HEAD & NECK

Question 1

PARAPHARYNGEAL SPACE LESIONS

Answer 1

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.

Question 2

PHARYNGEAL MUCOSAL SPACE

LESIONS: NASOPHARYNX

Answer 2

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

Question 3

PHARYNGEAL MUCOSAL SPACE

LESIONS: OROPHARYNX

Answer 3

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

Question 4

MASTICATOR SPACE LESIONS

Answer 4

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

Question 5

FOCAL PAROTID SPACE LESIONS

5

Answer 5

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).

Question 6

DIFFUSE PAROTID ENLARGEMENT

Answer 6

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

Question 7

CAROTID SPACE LESIONS

Answer 7

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;

Question 8

PERIVERTEBRAL SPACE LESIONS

Answer 8

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.

Question 9

POSTERIOR CERVICAL SPACE LESIONS

6

Answer 9

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)

Question 10

RETROPHARYNGEAL SPACE

LESIONS: FOCAL

Answer 10

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.

Question 11

RETROPHARYNGEAL SPACE

LESIONS: DIFFUSE

Answer 11

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

Question 12

ORAL CAVITY: ORAL MUCOSAL

SPACE LESIONS

Answer 12

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

Question 13

ORAL CAVITY: SUBLINGUAL SPACE LESIONS

6

Answer 13

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.

Question 14

ORAL CAVITY: SUBMANDIBULAR

SPACE LESIONS

Answer 14

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

Question 15

ORAL CAVITY: ROOT OF

TONGUE LESIONS

Answer 15

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.

Question 16

TRANSSPATIAL NECK LESIONS 6

Answer 16

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.

Question 17

Laryngeal lesions
main 8
others 5

Answer 17

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).

Question 18

THYROID ENLARGEMENT

9

Answer 18

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.

Question 19

Features associated with benign nodules

Answer 19

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

Question 20

Features associated with malignant nodules

Answer 20

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

Question 21

SONOGRAPHIC FEATURES OF NORMAL

VERSUS ABNORMAL LYMPH NODES

Answer 21

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).

Question 22

BONY LESIONS OF MANDIBLE/MAXILLA: CYSTIC

10

Answer 22

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.

Question 23

BONY LESIONS OF MANDIBLE/
MAXILLA: SOLID
Lytic 12

Answer 23

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

Question 24

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

Answer 24

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.

Question 25

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

Answer 25

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.

3. 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.
4. 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.
5. Ameloblastic fibroodontoma—rare; well-defined lucent lesion
   containing a dense mass of enamel and dentin (a hybrid of
   ameloblastic fibroma and complex odontoma).

Question 26

NASAL SEPTAL PERFORATION

Answer 26

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

Question 27

PARANASAL SINUS LESION WITHOUT
BONE DESTRUCTION
Inflammatory

Answer 27

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

Question 28

PARANASAL SINUS LESION WITHOUT
BONE DESTRUCTION
Neoplastic

Answer 28

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

Question 29

PARANASAL SINUS LESION WITH

BONE DESTRUCTION

Answer 29

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

Question 30

ORBIT: LESIONS INVOLVING THE GLOBE

Answer 30

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

Question 31

ORBIT: LESIONS OF THE OPTIC NERVE OR SHEATH

6

Answer 31

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

Question 32

ORBIT: LESIONS ARISING WITHIN

INTRACONAL FAT

Answer 32

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.

Question 33

ORBIT: CONAL LESIONS

Answer 33

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

Question 34

ORBIT: EXTRACONAL LESIONS
Lesions arising within the orbital cavity
7

Answer 34

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)

Question 35

ORBIT: EXTRACONAL LESIONS

Lesions arising from the orbital wall

Answer 35

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

Question 36

EXTERNAL AUDITORY CANAL LESIONS

Answer 36

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%.

Question 37

MIDDLE EAR LESIONS

Answer 37

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.

Question 38

PETROUS APEX LESIONS

Normal variants

Answer 38

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

Question 39

PETROUS APEX LESIONS

Well-defined and expansile + bone remodelling

Answer 39

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

Question 40

PETROUS APEX LESIONS

Destructive

Answer 40

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*

Question 41

PETROUS APEX LESIONS

Other

Answer 41

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

Question 42

DIFFUSE OR MULTIFOCAL SKULL
BASE LESIONS
8

Answer 42

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.

Question 43

UNIFOCAL SKULL BASE LESION

7

Answer 43

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.

Question 44

CLIVUS LESIONS

6

Answer 44

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.

Question 45

JUGULAR FORAMEN LESIONS

Answer 45

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