overestimate degree of spinal stenosis compared to myelography/CT due to susceptibility, CSF motion and truncation artifact. Tx laminectomy (resection of lamina, spinous process, ligamentum flavum).
Retrodural space of Okada (v) – space posterior to ligamentun flavum, may be continuous with both facets, interspinous space. More common with chronic degeneration.
Defect in pars interarticularis esp L5, in 10% of asymptomatic patients, but may cause instability and low back pain. ?Acquired in childhood from stress fracture, more common in extreme lumbar extension (eg gymnastics). Rare cervical spondylolysis probably congenital. Most common cause of identifiable lower back pain in children. Best seen on CT transverse slices at level of mid body through the pedicles, showing break in bony lamina(e). On oblique views defect is break in neck of the ‘scottie dog’. SPECT will show acute/symptomatic defects, MR will show bone marrow oedema.
Subluxation of a vertebral body, usually anterior (anterolisthesis). If severe, may cause central canal stenosis and/or neuroforaminal stenosis. Meyerding grade 1-4 depending of posterior corner cephalad vertebral body offset compared to the caudal vertebral body which is divided into quarters, grade 5 (spondyloptosis) complete with inferior migration. Change in orientation of the neural foramina from vertical to horizontal, sharp angulation of the nerve root (pediculate kinking). Associated disc herniations are unusual at that level, but common at level above. Pseudoherniation (uncovering of the disk) as the vertebral body displaces anteriorly with respect to the disk. Doesn’t tend to progress after 20yo. Increases disc degeneration. Causes include:
- Congenital – Dysplastic or abnormal orientation of facets, kyphosis.
- Spondylolysis (spondylolytic spondylolisthesis) – May be severe if bilateral.
- Facet joint DJD with joint instability and subluxations esp L4/5. Increased risk with diabetes. Usually mild.
- Postsurgical – Altered stress after fusions, laminectomies etc.
- Pedical fractures after trauma.
- Osteoporosis, metastases, infection, osteopetrosis, arthrogryposis.
Segmental instability may be due to listhesis (most from facet joint disease) or pars defects. Pain does not respond to steroid injections.
Facet Joint Synovial Cyst
(Juxta-articular cyst). Rounded posterolateral extradural cyst, extending from facet joint, associated with degenerative disease. Associated with spondylolisthesis and abnormal facet joint movement. Most are synovial cysts (from tear of synovium), some are ganglion cysts (with connective tissue capsule). Most lumbar (esp L4/5 or L5/S1). Occasionally haemorrhage causing acute symptoms. May contain gas or wall calcification.
Upward protrusion of odontoid peg into infratentorial space. McGregor’s line extends from posterior hard palate to undersurface occiput; Chamberlain’s line extends from hard palate to mid opisthion; dens should not extend >5mm or half its height above these lines. Caused by Paget disease, rickets, fibrous dysplasia, osteogenesis imperfecta, hyperparathyroidism, osteomalacia, achondroplasia, cleidocranial dysplasia, Morquio syndrome, RA. Basilar impression = when cause is from bone-softening disease.
DDx Platybasia – flattening of skull base, when Wencke basal angle (lines from nasion to tuberculum sellae and along tuberculum/clivus/basion) is >143deg. Seen in Klippel-Feil, cleidocranial dysostosis, achondroplasia.
Diffuse Idiopathic Skeletal Hyperostosis (DISH)
(Forestier disease). Calcification/ossification of the ALL with proliferative enthesopathy (hyperostosis) at attachment to the vertebral body. Ossification along the anterior ± lateral spine, paraarticular osteophytes, OPLL in 50%. Osseous bridging of at least 4 contiguous vertebral bodies. Relative absent disc and facet joint disease. Hypertrophy and ossification at the spinous processes. Posterior osteophytes if present are small. Increased risk of spinal fracture, low threshold for CT/MR in context of back pain and trauma; fractures tend to occur through the mid vertebral body, or junction of ankylosed segment with relaively normal spine at the intervetebral disk. DDx ankylosing spondylitis (involves SIJ, facet joints, squaring).
Ossification of the Posterior Longitudinal Ligament (OPLL)
Inflammatory degenerative disease esp Japanese, Polynesians. M=F, 40s-60s. Occurs in 50% of patients with DISH. May compress spinal cord. Continuous ossification over several vertebral levels (cf calcified disk, osteophytes, meningioma). May contain marrow fat, may be associated with ligamentum flavum calcification/ossification. DDx ossification of the posterior ligaments from fluorosis.
Very high risk of spinal fractures even with minor trauma due to osteoporosis and magnified force along fused spine (in effect a lever arm). Most prone area to fracture is through the calcified disc.
(Charcot spine). From cervical syrinx, diabetes, traumatic spinal cord injuries, tabes dorsalis, postsurgical. L-spine most common. Patients are unaware of the severe degeneration and continue to use the joint causing progressive destruction, sclerosis (density), fragmentation (destruction), listhesis (dislocation).
Acute Calcific Tendonitis of the Longus Muscles
Neck pain, dysphagia. Unilateral or bilateral calcifications within longus colli and capitis, high T2 in prevertbral or retropharyngeal space. Tx NSAIDS.
Lateral curvature of spine, may be associated with kyphosis/lordosis or rotatory deformity. Severe scoliosis may lead to respiratory compromise, neurologic Sx, pain. MR to assess neural compromise. Painful scoliosis may be due to underlying tumour, stress fracture or infection.
- Idiopathic (85%) – Usually late childhood/adolescence, M:F 1:7. Degree may change rapidly during rapid growth (puberty). Prevalence 2-4%, increased risk with family history. Diagnosis of exclusion. Usually primary/major thoracic/thoracolumbar curve with secondary/minor compensatory curve above and below. May be double major S-shaped. R-sided curvature more common in older children.
- Congenital scoliosis – Presents earlier and more severe, more abrupt short-segment curves, progresses more rapidly than idiopathic. Vertebral body anomaly with 1 of the 3 ossification centres (1 body 2 posterior elements) may fail to form or fuse with adjacent segment causing segmentation abnormal eg hemivertebra. May be associated with VACTERL (vertebral, anorectal, cardiac, tracheoesophageal fistula, renal, limb anomalies), tethered cord or diastematomyelia.
- Leg-length discrepancy – Significant if >10-20mm. Pelvic tilt on standing XR. Unilateral leg shortening from trauma (esp physeal injury), SUFE, congenital (eg infantile coxa vara); unilateral leg lengthning from hyperaemia near physis (inflammatory arthritis, high-flow vascular malformation, fracture), hemihypertrophy. Tested by long-cassette sliding table technique, or CT scanogram (less dose) with femoral/tibial measurements between tops of femoral heads, distal medial femoral condyles, tibial plafond. Tx lengthening procedures or epiphysiodesis (fusion of physis).
- Neuromuscular scoliosis – Neurologic impairment or muscular dystrophy causing paraspinal muscle imbalance (spasticity or flaccidity), typically long C-shaped. From cerebral palsy, muscular dystrophy, paralysis, arthrogryposis. Associated with dysplasia/dislocation of hips.
- Syndromatic scoliosis – Associated with connective tissue disorders (Marfan syndrome, Ehlers-Danlos syndrome), NF1, RA, Down syndrome. In NF may progress rapidly and become unstable with subluxation and paralysis. Commonly kyphotic esp midthoracic. Associated with dural ectasia (post vertebral body scalloping, enlarged neural foramina, widened interpediculate distance), rib abnormalities (twisdted narrow ribbon ribs).
- Tumours – Esp osteoid osteoma in posterior elements, concave to nidus (muscle spasm).
- Radiotherapy – Arrested growth. Associated with hypoplastic ribs.
- Degenerative – Asymmetric disc or facet disease.
Thoracolumbar spine on single cassette with patient standing (or sitting or brace); PA (reducing dose to breast, AP may be done initially to better assess vertebrae) ± lateral, bilateral bending views or distraction views. Cobb angle from superior endplate above and inferior endplate below (pedicles if endplates not well seen) creating greatest angle; scoliosis if >10deg. Dextroscloliosis is convex to right, levoscloliosis to left. Level of apex also noted. Bilateral bending views to determine if fixed (structural) or flexible (functional). Risser index is degree of skeletal maturity assessed at iliac apophysis; grade 1 lateral 25% ossified, grade 2 lateral 50%, grade 3 lateral 75%, grade 4 entire apophysis, grade 5 fused with iliac wing. Increased maturity has less chance of further soliosis or progression. Tx >25deg external brace; rapid progression or >50deg surgery to prevent complications, using spinal rods, lamina wires/hooks and pedicle screws.
Congenital variation wih posterior tip of one facet more medial than anterior tip. This causes ipsilateral slippage on the more sagittally orientad facet with rotation. May be mild and asymptomatic.
Mass effect from swelling, haemorrahge and scar may simulate disc herniation; may initially be worse than preoperatively, but reduces over up to 6 months; doesn’t correlated with outcome. Post-op there is enhancement of the facet joints, paraspinal muscles, previouslly compressed nerve roots (extending towards conus), post-discectomy space, vertebral endplates; may persist for months. All have scar/granulation tissue by 4 months, which enhances (cf nonenhancing disc material).
Failed back surgery syndrome in 5-40% after lumbar disc surgery. Imaging should be done with enhanced T1 FS. Causes include:
- Inadequate surgery – Eg missed free disc fragment, insufficient decompression of nerve root.
- Postoperative epidural scarring/fibrosis – Enhances due to inflammation (cf disc minimal peripheral enhancement, may enhance after 20min). May cause traction on dura.
- Bone graft complications
- Residual or recurrent disc
- Postoperative spondylolisthesis with instability
- Hardware failure, hardware abutting thecal sac or nerve root
- Postoperative infection, haematoma, trauma to roots
- Dural tear – Leak of CSF from wound or forming a pseudomeningocele (DDx abscess, seroma, organising clot).
Hydromyelia is dilatation of the central canal (lined by ependyma); syringomyelia (syrinx) is cavitation outside the cental canal lined by glial cells; difficult to distinguish between these on imaging – hence the term syringohydromyelia. May be developmental (Arnold-Chiari malformation), trauma, tumour, inflammatory or ischaemic. Presyrinx is altered CSF flow prior to development of syringomyelia, spinal cord becomes oedematous and expanded. Reversible if CSF pressure treated. Exosyrinx – eccentric intra- and extra-medullary syrinx. Well-defined, signal follows CSF. May have glial adhesions creating linked-sausage appearance. Unless definite benign Hx (eg contusion, Chiari I), give Gad to search for a tumour nidus. May enhance on delayed imaging. Causes include:
- Hydromyelia communicating with 4th ventricle – From obstruction of CSF at 4th ventricle outlets, associated with hydrocephalus.
- Hydromyelia which doesn’t communicate with the 4th ventricle – Altered CSF dynamics from Chiari I, IDEM tumours, arachnoid cysts, arachnoiditis, cervical spinal stenosis, basilar invagination, diastematomyelia, Klippel-Feil, Page disease, spinal dysraphism, tethered cord syndrome.
- Syringomyelia – Centred in spinal cord parenchyma in watershed regions from injury. From trauma, infarction, spinal cord neoplasms, myelitis. Trauma/haemorrhage/infarction may cause myelomalacia (cord cavitation), with altered CSF dynamics (from adhesions etc) causing syrinx formation. Cystic myelomalacia follows CSF on all sequences, is treatable cause of myelopathy. Noncystic/microscopic myelomalacia has high PD and T2.
DDx oedema (indistinct borders, brighter T1 and lower T2 than CSF), high signal truncation (Gibbs) artifact from overshoot/’ringing’ of Fourier transform at abrupt high contrast interfaces.
<2mm can say dilatation central canal – no need for followup Those >2mm can call hydromyelia, recommend contrast enhanced MRI – if this is negative then benign incidental hydromelia with no followup needed
Adult Tethered Cord
(Tight filum terminale syndrome). Young women with diffuse back and perianal pain, leg weakness, urinary dysfunction. Conus below L2, thickened filum (>2mm). May be tethered by spina bifida occulta, filum lipoma or intradural lipoma.
Transdural Spinal Cord Herniation
Rare spontaneous, post-traumatic or postoperative. Symptomatic up to several years after event with myelopathy, radiculopathy, Brown-Sequard syndrome. Cord herniates through a dural defect. Nuclear trail sign – sclerosis in vertebral endplate or disc from previous herniated nucleus. Cord is small, rotated, displaced with dilated CSF. High T2 in the cord if strangulated.
From obesity, steroids, Cushing syndrome. Increased posterior fatty tissue, may cause cord compression.
- Arachnoid cyst – Isointense to CSF. Usually asymptomatic, but may cause radicular compression if under pressure. May be congenital or acquired (previous inflammation, trauma). May or may not fill with intrathecal contrast. DDx epidermoid cysts which have restricted diffusion.
- Tarlov cyst (perineural cyst) – Dilated nerve root sleeve containing the nerve, arachnoid-lined, may have associated bony erosion. From ball-valve effect at ostium of nerve root sheath. May or may not fill with intrathecal contrast. May or may not be symptomatic.
- Anterior sacral meningocoele – Leptomeningeal diverticulum (not from neural tube defect), not associated with a nerve root (cf Tarlov cyst). Currarino’s triad if associated with anorectal malformation (eg imperforate anus), bony sacral defect (eg scimitar sacrum) and presacral mass (cyst/teratoma/meningocoele).
- Epidermoid cyst – Usually extramedulalry, rarely intramedullary. Congenital from displaced ectodermal inclusions ?faulty closure of neural tube. Acquired from lumbar puncture with inclusion of skin tissue. Discrete mass with variable signal, may calcify. Diffusion restriction.
- Neuroenteric cyst – Communication to mediastinum (with enteric duplication cyst), associated with a vertebral body anomaly.
- Dermoid cyst – Contains fat.
- Ependymal cyst – Follows CSF.
- Synovial cyst
Enlarged dural sac and/or root sleeves, most commonly lumbosacral. Seen in Marfan syndrome, NF, Ehlers-Danlos syndrome, mucopolysaccharidoses, achondroplasia, ankylosing spondylitis. Scalloping of the posterior vertebral bodies, widened interpedicular distance, widened neural foramina, thinning of pedicle and lamina cortex.
Posterior dura compresses cord in in mid/lower C-spine during flexion. MR in flexed possition will show anterior migration of posterior dura with engorged venous plexus in the posterior epidural space. Progresses over years to cause atrophy of the cord.
Plain radiographs are adequate in low-risk cases, CT suggested for severe trauma to check for subtle lesions, and complex fractures as seen on XR. 5% have other noncontiguous spinal fractures.
Stability is capacity of spine to limit displacement so there is no compromise to spinal cord and nerve roots during normal loads. Clinical instability is greater than normal ROM at a spinal segment. In the C-spine instability is anterior listhesis of >3.5mm, vertebral body angulation >11deg. Anterior column is ALL and anterior half vertebral body/disc. Middle column PLL and posterior half body/disc. Posterior column in posterior elements, facet joints and ligaments. Generally disruption of only one column doesn’t result in instability. Compression fractures usually only involve anterior column, burst fracture anterior and middle, flexion-distraction middle and posterior, fracture-dislocation all columns.
Benign features of acute compression fractures include cortical fracture without destruction (puzzle sign), retropulsion into spinal canal, fracure lines within cancellous bone, thin diffuse paraspinal mass, intravertebral vacuum effect, low T1 which returns to normal after 4-6 weeks. Features of malignant fractures include destruction of anterolateral or posterior cortex, destruction of cancellous bone, destruction of the pedicle, focal paraspinal mass, epidural mass, diffuse replacement with low T1, diffusion restriction from marrow packing (controversial). If unsure can repeat MR in 4-6 weeks to check for resolution of low T1 and reduced enhancement.
Contusions usually at sites of fracture, from bony impingement and cord compression, may be from hyperflexion/hyperextension. Injury to thoracic levels or below usually cause paraplegia; cervical quadriplegia; above C4 respiratory compromise from paralysis to diaphragm. Spinal cord oedema and haemorrhage. Low T1 high T2 has best prognosis and is potentially reversible. High T1 and T2 with haemorrhage has poorest prognosis. Enhancement between 2-3/12 from early necrosis, absorption, reorganisation. Cord avulsion may occur from sudden distraction force along long axis, esp cervicaohoracic junction. Associated with anterior and posterior longitudinal ligament partial/complete tear with oedema, causing instability. May progresses to atrophy, myelomalacia, may enlarge with CSF entry, posttraumatic syrinx from adhesions disturbing CSF flow (may later require shunting), arachnoiditis, arachnoid cyst.
Spinal cord injury without radiologic abnormality (SCIWORA) – Post-traumatic myelopathy with normal imaging. Esp children with C-spine injuries, ?ligamentous laxity. Usually hyperextension. MR may show ligamentous injury or cartilage fractures.
Subdural haematomas rare in spine, usually due to coagulopathy. Dura separated by bone by epidural fat, ventral space also contains rich plexus of veins which may tear. Haematomas grow with time.
Nerve Root Avulsion
Avulsion of spinal nerve root from connection to cord, most common in cervical spine (wider range of motion), esp roots serving brachial plexus. May occur from birth trauma from traction on shoulder resulting in Erb palsy from injury to C5-7 roots (shoulder adducted and internally rotated, elbow extended and pronated, wrist flexed) or trauma causing traction on upper limb. CSF typically leaks into epidural space through rent in arachnoid and dura. Absent roots, cord displaced to contralateral side. The pseudomeningoceles may later lose communication with CSF space forming an epidural mass.
- Neutral lateral
- AP from C3 to T1
- AP atlantoaxial region (open-mouth odontoid view) – Normal spaces lateral to dens equal. Rotation causes ipsilateral space widening.
- AP obliques
- With clinical neuropathy â€“ CT or MRI.
- Flexion and extension – If other views normal, must be done completely unaided (conscious and alert patient will not injure themselves with voluntary movement as injury -> muscle guarding).
- ‘Swimmer’s view’ – Useful for evaluating alignment of C6-T1, but not very useful for detecting fractures in this region.
Trauma C-Spine review (AABCS):
- Adequacy – C1-T1 visualised.
- Alignment – Normally lordosis, but loss of this if on backboard or in collar, muscle spasm. Lines include anterior longitudinal line, posterior vertebral line, spinolamina line (should always be continuous) and tips of spinous processes (variable but C7 is always the largest). In children there may be physiological offset of 2-3mm at C2/3 and C3/4 (of all but spinolamina line).
- Basion-axis interval (BAI) – Between posterior axial line (PAL) and basion in midsagittal line; normal <12mm (not reliable).
- Basion-dental interval (BDI) – Between basion and closest aspect of dens in midsagittal line; normal <12mm (should be <9mm).
- Powers ratio – Distance from basion to mid posterior arch (BC): distance from opisthion to mid anterior arch (AO); normal BC/AO <1.
- Predental space (atlandodental interval ADI) – Anterior arch C1 <3mm from dens without change in flexion, <5mm in children (may change by 1-2mm with flexion. Greater suggests transverse ligament injury.
- Atlando-occipital interval – Distance between perpendicular articular surfaces of occipital condyle and lateral masses C1; normal <1.5mm.
- Odontoid process should tilt posteriorly.
- Open-mouth odontoid peg view should show lateral margins of C1/2 aligned, or move as a unit with rotation. Bilateral-lateral offset of C1 suggests ring fracture, but may be normal in children.
- Facet joints should be superimposed (if perfectly lateral) or at least uniform overlap thoughought, abrupt change indicates longitudinal axis rotation. Facet articular surfaces must also be congruent with complete coverage.
- Disc spaces (Cartilage) – Areas of widening of narrowing may indicate fracture; narrowing usually OA (IF osteophytes and sclerosis also present). May have corresponding distraction of spinous processes.
- Prevertebral Soft tissues – Posterior airway. <7mm anterior to C1-3/4, <21mm (or one vertebral body) anterior to C3/4-C7. In children <2/3 C2 width at C3-4 and <14mm at C6.
- Ocipitalisation of the atlas – Lack of segmentation of atlanto-occipital junction with apparant atlantoaxial subluxation, abnormal large C1/2 interspinous space with atlas very close to occiput. Odontoid peg appears bizarre. Flexion view shows the fixation.
- Lack of ossification or fusion – Bifid C1 body, synchondroses neural arches of C1 and C2 which extends below base of odontoid.
- Os terminale – At tip of odontoid peg, V-shaped tip before ossification.
- Os odontoideum – Large ossicle separated from hypoplastic odontoid, fixed to arch of atlas within the transverse ligament, compensatory hypertrophy of anterior arch C1. ?Old ununited fracture ?enlarged os terminale. Position is orthotopic if in position of odontoid process, or dystropic if at foramen magnum near base of occiput. Tx usually posterior antlantoaxial fusion.
- Occipital condyle fracture – Often requires CT, may involve hypoglossal canal or jugular foramen. Type I impaction with asymmetric axial load; type II basilar type from distraction through alar and apical ligaments; type III avulsion type.
- Craniocervical dissociation (occipital vertebral dissociation, atlanto-occipital dislocation) – Severe trauma, true dislocation often fatal. Subluxation is rare. Higher risk in children (?small occipital condyles and horizontal atlanto-occipital joints), Down syndrome, Marfan syndrome, bony metastases. Basion to tip of peg >12mm, unreliable <13yo. Associated with pontomedullary laceration, contusion/laceration of inferior medulla and spinal cord, midbrain injury, SAH, SDH, dissection.
- Jefferson fracture – Axial injury (blow to apex of skull) -> burst fracture of C1 in >/= 2 places (fixed ring, classically 4 site at junctions of arches to lateral masses) involving anterior and posterior arches. On plain radiograph lateral masses C1 extend beyond margins C2 body. May be stable if there is only minimal displacement and no disruption of transverse atlantal ligaments.
- Atlantoaxial distraction – Severe extension with disruption of capsules, alar ligaments, transverse ligament, tectorial membranes, occasionally type I dens fracture. Widening of C1-2 space.
- Altantoaxial rotation (rotatory fixation of the atlantoaxial Joint, atlantoaxial rotatory displacement, rotary atlantoaxial subluxation) – Controversial, from rotation injury locking C1/2 facets, usually in childhod with torticollis. On peg view one of the spaces lateral to dens is wider and closer to midline with opposite narrower and laterally offset. Space stays wider even with contralateral head rotation. Occasionally associated with C1-2 transverse ligament disruption (increasing distance anterior to dens). Usually spontaneous or mild trauma (eg unusual sleeping position). Tx soft collar and/or gentle traction.
- Atlantoaxial dislocation – From trauma (rupture of transverse ligament), transverse ligament or odontoid peg abnormality (os odontoideum, ossculum terminale, agenesis of odontoid base or apical segment), Grisel syndrome (rotatory subluxation from inflammatory mass in tonsillitis/pharyngitis), Down syndrome, Marfan syndrome, NF, ankylosing spondylitis, RA, CPPD (thickening of transverse ligament), tumours. Fatal or asymptomatic. Complete dislocation of C1-2 facets.
- Odontoid peg fracture – Type 1 involves tip (usually stable); type 2 through waist/base (most common, unstable); type 3 extends below base into cancellous bone of C2 body (unstable). May cause anterior angulation or straightening of peg (should be angled postriorly).
- Hangman\’s fracture (traumatic spondylolisthesis) – Unstable, from hyperextension and distraction (eg hitting head on dashboard). Bilateral neural arch fractures usually at C2 (may occur at other levels). C2 body usually displaced anterior and spinous process posteriorly compared to C3. Effendi type 1 involves posterior C2 with <3mm displacement and <15deg angulation and intact disc /ALL/PLL (most common); type 2 significant displacement/angulation (disc probably disrputed, unstable); type 3 severe displacement/angulation with disloacted and locked facets. Good neurologic prognosis (fracture posterior C2 is effective decompression).
- Fracture of the posterior arch of the atlas – Hyperextension with fracture between occiput and spinous process C2.
- Anterior wedge compression fracture – Usually only anterior column, stable. Increased posterior height of disc space with fanning of spinous processes accentuated on flexion films suggests PLL disruption and instability.
- Flexion teardrop (teardrop burst) fracture – Severe flexion and compression, disrupting posterior ligaments. Sagittal and coronal comminuted vertebral body fractures with triangular avulsion fracture fragment at the anteroinferior border (generally width > height). Posterior body fragment displaced into spinal canal, 80% associated with neurological injury. Extent of injury usually underestimated on XR. Unstable.
- Unilateral facet dislocation (unilateral locked facet) – Flexion, distraction and rotation. Perched facet causing abrupt change in facet overlap (bow-tie sign), usually at C4/5 or C5/6. 35% associated with fracture, usually of the facet. There may be no significant vertebral body subluxation.
- Bilateral facet dislocation (bilateral locked facets) – Flexion and distraction. Vertebral body displaced usually 50%. High incidence of cord injury.
- Clay-Shoveler\’s fracture – Avusion fracture C6, C7 or T1 spinous process by the supraspinous ligament. Stable.
- Acute disc protrusion – Loss of disc height, anterolisthesis.
Hyperextension injuries are more subtle, injuries can spontaneously reduce. May be associated with vacuum phenomenon at annulus fibrosis.
- Extension sprain injuries – Stretch or tear of ALL, disruption of anterior annulus fibrosis.
- Extension teardrop fracture – Avulsion of anteroinferior vetebral body by ALL usually at C2 or C3, generally height > width. Commonly associated with Hangman’s fracture. Stable on flexion, unstable in extension.
- Facet compression fracture.
- Spinal cord injury without fracture or dislocation.
- Whiplash injury – From hyperextension and subsequent hyperflexion. Whiplash syndrome includes HA, neck pain, interscapular pain, paresthesia, vertigo, lethargy. ?Facet joint occult fracture, capsular rupture or intra-articular haemorrhage. May have kyphotic angle on flexion and extension views from muscle spasm.
- Radicular symptoms following cervical spine injury.
- Neurocentral joint degeneration .
- Rheumatoid arthritis, esp atlantoaxial subluxation.
Thoracic and Lumbar Spine
- AP ± weight bearing
- Lateral – Thoracic long exposure, cross-table if unable to stand.
- Lateral centred on the thoracolumbar junction
- Coned lateral lumbosacral junction
- 30° angled sacroiliac joints
- Oblique views
Interpedicular distances should gradually widen, disc spaces increase to greatest at L4-5. Type A fractues axial load with compression fracture; B anterior and posterior elements with soft tissue injury in transverse plane; C superimposed rotational component.
Most injuries occur at T12-L2. Flexion forces are converted into compression by strong middle and posterior columns.
- Anterior wedge compression fracture – Common esp thoracolumbar junction. Difficult to tell if acute or old. Can be asumed old injury if seen on previous or if no pain on examination. Posterior wall of vertebral body and PLL are intact. Type A both endplates; B (most common) superior endplate; C inferior endplate; D buckle of anterior cortex with both endplates intact. Kummel disease – acute fracture left unprotected with delayed (usually 1-2/52) further collapse with neurologic deficit. Tx back brace until pain-free. Further imaging with CT/MR not required.
- Burst/comminuted fracture – Involves anterior and posterior elements. Loss of vertebral body height with splayed fragments, interpedicular widening. Facets may be fractured, subluxed, perched, dislocated or locked. Need CT to check for bony fragments in spinal canal. 40% associated with another spine fracture, so entire spine should be radiographed. Type A (40%, from axial compression) comminuted both endplates, pedicles and posterior elements, minimal kyphosis; B (40%, from flexion-compression) superior endplate with retropulsion of post-sup corner; C (rare, from flexion-compression) inferior endplate with retropulsion of post-inf corner; D type A with rotation; E (compression and lateral bending) lateral burst.
- Chance (lap-belt) fracture – Hyperflexion at waist, distracting posterior elements and ligaments, usually T12, L1 or L2. May spontaneously reduce. Transverse fracture through posterior elements and vertebral body (± compression) or disc space. May have fractures through pedicles, lamina or transverse processes. Associated with abdominal wall haematoma, intra-abdominal injury.
- Cervicothoracic transverse process fracture – Lap and shoulder belt concentrates forces at cervicothoracic junction with twisting component.
- Lateral compression fracture – From lateral flexion, asymmetrical vertebral body compression often associated with scoliosis.
- Hyperextension injuries uncommon, may disrupt ALL, cause posterior element and facet compression.
- Transverse process fracture – May be isolated, if multiple may be associated with intra-abdominal injury.
Sacral Insufficiency Fracture
Esp after radiotherapy or severe osteoporosis (postmenopausal or steroid-induced). H-shaped fracture along sacral ala, down plane of sacral foramina. Honda sign on bone scan. DDx stress fracture. Tx sacropalsty (cement injection), bed rest or hardware stabilisation.
Injection of cement (methylmethacrylate) into vertebral body fractures (benign or malignant) or haemangiomas via transpedicular approach. Kyphoplasty inflates balloon within compressed body followed by methylmethacrylate. Fractures with marrow oedema or hot on bone scan most likely to benefit from these. Cx leak into veins (compressing spinal cord, nerves or causing PE), leak into disc space (increasing risk of adjacent vertebral fracture).
Normal peripheral nerves are similar in size to adjacent vessels, signal similar to muscles, smooth outline, preserved surrounding fat plane, no enhancement (except adjacent vessels)Peripheral nerve injury will lead to widening between axons and hence increased anisotropy on DTI.
- Perinatal injuries – Increased risk with shoulder dystocia, maternal diabetes, high birth weight, breech, mechanical assistance. Loss of visualisation of nerve root, ipsilateral pseudomeningocele, contralateral spinal cord displacement, rarely spinal cord injury. May have dural tear without root avulsion.
- Erb (Duchenne) palsy – Avulsion of C5-6 nerve roots causing weakness of shoulder and intrinsic muscles of hand.
- Klumpke injury – Avulsion of C7-T1 afecting hand muscles. May be associated with Horner syndrome if involves sympathetics or stellate gnalgion at C7-T1 level.
- Cervical ribs – In 1-2%, bilateral in 25%, symptomatic in 10%. Incomplete ribs may have band to clavicle, trappping the plexus.
- Brachial plexitis – Usually viral or after radiotherapy. High T2, variable enhancement.
- Lymphatic malformation – Multiloculation, fluid-fluid levels, bright T1 and T2. Doesn’t usually enhance.
- Venous malformation
- Neurogenic tumour – Fusiform, neurofibromas > schwannomas, may be associated with NF1.
- Desmoid tumour – High T2 with avid enhancement.
- Primary malignant tumours – Fibrosarcoma, liposarcoma, rhabdomyosarcoma (children), malignant PNST (eg neurofibrosarcoma), lymphomas
- Secondary malignanancy – Contiguous spread from Pancoast tumour, breast cancer nodal metastasis, lymphoma, oesopagus, thyroid, trachea, H&N tumours. Loss of fat planes between brachial plexus and scalene muscles.