Musculoskeletal Principles

Bones

Mature bone made of organic matrix (osteoid) of collagen and other proteins mixed with mineral calcium hydroxyapatite. Thick outer cortex and inner cancellous/trabecular bone. Periosteum covers surfaces except joints (cartilage), joint capsule and ligament atachments. In children it is loosely adherent except at physes, hence allowing blood/pus/tumour to accumulate. Constant turnover with osteoclasts resorbing old aging bone (may contain microfractures), osteoblasts forming new bone, with 10% of skeleton replaced/remodelled annually. Wolff’s law – increase in bone stress shifts balance to greater bone production ?due to microfractures. Cells types include:

  • Osteoprogenitor cells – Pluripotent mesenchymal stem cells near bony surfaces.
  • Osteoblasts – At surface. Sythesize, transport and arrange proteins (type 1 collagen and other proteins) of the bony matrix and initiate mineralisation. Initial random weave of woven bone (at times of rapid bone formation, pathological in adults) or orderly layered lamellar bone (stronger).
  • Osteocytes – Communicate with other cells on bone surface via network of cytoplasmic processes within the bone canaliculi. Control calcium and phosphate levels. Mechanotransduction – detects mechanical forces and translates into biological activity.
  • Osteoclasts – Derived from monocyte-macrophage precursors, forms a resorption pit (analogous to a lysosome) with surrounding cell membrane preventing leakage of digestion products.

T1 used for finding bony lesions (replacement of bright marrow fat).

Skeletal Development

Aggregation of mesenchymal cells in 1st T. Bones formed by intramemrabnous ossification by direct transformation (skull, mandible, most facial bones, lateral clavicles) or enchondral ossification of initial cartilage model at physes (remainder of skeleton). The immature woven bone is remodelled by osteoclasts and osteoblasts into mature lamellar bone at primary ossification centres. Secondary ossification centres at the epiphyses, separated from primary ossification by the physis. Physis – clusters of chondrocytes at epiphyseal margin of physis (resting zone), divide and enlarge (provisional zone), cease to divide but continue to enlarge (maturation zone), greatley enlarge (hypertrophic zone) then calcify (provisional calcification), chondrocytes die and are replaced by osteoblasts (osteogenic zone) starting ossification at the physeal/metaphyseal junction; contributing to longitudinal growth. Bone bark – lateral margin of physis which occasionally calcifies.

Tubulation is lateral growth (periosteal new bone) and remodeling at metaphysis into tubular shape (osteoclasts and osteoblasts), creating a normal cancave metaphyseal margin. Undertubulation (Erlenmeyer flask deformity) causes wide metaphyses; seen in rickets, osteopetrosis (reduced osteoclastic activity), fibrous dysplasia, dwarfism, storage diseases (marrow packing), multiple osteochondromas. Overtubulation (gracile bones) have narrow metaphyses and long narrow diaphysis with short epiphyseal-diaphyseal transition; in neuromuscular conditions (reduced weight-bearing eg cerebral palsy, myelomeningocoele, arthrogryposis), osteogenesis imperfecta, JIA, Marfan’s, homocystinuria.

At skeletal maturity chondrocytes in resting zone stop dividing, ceasing cartilage thus bone formation, may be left with dense transverse line (physeal scar). Growth recovery lines (stress/Park/Harris lines) are thin sclerotic lines in metaphysis associated with recovery phase after stress, eventually removed by remodeling in adulthood. Broad ill-defined bands abutting the physis may be normal in weight-bearing bones; in all bones is abnormal eg heavy-metal poisoning. Lucent metaphyseal bands seen in rickets, leukemia, metastatic neuroblastoma.

Epiphyseal cartilage (growth cartilage) is mostly fibrocartilage (lower T2 than articular cartilage), highly vascular (enhances).

Fractures

Bones are anisotropic, stronger in compression, weaker in tension and shear. Rotation and bending are combinations of these forces. Fracture threshold is inversely proportional to rate of load applied (hence more resistent to slowly increasing force). Stress riser – small defect (eg screw tract, nutrient foramen) where force is concetrated, lowering fracture threshold. Fracture descriptions include location, position, alignment, comminution, joint involvement, open (compound) or closed (skin disruption), foreign body, pre-existing lesion (pathologic fracture, tend to be transverse).

  • Complete fracture
    • Transverse – From tension, high force shear.
    • Oblique – Compression, shear in line of force.
    • Spiral – Rotation/twisting.
  • Incomplete fracture – Mostly children, osteomalacia or osteoporosis. Bones can permanently deform (numerous microfractures) without fully breaking.
    • Buckle – Focal compression. Torus fracture is complete circumferential buckle.
    • Greenstick – From bending, distraction of convex side.
    • Pure plastic bowing deformity – Innumerable microfractures.
  • Comminuted fracture
    • Segmental comminuted – Two separate sites in same bone.
    • Butterfly comminuted – From bending, with wedge-shaped ‘butterfly’ fragment.
  • Intra-articular fracture – Extends to articular surface. Associated joint effusion with fluid-fluid (haemarthrosis with cellular fluid dependent) or fat-fluid level (marrow fat). Cx post-traumatic osteoarthritis, esp if step-off/gap is >2mm.
    • Die punch fragment – Articular surface fragment driven into epiphysis, most commonly tibial plateau fracture.
    • Osteochondral fracture – Compression or shear fracture of cartilage and subchondral bone.
  • Other fractures
    • Avulsion fracture – Tension by tendon/ligament.
    • Chip fracture – Small cortical fragment from focal impaction/shearing.

Alignment described by position of distal fragment

  • Displacement – Perentage cross-sectional diameter of dominant fragment. If >100% then may cause overriding/bayonet appostion.
  • Distraction – Separation
  • Angulation – Medial/varus or lateral/valgus.
  • Rotation/torsion

Physeal Injuries

Physes (epiphyseal/apophyseal growth plates) contribute to bone growth via enchondral ossification, producing cartilage model then osteoblastic replacement with bone. Injury may cause healing with bone bridging or chondrocyte injury with growth arrest or deformity. Loss of metaphyseal blood vessles (trauma, infection etc) inhibits ossification of the cartilage template, thus widening of the physis, growth deformity/disturbance. Physes involved in 15% paediatric fractures, may -> growth arrest. Salter-Harris classification (‘SALTR’) has increasing Cx with type.

  • Type 1 – ‘Slipped’ through physis, <5yo, epiphysis may be displaced, soft tissue swelling.
  • Type 2 – Metaphysis and physis (‘Above), 75% of physeal injuries. Traingular metaphyseal bony fragment attached to physis and epiphysis.
  • Type 3 – Physis and epiphysis (‘beLow’). Higher risk of growth arrest.
  • Type 4 (vertical) – Epiphysis, physis and metaphysis (‘Through’). High risk of growth arrest.
  • Type 5 – Crush to all/part of physis (‘Rammed’).

Growth arrest may from bony bridge/bar accross physis, SH4 or traumatic/ischaemic injury to physeal chondrocytes (also seen in extreme vascular insult eg DIC, most prone in central physis); trivial in teenager but devastating in a young child. If central, no angular deformity but may cause ball-in-cup. Growth recovery line – original fracture line, with relative reduced bony growth at region of physeal injury, appears to merge with bony bridge. Bar best seen on 3D spoiled GRE FS (same as articular cartilage). Tx in older children (close to normal fusion) is fixation (epiphysiodesis) to prevent angulation. Tx in younger patients is physeal salvage with resection of bone bridge with drill; unsuccessfull if bridge >50% of physis hence may need to fuse contralateral physis to prevent limb-length discrepancy.

Stress injury may cause ‘chronic SH1’ with widening and irregularity, esp distal radius/ulnar in gymnasts, proximal humerus in throwing, lower legs of runners.

Stress Fractures

Fatigue fracture (often synonymous with stress fracture) is abnormal or repeditive stress on normal bone. Muscles, tendons and ligaments help to redistribute forces, hence muscle fatigue reduces protection. Microfractures stimulate new bone formation (Wolff’s law) with osteoclasts acting 1st to remove weaker/injured old bone, hence bones become weaker for 1st few weeks, when microfractures can coalesce into discrete fracture. Can occur in almost any weight-bearing bone, esp femoral neck, posteromedial tibial shaft (runners), metatarsals (march fracture in new military recruits), tarsals, femoral shaft, pelvis (parasymphyseal, pubic rami, supra-acetabular), lumbar spondylolysis. Upper limb much less common. If atypical location/history need to follow-up or biopsy; DDx infection, tumour.

  • Stress reaction (shin splint in tibia) – Early stress injury distributed along segment of cortex, may show faint cortical resorption, periosteal reaction, periosteal new bone formation. T1 normal.
  • True stress fracture – Focal segment may weaken more rapidly, acting as stress riser hence progress further, also reducing stress elsewhere allowing healing. Low T1 as marrow is replaced by callus/haemorrhage/fibrosis.
  • Complete fracture if left untreated

Bone scan is very sensitive, showing intense focal bone scan uptake. XR is specific showing periosteal reaction or linear sclerosis usually perpendicular to major trabecula from attempted healing. MRI most sensitve showing marrow oedema, specific when fracture line seen. Tx rest or immobilisation, earlier intervention results in more rapid healing.

Insufficiency fracture is normal stress on demineralised/abnormal bone from osteopaenia/osteoporosis, CRF, osteomalacia, neoplasia. Microfracture leads to bone marrow oedema syndrome which either resolves, subchondral insufficiency fracture or avascular necrosis. Difficult to detected due to osteopenia, with initial radiographs negative in 80%. Bone scans sensitive but nonspecific, improved with MRI. CT less sensitive but may show fracture line or early bone healing.

Pathologic fracture – Any fracture with normal stress in abnormal bone, technically includes insufficiency fracture but usually reserved for tumours.

Fracture Healing and Complicataions

Fracture follow-up radiographs should describe fragment position and alignment change, maturity of healing, complications.

Fracture reduction – Restoration of anatomical alignment, closed or open (operative access for fixation or assessment of intra-articular aligment).

Immobilisation

  • Internal fixation – Cortical plate with transverse screws, pin or screws across fracture, cerclage wires, Kirshner/K-wires, or intramedullary rod/nail. Cortical screws have fine thread, trabecular wider to gain purchase.
  • External fixation – Pins remote to fracture site, used when site is infected or fracture near end of bone.

Compression improves contact and reduces risk of nonunion, but technique may telescope or shorten a long bone.

  • Cortical compression plates – Slots for screw heads designed to force fragments toward centre of plate.
  • Lag screws – Gap between thread and head allowing compression as screw is tightened.
  • Dynamic fixation – Eg dynamic hip screw, dynamising an intramedullary nail by removing interlocking screws on one side (after healing initiated and partial stability).

Fracture healing is impaired by age, local bone and soft tissue devitalisation, location (months in tibia cf 6-8/52 elsewhere), mobilisation, lack of bone fragment apposition, infection, tumour at fracture, bone necrosis, poor nutrition, smoking, corticosteroids, NSAIDS. Healing is stimulated by microscopic motion (none in extremely rigid fixation).

  • Haematoma with fibrin mesh (soft-tissue callus, procallus) – Induces growth factors and neovascularisation, localised bone demineralisation, osteoclastic removal of necrotic margins of fracture causing blurring.
  • Bony callus – Immature woven bone formed within haematoma. Inadequate fixation causes abundant callus and is unable to mature.
  • Remodelling into mature lamellar bone – Portions of callus bone that are not physically stressed are resorbed. Remodelling improves with younger age, metaphyseal location, no or only angular deformity in same plane of motion as adjacent joint.

Complications:

  • Delayed union – Clinical diagnosis, fracture may be healing slowly but satisfactorily.
  • Nonunion – No evidence of bridging bone, smooth tapered rounded sclerotic margins. May be hypertrophic with excessive bone deposition or atrophic with demineralisation. Central portion of callus may undergo cystic degeneration, lined with synovial-like cells and create a pseudoarthrosis. Prevention/Tx augmented with autologous/donor bone graft, hydroxyapatite cast, pulverised coral (DDx methacrylate beads impregnated with antibiotics for infection, usually larger and used after removal of infected hardware).
  • Malunion – Healing with angulation or deformity, may cause limb-length discrepancy, obvious deformity, may limit function, cause pain. Angulation may be tolerated if it is in plane of adjacent joint movement, hence able to be compensated.
  • Avascular necrosis (AVN) – Esp proximal pole scaphoid, talar dome, femoral head. Extensive covering articular cartilage limits blood vessels to enter. Lack of normal demineralisation from hyperaemia and remains dense (mild sclerosis proximal pole of scaphoid may be normal). Tx grafting or surgical removal.
  • Soft tissue injury – Arterial, nerve, ligament.
  • Osteomyelitis – If open fracture or orthopaedic hardware. Osteolysis surrounding pin/screw or tract enlargement (DDx mechanical loosening), soft tissue gas.
  • Hardware failure – Inadequate reduction (increased strain on hardware), inadequate hardware or excessive loads on fracture before fracture healing.
  • Reflex sympathetic dystrophy (RSD, Sudeck’s atrophy) – Alteration in sympathetic nervous system causing regional hyperaemia, pain, osteoporosis, soft tissue atrophy, altered temperature control.
  • Myositis ossificans, heterotopic ossification

Excessive callus formation seen in:

  • Malalignment – Callus is greatest at the concave portion
  • Corticosteroids (exogenous or Cushing’s)
  • Neuropathic joint
  • Paralysis
  • Osteogenesis imperfecta
  • Renal osteodystrophy
  • Burn patients
  • Subperiosteal bleeding eg scurvy
  • Congenital insensitivity to pain

Bone Marrow Oedema Syndromes

Causes of oedema include trauma, infection, tumour, infarction or idiopathic. Yellow fat is predominantly fat with high T1; requires 30% loss to reduce T1. Red/haematopoietic marrow has increased vascularity with iso T1, mildly high T2FS/STIR, mild enhancement. T1 is most sensitive for pathology.

Joints and Soft Tissues

Synovial joints (diarthorosis) have hyaline cartilage covering bones (cushions, reduces friction), synovium lining capsule (produces fluid lubricating and nourishing cartilage) and stabilising ligaments. Cartilaginous joints have fibrocartilage over articulating bone. Fibrous joints are the strongest. Enthesis are site of attachments of ligaments or tendons, Sharpey’s fibres form the intraosseous root.

Subluxation is partial loss of articular contact; from ligament injury, laxity or cartilage thinning. Dislocation (luxation) is complete loss of articular contact. Diastasis is separation of a slightly mobile joint or fracture fragments. Intra-articular bodies may cause pain and locking, including bone/cartilage/meniscal fragment, may be loose or fixed to synovium.

Impingement is abnormal tissue compression, usually of soft tissues in/near joint, clinical diagnosis.

Bursa is a synovium-lined potential space reducing friction, normally difficult to see. Bursitis from trauma, calcium salt deposition (calcific bursitis), infection or generalised synovial inflammation (eg RA). Adventitial bursa is pathological, formed at bony prominances, lacks epithelial lining.

Soft tissue calcification:

  • Trauma – Myositis ossificans (timing), burns (associated contractures, acro-osteolysis), frostbite (acro-osteolysis, thumb spared), head injury, paraplegia/quadriplegia (esp hips).
  • Tumour – Synovial cell carcinoma, liposracoma, fibrosarcoma/MFH, soft tissue osteosarcoma, phleboliths.
  • Collagen vascular disease – Scleroderma (SC, acro-osteolysis), dermatomyositis (sheet-like in muscle/fascial plane), SLE (uncommon, esp legs), CREST, calcinosis cutis.
  • Arthritis – CPPD, HADD, gout, synovial osteochondromatosis.
  • Congenital – Tumoral calcinosis, myositis ossificans progressiva, pseudohypoparathyroidism, pseudo-pseudohypoparathyroidism, progeria, Ehlers-Danlos disaese.
  • Metabolic – Hyperparathyroidism, hypoparathyroidism, renal dialysis.
  • Infection – Granulomatous (TB, brucellosis, coccidioidomycosis), abscess, leprosy, cysticercosis, Echinococcus.
  • Drugs – Hypervitaminosis D, milk-alkali syndrome.

Tendons and Ligaments

Dark on all MR sequences (highly ordered anisotropic, dissipating energy), may some have intermediate signal at/near insertion/origin or where it fans out. Magic angle effect/phenomenon – intermediate/bright signal when orientated 55o to β0 on short-TE (GRE, T1, PD), esp ankles as curve around malleoli, supraspinatus curving over humeral head; not seen on T2. ?? for assessment, T2 for troubleshooting. US hyperechoic of uniform fibres if beam perpendicular. Poor blood supply, healing by mucoid degeneration or fibrosis, causing tendon to become thicker or thinner, injuries acumulate over years.

  • Sprains are incomplete disruption, with oedema amongst intact fibres. Sprains more common in adolescents-middle age, fractures more common in very young and elderly.
  • Partial tear – Focal defect or thinning, some lax/wavy fibres. Some chronic tears may only show thickening or thinning.
    • Intrasubstace tear – Doesn’t extend to surface. Interstitial tear is longitudinally orientated, laminar/cleavage tear is sheet-like in flat tnedon.
  • Complete tear (full-thickness, full-width) – Laxity with all fibres interupted, high T2/hypoechoic fluid or granulation tissue, fragments move seprately ± retraction. Fatty muscle atrophy if chronic.
  • Tendinosis – Chronic tendon tearing and repair, some also include complete tear. Thickened (occasionally thinned) tendon with increased T1/T2 or reduced echogenicity. If repair predominates over injury may be homogenously reduced T1/T2, if mucoid degeneration or interstitial tears then heterogeneous.
  • Subluxation – From bony groove or overlying retinaculum, esp extensor carpi ulnaris (ulnar styloid), peroneus longus/brevis (lat malleolus), tibialis posterior (med malleolus), long head biceps (subscapularis tear). If recurrent can cause tendon degeneration.
  • Tendinitis – Tender, painful tendon.
  • Calcific tendinitis – Amorphous calcium deposits.
  • Tenosynovitis – Inflammation of tendon sheath with increased fluid. From generalised synovitis (eg RA) or tendon degeneration, inflammation, tear, overuse, trauma, infection. Stenosing tenosynovitis is irregular scarring/fibrosis of tendon with adhesion to sheath, loculated fluid.

Articular Cartilage

Complex matrix of collagen and large molecule proteoglycans, chondrocytes and bound water. Deepest layer of collagen is radial (perpendicular to bone), middle random, thin superficial later parallel to surface; hence even distribution of load to subchondral bone and low friction. Avascular, relying of diffusion of nutrients via synovial fluid, and some from ECF of bone, hence motion drives nutrients. Thickness ~5mm in knee, much less elswhere, ~1.5mm at ankle. Incapable of regeneration, but there may be limited repair if subchondral bone is breached (eg surgery to induce repair) with production of fibrocartilage (cf hyaline cartilage). Damage/defects -> inadequate cushioning, subchondral trabecular microinjury -> adaptive changes including osteophytes, subchondral fibrosis, sclerosis.

XR can only show joint space narrowing (crude, late sign), some residual cartilage or loose bodies may hold space open. Best sequence intermediate FSE of TE 45ms, intermediate intensity (slighlty lower in deep layer due to anisotropy); defect causes increased signal or reduced thickeness, accentuated with FS. CT/MR arthrography shows surface defects better. FS 3D spoiled gradient echo improves resolution enabling better morphology assessment, cartilage is bright (defects dark), but limited assessment of other tissues. Gold standard assessment is arthroscopy. Defect description includes size, grade, location, subchondral bone oedema/sclerosis/cysts, associated synovitis/meniscal tears/etc. MRI modified (from arthroscopic) 4-grade (Outerbridge) classification:

  • Grade 1 – Degradation damaged cartilage imbiding (‘drinking’) joint fluid. Normal or mildly increased T2, may take up contrast.
  • Grade 2 – Defect <50% or localised swelling of cartilage.
  • Grade 3 – Defect >50%
  • Grade 4 – Full-thickness, usually associated with underlying sclerosis/fibrosis/oedema. ?Grade 4 if subchondral cyst/oedema present regardles of defect depth.

Fissure – crack in surface of variable depth. Delamination – separation from bone; if partially disrupted then flap tear, if fully disrupted then grade 4 defect. Osteochondral fragment (cartilage and subchondral bone) reattachment heals better than cartilage alone.

Treatments:

  • Osteochondral autologous transplantation (OATS/AOTS, mosaic-plasty) – Osteochondral plug from non-weightbearing parts (donor) transplanted to defect, usually limited to <2cm2.
  • Cadavaric osteochondral allograft – For larger lesions, prone to poor incorporation and rejection.
  • Autologous chondrocyte implatation (ACI) – Harvests chondrocytes, grown ex vivo then implanted under periosteal flap.
  • Disruption of exposed subchondral bone with small holes, abrasion or microfractures, inducing fibrocartilage production (inferior to normal articular cartilage).

Acute chondrolysis – Rare sudden diffuse uniform loss of articular cartilage, usually after trauma/surgery esp hip, occasionally idiopathic in immobilised patients. Unknown aetiology ?change in load bearing reducing nutrient diffusion to cartilage. DDx infection.

Chondrocalcinosis – Articular cartilage calcification from crystal arthropaties (esp CPPD), haemochromatosis, elderly/degenerative.

Muscles

Normally intermediate T1, low/intermediate T2. STIR or T2FS for oedema, masses or collections. T1 for fatty infiltration (chronic irreversible injury) or methaemoglobin (subacute haematoma). GRE for old haematoma with haemosiderin in macrophages at margins. Gad for necrosis or abscess. Biopsy area of oedema without fatty infiltration, hence active inflammatory infiltration.

  • Muscle strain – Microscopic fibre tearing at musculotendinous junction, from forceful contraction against load. Esp muscles that elongate during contraction eg hamstrings, biceps. Mild (grade 1) oedema between fibres centered at musculotendinous junction; moderate (grade 2) more oedema with fluid collections; severe (grade 3) disruption of musculotendinous junction with loss of function.
  • Contusion – Oedema and small collections at site of injury.
  • Intramascular haematoma – May have fluid-fluid level, high T1 (methaemoglobin) or low T1 (haemosiderin).
  • Heterotopic ossification – Any extra-skeletal ossification, common around hip after arthroplasty or femoral nail, profoundly reduced joint motion (eg paralysis). May limit ROM.
    • Myositis ossificans – From blunt trauma ?aetiology. Immature granulation tissue, ossifying after several weeks. Early mass-like mimicking sarcoma at imaging and biopsy, may cause periostitis. Amorphous calcification -> peripheral ossification -> resolve, diminish or migrate to merge with adjacent bone, or remain unchanged.
  • Muscle denervation – After 2-4/52 diffuse oedema, if innervation restored returns to normal. After several weeks, irreversible wasting with fatty atrophy. DDx chronic complete tendon tear, long-term high-dose corticosteroids.
  • Degenerative neuromuscular conditions – Active oedema then end-stage fatty atrophy.
    • Denervation atrophy – Spinal muscular atrophy (inflammatory motor neuron disease).
    • Diseases of the neuromuscular junction – Myasthenia gravis, Lambert-Eaton myasthenic syndrome (paraneoplastic).
    • Muscular dystrophies – Eg X-lined muscular dystrophy (Duchenne muscular dystrophy, Becker muscular dystrophy).
    • Ion channel myopathies (chennalopathies)
    • Congenital myopathies
    • Myopathies associated with inborn errors of metabolism – Lipid myopathies, mitochondrial myopathies.
  • Autoimmune conditions – Active oedema then end-stage fatty atrophy. Dermatomyositis, polymyositis, inclusion body myositis. Late stage dermatomyositis or polymyositis – streaky/sheet-like calcification within fasciae.
  • Infection – Focal/diffuse oedema, may form abscess if pyogenic (central fluid with enhancing margin), gas suggests highly aggressive organism (eg Clostridium).
  • Diabetic myonecrosis – Extremely painful ?aetiology, similar appearance to severe infectious myositis, complex appearance.
  • Radiation – Long-lasting soft-tissue oedema with sharp margins.
  • Acute compartment syndrome – Esp leg and volar forearm which is invested in indistensible superficial fascia. From fracture, trauma, surgery causing swelling, haemorrhage. Increased pressure may cause ischaemia, more oedema and swelling -> atrophy, scar, contracture, irreversible loss of function if untreated. Tx fasciotomy.
    • Exertional compartment syndrome – Intermitent, reproducible during exercise. Oedema (may be subtle) during or immediately after activity.
  • Myofascial defect – Bump/protrusion along surface (esp calf) through defect in fascia. Usually incidental, may be symptomatic during exercise, exacerbated with contraction.

Nerves

Peripheral nerves composed of fascicles (bundles of fibres), fatty myelin sheath. High-resolution MRI/US can demonstrate individual fascicles. Injury from direct trauma, compression, tension, tumour, autoimmune, infection (leprosy, diptheria), diabetes, radiation or hereditary motor and sensory neuropathies (HMSNs eg HMSN I Charcot-Marie-Tooth). May show oedema, enhancement or swelling, muscle denervation. Electromyelography (EMG) generally superior than imaging apart from masses (eg neurofibroma, schwannoma, extrinsic mass).

Peripheral nerve entrapment syndromes:

  • Median nerve
    • Carpal tunnel syndrome – In carpal tunnel from congenital narrowing, overuse, synovitis (eg RA), mass, hypothyroidism, fracture, idiopathic.
    • Pronator syndrome – In pronator teres.
    • Ligament of Struthers – Normal variant.
  • Radial nerve
    • Posterior interosseous nerve syndrome – deep branch in supinator muscle.
    • Humerus shaft fracture
    • Sleep palsy – from sleeping on side.
  • Ulnar nerve
    • Cubital tunnel syndrome – From nerve subluxation, mass, trauma, inflammation.
    • Guyon’s canal syndrome – Mass trauma, inflammation.
  • Axillary nerve in quadrilateral space syndrome (fibrotic bands, mass)
  • Suprascapular notch syndrome (mass, inflammation in spinoglenoid or suprascapular notch)
  • Posterior tibial nerve in tarsal tunnel syndrome – Nerve subluxation, mass, trauma, inflammation
  • Sciatic nerve in piriformis syndrome
  • Lateral femoral cutaneous nerve in Meralgia paresthetica – Compression over inguinal ligament adjacent to ASIS.

Foreign Bodies

Includes surgical implants. US can localise supeficial objects. MR insensitive to small nonmetalic objects. Glass is always radiopaque. Microscopic metallic fragments common after arthroscopy esp if drill/burr used, only seen on MR as artifact. Wood is radiolucent/gas density if dry, water density if fresh, often invisible on MR. May develop surrounding granulation, sterile fluid or pus.

Cobalt chromium steel alloys have much greater artifact than titanium and zirconium oxide alloys. MRI techniques to minimise metal artifact:

  • Low strength magnet.
  • Increased receiver bandwidth, matrix
  • Frequency encoding direction parallel to long axis of object
  • FSE esp PD rather than convenstional SE
  • No GRE or chemical FS
  • STIR instead to T2FS

Musculoskeletal Procedures

Joint Injection/Aspiration

Only major risk is infection (1:2,000). Intra-articular lignocaine is painful and can rapidly enter bloodstream. MR arthrogram can use saline or dilute gadolinium (1:100-250); CT full-strength iodinated. Iodinated contrast shortens T2 reducing signal on all sequences, hence use only a small amount if going to have MR. Can attach tubing to dilute gad solution and draw up 1-2mL full-strength iodinated contrast only into the tubing (hence less used, and if extraarticular then less gad in tissues). Overdistention of joint (if any resistence is felt) will cause decompression into soft tissues. Vasovagal reactions common.

  • Shoulder – Supine palm up at side with sandbag to stabilise. With fluoroscopy needle straight down over medial inferior anatomic neck adjacent to joint space until hit bone (ant labrum overlies ‘joint space’ and is very painful). 20-22G needle, 10-15mL. Subscapularis tendon may be firm simulating bone.
  • Elbow
    • Post – Supine, hand on abdo in flexion. No fluoro req. Needle in centre of triangle made by lateral epicondyle, olecranon and radial head. 25G needle, 6-8mL.
    • Lat ‘straight down’ – prone, arm above head, 90deg flexion with thumb up. Fluoro needle over radiocapitellar joint. 25G needle, 6-8mL. Avoid if ?lat joint abnormal.
  • Radiocarpal – Prone, arm above head, mild wrist flexion over towel in mild ulnar deviation. Needle ~5mm distal to radiocarpal joint space angled 45deg to slip between scaphoid and dorsal lip radius. Needle 25G, 4-6mL. Can carefully go lateral (keeping wrist flexed) to check intraarticular. In TFCC tear contrast will -> DRUJ; scapholunate/lunotriquetral tear -> midcarpal joint.
  • Midcarpal – Prone, arm above head, palm down. Needle in centre of four corners of lunate, capitate, hamate, triquetral; or space between sacphoid, capitate, trapezium. Only advance ~10mm. Needle 25G, 6mL.
  • DRUJ – Prone, arm above head, palm down. Needle at edge of ulnar at DURJ, walked into joint. Needle 25G, 1mL.
  • Hip – Supine, hip straight (or slightly flexed), internally rotated. Needle straight down over centre of thinnest part femoral neck (most redundant capsule) or over lateral head-neck junction down to bone. For iliopsoas bursagram same location but withdraw 5-10mm from bone. Needle 20-22G spinal or possibly 18G for aspiration, 10-15mL.
  • Hip arthroplasty – Straight down direct anterior on head/neck junction or anterolateral approach advancing fom above greater trochanter towards head/neck junction; down to metal. If no fluid aspirated then can use small amount of contrast then lavage of 10mL saline before re-aspirating and repeated until fluid can be aspirated. Fluid in hip may be in dependent position behind prosthesis, may internally rotate or massage posterior part of joint while aspirating.
  • Knee – Supine, slight flexion over pillow with relaxed quadriceps. No fluoro req. Push patella medial (opening medial patellofemoral joint space), needle between lower half medial patellar facet and anteromedial femoral condyle; can also do lateral approach. Needle 18-22G, 20-30mL. Aspirate as much effusion as possible by milking before injection, as may hold large amount of fluid.
  • Tibiotalar – Lying on side. Lateral projection, fluro needle from anterior approach, avoiding dorsalis pedis and anterior tendons by palpation. Needle 25G, 4-8mL.

Biopsy

Sample must be representative, in area of enhancement, most aggressive areas or oedema. For sarcomas entire needle track (and compartments) must be resected. Coaxial technique (outer needle outside tumour) reduces, but doesn’t elimiate seeding. Tract should cross only one compartment, avoid neurovascular bundles, joints (suprapatellar bursa extends far proximal and lateral), physis. Approach must avoid tissue required for reconstruction (pectoralis, glutei, rectus, quadriceps). In shoulder anterior 1/3 deltoid avoiding pectaralis (for reconstruction) and posterior deltoid (supplies anterior deltoid so resection denervates anterior deltoid).

Bone biopsy – Liberal LA at periosteum. Bone-cutting needle, remove stylet when tip at lesion, core for ~20mm, wiggle needle to break core then aspirate while pulling needle out. For lytic lesions FNA first as may be impossible to obtain core. Percutaneous biopsy of cartilagenous tumours not suggested as very little blood supply required for recurrence in tract and histological evaluation of the small sample confused between enchondroma and low-grade chondrosarcoma.

Trephined needles have crown-shaped cylindrical tip that grinds a defect around the core.