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Flashcards in HEAD & NECK Deck (45)
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1
Q

PARAPHARYNGEAL SPACE LESIONS

A
  1. Deep lobe parotid neoplasm—widens stylomandibular notch and
    displaces parapharyngeal fat medially. See Section 12.5.
  2. Masticator space pathology—displaces parapharyngeal fat
    posteriorly. See Section 12.4.
  3. Carotid space mass—displaces parapharyngeal fat anteriorly. See
    Section 12.7.
  4. Pharyngeal mucosal space mass—tumours of the nasopharynx or
    oropharynx can infiltrate the parapharyngeal fat or displace it
    laterally.
2
Q

PHARYNGEAL MUCOSAL SPACE

LESIONS: NASOPHARYNX

A
  1. Nasopharyngeal carcinoma—SCC or undifferentiated. Infiltrative
    intermediate T2 signal mass enhancing less than normal mucosa,
    centred on fossa of Rosenmüller. Produces middle ear effusion via
    eustachian tube dysfunction. Can invade nasal cavity, prevertebral
    muscle, pterygopalatine fossa, skull base and intracranial space (via
    foramen lacerum and perineural spread along CN V3). Nodal
    disease commonly retropharyngeal, posterior triangle and posterior
    deep cervical chain. Distant metastatic disease in 20% (lung, bone,
    liver) means PET-CT mandatory as part of work-up.
  2. Lymphoma*—NHL. Bulky homogeneous intermediate T2 signal
    mass, variable enhancement. May extend into PPS,
    retropharyngeal space or skull base.
  3. Lymphoid hyperplasia —normal finding in teens and 20s. May
    relate to viral infection including HIV. Symmetrical, shows vertical
    ‘tiger stripe’ enhancement, often with small mucous retention cysts
    at the bases. No extension beyond nasopharynx.
  4. Tornwaldt cyst—thin-walled midline submucosal cyst with variable
    T1/T2 signal depending on protein content. No internal
    enhancement.
  5. Juvenile angiofibroma—benign locally invasive vascular tumour
    seen almost exclusively in adolescent or young adult males. Avidly
    enhancing mass centred on the nasopharynx and sphenopalatine
    foramen, often extending into the pterygopalatine fossa, nasal
    cavity, paranasal sinuses, masticator space, inferior orbital fissure
    and middle cranial fossa (via vidian canal or foramen rotundum).
    Bone remodelling > destruction.
  6. Minor salivary gland malignancy—infiltrative enhancing mass
    with propensity for perineural and perivascular spread
3
Q

PHARYNGEAL MUCOSAL SPACE

LESIONS: OROPHARYNX

A
  1. Tonsil SCC—lingual (tongue base) or faucial (palatine). Associated
    with smoking and HPV. Mucosal ulceration or mass evident on
    inspection. On MRI, the mass is isointense on T1 and iso/↑ to
    muscle on T2, + enhancement. Level II and III adenopathy is
    common at presentation. HPV−ve tumours tend to be more
    ill-defined and invasive (e.g. into adjacent muscle); enhancement
    helps delineate extent. HPV+ve tumours (p16+ve on histology)
    tend to be more well-defined, exophytic and enhancing, with
    cystic nodal metastases.
  2. Palatine tonsil inflammation/abscess—enlarged poorly
    enhancing tonsil. Nonenhancing central low attenuation ± gas
    indicates abscess, which may extend beyond constrictor into PPS.
  3. Lymphoma*—extranodal NHL involving lingual or palatine tissue
    (Waldeyer’s ring). Cervical adenopathy also seen in most. Imaging:
    bulky homogeneous nonnecrotic mass, isoattenuating to muscle,
    intermediate T2 signal.
  4. Minor salivary gland malignancy—variable appearance
    depending on histology.Head and neck 351
    12
  5. Crohn’s disease*—can rarely involve the oropharynx, causing
    diffuse mucosal thickening and oedema
4
Q

MASTICATOR SPACE LESIONS

A
  1. Abscess—secondary to dental infection/manipulation →
    osteomyelitis of posterior body of mandible → cortical dehiscence
    → extension of pus into masticator space. Clinical: trismus,
    tenderness and fever. CT: cortical destruction ± periosteal reaction
    at posterior body/ramus. ‘Empty socket’ if following dental
    extraction. ‘Dirty’ fat planes. CT/MRI: swollen and enhancing
    muscles (myositis) + rim enhancing fluid attenuation abscess ±
    enhancing phlegmon. T1↓ in marrow, STIR↑ in marrow and soft
    tissue. May extend into supra-zygomatic masticator space ±
    associated epidural/subdural empyema.
  2. Bony lesions of mandible—see Sections 12.21 and 12.22.
  3. Incidental benign conditions.
    (a) Masticator muscle hypertrophy—smooth, diffuse
    enlargement of masticator muscle due to bruxism, habitual
    gum chewing or temporomandibular joint dysfunction. Often
    bilateral, usually asymmetrical. Clinical: nontender lateral facial
    mass which enlarges with jaw clenching. CT/MRI: enlarged
    (>1.5 cm depth) masseter muscle isoattenuating and
    isointense to normal skeletal muscles on pre- and postcontrast
    sequences.
    (b) Masticator space pseudolesions—incidental small masticator
    muscle → pseudohypertrophy of contralateral side. Clinical: no
    facial mass on jaw clenching.
    (c) Pterygoid venous plexus asymmetry—unilateral prominence
    of deep facial venous plexus from cavernous sinus and orbit.
    CT and MRI: prominent asymmetrical serpiginous vessels in
    masticator space, enhancing like other veins.
  4. Motor denervation cranial nerve (CN) VIII—cause: benign or
    malignant tumours, surgical trauma. Phases:
    (a) Acute (≤1 month)—enlarged muscle with STIR↑ (oedema)
    and ↑enhancement.
    (b) Subacute (≤12–20 months)—↓oedema, partial atrophy. STIR
    normal or mildly ↑. T1↑ due to fatty change. No or mild
    enhancement.
    (c) Chronic (>12–20 months)—fatty atrophy of muscle. T1↑↑.
    No oedema or enhancement.
  5. Sarcoma—rhabdomyosarcoma, leiomyosarcoma, liposarcoma,
    Ewing sarcoma, osteosarcoma, chondrosarcoma or synovial
    sarcoma. Mean age: 35 years. Can be associated with Gardner
    syndrome. CT/MRI: aggressive, ill-defined mass ± bone
    destruction.
  6. Perineural tumour extension—enhancement of CN VIII in
    masticator space → foramen ovale → Meckel’s cave. Can be seen
    with SCC, melanoma, sarcoma, NHL and adenoid cystic carcinoma
    (of parotid gland).
  7. Schwannoma of CN VIII—age: third to fourth decade (younger in
    NF2). CT: smooth enlargement of foramen ovale. MRI: variable T1/
    T2 signal depending on cystic change or haemorrhage.
    Homogeneous or heterogeneous enhancement. Well-defined,
    ovoid or fusiform/tubular shape ± signs of motor denervation
5
Q

FOCAL PAROTID SPACE LESIONS

5

A
  1. Pleomorphic adenoma—80% of parotid tumours. Well-defined
    lobulated mass, homogeneous when small, heterogeneous when
    large. Hypoechoic on US ± posterior acoustic enhancement. CT/
    MRI: prominent homogeneous enhancement when small (less so
    when large) ± calcification. T1↓, T2↑↑ (especially myxoid type),
    often with a T2↓ rim (fibrous capsule).
  2. Warthin tumour—second most common parotid tumour, often in
    the tail (may be mistaken for lymph node if exophytic). Bilateral or
    multifocal in 20%; most common cause of multiple solid parotid
    masses. Peak in sixth decade; the vast majority are smokers.
    Well-defined and heterogeneous. Greater tendency for cystic
    change than other salivary gland tumours. Often hypervascular on
    US with multiple small irregular sponge-like anechoic areas. Large
    tumours (>5 cm) are more cystic. CT: no calcification; cyst + mural
    nodule strongly suggestive. MRI: heterogeneous T1/T2 signal.
    Minimal enhancement on CT/MR.
  3. Nodal metastases or lymphoma*—metastases usually from scalp,
    external auditory canal (EAC), cheek skin SCC or melanoma.
    Ill-defined irregular lymph nodes (LNs), often with other abnormal
    periparotid, occipital or level II/V nodes. Lymphoma may be adenopathy from generalized disease or MALT lymphoma in Sjögren’s syndrome.
  4. Salivary gland carcinomas—mucoepidermoid, adenoid cystic,
    malignant mixed tumour, acinic cell, adenocarcinoma, ductal
    carcinoma, SCC. When small or low grade, indistinguishable from
    pleomorphic adenoma or LNs. Ill-defined margins are clue to
    diagnosis. T2↓ in a solid mass suggests malignancy. Look for
    perineural spread to temporal bone along CN VII.
  5. First branchial cleft cyst—either preauricular/intraparotid (± sinus
    tract to middle ear or medial EAC) or posterior/inferior to angle of
    mandible (± sinus tract to lateral EAC).
6
Q

DIFFUSE PAROTID ENLARGEMENT

A
  1. Parotitis—acute (viral/bacterial) or acute-on-chronic (due to
    obstructing calculus). Unilateral enlargement of hyperattenuating
    parotid + subcutaneous stranding. Chronic: small heterogeneous
    gland ± calculi in dilated ducts. NB: mumps parotitis is usually
    bilateral.
  2. Sjögren’s syndrome*—multiple bilateral cysts and hypoechoic
    nodules, ± submandibular/lacrimal gland involvement.
    Look carefully for solid lesions as increased risk of MALT
    lymphoma.
  3. Benign lymphoepithelial lesions of HIV—mimics Sjögren’s, but
    other glands are spared. Look for adenoidal hypertrophy and
    reactive adenopathy of HIV.
  4. Sarcoidosis*—mimics Sjögren’s; no increase in NHL risk. Cervical
    and mediastinal adenopathy is suggestive.
  5. Lymphoma*—usually part of systemic NHL with uni/bilateral solid
    nodules. Primary NHL is much less common
7
Q

CAROTID SPACE LESIONS

A
  1. Carotid body paraganglioma—most common paraganglioma of
    head and neck; located at carotid bifurcation + characteristic
    splaying of internal carotid artery (ICA) and external carotid artery
    (ECA) (‘lyre’ sign). Rarely associated with MEN 2A/B, Carney triad,
    tuberous sclerosis, NF1 or vHL—often multicentric when
    syndromic. Dense vascularity, avid contrast enhancement on CT/
    MR. MRI: T1↓ usually with ‘salt and pepper’ appearance due to
    punctate haemorrhages/slow flow (salt) and flow voids (pepper).
    T2↑ with multiple flow voids. Angiography: lyre sign with an
    intense blush in tumour ± ‘early vein’ due to arteriovenous
    shunting. Usually supplied by ascending pharyngeal artery.
    Scintigraphy: not specific, but MIBG and octreotide uptake can be
    useful for multiple lesions.
  2. Vagal schwannoma—fusiform, lies along the course of the vagus
    nerve; tends to displace both ICA and ECA anteriorly ± medially
    together, rather than splaying them. Imaging: T2↑, intense
    enhancement ± intramural cysts.
  3. Jugular vein thrombosis—expansion and lack of contrast/flow
    void in internal jugular vein (IJV). Causes: IV drug abuse,
    indwelling IJV catheter or deep neck space infection (Lemierre’s
    syndrome).
  4. Glomus vagale paraganglioma—identical appearance on CT/MR
    to carotid body paraganglioma, but located higher below the skull
    base. Displaces ICA and ECA anteriorly (without splaying) and IJV
    posteriorly. Vocal cord paralysis is common. Does not widen the
    jugular foramen.
  5. Pseudoaneurysm—post trauma or carotid dissection. Imaging:
    focal dilatation of carotid artery + mural thrombus or calcification.
    Flow void changes on MRI, complex wall sign; CTA or MRA
    correlation required.
  6. Neurofibroma—solitary tumours are fusiform, well-defined and
    usually sporadic. CT: ↓ attenuation. Plexiform tumours are seen in
    NF1;
8
Q

PERIVERTEBRAL SPACE LESIONS

A
  1. Vertebral body metastasis—MRI: replacement of normal marrow
    signal. CT: lytic or sclerotic vertebral body lesions with perivertebral
    soft-tissue extension.
  2. Infection—clinical: local pain, raised inflammatory markers. Discitis
    or vertebral body osteomyelitis + contiguous inflammatory mass.
    Epidural extension may cause cord compression or radicular
    symptoms. CT: peripherally enhancing fluid collection/abscess.
  3. Schwannoma—may appear embedded in scalene muscles. CT:
    may extend into spinal canal + smoothly enlarged neural foramen.
    MRI: T2↑, heterogeneous enhancement and cyst formation when
    large.
  4. Chordoma—rare in cervical vertebral body; destructive enhancing
    mass + perivertebral extension. MRI: characteristic T2↑↑.
  5. Plexiform neurofibroma—seen in NF1, involves multiple nerve
    roots. CT: isoattenuating to cord and nerve roots, may follow path
    of brachial plexus. MRI: isointense to nerve roots or cord, variable
    enhancement. Characteristic ‘target’ sign: T2↑ in periphery, T2↓ in
    centre.
9
Q

POSTERIOR CERVICAL SPACE LESIONS

6

A
  1. Lymphadenopathy—e.g. metastatic SCC, thyroid malignancies,
    lymphoma, suppurative LNs, granulomatous disorders (including
    TB, sarcoidosis and cat-scratch disease) and Rosai-Dorfman disease.
  2. Third branchial cleft cyst—congenital cyst posterolateral to carotid space.
  3. Nerve sheath tumour—e.g. schwannoma, neurofibroma.
  4. Nodular fasciitis—rapidly growing painful soft-tissue mass, usually
    related to the subcutaneous or muscular fascia. Variable enhancement and T1/T2 signal
  5. Thoracic duct cyst—in left supraclavicular fossa. Fluid attenuation
    and signal.
  6. Venous diverticulum—arises from the confluence of IJV and subclavian vein. Can mimic a supraclavicular node on CT, as it may not fill well with contrast. Diagnosis confirmed on US (may need Valsalva to visualize)
10
Q

RETROPHARYNGEAL SPACE

LESIONS: FOCAL

A
  1. Reactive lymph node—common in children.
  2. Metastatic lymph node—SCC of naso/oro/hypopharynx. If large
    but not necrotic, more likely nasopharyngeal carcinoma. Also may
    be from sinonasal or thyroid malignancies.
  3. Lymphoma*—often with Waldeyer’s ring involvement; solid and
    homogeneous even when large.
  4. Multinodular goitre—extends from enlarged thyroid, often with
    cysts and calcifications. Look for tracheal displacement/narrowing.
  5. Ectopic parathyroid adenoma—4D CT or SPECT aids
    differentiation from LN.
  6. Sympathetic schwannoma—slow-growing; fusiform enhancing
    mass medial to ICA.
11
Q

RETROPHARYNGEAL SPACE

LESIONS: DIFFUSE

A
  1. Abscess—crucial to avoid delay in diagnosis, as this may cause
    airway compromise or extend into danger space. Usually from
    pharyngitis or tonsillitis, in children, elderly or the
    immunocompromised. Rim-enhancing fluid collection; mass effect
    on surrounding structures helps differentiate from effusion.
  2. Effusion—fluid from impaired lymphatic drainage, often due to IJV
    thrombosis, radiotherapy or pharyngitis. Nonenhancing fluid
    collection with only mild mass effect.
  3. Suppurative adenopathy—hypoechoic/hypoattenuating enlarged
    LNs.
  4. Longus colli tendonitis—neck pain and stiffness. Acute
    inflammatory process with nonenhancing reactive RPS effusion and
    pathognomonic calcific deposits in longus colli insertion at C1–C2
    levels.
  5. Hypopharyngeal SCC—posterior wall or pyriform sinus SCC can
    extend posteriorly into and distend the RPS. Look for prevertebral
    involvement and RPS node
12
Q

ORAL CAVITY: ORAL MUCOSAL

SPACE LESIONS

A
  1. SCC of different OMS subsites.
  2. Minor salivary gland carcinoma—second most common
    submucosal mass, most often in the hard palate. Look for
    perineural spread along CN V2 branch.
  3. Radiation mucositis—acute/subacute phase. Diffuse mucosal
    enhancement
13
Q

ORAL CAVITY: SUBLINGUAL SPACE LESIONS

6

A
  1. Simple ranula—postinflammatory unilateral sublingual mucous
    retention cyst. Imaging similar to lymphatic malformation, epidermoid and sialocoele.
  2. Abscess—caused by tooth abscess or submandibular duct stone.
    Rim-enhancing fluid collection with duct stone or tooth abscess.
  3. Sublingual gland sialadenitis—enlarged, enhancing sublingual glands.
  4. Sublingual gland carcinoma—90% of sublingual gland masses are
    malignant. Most commonly adenoid cystic, mucoepidermoid, or acinic cell. CT/MR: heterogeneous invasive mass, variable enhancement. Tends to recur late (5–10 years).
  5. Sialocoele—cystic lesion due to trauma, surgery, stone or stenosis of submandibular duct. True sialocoele: distended duct. False: ruptured duct + pseudocyst due to extravasated saliva. May enhance peripherally after 2 weeks.
  6. Dermoid—from ecto- and mesodermal remnants. Mixed density,
    may contain fat (T1↑) or calcifications (T1↓).
  7. Epidermoid—ectoderm only. Homogeneous fluid density; T1↓,
    T2↑, restricted diffusion.
14
Q

ORAL CAVITY: SUBMANDIBULAR

SPACE LESIONS

A
  1. Submandibular gland (SMG) sialadenitis—swollen, painful SMG
    ± calculus and dilated duct if acute; atrophic SMG if chronic.
  2. Diving ranula—simple ranula of SLS ruptures into SMS through
    mylohyoid defect, forming a thin-walled, comet-shaped
    pseudocyst.
  3. Pleomorphic adenoma of SMG—50% of SMG tumours.
    Heterogeneous, well-defined, T1↓, T2↑, variable enhancement,
    ± calcifications, haemorrhage or necrosis. Hypoechoic on US.
  4. SMG carcinoma—usually adenoid cystic or mucoepidermoid.
    Invasive mass arising from SMG. Look for perineural spread in
    adenoid cystic carcinoma.
  5. Sjögren’s syndrome*—parotids, SMGs and lacrimal glands are
    usually involved. See Section 12.6.
  6. Benign lymphoepithelial lesions of HIV—more common in
    parotid glands. See Section 12.6.
  7. Accessory salivary tissue—similar attenuation/signal as adjacent
    SMG, extends into anterior SMS through mylohyoid defect.
  8. Second branchial cleft cyst—cystic mass in posterior SMS in a
    child or young adult. Usually thin-walled unless infected.
  9. Küttner pseudotumour—chronic sclerosing sialadenitis, seen as
    part of IgG4-related disease. Produces firm swelling and pain, or
    asymptomatic. MRI: T1↓, T2/STIR↑. US: hypoechoic, usually
    well-defined
15
Q

ORAL CAVITY: ROOT OF

TONGUE LESIONS

A
  1. Abscess—no LNs in root of tongue (ROT), so abscess results from
    haematogenous spread, foreign body or dental disease.
    Rim-enhancing mass splitting genioglossus muscles.
  2. SCC invasion—infiltrative mass arising from floor of mouth or oral
    tongue.
  3. Thyroglossal duct cyst—unilocular midline ROT cyst. T2↑, T1↓ (or
    ↑ if proteinaceous contents). Thin rim of enhancement.
  4. Dermoid and epidermoid—see Section 12.13.
  5. Ectopic thyroid tissue—well-defined ROT mass with signal/density
    similar to thyroid gland: hyperattenuating on CT, T1/T2↑ relative
    to tongue muscles on MRI. Homogeneous enhancement. NB: this
    may be the patient’s only functioning thyroid tissue. Can undergo
    goitrous, nodular or malignant change.
  6. Foregut duplication cyst—congenital cystic lesion between
    genioglossus muscles, lined with alimentary tract epithelium.
    Well-defined thick-walled cyst, variable contents, may mimic
    epidermoid due to protein content. US: visible bowel wall layers.
16
Q

TRANSSPATIAL NECK LESIONS 6

A
  1. Venous malformation—congenital slow-flow vascular mass.
    Lobulated, infiltrative margins, phleboliths on CT, T2↑ on MRI,
    moderate enhancement.
  2. Venolymphatic malformation—congenital; lymphatic and venous
    components. Lymphatic components show fluid characteristics ±
    blood-fluid levels. Venous components show solid enhancement
    and phleboliths.
  3. Infection—often odontogenic, may spread from superficial to
    deep, and from deep spaces into mediastinum. Heterogeneous
    rim-enhancing mass. Check airway and vascular patency.
  4. SCC—most common head and neck neoplasm. Deep spread = T4
    stage. Nodal conglomerates may involve multiple spaces.
  5. Lymphatic malformation—congenital uni/multilocular cystic mass.
    Well-defined, thin-walled, fluid attenuation on CT, blood-fluid
    levels on MRI. No enhancement.
  6. Plexiform neurofibroma—seen in NF1.
17
Q

Laryngeal lesions
main 8
others 5

A
  1. SCC—classified as supraglottic, glottic, subglottic or transglottic
    (>1 site). Linked to smoking and alcohol. Irregular, enhancing,
    exophytic or infiltrative soft-tissue mass. Look for effacement of
    paralaryngeal fat and cartilage invasion. Nodal disease is common.
  2. Vocal cord paralysis—usually unilateral, L>R due to longer
    recurrent laryngeal nerve on L side. May be life-threatening if
    bilateral. Caused by damage to recurrent laryngeal or vagus nerve,
    either due to tumour infiltration, trauma (e.g. postthyroidectomy),
    carotid dissection or dilated cardiovascular structures (e.g. aortic
    aneurysm). The involved cord is medialized with anteromedial
    deviation of the ipsilateral arytenoid cartilage and aryepiglottic
    fold.
  3. Laryngocoele—air- or fluid-filled cystic dilatation of laryngeal
    ventricle. May be contained within larynx (internal) or herniate
    through thyrohyoid membrane beyond confines of larynx
    (external). Usually due to increased intralaryngeal pressure, e.g.
    due to chronic cough, occupation (glass blowers, wind
    instruments) or an obstructing laryngeal tumour.
  4. Laryngeal reflux—of stomach acid, causing diffuse oedema and
    mucosal enhancement of larynx and hypopharynx.
  5. Other tumours—e.g. chondrosarcoma (T2↑, chondroid
    calcification, minimal enhancement), paraganglioma (discrete
    hypervascular mass), papilloma (polypoid, seen in papillomatosis
    related to HPV infection; biopsy required to exclude carcinoma),
    melanoma (primary or metastatic), inflammatory pseudotumour
    (nonspecific mass).
  6. Wegener’s granulomatosis*—classically causes subglottic stenosis
    ± inflammatory mass. Look for associated bony erosions in the
    paranasal sinuses.
  7. Rheumatoid arthritis*—can affect the cricoarytenoid and
    cricothyroid joints, resulting in sclerosis, fixation ± ankylosis. A
    poorly enhancing inflammatory mass ± cartilage erosion may also
    be seen, mimicking malignancy.
  8. Amyloidosis*—submucosal soft-tissue mass or diffuse infiltration +
    homogeneous enhancement ± calcification. Usually T2 isointense
    (cf. chondrosarcoma). Most commonly supraglottic. No cartilage
    destruction.
    Other lesions
  9. Thyroglossal duct cyst—most common congenital neck cyst. May
    be suprahyoid (in tongue base), level with hyoid or infrahyoid
    (most common); usually paramedian and intimately related to
    strap muscles. US: anechoic and thin-walled (unless infected), no
    internal vascularity. In adults, may contain debris. CT: thin-walled,
    smooth, well-defined, fluid attenuation. MRI: T2↑, may be T1↑ if
    haemorrhagic, infected or proteinaceous. No enhancement if
    uncomplicated, otherwise thin rim enhancement.
  10. Lymphadenopathy—e.g. lymphoma (homogeneous; when in level
    VI, often also in mediastinum) or nodal involvement by
    differentiated thyroid cancer (heterogeneous; may be calcified in
    papillary and medullary cancer, or cystic in medullary cancer).
  11. Parathyroid adenoma—benign, most common cause of primary
    hyperparathyroidism. Majority are solitary, located posterior or
    inferior to thyroid. May rarely be ectopic, e.g. in mediastinum,
    carotid sheath, retropharyngeal, or intrathyroid. US: ovoid,
    homogeneous, hypoechoic to thyroid. Doppler US: characteristic
    feeding vessel from the poles with vascular rim. NM: ↑ Sestamibi
    uptake. SPECT may improve anatomical localization. 4DCT is more
    sensitive than US or scintigraphy for localization; low attenuation
    precontrast, avid arterial enhancement with washout on delayed
    phase.
  12. Fourth branchial cleft cyst—cystic neck mass adjacent to or
    within thyroid, ± fistula to skin ± recurrent suppurative thyroiditis
    (intrathyroid abscess). L>R. Imaging: CT best, consider with oral
    barium (may show connection from cyst to pyriform sinus).
  13. Thymic remnant—ectopic thymic tissue seen along the path of
    descent (thymopharyngeal duct).
18
Q

THYROID ENLARGEMENT

9

A
  1. Multinodular goitre—diffuse nodular enlargement with benign
    change, fibrosis, haemorrhage, cysts and calcifications. Patients are
    usually euthyroid. Look for retrosternal extension and tracheal
    compression.
  2. Thyroiditis—may be the following:
    (a) Autoimmune—related to thyroid antibodies:
    (i) Hashimoto’s thyroiditis—lymphocytic thyroiditis.
    Typically in middle-aged women, usually hypothyroid +
    goitre, but can be hyperthyroid in ~5%. First gradual
    painless enlargement, then atrophy and fibrosis. US:
    depends on phase and severity. Enlarged heterogeneous
    gland + hypoechoic nodular texture with reactive LNs
    especially in level VI. Doppler vascularity is usually
    normal/low. Increased risk of papillary thyroid cancer and NHL.
    (ii) Graves’ disease—most common cause of thyrotoxicosis,
    usually in middle-aged women. US: enlarged and patchy
    hypoechoic thyroid ± marked hypervascularity on
    Doppler (‘thyroid inferno’). NM: enlarged gland with
    homogeneous ↑ uptake on 123I and 99mTc-pertechnetate
    scintigraphy.
    (iii) Riedel’s thyroiditis—rare, part of IgG4-related disease.
    Painless, may grow rapidly + dysphagia/stridor, hard fixed
    ‘woody’ thyroid. Parenchyma replaced by fibrosis, which
    extends into surrounding tissues; can mimic anaplastic
    thyroid carcinoma. US: homogeneously hypoechoic
    thyroid with ill-defined margins. CT: enlarged
    hypoattenuating gland + compression of local structures.
    MRI: ↓ on T1 and T2, variable enhancement.
    (iv) Postpartum thyroiditis—seen in 5%–9% of women in
    the first year after childbirth or abortion; usually transient,
    lasting several weeks to months. Clinical: hyper- or
    hypothyroid. US: variable, often hypoechoic thyroid.
    (b) De Quervain’s subacute granulomatous thyroiditis—selflimiting thyroiditis, often after a viral URTI. US: usually
    nonenlarged gland, ill-defined geographic hypoechoic and
    hypovascular areas interspersed with normal parenchyma. The
    key to diagnosis is that the thyroid is tender and painful.
    (c) Suppurative thyroiditis—rare, as the thyroid is normally
    resistant to infection. Can occur in an abnormal thyroid gland
    (e.g. Hashimoto’s) or due to infection of a fourth branchial
    cleft cyst (see Section 12.17). A rim-enhancing abscess may be
    seen.
  3. Primary thyroid carcinoma—90% of thyroid malignancies. Risk
    factors: prior irradiation (especially for papillary type), family
    history of thyroid cancer. NB: incidental FDG-avid thyroid nodules
    on PET/CT have ~40% risk being a primary thyroid malignancy.
    Four main types:
    (a) Papillary—most common (60%–80%). F>M, peak in third to
    fourth decades. US: solitary hypoechoic ill-defined mass +
    microcalcification. 50% have local adenopathy at presentation,
    usually ipsilateral levels III and IV, tend to become cystic ±
    microcalcification. NM: usually concentrates radioiodine but
    not pertechnetate. Prognosis is excellent even with metastatic
    disease.
    (b) Follicular—10%–20%. F>M, peak in fifth to sixth decades. US:
    hypoechoic solid tumour. Nodal spread occurs late,
    haematogenous metastases are more common. NM: typically
    concentrates pertechnetate but not radioiodine. FNA cannot
    differentiate between follicular adenoma and carcinoma;
    surgical resection is required.
    (c) Medullary—5%. Most are sporadic, seen in third to fourth
    decades. When familial (e.g. part of MEN 2A/B syndromes),
    tend to be multiple and in younger patients. US: hypoechoic
    mass with punctate (coarse) calcification in primary and
    involved LNs (cf. fine calcification in papillary type), and in
    distant metastatic sites on CT. Calcitonin levels are invariably
    high and can be used for follow-up.
    (d) Anaplastic—1%–2%. Highly aggressive, worst prognosis,
    5-year survival ~5%. Typically elderly (sixth to seventh
    decades), F>M, ± previous multinodular goitre. Infiltrative mass
    ± microcalcification. Nodal ± distant metastases common at
    presentation.
  4. Thyroid adenoma—benign, often incidental finding. Well-defined
    mass, may be heterogeneous ± cystic degeneration.
  5. Thyroid lymphoma*—NHL, ~2.5% of thyroid malignancies.
    Primary or secondary, peaks at 50–70 years, F>M. Hashimoto’s
    thyroiditis is a major risk factor, but still rare in this group. Clinical:
    rapidly enlarging goitre, compressive symptoms and cervical
    lymphadenopathy. B-symptoms rare, ~50% euthyroid. US: may be
    a hypoechoic nodular mass, diffuse heterogeneous infiltration or
    both. Calcification rare. CT: goitre, hypoattenuating to adjacent
    muscle, heterogeneous enhancement. More compressive than
    invasive. MRI: T1/T2 iso- to ↑, ± pseudocapsule.
  6. Thyroid metastasis—rare. Most often from breast, kidney, colon
    or lung. Nonspecific on imaging. Often detected on FDG PET/CT.
  7. Paraganglioma—can rarely occur within the thyroid. Well-defined,
    hypervascular + intratumoural vessels (rare with other thyroid
    masses).
  8. Fourth branchial cleft cyst
  9. Parathyroid adenoma (mimic)—at posterior aspect of thyroid, or
    rarely within the thyroid.
19
Q

Features associated with benign nodules

A
  1. Spongiform/honeycomb appearance comprising >50% of the
    nodule.
  2. Purely cystic, or solid-cystic with colloid (ring-down/comet-tail
    artefact).
  3. Eggshell calcification.
  4. Iso- or mildly hyperechoic with a hypoechoic halo.
  5. Peripheral vascularity on colour flow/Doppler
20
Q

Features associated with malignant nodules

A
  1. Solid hypoechoic nodule ± hyperechoic foci (microcalcification).
  2. Irregular margin, intranodular vascularity and absent halo.
  3. Taller than wide (i.e. anteroposterior > transverse diameter).
  4. Interrupted eggshell calcification with hypoechoic soft-tissue
    extension beyond it
21
Q

SONOGRAPHIC FEATURES OF NORMAL

VERSUS ABNORMAL LYMPH NODES

A
  1. Size—short axis is measured. Poor predictor for malignancy when
    used alone. Higher size cut-off yields higher specificity but lower
    sensitivity. Upper neck nodes are larger than lower neck nodes.
    Cut-off of 7 mm for level I and 8 mm for all other cervical nodes is
    recommended for 70% accuracy.
  2. Shape—metastatic, lymphomatous (Hodgkin/NHL) and
    tuberculous nodes are rounded. Normal or reactive nodes are
    usually oval or flat. Short/long axis ratio can be measured: <0.5 =
    oval; ≥ 0.5 = round. However, normal submandibular and parotid
    nodes are usually round.
  3. Echogenic hilum—normal feature. May be absent in metastatic,
    lymphomatous and tuberculous nodes, but not always.
  4. Nodal border—in proven malignant nodes, irregular ill-defined
    borders and hypoechoic change around LNs indicate extranodal
    extension (ENE). Clinical and histological evidence of ENE is now
    part of AJCC 8th edition; however, radiological appearances
    suggesting ENE may aid treatment planning at an earlier stage.
  5. Echogenicity—metastatic nodes are usually hypoechoic. Papillary
    cancer metastases are hyperechoic (thyroglobulin deposition).
    Tuberculous nodes are hypoechoic. Lymphomatous nodes are
    hypoechoic (often markedly) with posterior acoustic enhancement
    ± intranodal reticulation/micronodular pattern.
  6. Calcification—common in metastases from papillary (fine and
    peripheral) and medullary (coarse) thyroid carcinomas.
    Calcification may be seen in other metastatic LNs after
    radiotherapy or rarely after chemotherapy.
  7. Intranodal necrosis—late event in tumour invasion, may appear
    cystic or echogenic (coagulative necrosis). Cystic necrosis is
    common in SCC metastases (especially p16+ve), papillary thyroid
    carcinoma and TB. Coagulative necrosis is uncommon and may be
    seen in malignant or inflammatory nodes.
  8. Vascular pattern—normal and reactive nodes tend to show hilar
    vascularity or appear avascular. Metastatic nodes tend to have
    peripheral vascularity. Mixed vascularity is also common in
    lymphomatous nodes.
  9. Ancillary features—matting (common in TB) and adjacent
    soft-tissue oedema (may be seen around metastatic, suppurative or
    tuberculous nodes).
22
Q

BONY LESIONS OF MANDIBLE/MAXILLA: CYSTIC

10

A
  1. Periapical (radicular) cyst—well-defined ovoid ≤1 cm cyst at the
    apex of a dead (nonvital) tooth, due to inflammation and
    necrosis from dental caries (often visible as erosion of the crown
    enamel). Most common odontogenic cyst.
  2. Nasopalatine duct cyst—asymptomatic incidental developmental
    cyst arising from nasopalatine duct. Well-defined ≥1 cm midline
    cyst in the anterior maxilla (incisive canal).
  3. Dentigerous cyst—developmental cyst associated with the
    crown of an unerupted or impacted tooth. Most in mandible,
    especially at third molar. Variable size, usually unilocular with a
    thin sclerotic border. Maxillary cysts expand into maxillary sinus.
    No enhancement or solid component on CT/MR.
  4. Odontogenic keratocyst—benign cystic lesion with aggressive
    behaviour and high recurrence rate. 75% in posterior mandible,
    near third molar. In maxilla, most often near canine. May be
    multiple in Gorlin-Goltz syndrome. OPG/CT: solitary expansile
    unilocular cyst + sclerotic rim, may be near an unerupted tooth
    but not related to crown; ± displacement of developing tooth or
    resorption of roots. CT/MR: no solid nodule or mass, ± thin
    enhancing rim. Due to the keratin content, these usually have
    soft-tissue attenuation on CT and variable T1/T2 signal. May
    contain internal foci of calcification (calcifying odontogenic cyst).
  5. Ameloblastoma—benign, locally aggressive neoplasm arising
    from tooth-bearing area of jaws. Age: 30–50 years. Most in
    mandible, especially near third molar and ramus. In maxilla, most
    often near premolar and first molar. OPG/CT: usually multilocular
    (‘bubbly’) and expansile with cortical scalloping and resorption of
    adjacent teeth. Possible associated unerupted molar tooth. No
    internal calcification. CT/MR: enhancing mural nodule and septa.
    Malignant transformation in 1% (ameloblastic carcinoma).
  6. Residual cyst—at site of dental extraction, abutting alveolar
    crest. Absent overlying tooth.
  7. Simple bone cyst—age: 10–30 years. 50% have history of
    trauma. Mandible&raquo_space; maxilla. OPG/CT: nonexpansile unilocular
    cyst with marginal sclerosis, no internal septation and no
    association with teeth. MRI: T2↑ with fluid-fluid levels, mild rim
    enhancement
  8. Aneurysmal bone cyst—age: <20 years. Can occur
    spontaneously or related to trauma or other lesions, e.g. giant
    cell tumour (secondary ABC). Most at mandibular ramus. OPG/
    CT: uni- or multilocular, expansile + cortical thinning ±
    dehiscence. Sharp margins, even with cortical destruction, ±
    shallow reactive bone. Partially cystic meshwork divided by coarse
    septa. MRI: T2↑ with fluid-fluid levels and ‘bubbly’ appearance.
    ‘Honeycomb’ pattern of enhancement, no mural nodules (cf.
    ameloblastoma).
  9. Primordial cyst—a dental follicle without a developing tooth.
  10. Stafne cyst (mimic)—a medial cortical defect (containing fat or
    salivary gland tissue) in the posterior mandible measuring <2 cm,
    unrelated to the teeth. May mimic a cyst on OPG, diagnosis can
    be confirmed on CT/MR.
23
Q

BONY LESIONS OF MANDIBLE/
MAXILLA: SOLID
Lytic 12

A
  1. Malignant infiltration by adjacent tumour—SCC most
    common. CT/MRI: destructive bony lesion with adjacent
    soft-tissue mass.
  2. Myeloma—most common in posterior mandible. Lytic
    punched-out lesion without sclerosis or bone expansion.
  3. Metastasis—e.g. from breast or lung, often multiple. Mandible
    (especially molar region) > maxilla. MRI: marrow replacement
    with T1↓, STIR↑ + enhancement.
  4. Lymphoma*—primary or systemic NHL. Infiltrative or destructive
    lesion + soft-tissue mass ± adenopathy. The degree of bone
    destruction is often less than with other malignant processes.
  5. Leukaemia—common in acute leukaemia. Loss of definition of
    lamina dura, lytic bony destruction or diffuse osteopenia.
  6. Eosinophilic granuloma—in children. Well- or ill-defined, ±
    soft-tissue mass ± surrounding reactive sclerosis and periosteal
    reaction.
  7. Ewing sarcoma—age 5–25 years. Mandible > maxilla. Ill-defined
    bony destruction ± periosteal reaction (may be sunburst). Large
    soft-tissue mass.
  8. Other malignant tumours—e.g. odontogenic carcinoma,
    ameloblastic carcinoma, various sarcomas. Ill-defined destructive
    mass. Rare.
  9. Giant cell granuloma—benign, mean ~25 years. Mandible
    (especially midline) > maxilla. CT: expansile lytic mass with coarse
    or thin wavy septations, often at right angle to cortex ± cortical
    scalloping and dehiscence ± tooth root resorption. MRI: T2↓ or
    isointense ± fluid-fluid levels (intralesional ABC), heterogeneous
    enhancement.
  10. Ameloblastic fibroma—benign well-defined lucent lesion. May
    be multilocular, mimicking ameloblastoma, or unilocular and
    associated with the crown of an unerupted tooth, mimicking
    dentigerous cyst.
  11. Odontogenic myxoma—benign well-defined multilocular lucent
    lesion indistinguishable from ameloblastoma.
  12. Nerve sheath tumour—e.g. schwannoma, neurofibroma. May
    widen inferior alveolar nerve canal.
  13. Intraosseous arteriovenous malformation—multilocular lucent
    lesion on OPG. Vascular nature revealed on CT/MR
24
Q

BONY LESIONS OF MANDIBLE/
MAXILLA: SOLID
Sclerotic, calcified or ossified

A

Unrelated to the teeth
1. Osteoma—small well-defined homogeneously sclerotic lesion
unrelated to the teeth, may be exophytic. No hypodense halo. If
multiple, consider Gardner syndrome.
2. Metastasis—e.g. from prostate or breast. Usually multiple + bone
metastases elsewhere.
3. Exostosis—also known as torus. Similar to exostoses in other
bones. Can arise from mandible or maxilla, grows inwards into the
oral cavity.
Related to the teeth
1. Condensing osteitis—reactive ill-defined nonexpansile periapical
sclerosis around a diseased tooth.
2. Odontoma—benign hamartoma. May be simple (supernumerary
tooth), compound (a cluster of small tooth-like denticles) or
complex (dense amorphous mass of enamel and dentin).
Well-defined with a hypodense halo. Often associated with an
impacted tooth.
3. Cementoblastoma—in children and young adults. Well-defined
round sclerotic lesion fused to the apical portion of a tooth, with a
radiolucent halo.

25
Q

BONY LESIONS OF MANDIBLE/
MAXILLA: SOLID
Ground-glass, mixed or variable density

A

Unrelated to the teeth. NB: these may appear related to the teeth if large.
1. Fibrous dysplasia (FD)—face and calvarium involvement in 25%
of monostotic FD and >50% of polyostotic FD (e.g.
McCune-Albright and Mazabraud syndromes). Maxilla > mandible
> rest of skull. OPG/CT: typically an ill-defined expansile
ground-glass density lesion, but may also be cystic (lucent +
sclerotic border, active disease) or pagetoid (mixed lucent and
sclerotic). MRI: variable appearances. Ossified and fibrous areas are
T1/T2↓; cystic areas are T2↑. Fibrous areas may enhance. Bone
scan and PET-CT: nonspecific ↑ uptake depending on activity.
Malignant transformation (e.g. osteosarcoma) is rare. May be
associated with ABC. Pagetoid FD mimics Paget’s disease; however,
Paget’s occurs in the elderly and involves skull vault and base,
usually sparing the facial bones.
2. Osteonecrosis—can occur after local radiotherapy (peaks at
6–12 months, can persist for years) or in patients on
bisphosphonates (especially after tooth extraction). Mandible >
maxilla. CT: ill-defined bone destruction with mixed lysis and
sclerosis ± sequestra ± gas bubbles. MRI: T1↓ and STIR↑ +
marrow enhancement and surrounding soft-tissue thickening.
3. Renal osteodystrophy—mixed bone sclerosis and resorption with
loss of definition of lamina dura (‘floating teeth’) ± lytic brown
tumour.
4. Osteosarcoma—mean ~35 years. Mandible > maxilla. Ill-defined
destructive lesion with osteoid matrix and periosteal reaction. May
be related to previous radiotherapy.
5. Paget’s disease
—may rarely involve maxilla > mandible, usually
with skull involvement. Most commonly symmetrical. OPG/CT:
trabecular thickening with ground-glass and sclerotic islands.
Hypercementosis around tooth roots.
6. Ossifying fibroma—benign fibroosseous lesion. Typically a
well-defined, solitary, expansile ground-glass density mass ± a
sclerotic margin. May also appear lucent (early) or ossified
(cementoossifying subtype). May mimic FD but appears more
well-defined, tends to displace or erode teeth and peaks at an
older age (20–40 years). Mandible > maxilla > other bones. MRI:
variable T1/T2 signal ± fluid-fluid levels + enhancement of fibrous
component. If multiple, consider hyperparathyroidism-jaw tumour
syndrome.
7. Osteoblastoma/osteoid osteoma—mixed lucent and sclerotic
lesion ± lucent nidus, usually in patients <20 years. Typically
painful, unlike most other fibroosseous lesions.
8. Intraosseous haemangioma—rare; usually lucent with multiple
coarse trabeculations ± phleboliths.

Related to the teeth
1. Osteomyelitis—see Section 12.4. Mandible&raquo_space; maxilla. May be
destructive or sclerotic (Garré’s sclerosing osteomyelitis) ±
sequestra, gas bubbles, fistula, abscess and periostitis.
2. Cementoosseous dysplasia—benign hamartomatous lesion mostly
seen in middle-aged Afro-Caribbean or East Asian women. May be
lytic (early), sclerotic (late) or mixed, ± radiolucent halo. Periapical
location; may be focal or florid (involving ≥2 jaw quadrants).
Mandible > maxilla.

  1. Pindborg tumour—rare; well-defined and lucent + variable
    scattered or trabecular calcifications (may have a ‘driven snow’
    appearance). May be associated with an unerupted tooth.
  2. Adenomatoid odontogenic tumour—rare; well-defined lucent
    lesion related to the crown of an unerupted tooth. Maxilla >
    mandible. Can mimic dentigerous cyst, but usually contains flakes
    of calcification.
  3. Ameloblastic fibroodontoma—rare; well-defined lucent lesion
    containing a dense mass of enamel and dentin (a hybrid of
    ameloblastic fibroma and complex odontoma).
26
Q

NASAL SEPTAL PERFORATION

A
  1. Trauma—external, self-inflicted (e.g. nose picking) or iatrogenic
    (e.g. septoplasty, nasal packing, cauterization for epistaxis,
    nasotracheal intubation). Laceration or septal haematoma →
    elevation of mucoperichondrium from the septal cartilage →
    ischemia, necrosis and perforation.
  2. Cocaine necrosis—vasoconstriction → ischemic necrosis.
  3. Wegener’s granulomatosis*—most patients will have
    involvement of nose (septum > turbinates) and sinuses ± orbit,
    nasopharynx, larynx, oral cavity, temporal bone and salivary
    glands. CT/MRI: enhancing nodular soft-tissue masses in nasal
    cavity ± chronic sinusitis. Commonly causes nasal septal
    perforation ± destruction of turbinates, lateral nasal wall and hard
    palate (sinonasal–oral fistula). Sclerotic bone thickening of the
    sinus walls. MRI: nodular masses are T2↓ relative to inflamed T2↑
    mucosa.
  4. Rhinitis medicamentosa—vasoconstrictive and steroid nasal
    sprays → ischemic necrosis and perforation.
  5. Invasive fungal sinusitis
  6. Sarcoidosis*—sinonasal disease is uncommon. Generalized
    mucosal thickening often centred on the anterior nasal cavity and
    nasal septum + bone erosion.
  7. Sinonasal SCC—see Section 12.25. May destroy nasal septum.
  8. Lymphoma*—usually natural killer cell NHL. Age 60–80 years.
    Nasal cavity > sinuses, ± involvement of nasopharynx, oropharynx
    and LNs. Infiltrative mass ± bone destruction or remodelling. CT:
    may be high attenuation. MRI: T2↓ or intermediate due to high
    cellularity. Variable enhancement.
  9. Melanoma—arises from melanocytes in sinonasal mucosa.
    Typically in Caucasians aged 50–90 years. Nasal cavity > sinuses.
    Infiltrative, avidly enhancing mass with bony destruction ±
    remodelling. Classically T1↑ (if melanotic) and T2↓. Blooming on
    T2* due to haemorrhage. Amelanotic melanoma has variable
    T1/T2 signal.
  10. Nasal septal abscess—due to acute rhinosinusitis. Can cause
    septal perforation
27
Q

PARANASAL SINUS LESION WITHOUT
BONE DESTRUCTION
Inflammatory

A
  1. Chronic rhinosinusitis—sinonasal inflammation for ≥12
    consecutive weeks. Ethmoid > maxillary > frontal and sphenoid.
    CT: mucosal thickening + bony sclerosis and thickening without
    destruction or sinus expansion. Sinus secretions may be
    hyperdense if high protein or fungal content, ± occasional
    calcification. MRI: variable T1 signal (↑ if proteinaceous). Mucosa is
    T2↑, secretions vary depending on water content. Smooth mucosal
    enhancement. Complications: osteomyelitis, subgaleal abscess
    (Pott’s puffy tumour), subperiosteal abscess, myositis of extraocular
    muscles, pre- or postseptal cellulitis or abscess, optic neuritis,
    meningitis, epidural or subdural abscess, cerebritis, brain abscess,
    cavernous sinus thrombosis.
  2. Acute rhinosinusitis—sinonasal inflammation ≤4 weeks, most
    commonly ethmoid and maxillary. CT: air-fluid level ± bubbly or
    strand-like secretions in sinus with mucosal thickening and
    obstruction of ostiomeatal complex. Enhancement of inflamed
    mucosa, nonenhancing central secretions. MRI: mucosa and
    secretions T2↑ and T1↓. If secretions are proteinaceous, T1↑ and
    T2↓. Same potential complications as above.
  3. Retention cyst—well-defined rounded cyst, usually in the maxillary
    sinus. Fluid attenuation on CT and fluid signal on MRI (may be
    proteinaceous). The rest of the involved sinus is typically aerated
    (cf. mucocoele). May be associated with sinusitis.
  4. Mucocoele—completely opacified and expanded sinus with
    smooth remodelling of walls due to obstruction of sinus ostium.
    Frontal > ethmoid (may extend into orbit) > maxillary > sphenoid
    (may extend into cranial cavity). Cause: polyps, sinusitis, trauma,
    surgery or tumour. CT: fluid or soft-tissue attenuation (if desiccated
    secretions or fungal colonization). Sinus wall may be normal, thin
    or focally absent. MRI: fluid signal (may be proteinaceous).
    Minimal peripheral enhancement only. Thick peripheral mucosal
    enhancement suggests superadded infection (mucopyocoele).
    Nodular enhancement suggests an underlying tumour.
  5. Sinonasal polyposis—inflammatory swelling of sinonasal mucosa
    that buckles to form ‘polyps’. Usually multiple and bilateral,
    involving both nasal cavity and sinuses. Often obstructs sinus
    drainage pathways in the superior nasal cavity, resulting in sinusitis.
    CT: soft-tissue attenuation, may be hyperattenuating if ↑ protein or
    colonization with fungus; ± bony remodelling or erosion. MRI:
    usually T1↓ and T2↑ of mucosa and associated secretions; T1↑ if
    secretions are proteinaceous. Peripheral mucosal enhancement
    with central nonenhancing secretions.
  6. Solitary sinonasal polyp—inflammatory polyp arising from sinus,
    herniating through major or accessory ostium into nasal cavity ±
    prolapse into nasopharynx. Antrochoanal polyp is the most
    common, arising from the maxillary sinus. Sphenochoanal and
    ethmochoanal polyps are rare. Most common in adolescents and
    young adults. CT: dumbbell-shaped low attenuation mass arising
    from maxillary antrum, extending through widened ostium or
    accessory ostium into ipsilateral nasal cavity + bone remodelling.
    Can be ↑ density if fungal colonization. MRI: variable T1 signal (↑
    if proteinaceous), T2↑. Thin peripheral enhancement.
  7. Allergic fungal sinusitis—chronic noninvasive fungal sinusitis in an
    immunocompetent nondiabetic young adult with a long history of
    chronic rhinosinusitis, allergy ± polyposis. Multiple sinuses involved,
    may be unilateral or bilateral. Ethmoid > maxillary > frontal >
    sphenoid, ± sinus expansion with bony remodelling or erosion.
    CT: ↑ attenuation in opacified sinus with hypoattenuating rim of
    mucosa. MRI: variable T1 signal depending on protein, water and
    fungal content. T2↓↓ centrally due to dense fungal concretions and
    heavy metals. Peripheral enhancement of inflamed mucosa.
  8. Mycetoma—chronic noninvasive form of fungal sinusitis where
    material in the sinonasal cavity is colonized by fungus. Indolent
    clinical course. More common in the elderly. Usually affects a
    single sinus; maxillary > sphenoid > frontal > ethmoid. CT: thick
    mucosa with central high attenuation ± calcification ± thick
    sclerotic sinus wall. MRI: T2↓↓, can be mistaken for air.
  9. Silent sinus syndrome—chronic occlusion of the maxillary sinus
    ostium → resorption of sinus gas → retraction of maxillary sinus
    walls and reduced sinus volume (atelectasis). Symptoms of sinusitis
    are characteristically absent. CT/MRI: small volume and opacified
    maxillary sinus with retraction of walls including the orbital floor,
    resulting in enophthalmos
28
Q

PARANASAL SINUS LESION WITHOUT
BONE DESTRUCTION
Neoplastic

A
  1. Osteoma—benign bone-forming tumour that typically arises from
    the sinus wall and protrudes into the lumen. Almost exclusive to
    the craniofacial skeleton; frontal and ethmoid&raquo_space; maxillary and
    sphenoid sinuses. Usually incidental and asymptomatic; can rarely
    obstruct sinus drainage, causing sinusitis or a mucocoele. CT:
    well-defined and uniformly sclerotic, may be ground-glass.
    Multiple in Gardner syndrome.
  2. Inverted papilloma—benign epithelial tumour of sinonasal
    mucosa with histology showing epithelial proliferation into
    underlying stroma. 10% either degenerate or coexist with SCC.
    Age 40–70 years. Usually arises from lateral nasal wall in middle
    meatus ± extension into maxillary antrum ± bone remodelling and
    obstructive sinusitis. Uncommonly arises from sinuses. Often has
    entrapped bone/tumourous calcification ± focal hyperostosis of
    adjacent bone at site of origin. CT/MRI: convoluted ‘cerebriform’
    pattern of enhancement. Secretions and areas of necrosis do not
    enhance. High rate of local recurrence after surgical resection.
  3. Juvenile angiofibroma—see Section 12.2.
  4. Pleomorphic adenoma—can rarely arise from minor salivary gland
    tissue in the nasal cavity, extending into paranasal sinuses.
    Nonspecific soft-tissue mass + bone remodelling.
  5. Nerve sheath tumour—e.g. schwannoma or neurofibroma.
    Well-defined, expansile, variably enhancing mass centred on the
    nasoethmoid region + adjacent bone remodelling
29
Q

PARANASAL SINUS LESION WITH

BONE DESTRUCTION

A
  1. Sinonasal SCC—most common sinonasal malignancy; sinuses
    (especially maxillary) > nasal cavity. Age 50–70 years. Infiltrative
    mass with destruction of sinus wall. The mass shows intermediate
    T2 signal and heterogeneous nodular enhancement (cf. benign
    mucosal thickening which is T2↑ with smooth uniform
    enhancement).
  2. Invasive fungal sinusitis—different clinical presentations and course:
    (a) Acute invasive fungal sinusitis—immunocompromised
    patient, rapidly progressive or fatal within days to weeks, ±
    orbital and intracranial extension.
    (b) Granulomatous invasive fungal sinusitis—immunocompetent
    patient. Slowly progressive over >12 weeks. Enlarging cheek,
    orbit or sinonasal mass. Primarily seen in the Middle East and
    on the Indian subcontinent.
    (c) Chronic invasive fungal sinusitis—slowly progressive over
    >12 weeks, usually in patients with AIDS, diabetes or on
    steroids. CT: soft-tissue opacification and mucosal thickening
    of sinuses. High attenuation secretions ± septal/sinus wall
    erosion ± narrowing or occlusion of adjacent arteries or veins ±
    intraorbital or meningeal extension. MRI: variable T1 signal
    depending on protein/water content. Fungal elements are
    T2↓↓ with surrounding soft tissue T2↑ and enhancement.
  3. Olfactory neuroblastoma—rare, slow-growing, malignant tumour
    arising from olfactory neuroepithelium in the roof of the nasal
    cavity. Dumbbell-shaped enhancing tumour with upper portion in
    the anterior cranial fossa, waist at level of cribriform plate and
    lower portion in upper nasal cavity, + bone destruction (especially
    cribriform plate) and remodelling ± areas of haemorrhage and
    necrosis. A peritumoural cyst at the margin of the intracranial
    component is characteristic. Two peaks: in young adults and
    middle age. Tends to recur after treatment (may be years later).
  4. Wegener’s granulomatosis*—see Section 12.23.
  5. Lymphoma*—see Section 12.23.
  6. Other carcinomas—e.g. undifferentiated, adenoid cystic,
    adenocarcinoma. Aggressive ill-defined mass with bony destruction
    ± perineural spread. Age 40–80 years.
  7. Sarcoidosis*—see Section 12.23.
  8. Osteosarcoma—age 30–50 years (older than osteosarcoma of long
    bones). Mandible > maxilla. CT/MRI: aggressive mass with calcified
    osteoid matrix and periosteal reaction ± soft-tissue component.
  9. Chondrosarcoma—age 50–80 years. Arises from the nasal septum.
    CT: well-defined mass with a nonsclerotic margin ± chondroid
    matrix calcification. Most show bony destruction. MRI: T1↓ or
    intermediate, T2↑ ± foci of T2↓ (calcification). Heterogeneous
    enhancement
30
Q

ORBIT: LESIONS INVOLVING THE GLOBE

A
  1. Haemorrhage—due to trauma or surgery. Usually vitreal or
    suprachoroidal, rarely retinal. CT: patchy or lenticular
    hyperattenuation in vitreous or suprachoroidal space ± evidence
    of trauma, e.g. globe rupture, dislocated lens or bone fracture.
    MRI: acute haematoma T1/T2↓; subacute haematoma T1↑.
  2. Retinal or choroidal detachment—accumulation of fluid or
    haemorrhage within detached layers of retina or in
    suprachoroidal space. Retinal: leaves of retina converge at optic
    disc, forming a ‘V’ shape. Anterior end extends towards (but not
    anterior to) ciliary body. Choroidal: does not converge at the
    optic disc, forming two separate lenticular shapes. Anterior end
    can extend beyond ciliary body. CT/MR: attenuation and
    intensity depends on content (fluid, protein or blood). Usually ↑
    density on CT and T1↑ on MRI.
  3. Orbital pseudotumour—various patterns; can involve the globe
    causing irregular scleral thickening and enhancement, usually
    extending posteriorly to involve the optic nerve sheath. See also
    Section 12.29.
  4. Melanoma—most common primary intraocular tumour in adults.
    Usually arises from choroid. CT/MRI: dome or mushroom shaped
    enhancing mass with broad choroidal base ± choroidal or retinal
    detachment. No calcification (unless following therapy). T1↑
    (unless amelanotic), T2↓.
  5. Endophthalmitis—purulent inflammation of intraocular fluid due
    to contiguous spread of infection, usually from pre- or postseptal
    cellulitis, trauma or surgery. More common in children and
    young adults. CT/MRI: thickening and enhancement of uvea/
    sclera ± restricted diffusion ± features of panophthalmitis
    (intraconal fat stranding, oedema and enhancement of
    extraocular muscles, subperiosteal or intraorbital abscess, septal
    thickening). Complications: cavernous sinus thrombosis,
    intracranial spread of infection.
  6. Ocular calcification—e.g. drusen (at optic disc), choroidal
    osteoma (close to optic disc), phthisis bulbi (shrunken ‘end-stage’
    eye).
  7. Surgical inserts—e.g. scleral buckle (dense ring around sclera) or
    vitreous silicone oil (rounded uniformly dense material within
    vitreous cavity, T1↑ on MRI). Both are treatments for retinal
    detachment.
  8. Staphyloma/coloboma—both are focal posterior outpouchings
    of the globe, usually bilateral; staphyloma is due to acquired
    scleral thinning related to severe myopia; coloboma is due to a
    congenital scleral defect.
  9. Choroidal haemangioma—benign hamartoma. Avidly enhancing
    ± calcification; may be circumscribed and lentiform (middle-aged
    patients, sporadic) or diffuse mild choroidal thickening (younger
    patients, associated with Sturge-Weber syndrome).
  10. Lymphoproliferative lesions— Can rarely
    involve the globe.
  11. Ocular metastases—e.g. from lung or breast. Rare; may be
    multiple and bilateral.
  12. Sarcoidosis*—Can involve iris, ciliary body
    and/or choroid.
  13. Retinoblastoma—extremely rare in adults
31
Q

ORBIT: LESIONS OF THE OPTIC NERVE OR SHEATH

6

A
  1. Optic nerve sheath meningioma—age: fourth to fifth decade
    (~10 years in NF2). Usually tubular but may be pedunculated or
    fusiform. Linear or punctate calcification is common (cf. glioma).
    Homogeneous ‘tram-track’ enhancement is typical but not
    pathognomonic. Typically spares distal-most segment of the optic
    nerve sheath—CSF may become trapped here, creating a perioptic
    cyst.
  2. Optic pathway glioma—age varies (occurs in children when
    associated with NF1). If bilateral, highly suggestive of NF1. CT/
    MRI: diffuse sausage-shaped or fusiform enlargement of optic
    nerve (often kinked) ± chiasm, with variable enhancement ± cystic
    spaces. May extend to hypothalamus, optic tracts and radiations.
    Calcification very rare. Look for cerebral features of NF1.
  3. Optic neuritis—age 15–50 years. Autoimmune optic nerve
    inflammation; 50%–60% will develop multiple sclerosis. Focal or
    segmental T2 hyperintensity of optic nerve ± enhancement ± mild
    nerve swelling. Look for cerebral features of MS.
  4. Orbital pseudotumour—various patterns; can involve the optic
    nerve sheath causing irregular thickening and enhancement (may
    be ‘tram-track’) ± involvement of retrobulbar fat.
  5. Lymphoproliferative lesions— May cause ‘tram-track’ enhancement.
  6. Sarcoidosis*— May cause ‘tram-track’ enhancement
32
Q

ORBIT: LESIONS ARISING WITHIN

INTRACONAL FAT

A
  1. Orbital pseudotumour—various patterns; can present as an
    ill-defined infiltrative enhancing intraconal mass ± involvement of
    other parts of orbit. Does not distort globe or erode bone. MRI:
    T1↓, T2 signal usually less than other orbital lesions due to cellular
    infiltrates and fibrosis.
  2. Cavernous haemangioma—encapsulated vascular malformation,
    usually an incidental finding on CT/MR. Most common in
    intraconal fat. CT: iso- or hyperattenuating (due to
    microcalcification). No phleboliths, unlike venous varix. Avid
    enhancement. MRI: T1 isointense or ↑. T2↑ ± internal septations.
    Dynamic post contrast: early patchy enhancement →
    homogeneous filling on delayed sequences.
  3. Venous varix—slow-flow venous malformation, distends with
    Valsalva. Tubular or tortuous retrobulbar lesion with intense
    enhancement ± phleboliths.
  4. Lymphoproliferative lesions—see Section 12.30.
  5. Sarcoidosis*—see Section 12.30.
  6. Erdheim-Chester disease*—orbital involvement is common,
    usually manifesting as bilateral infiltrative enhancing intraconal
    masses, which are T1/T2↓ on MRI. The pattern of disease
    elsewhere aids differentiation from orbital pseudotumour.
  7. Nerve sheath tumour—e.g. schwannoma, neurofibroma.
    Well-defined intraconal mass.
33
Q

ORBIT: CONAL LESIONS

A
  1. Thyroid ophthalmopathy—most common orbital disorder and
    cause of proptosis. Autoimmune process associated with Graves’
    disease involving extraocular muscles, fat and connective tissue ±
    lacrimal glands. Typically bilateral and symmetrical. Muscle
    involvement: inferior > medial > superior > lateral > obliques (I’M
    SLO). Muscle belly thickness ≥5 mm is abnormal. Tendons are
    typically spared (cf. orbital pseudotumour). Acute phase: T2↑ in
    muscles (oedema, best seen on T2 fatsat). Chronic phase: T2↓ due
    to fibrosis. Increased orbital fat → stretching of optic nerve.
  2. Orbital pseudotumour—most common painful orbital mass in
    adults, usually unilateral. Various patterns; extraocular muscle
    involvement is the most common, especially superior and medial
    rectus, superior oblique and levator palpebrae. Shaggy thickening
    and enhancement of involved muscles + tendinous insertions.
    Associated with IgG4-related disease.
  3. Lymphoproliferative lesions—see Section 12.30.
  4. Sarcoidosis*—see Section 12.30.
  5. Metastasis—most commonly from breast, lung, melanoma.
    Nonspecific mass, usually in the presence of metastases elsewhere.
  6. Extraocular myositis—usually due to sinusitis + orbital cellulitis
    (see Section 12.24). Muscle and fat infiltration + enhancement ±
    subperiosteal abscess. Most commonly medial rectus secondary to
    ethmoid sinusitis.
  7. Rhabdomyosarcoma—usually <15 years. Infiltrative mass ±
    extension into eyelid and paranasal sinuses
34
Q

ORBIT: EXTRACONAL LESIONS
Lesions arising within the orbital cavity
7

A
  1. Lymphoproliferative lesions—second most common orbital
    disorder. Spectrum of benign lymphoid hyperplasia to malignant
    lymphoma (± systemic disease). Age >60 years. Can involve any
    part of orbit, most commonly anterior extraconal space and
    lacrimal gland. Mostly unilateral. CT: slightly hyperattenuating due
    to high cellularity + homogeneous enhancement. MRI: mildly T1/
    T2↑ relative to muscle. Bone destruction if aggressive histology.
  2. Orbital pseudotumour—lacrimal gland involvement is the second
    most common pattern: diffuse enlargement + ill-defined margins +
    enhancement. Orbital apex involvement can also occur ±
    intracranial extension through fissures into cavernous sinus
    (Tolosa-Hunt syndrome). See also Section 12.29.
  3. Pleomorphic adenoma—most common epithelial tumour of
    lacrimal gland. Age: second to fifth decades. CT/MRI: well-defined
    enhancing mass ± cystic change ± calcification ± scalloping of
    adjacent bone. Risk of malignant transformation.
  4. Malignant lacrimal gland tumour—e.g. adenoid cystic carcinoma
    (most common), malignant mixed tumour, adenocarcinoma, SCC.
    Ill-defined enhancing mass, often with bony destruction.378 Aids to Radiological Differential Diagnosis
  5. Sarcoidosis*—can involve any part of orbit, most commonly the
    lacrimal gland. Diffuse nonspecific lacrimal gland enlargement or
    ill-defined orbital masses with homogeneous enhancement.
    Lacrimal gland involvement may be isolated without systemic
    disease.
  6. Sjögren’s syndrome*—chronic systemic autoimmune
    exocrinopathy; usually involves salivary glands, but can also involve
    lacrimal glands, which become enlarged and heterogeneous.
  7. Dacryocystocoele—cystic mass at medial canthus + enlarged
    nasolacrimal duct. Rim enhancement suggests infection
    (dacryocystitis)
35
Q

ORBIT: EXTRACONAL LESIONS

Lesions arising from the orbital wall

A
  1. Subperiosteal abscess—due to orbital cellulitis or adjacent sinusitis
    (most commonly ethmoidal); see Section 12.24. In this setting any
    soft-tissue thickening adjacent to the orbital wall must be
    considered suspicious for an abscess, even in the absence of rim
    enhancement.
  2. Sinonasal mucocoele—see Section 12.24. May bulge into orbit.
  3. Sinonasal SCC—see Section 12.25. May invade the orbit.
  4. Metastasis to orbital wall—see Section 12.34.
  5. Dermoid and epidermoid—developmental ectodermal inclusion
    cyst, most common in children. Slowly progressive nontender
    mass → inflammation if ruptures. Located adjacent to sutures,
    especially frontozygomatic suture ± adjacent bone remodelling.
    Dermoid contains macroscopic fat ± calcification ± fluid-fluid levels.
    Epidermoid appears cystic + restricted diffusion.
  6. Sphenoid wing dysplasia—seen in NF1, ± other features, e.g.
    optic nerve glioma, plexiform neurofibroma, buphthalmos and
    cerebral T2 hyperintensities. X-ray: absent innominate line due to
    absent greater wing of sphenoid. CT/MRI: hypoplastic or absent
    sphenoid wing ± herniation of middle cranial fossa contents into
    the orbit ± associated arachnoid cyst.
  7. Fibrous dysplasia—see Section 12.22.
  8. Paget’s disease*—see Section 12.34.
  9. Intraosseous meningioma—e.g. in sphenoid wing; either primary
    or secondary intraosseous extension. CT: bony thickening and
    permeative sclerosis + enhancing dural mass or thickening
36
Q

EXTERNAL AUDITORY CANAL LESIONS

A
  1. Earwax plug—very common especially in elderly, often bilateral.
    Low attenuation on CT, usually with a rim of gas.
  2. Cholesteatoma—nonenhancing EAC mass with bone erosion ±
    bone fragments within lesion.Head and neck 379
    12
  3. Carcinoma—usually SCC but minor salivary gland tumours, e.g.
    adenoid cystic carcinoma can occur. Infiltrative enhancing mass ±
    bone destruction ± parotid space nodes. Usually extends inwards
    from pinna.
  4. Necrotizing otitis externa—painful, severe, invasive infection of
    EAC in elderly diabetics and immunocompromised patients due to
    Pseudomonas aeruginosa. Soft-tissue thickening in the EAC
    extending to the outer soft tissues (especially below skull base) +
    fat stranding ± abscess ± erosion or osteomyelitis of the mastoid
    bone ± skull base. Infection can spread into the intracranial cavity
    causing venous sinus thrombosis, subdural empyema or brain
    abscess.
  5. Congenital ear malformations—variable severity. External ear:
    EAC stenosis or atresia ± malformed pinna. Middle ear: small cavity
    ± calcified tympanic membrane ± malformed or fused ossicles.
    Inner ear usually normal.
  6. Osteoma—solitary pedunculated bony outgrowth, located laterally
    in EAC at junction of bony and cartilaginous portions.
  7. Exostosis—benign lobulated bony overgrowth circumferentially
    narrowing the EAC bilaterally, due to chronic cold water exposure
    (surfer’s ear).
  8. Medial canal fibrosis—crescent of fibrous soft tissue in the medial
    EAC overlying the tympanic membrane. No middle ear
    involvement or bony changes. Bilateral in 50%.
  9. Keratosis obturans—abnormal accumulation of desquamated
    keratin causing partial or complete filling of EAC ± mild expansion.
    No bony erosion (cf. cholesteatoma). Bilateral in 50%.
37
Q

MIDDLE EAR LESIONS

A
  1. Chronic otitis media—either erosive, tympanosclerotic, or both.
    Erosions and/or sclerosis of ossicles (especially erosion of the
    distal long process of incus), ± calcification elsewhere in middle
    ear cavity. Tympanic membrane retraction ± calcification. Under
    pneumatization of mastoid.
  2. Acquired cholesteatoma—focal accumulation of exfoliated
    keratin within stratified squamous epithelium. Two types based
    on site of origin (see below). CT: nondependent soft-tissue mass
    + local bone erosion. MRI: T1↓ (cf. cholesterol granuloma), T2↑
    and marked restricted diffusion. No enhancement, though
    surrounding granulation tissue may enhance. Complications:
    dural extension, meningitis, subperiosteal or intracranial abscess,
    labyrinthitis and venous sinus thrombosis. In postsurgical patients
    it is hard to differentiate recurrent cholesteatoma from
    granulation tissue, fluid and fibrosis on CT; on nonEPI DWI MRI,
    only recurrent cholesteatoma will show significant restricted
    diffusion.
    (a) Pars flaccida—80%. Arises in Prussak’s space (between
    scutum and malleus) + erosion of scutum and ossicles; if
    large, can cause dehiscence of lateral semicircular canal,
    tegmen tympani, tegmen mastoideum and facial nerve
    canal.
    (b) Pars tensa—20%. Arises medial to ossicles ± extension into
    sinus tympani, facial recess, aditus ad antrum ± mastoid air
    cells. Erosion of adjacent ossicles, mastoid antrum and
    anterior tegmen mastoideum.
  3. Cholesterol granuloma—mass of granulation tissue associated
    with recurrent haemorrhage and cholesterol deposition in
    patients with chronic otitis media. CT: expansile mass in middle
    ear ± mastoid air cells. Large lesions cause ossicular displacement
    ± erosion. MRI: characteristically T1↑ (methaemoglobin); T2↑
    centrally (granulation tissue) with a T2↓ rim (haemosiderin). No
    enhancement (beware of inherent T1↑ signal).
  4. Glomus tympanicum—benign paraganglioma arising from
    glomus body situated on cochlear promontory. Most common
    tumour of middle ear; age 40–60 years. May be associated with
    paragangliomas elsewhere. Clinical: pulsatile tinnitus, red
    anteroinferior mass on otoscopy. CT/MRI: avidly enhancing
    2–20 mm mass with a flat base on the cochlear promontory.
    Floor of middle ear cavity intact.
  5. Glomus jugulare—paraganglioma centred on jugular foramen.
    Typically large, can extend into middle ear cavity (glomus
    jugulotympanicum). May be multiple and familial (e.g. MEN 1,
    NF1). Clinical: pulsatile tinnitus ± cranial nerve palsies (especially
    CN IX), retrotympanic mass on otoscopy. CT/MRI: avidly
    enhancing mass in jugular foramen + bone destruction and
    dehiscence of jugular bulb ± extension of mass into middle
    ear. Tumours >2 cm show a ‘salt and pepper’ appearance
    due to foci of T1↑ (haemorrhage or slow flow) and T1↓
    (flow voids).
  6. Acute otomastoiditis with abscess—clinical: otalgia, otorrhoea,
    fever and hearing loss. CT: opacified mastoid air cells + cortical
    and trabecular erosion ± subperiosteal, epidural or brain abscess
    ± venous sinus thrombosis.
  7. Dehiscent jugular bulb—normal variant with superolateral
    protrusion of jugular bulb into middle ear cavity through
    dehiscent sigmoid plate. No bone destruction. Important
    incidental finding for surgical planning. Usually asymptomatic.
  8. Aberrant ICA—normal variant with posterolateral displacement
    of the petrous portion of the ICA, which protrudes into the
    middle ear cavity. Important to recognize for surgical planning.
    Mostly asymptomatic.
  9. Intraosseous meningioma—see Section 12.30. Temporal bone
    is a common site. Soft tissue may extend into middle ear cavity.Head and neck 381
    12
  10. Middle ear schwannoma—primary schwannoma arises from
    tympanic segment of CN VII, Jacobson nerve or chorda tympani.
    Secondary schwannoma arises from outside middle ear, e.g.
    jugular foramen schwannoma or acoustic schwannoma
    (CN VIII). Enhancing mass contiguous with long axis of
    parent nerve.
  11. Perineural tumour spread along CN VII—most commonly seen
    with adenoid cystic carcinoma of parotid. Ill-defined enhancing
    tubular lesion extending from parotid tumour through
    stylomastoid foramen → mastoid segment of CN VII ± extension
    proximally to internal auditory meatus. Best seen on MRI (fatsat
    T1+C).
  12. Endolymphatic sac tumour—sporadic or associated with vHL.
    May be bilateral. CT: permeative destructive mass centred
    posterior to labyrinth + central spiculated calcification. Thin
    calcified rim along posterior margin. MRI: T1↑ foci due to
    haemorrhage. Heterogeneous enhancement.
38
Q

PETROUS APEX LESIONS

Normal variants

A
  1. Asymmetrical marrow—degree of petrous apex pneumatization is
    variable and can be asymmetrical; nonpneumatized marrow space
    may simulate a mass. No bony expansion. MRI: T1↑ due to normal
    fatty marrow, with signal loss on fatsat sequences (cf. cholesterol
    granuloma).
  2. Trapped fluid—sterile residual fluid in pneumatized petrous apex
    due to previous otomastoiditis. T2↑, variable T1 signal depending
    on protein content. No bony expansion or erosion. No concurrent
    middle ear or mastoid inflammation.
  3. Petrous apex cephalocoele—herniation of posterolateral wall of
    Meckel’s cave into petrous apex. Fluid attenuation and signal on
    CT/MRI
39
Q

PETROUS APEX LESIONS

Well-defined and expansile + bone remodelling

A
  1. Cholesterol granuloma—most common petrous apex lesion. T1/
    T2↑ on MRI (see Section 12.32).
  2. Epidermoid cyst—also known as congenital cholesteatoma. T1↓
    (cf. cholesterol granuloma), T2↑ + restricted diffusion. No
    enhancement.
  3. Petrous apex mucocoele—T2↑, variable T1 signal depending on
    protein content (though not as T1↑ as cholesterol granuloma). No
    restricted diffusion (cf. epidermoid cyst) or enhancement.382 Aids to Radiological Differential Diagnosis
  4. Trigeminal nerve schwannoma—CT: smooth expansile
    remodelling of foramen ovale. MRI: enhancing tubular lesion in
    continuity with the trigeminal nerve in Meckel’s cave.
  5. Petrous ICA aneurysm—s
40
Q

PETROUS APEX LESIONS

Destructive

A
  1. Metastasis—e.g. from breast, lung, prostate, RCC. The petrous
    apex is the most common site of metastasis in the temporal
    bone.
  2. Petrous apicitis—suppurative infection of pneumatized petrous
    apex due to extension of mastoiditis. Age: children and
    adolescents. Clinical: otorrhea, deep facial/ear pain, fever ±
    Gradenigo syndrome (retroorbital pain + lateral rectus palsy + otitis
    media) ± cranial neuropathy (CN V–VIII). CT/MRI: fluid in petrous
    apex + bony erosion ± enhancing soft-tissue phlegmon or abscess.
    Complications: dural involvement, cavernous sinus thrombosis,
    fistula with bony labyrinth.
  3. Chondrosarcoma—see Section 12.35.
  4. Plasmacytoma*—lytic lesion with nonsclerotic margin. MRI: T1↓
    and T2↑ or intermediate; heterogeneous enhancement.
  5. Langerhans cell histiocytosis*
41
Q

PETROUS APEX LESIONS

Other

A
  1. Meningioma—see Section 12.35.
  2. Paget’s disease*—see Section 12.34.
  3. Fibrous dysplasia
42
Q

DIFFUSE OR MULTIFOCAL SKULL
BASE LESIONS
8

A
  1. Metastasis—most commonly from breast, lung, prostate. Can be
    solitary, multifocal or diffuse. Most common where bone marrow is
    abundant, i.e. clivus, nonpneumatized petrous apex and greater
    wing of sphenoid. CT: lytic, sclerotic or mixed. MRI: T1↓ lesion
    replacing high signal marrow; enhances post contrast.
  2. Paget’s disease*—calvarium > skull base > temporal bone. Diffuse
    bone thickening with lysis (early), sclerosis (late) or mixed density
    (may have a ‘cotton wool’ appearance). May rarely undergo
    malignant transformation to osteosarcoma.
  3. Fibrous dysplasia—see Section 12.22.
  4. Myeloma—CT: punched-out lytic lesions of calvarium, facial bones
    and skull base with no marginal sclerosis. MRI: T1↓ and T2↑ or
    intermediate, + enhancement and restricted diffusion. Bone scan:
    cold lesion.
  5. Osteomyelitis—acute or chronic, may relate to necrotizing otitis
    externa or previous radiotherapy. CT: bone destruction ± sequestra,
    can be lytic or sclerotic (if chronic). MRI: T1↓ and T2↑ in marrow
    + enhancement ± adjacent dural enhancement.
  6. Langerhans cell histiocytosis*—usually in children or young
    adults. CT: punched-out lytic lesions with bevelled margins ±
    surrounding sclerosis ± button sequestrum. Heterogeneous
    enhancement with soft-tissue mass and dural involvement ±
    thickening of pituitary infundibulum.
  7. Intracranial inflammatory pseudotumour—see Section 12.30.
    Extends from orbit to central and anterior skull base ± cavernous
    sinus, Meckel’s cave, falx, tentorium, pterygopalatine fossa, nose
    and nasopharynx.
  8. Lymphoma*—can cause diffuse or multifocal skull base
    involvement ± cervicofacial or systemic disease. Most commonly
    originates from nasal cavity or paranasal sinuses. Permeative bone
    destruction, sclerosis or both, with a homogeneous soft-tissue
    mass.
43
Q

UNIFOCAL SKULL BASE LESION

7

A
  1. Any multifocal skull base lesion— Any of these can be unifocal.
  2. Meningioma—avidly enhancing dural based mass + dural tail +
    bony hyperostosis and sclerosis ± invasion. May extend below skull
    base through neural and vascular foramina.
  3. Chondrosarcoma—arises from skull base synchondroses
    (petroclival, sphenopetrosal, petrooccipital or sphenooccipital).
    Lytic mass + chondroid calcification on CT, T2↑ on MRI + variable
    enhancement. Tumours are often indolent/low grade.
  4. ICA aneurysm—if large and involves cavernous portion, causes
    bony remodelling of adjacent sella, clivus and petrous apex.
    Continuity with ICA confirmed on CTA/MRA. Variable T1/T2 signal
    due to turbulent flow voids ± mural thrombus.
  5. Ossifying fibroma.
  6. Haemangiopericytoma—rare locally aggressive tumour of meninges. Avidly enhancing mass invading and eroding the skull ±dural tail ± internal flow voids. Can mimic meningioma but tends not to calcify or cause bony hyperostosis. Peak age 30–40 years, can also occur in children (cf. meningioma peak age >50 years).
  7. Giant cell tumour—extremely rare. Age: third to fourth decade.
    Sphenoid bone most common. CT: expansile lytic lesion with cortical thinning + soft-tissue component ± ‘soap bubble’ appearance. MRI: T2↓ (haemosiderin), heterogeneous enhancement.
44
Q

CLIVUS LESIONS

6

A
  1. Skull base lesions not specific to the clivus—e.g. fibrous
    dysplasia, Paget’s disease, metastasis, lymphoma, myeloma,
    meningioma.
  2. Nasopharyngeal carcinoma— May invade and
    destroy clivus ± intracranial extension.
  3. Pituitary macroadenoma—if large, can invade the clivus and
    sphenoid sinus. The mass is centred on an enlarged sella.
  4. Chordoma—peak age 30–50 years. Arises in the midline near
    sphenooccipital synchondrosis. CT/MRI: expansile lytic clival mass
    + soft-tissue component + bony sequestra floating within the mass
    ± intralesional haemorrhage. Classically T2↑↑ with heterogeneous
    or ‘honeycomb’ enhancement.
  5. Chondrosarcoma—see Section 12.35. Tends to be paramidline
    (cf. chordoma).
  6. Ecchordosis physaliphora—asymptomatic incidental finding on
    CT/MR. Benign notochord remnant, either within the clivus
    (well-defined and lytic on CT) or attached to it by an osseous
    stalk (characteristic appearance on CT). T2↑↑ on MRI with no or
    minimal enhancement (cf. chordoma). Histologically very similar
    to chordoma.
45
Q

JUGULAR FORAMEN LESIONS

A
  1. Glomus jugulare—see Section 12.32.
  2. Schwannoma—can arise from CN IX, X or XI. Mean age 45
    years. Large tubular or dumbbell-shaped tumour with jugular
    foramen enlargement and bony remodelling. Uniformly enhancing
    unless there is cystic change. May extend to adjacent carotid
    space.
  3. Necrotizing otitis externa—infection can spread to the jugular
    foramen either via the bones or soft tissues, ± IJV thrombosis.
  4. Skull base lesions not specific to the jugular foramen—e.g.
    meningioma, metastasis, myeloma, chondrosarcoma