>90% of paediatric masses are benign congenital or inflammatory; less likely lymphoma or rhabdomyosarcoma. >90% adult masses are malignant with 20-40yo most commonly lymphoma, >40yo most common SCC nodal metastasis.
Trans-spatial diseases include lymphatic (lymphangioma), neural (neurofibroma, schwannoma, perineural spread) and vascular (haemangioma) lesions.
- Neurofibromas – Low T1 centre, often involves more than 1 peripheral nerve.
- Lymphangiomas – Congenital, high T2, infiltrative, tends to be heterogeneous signal with blood degradation products.
- Haemangiomas – Congenital, high T2, infiltrative, may contain phleboliths.
- Perineural disease – Spread of tumour or infection (fungal, SCC, adenoid cystic carcinoma), enabling access to noncontiguous spaces.
Compression or involvement of cranial nerves may cause:
- CN10 – Patulous oropharynx.
- CN12 – Denervation glottic myositis (diffuse enhancement of one side) then fatty atrophy.
Branchial Cleft Cyst (BCC)
(Cervical lymphoepithelial cyst). Failure of one of the six branchial arches to regress.
- 1st BCC (7%) – The cleft/groove (ectoderm) forms EAC; pouch (endoderm) froms eustachian tube, mastoid cells, V3. Classically parotid gland, around EAC, occasionally deep parotid or submandibular gland. Arnot type I is intraparotid, type II anterior neck that may have tract through parotid gland to EAC. Sinus may extend to bone/cartilage junction of EAC or skin.
- 2nd BCC (90%) – Forms palatine tonsils, CN VII. Triangle between SCM, submandibular and carotid spaces. Anywhere along base of tonsillar fossa to between ICA and ECA, anterior to mid SCM, parapharyngeal, lateral to IJV. Painless mass usually <40yo, varies in size with time, enlarging with URTIs. Low or high (protenaceous fluid) on T1. Wall thickening, irregularilty and enhancement suggests active/prior infection. DDx necrotic nodes, abscess, cystic neural lesion, thrombosed vessels. Branchial cleft fistula may drain to palatine tonsil/fossa, mucosa or skin. Dimple towards the oropharynx.
- Bailey type I – Superficial to anterior SCM, deep to platysma.
- Bailey type II (most) – Between SCM and carotid sheath, abutting the sheath, may be adherent to the IJV.
- Bailey type III – Between ICA and ECA.
- Bailey type IV – Pharyngeal mucosa or submucosa, deep to carotid aa, may be in parapharyngeal space.
- 3rd BCC (2%) – Forms thymus, inferior parathyroid gland, CN IX. Anterior to lower SCM. Fistula may drain between CCA and vagus nerve to piriform sinus.
- 4th BCC (1%) – Forms thryoid parafollicular C cells, superior parathyroid, CN X. Anterior to lower SCM, left in >90%, follows recurrent laryngeal nerve. Fistula around great vessels and aortic arch to thyroid gland, skin or apex of piriform sinus.
(Infantile haemangioma). True neoplasm of endothelial cells. May or may not be present at birth, has rapid proliferative phase after birth then involutes in early childhood with 50% resolving by 5yo. More common in Caucasian girls. Skin, subcutaneous or deep spaces of the head and neck. Low T1, high T2, enhances. Involution causes fibrofatty infiltration. Tx steroids, beta-blockers, chemotherapy, laser or nothing. Kasabach-Merrit syndrome – infantile haemangiomas associated with consumptive coagulopathy, high-output CHF and respiratory distress ± splenomegaly.
Venous Vascular Malformation
(Previously ‘haemangioma’ misnomer). Dysplastic vessels present at birth, grow during childhood and persist. Most slow-flow venous, may be mixed with lymphatic malformation (the more lymphatic the more cystic). Lobulated, low T1, high T2, heterogeneous enhancement. May have calcified phleboliths. May see flow voids. 20% associated with brain DVA.
- Maffuci syndrome – Venous malformations and enchondromatosis.
- Klippel-Trenaunay-Weber syndrome – Mixed capillary-venous-lymphatic malformations with hemihypertrophy.
- PHACES syndrome – Posterior fossa malformations (Dandy-Walker, cerebellar hypoplasia), haemangiomas, arterial anomalies (hypoplasia, persistent embrologic a, moyamoya), cardiac defects, eye abnormality, sternal/ventral defects. Cutaneous haemangiomas in brain, head and neck (mostly face).
(Lymphangioma). Benign, nonencapsulated malformations/sequestrations of lymphatic channels. Lymphatics develop from sacs derived from the venous system, if fails to communicate with veins they dilate, accumulating lymph. If extensive, causes foetal hydrops, imcompatible with life. Associated with Turner syndrome, foetal alcohol syndrome, Noonan syndrome, Down syndrome, trisomy 13. 90% present <2yo (greatest lymphatic development). Capillary (capillary sized thin-walled channels), cavernous (moderate dilated with fibrous adventitia) or cystic hygroma (enormously dilated). Painless compressible mass without displacing/compressing outher structures, may trans-illuminate. Varibale T1 and T2 (proteinaceous-chylous-haemorrhagic content). Common posterior triangle of neck. Multiloculated with septations, haemorrhage-fluid levels, heterogenous signals from blood degradation products. Propensity to haemorrhage into themselves causing acute increase in size. May be trans-spatial.
Internal jugular chain is the final common drainage pathway for the entire H&N; the jugulodigastric node is the highest (drainaing tonsil, oral cavity, pharynx, submandibular nodes) measuring up to 15mm. All other nodes up to 10mm (above this 70% are metastases, 30% are benign reactive hyperplasia). Features suggesting malignancy include peripheral enhancement with central necrosis, extracapsular spread with infiltration of adjacent tissues, matted conglomerate mass of nodes, uptake on PET, heterogeneity (cystic change or necrosis), rounded shape.
- Calcified nodes – TB, other granulomatous diseases (fungi, sarcoidosis, Thorotrast granulomas), treated lymphoma, anthrosilicosis, metastatic thyroid, adenocarcinoma or SCC.
- Intensely enhancing nodes – Castleman disease, thyroid carcinoma, Kaposi sarcoma, some lymphomas, Kimura disease.
- Waldeyer’s ring lymphoid hyperplasia with adenopathy – AIDS, mononucleosis, lymphoma, sarcoidosis, pharyngeal carcinoma with metastases.
Young adults, 20-40yo. Usually homogeneous and bland. Necrosis uncommon (cf carcinoma). May spread to skull base via cranial nerve foramina. Positive on PET.
- Non-Hodgkin lymphoma (NHL, 75%) – Waldeyer’s ring involved in 50%. Nodal spread may be discontinuous, commonly involves other regions.
- Hodgkin lymphoma (25%) – Isolated cervical or additional mediastinal nodes. Commonly has a history of mononucleosis. Organised nodal spread.
Post-Transplant Lymphoproliferative Disorder (PTLD)
Ranges from benign lymphoid hypertrophy, myeloma, monoclonal lymphoma, polyclonal lyphoma. Enlarged nodes in abdomen, chest and neck (including adenoids and tonsils) in whole organ transplant recipients. In absence of T cells, EBV induces proliferation of B cells, and a monoclonal dominant may develop. May develop months-years after transplant. May present as necrotic mass in nasopharynx.
(Antiofollicular hyperplasia). Uncommon lymphoproliferative disorder with proliferation of B-cells, not malignant but similar to lymphoma. 70% in chest, 10% head and neck. Usually asymptomatic, <30yo. Hypervascular nodes with avid enhancement, non-necrotic, may have central stellate nonenhancement.
- Mononucleosis (EBV) – Multiple enlarged non-necrotic nodes. Usually bilateral, involves Waldeyer’s ring. DDx HIV (intraparotid cysts), sarcoidosis (diffuse parotid enlargement, bihilar adenopathy).
- Cat Scratch fever – Bartonella henselae G-neg intracellular bacterium from cat scratch or flea bite. Bilateral lymphadenopathy including intraparotid nodes, perinodal oedema. Usually self-limiting, but may progress to encephalopathy and neuropathy. Parinaud oculoglandular syndrome is unilateral conjunctivitis, polypoid granuloma of palpebral conjuctiva, preauricular parotid and periparotid lymphadenopathy.
- Kikuchi disease – Histiocytic necrotising lymphadenotis in young Asian adults ?viral. Adenopathy, fever, leukopenia. Large necrotic and nonnecrotic enhancing and nonenhancing adenopathy. DDx lymphoma, metastases, TB.
- Kimura disease – Diffuse hypervascular cervical adenopathy (esp Ib), eosinophilia, enlarged salivary glands. Asian men 10-30yo. Nodes are round, solid, hypoechoic, homogeneous, hypervascular. Affects all parts of Waldeyer’s ring.
- Tuberculous adenitis (scrofula) – Painless posterior neck mass in Southeast Asians. Usually from milk contaminated with Mycobacterium bovis causing subclinical pharyngitis, in USA usually M.tuberculosis, occasionally atypical mycobacteria (esp M.scrofulaceum). Uncommonly also has pulmonary TB. Bilateral hypodense necrotic nodes esp level V, ringlike thick enhancement, multiloculated, adjacent oedema causing ill-defined margins, often calcifies.
Parapharyngeal Space (PPS)
Triangular, fat-filled, from skull base to submandibular gland. Surrounded by carotid space (posterior), parotid space (lateral), masticator space (anterior) and superficial mucosal space (medial); compressed/obliterated by masses in these locations. Contains fat, V3, internal maxillary a, ascending pharyngeal a. Primary lesions in this space are uncommon, must be completely surrounded by fat.
- Salivary gland tumour most common esp pleomorphic adenoma. May be ectopic or extension from adjacent deep lobe of parotid or arise from minor salivary gland
- Infection – From mucosa (tonsillitis, pharyngitis), masticator space (odontogenic) or parotid spaces.
- Glomus tumours
- 2nd BCC (rare)
- Synovial sarcoma – Fluid levels, intratumoral haemorrahge, calcification, multiloculated.
Masses may separate or anteriorly displace the carotid and jugular vein, displace styloid muscles anterior (narrowing stylomandibular notch cf widening in deep parotid lesions), displace parapharyngeal fat anteriorly. Contains CN9-11, sympathetic nerves, jugular chain nodes, corotid a, jugular v. Lesions include:
- Glomus tumours
- LN – Metastases, lymphoma, infection.
- 2nd BCC
- IJV thrombophlebitis – Iatrogenic or from peritonsillar inflammation (Lemiere syndrome), Ludwig’s angina. Halo of oedema around the thrombosed vein, enhancing vessel wall.
- Carotid artery pseudoaneurysm – From paraphayryngeal abscess, syphilis, fibromuscular dysplasia, carotid dissection, Ehlers-Danlos syndrome, trauma, surgery, neoplastic ‘blow-out’ (occasionally after radiotherapy), idiopathic.
- Carotidynia – Syndrome of tenderness, swelling, increasd pulsatations. Self-limited. Enhancing tissue around distal CCA and bifurcation. DDx GCA, dissection, FMD, Takayasu, IMH.
- Asymmetry of the internal jugular veins – Common, usually R 2x > L. Variable signal which may be bright or signal void.
- Tortuosity of the carotid arery – Esp elderly.
Nerve Sheath Tumours
- Schwannomas are encapsulated tumours from nerve sheaths, without infiltrating the nerve. Often from vagus nerve, displacing the carotid a and parapharyngeal fat anteriorly. Usually well-defined, hypodense, moderate enhancement. Variable T2 (depending on Antoni A or B tissue). May be cystic, haemorrhagic.
- Neurofibromas are unencapsulated, usually multiple permeating the substance of the nerve.
(Glomus tumours). Rare, 40s-50s. Vascular tumour from globus neural crest derivatives. Most are in the adrenal medulla as pheochromocytomas; 70% of extra-adrenal tumours are in the head and neck (aorticopulmonary chain), others in the paravertebral paraganglia (eg organs of Zuckerkandl, rarely bladder). Nests/zellballen of round/oval chief cells surounded by delicate vascular septae. Painless, slow-growing, may be pulsatile with bruit, tinnitis. May have associated CN9-12 neuropathy. 3-5% have metanephrine secretions (HTN). Dramatic arterial enhancement with rapid uptake and rapid washout (DDx haemangioma, aneurysms, AVM, angiofibroma), cf slower enhancement with schwannomas. May have flow voids with salt-and-pepper appearance (salt being small haemorrhages; pepper being flow voids). Strong capillary blush on angiography. ‘Moth-eaten’ destruction of bone. Takes up Indium-111 octreotide (cf schwannomas and other masses). DDx other neuroendocrine lesions eg medullary thyroid carcinomas, thyroid adenomas, Merkel cell tumours, carcinoid tumours, schwannoma (esp CN9-11), meningioma. Malignant transformation in 6%. Multiple in 10%. 7% are inherited (eg AD MEN2) where they are multiple in 30%, bilateral in 10%. Tx resection ± preoperative embolisation. 50% are ultimately fatal due to infiltrative growth.
- Carotid body tumour (chemodactoma) – Carotid body is ~5mm within adventitial layer of CCA at level of bifurcation. Chemoreceptor (O2, CO2, pH) stimulating RR, sympathetics. Carotid body tumour is pulsatile mass, splaying ICA and ECA without any narrowing.
- Glomus jugulare – May grow through skull base into carotid space, usually infiltrating lumen of jugular vein. Almost always destroys bone, with destruction of the carotico-jugular spine (between the ICA and IJV) characteristic.
- Glomus vagale (glomus intravagale tumour, vagal paraganglioma) – May displace carotid aa anteriorly. From nodose ganglion (upper neck vagal ganglia within carotid sheath). Most above hyoid bone. May involve CN9-12. Tx requires sacrifice of vagus nerve causing vocal cord paralysis.
- Glomus tympanicum – From Arnold and Jacobson nerves of middle ear. Usually small at the cochlear promontory.
Extends from EAC to angle of mandible. Contains parotid gland, intraparotid LN (~10-20), CN7, ECA, retromandibular v. Masses deviate parapharyngeal space anteromedially, styloid muscles and carotid space posteriorly with widening of the stylomastoid foramen. The facial nerve passes close to the retromandibular vein, within the stylomandibular plane (line drawn between styloid process and mandibular condyle), dividing the deep and superficial lobes.
65-80% of salivary gland tumours occur in the parotid, 10% in the submandibular gland, the rest in the sublingual or minor salivary gland. 80% of parotid gland tumours are benign (pleomorphic adenoma, Warthin tumour), 20% malignant (adenocystic carcinoma, adenocarcinoma, SCC, mucoepidermoid carcinoma). 40% of submandibular, 50% of minor salivary gland and 80% of sublignual tumours a malignant. The larger the salivary gland (ie parotid) the higher rate of benignity in adults, malignancy in children. Imaging cannot definitively differentiate benign from malignant (except infiltration into other spaces, facial nerve). Multiple lesions seen in inflammatory or malignant adenopathy, Warthins tumour.
Circumscribed lesions are either benign or low-grade malignant. Ill-defined lesions are usually malignant. The margin is best evaulated on MRI or non-contrast CT (difficult on C+CT). Paediatric parotid tumours are rare; most commonly are malignant.
Other salivary gland lesions include:
- Capillary haemangioma of infancy.
- 1st Branchial Cleft Cyst
- Calculous Disease
- Sialosis – Painless enlargement of the parotid from diabetes, alcohol, hypothyroidism, medications (phenothiazines, diuretics), obesity, starvation or idiopathic. Usually bilaterally symmetric, reversible.
- Mucocele (sialocele) – Most common salivary gland lesion, from blockage or rupture of a duct. Saliva leaks into surrounding stroma. Most found on the lower lip after trauma, change in size with meals. Tx complete excision of the cyst and minor salivary gland lobule of origin; incomplete excision results in recurrence.
- Sarcoidosis – Bilateral enlarged glands with multifocal nodules.
- Neurogenic tumours (schwannoma, neurofibroma) – Along CNV or CNVII.
Other parotid lesions:
- Intraparotid node metastases – Drain from skin over the scalp, temporal, external ear.
Sialadenitis and Sialodochitis
Sialadenitis from calculous disease (most common), infection (mumps, HIV, coxsackie, inflenza, Streptococcus, Haemophilus, Staphylococcus, TB, Candida, cat scratch fever), idiopathic postpartum. May be associated with sialectasis (dilated ducts), microabscesses (rim-enhancing hypodensities/high T2, often multiple). Infection may be predisposed by poor dental hygiene.
Sialodochitis is inflammation of main salivary ducts, usually autoimmune. Punctate globular/cavitary/destructive appearance to ducts with pools of contrast in the gland. Fatty replacement over time. Lymphoepithelial cysts and nodules.
- Sjögren type 1 (Mikulicz disease) – Limited to salivary glands with chronic sialadenitis and sialodochitis, fibrous tissue, xerostomia (dry mouth). Middle-aged women.
- Sjögren type 2 (Sjögren syndrome) – Associated with collagen vascular disease (esp RA, SLE), lacrimal glands with dry eyes, dry mouth and arthritis. 10x increased risk of lymphoma (usually NHL).
?Partial obstruction of terminal ducts by surrounding lymphocytic infiltration. Multiple in collagen vascular disease (Sjogren syndrome) and HIV. AIDS-related parotid cysts are multiple cystic with associated solid lesions (DDx LN, lymphoma). Associated diffuse generalised lymphadenoatphy, low T1 bone marrow.
Benign Mixed Tumour (BMT)
(Pleomorphic adenoma). Mixed ductal/epithelial and myoepithelial cells with varying degreses of myxoid, hyaline, chondroid and osseous tissue. 80% of benign parotid gland tumours, 80% of salivary gland pleomorphic adenomas occur in the parotid (less common in submandibular, rare in minor glands), 80% of parotid tumours in the superficial lobe. Middle-aged women, increased risk with irradiation. Usually well-defined round solid, very bright T2 similar to CSF, low T1. Small lesions demonstrate homogeneous enhancement, but larger lesions heterogeneous enhancement (slightly more homogeneous with delay C+). Complete capsule of low T2 with lobulated contour. May have tentacles with irregular margin. Variable cystic degeneration and calcificaiton (uncommon in other parotid tumours). 80% remain benign, 20% undergo malignant change (carcinoma ex pleomorphic adenoma, malignant mixed tumour; usually adenocarcinoma or undifferentiated carcinoma). Tx resection. If not fully resected, but undergo seeding in the surgical bed with multiple recurrent enhancing nodules.
(Papillary Cystadenoma lymphomatosum). Most common elderly men, M>>F. Multiple in 10%, bilateral in 10%. Smoking increases risk 8x. Almost exclusively parotid glands, most in the superficial gland. Benign. May have tumoural cyst, low T1, heterogeneous T2. Uptake of Tc99m-pertechnetate (similar to oncocytomas).
Rare, benign epithelial tumour of oncocytes (rich in mitochondria), almost exclusively parotid gland. Bright T2, takes up Tc99m. Other oncycytomas include renal (benign) and thyroid (Hurthe cell adenoma, benign or malignant).
Malignant Salivary Gland Neoplasms
Palpable discrete painless mass in 98%, may cause facial nerve dysfunction (esp adenoid cystic and undifferentiated carcinomas), cervical adenopathy.
Staging: N and M staging follows SCC.
- Tx – Cannot be assessed.
- T0 – Primary not evident.
- T1 – </= 20mm
- T2 – 20-40mm
- T3 – >40mm or extraparenchymal extension (clinical or macroscopic, not microscopic).
- T4a – Invades skin, mandible, ear canal or facial nerve.
- T4b – Invades skull base, pterygoids or encases carotid a.
- Mucoepidermoid carcinoma (30%) – Most common malignant parotid tumour, most occur in parotids. Most common radiation induced parotid tumour. Variable mixtures of squamous, mucus-secreting and intermediate cells. May be ill-defined or well-defined with psudocapsule, may be up to 80mm. Low-grade tumours are high T2, high grade low T2.
- Adenoid cystic carcinoma – Most common malignant submandibular/sublingual/minor salivary gland tumour. 50-60% have perineural spread; along CN7 into temporal bone or CN5 to Meckel’s cave. Low T1, variable T2. May be well-defined. Slow-growing but relentless, with 50% eventually disseminating to bone, liver or brain; occasionally decades ofter resection.
- Squamous cell carcinoma – ?From metaplasia of ductal columnar epithelium into squamous cells (only in parotid gland) or extracapsular invasion from nodes (primary in overlying skin and ear). Almost always low T2 unless necrosis.
- Adenocarcinoma – From glandular tissue, some from pleomorphic adenomas. Varibale mucinous, cystic and solid components. Poor prognosis.
- Acinic cell carcinoma – Cells resemble normal serous acinar cells of salivary glands, most arise in the parotids. May be multifocal with 3% bilateral.
- Undifferentiated carcinoma – Rare, poor prognosis.
Superficial layer of deep cervical fascia surounds muscles and mandible. From angle of mandible to skull base, temporalis. Contains muscles of mastication (temporalis, medial and lateral pterygoids, masseter), ramus and body of mandible, inferior alveolar nerve, internal maxillary a. Masses displace the parapharyngeal space posteromedially, styloid muscles posteriorly. Most lesions are odontogenic absecess, osteomyelitis, direct spread of SCC, lymphoma, minor salivary tumour, muscle/bone sarcoma. Most malignancies are from direct extension. Other lesions include:
- Branchial cleft cysts
- Lymphangiomas – Loculated, infiltrative, multicystic, nonenhancing, high T1 and T2.
- Venous vascular malformations – Solid, enhance, low T1, high T2.
- Capillary haemangioma – Generally superfical, may extend into muscle and fat of masticator space. Very high T2, avid enhancement.
- Pseudotumours (common):
- Accessory parotid gland – May occur along anterior masseter. Hypodense, high T1.
- Muscle hypertrophy – From bruxism (clenching/grinding teeth), usually bilateral.
- Atrophy from V3 compromise – From tumours (eg neurogenic), perioperative injury, trauma.
- Odontogenic – Abscesses, osteomyelitis, cellulitis associated with carious teeth.
- Fibrous dysplasia – Enlarged mandible.
- Neurogenic tumours – Schwannoma and neurofibromas.
- Mandible tumours – Osteosarcoma, chondrosarcoma, Ewing sarcoma, ameloblastoma.
- SCC – From oral cavity (esp retromolar trigone), oropharynx or nasopharynx.
- Metastases to mandible – Esp renal, breast, lung, thyroid, neuroblastoma (children).
- Soft tissue sarcomas – Rhabdomyosarcomas in children (intratumoral haemorrhage in 30%, high T2), fibrosarcomas, osteosarcomas.
- Lymphoma – Esp NHL.
Temporomandibular Joint (TMJ) Syndrome
(Chronic maxillofacial pain syndrome). F>>M, often precipitated by trauma. 80% of those with symptoms have a dislocation, but 35% of asymptomatic patients have anterior dislocation. May have associated TMJ effusion. May have degenerative changes with narrowing, osteophytic ‘bird-beaking’, sclerosis, chronic avascular necrosis of the condylar head. The larger posterior band of TMJ meniscus is normally at the 11 or 12 o’clock position in relation to the condylar head.
- Anterior meniscal dislocation (most common) – Posterior band of meniscus dislocated anteriorly at 9/10 o’clock, may have fat in front of the condyle on closed-mouth. May reduce on opening with an ‘opening click’, redislocating on closing ‘closing click’. May restrict the joint’s motion (closed-lock).
- Rotational dislocation – Medial or lateral component to the anterior dislocation. Isolated medial/lateral (sideways) dislocation is rare.
- Stuck disk – Doesn’t move in open or closed mouth positions, usually fibrosed and immobile. May be anteriorly displaed.
- Disk perforation – Unable to be detected by MR, requires arthrography or arthroscopy. Usually associated with joint effusion, transverse component of meniscal dislocation.
- Athritidies – RA (usually has erosions and soft tissue), septic arthritis, gout, pseudogout, PVNS, synovial chondromatosis, tumoral calcinosis.
Retropharyngeal Space (RPS)
Potential space between superficial mucosal space, pharyngeal constrictors and prevertebral space. Contains lateral (nodes of Rouvier, abnormal when seen >30yo) and medial retropharyngeal LN (uncommon), fat. ‘Danger space’ as it may serve as a conduit spreading infection into the mediastinum. Masses displace parapharyngeal fat anterolaterally, longus muscles posteriorly, and styloid muscles anteriorly. Lesions include:
- LN metastases
- Acute leukemia – Diffuse infiltration.
- Fibromyxoma – Oval shaped mass.
- Retropharyngeal carotid artery – From incompetent medial aspect of the deep cervical fascia.
From pharyngitis (adenoids/tonsils) or sinusitis (children) spreading to a RPS node. Retropharyngeal cellulitis/lymphoedema occurs if the capsule of the node is breached. Suppurative necrotizing adenitis does not cross the midline (nodes are usually paramedian). Retropharyngeal abscesses may be midline, loculated, ring-enhancing. Ill-defined tissue may be nondrainable phelgmon. May cause ICA thickening, spasm or thrombosis. If breaches IJV may cause thrombophlebitis (Lemierre syndrome) and emboli to lungs. May cause rotatory subluxation of the atlantoaxial joint (Grisel syndrome) causing torticollis.
Prevertebral fascia surrounds muscles. Contains cervical vertebrae, prevertebral mm, paraspinal mm, phrenic n. Maseses displace longus colli anteriorly, styloid muscles anteriorly, rarely displaces parapharyngael fat. Lesions include:
- Infection – Including osteomyelitis and discitis.
- Vertebral osteophyte
- Bone metastases
- Calcific tendonitis of longus colli – (HADD). Thickening and oedema within the prevertebral/retropharyngeal space, may see calcification near attachment at the arterior arch of atlas. Usually self-limiting, may cause chronic back pain. Important to differentiate from retropharyngeal abscess,
- Nodular fasciitis – Lateral neck mass, may enhance, intermediate T2. ?Low-grade soft tissue tumour.
- Necrotizing fasciitis
- Aggressive fibromatosis (desmoid tumour) – Low T1 and T2, isodense, variable enhancement. ?Precursor to MFH.
- Lipoma – Esp lateral subcutaneous tissues, supraclavicular fossa, posterior perivertebral space. DDx lipoblastoma (<3yo with embryonal fat tissue and liposarcomas), Madelung disease (masssive symmetric lipomatosis of the posterior neck).
- 1st Branchial Cleft Cyst
- Dermoid cyst – Typically anterior floor or mouth, cobblesone architecture on MR.
- Venous vascular malformation
- Neurogenic tumour (schwannoma, neurofibroma) – Along CNV.
- Pleomorphic Adenoma
- Malignant Salivary Gland Neoplasms – Adenoid cystic, mucoepidermoid carcinoma or adenocarcinoma.
Ludwig’s angina is rapidly spreading bilateral submandibular space infection involving both sublingual and submaxillary compartments.
(Floor or mouth).
(Sialolithiasis). Most commonly submandibular gland (4x more common than parotid) due to mucinous secretions and uphill drainage more likely to stasis. Sublingual and minor salivary gland calculi rare. Unilateral. Increased risk with dehydration, reduced secretory function (drugs eg phenothiazines). 80% visible on radiograph. Painful glands worse with chewing. May have bacterial superinfection (esp S.aureus, Strep.viridans), with necrosis and abscess formation. Sialadenitis with enlarged gland and effacement of surrounding fat planes. Calculi not seen on NECT may require sialography (conventional or MR), which also detects strictures (after passage of calculus, autoimmune disease). Tx medications to promote salivation, transoral resection or sialodochoplasty. DDx autoimmune chronic sialadenitis (pruned, truncated main duncts with punctate/globular peripheral collections), mucous plug causing siadenitis (Kussmaul disease), impacted food debri, oedema ajacent to the orifice after trauma causing obstruction.
Kuttner tumour – Focal pseudomass in submandibular gland with glandular calcifications from chronic calculous sialadenitis.
(Mucus escape cyst). Mucocele/sialocele of the sublingual gland. Obstruction of sublingual gland or minor salivary gland at floor of mouth, from previous infection, trauma or calculi. Simple ranula just involves the sublingual space above mylohyoid, lined by epithelium (approached intraorally). Plunging ranula also involves submandibular spaces, either extending around the posterior border of mylohyoid, or through a defect in the muscel (boutonnière defect); is not epithelial lined and is surgically treated by submandibular or transvervical ± intraoral approach. Wall usually enhances, may have pointed anterior edge at site of obstruction. Rupture causes infection in neck.
Allergic, viral, bacterial or chemical insult (eg smoking, GORD); most as part of URTI or heavy smoking. Most infections are self-limited, but oedema may cause laryngeal obstruction esp H.infuenze or β-haemolytic strep in young children with small airways. Croup is laryngotracheobronchitis. Smoking induces squamous metaplasia, increased risk of SCC.
Vocal Cord Paresis
Atrophy of the thyroarytenoid muscle, dilated laryngeal ventricle, medial displacement, dilated ipsilateral piriform sinus and vallecula, medialisation of the vocal cord and aryepiglottic fold, anteromedial rotation of the arytenoid cartilage, posterior cricoarytenoid atrophy.
High vagus lesions also cause abnormal swallowing and gag reflex (sensory CN9, motor CN10), associated CN9/11/12 abnormality with pharyngeal muscle atrophy, deviated uvula. Causes include metastases to jugular foramen, glomus tumours, schwannomas, nasopharyngeal carcinomas, chordomas.
Low vagus lesions are not associated with pharyngeal abnormality; need to image pathway of vagus and recurrent laryngeal nerves (R loops under SCA, L under arch and pass up tracheoesophageal grooves). Causes include:
- Around carotid sheath – SCC, thyroid mass, glomus vagale, schwannomas, dissection and pseudoaneurysms, lymphadenopathy.
- Mediastinum – Lymphoma, bronchogenic carcinoma, lymphadenopathy, patent ductus arteriosus, mitral stenosis with PA dilatation, aneurysms, dissections.
- Tracheosophageal groove – Thyroid (cancer, goiter, truama), parathyroid (adenoma, carcinoma), oesophagus (Zenker’s diverticulum, perforation).
Typically impact of larynx against steering wheel. Injuries include:
- Fracture of thyroid cartilage
- Cricoarytenoid dislocation
- Mucosal tear, may cause pneumomediastinum or subcutaneous gas in paraglottic space
Airway compromise if there is swelling or involvement of the cricoid cartliage. Complications include infection and chondritis.
Dilated appendix/saccule of laryngeal ventricle (separating false and true cords, appendix is anterior blind pouch) from chronically increased intraglottic pressure (wind instruments, glass blowers, excessive coughers) or neoplasm obstructing the laryngeal ventricle/saccule. Usually air-filled, may be obstructed and fill with fluid (saccular cyst). Internal, external (rare isolated) or mixed (most) depending if they protrude above the thyroid cartilage through the thyrohyoid membrane. May extend superolaterally into the parapharyngeal space. Deep to strap muscles and comminicates with laryngeal ventricle (cf thyroglossal duct cyst). If infected becomes pyolaryngocele.
DDx Pharyngoceles from chronic increased intrapharyngeal pressure eg horn blowers.
Neonatal inspiratory stridor from floppy laryngeal cartilages collapsing with negative pressure. Best seen at fluoroscopy. Usually improves with age.
Focal deposition of amyloid, usually AL type. Very low T1 and T2, no enhancement, rarely calcifies. May also affect tongue and oropharynx, trachea, orbit or nasopharynx.
Reactive Vocal Cord Nodules
(Polyp). Most occur in heavy smokers or great strain on vocal cords. Singers’ nodules are bilateral, polyps unilateral. Adults, M>F. Smooth raounded, sessile or pedunculated, generally <few mm. Covered by squamous epithelium with loose myxoid connective tissue core. May ulcerate if apposed with inflammation causing hoarseness. Almost never causes SCC.
Benign small neoplasm on vocal cord, usually raspberry-like <10mm. When on free edge may ulcerate with haemoptysis. Rarely cause SCC.
Laryngotracheal papillomatosis (juvenile laryngeal papillomatosis) – Most commonly children, HPV 6 or 11 from descent in birth passage. Most commonly true cords. Tx laser with common recurrence. Often spontaneously regress at puberty.
Rare, after radiotherapy. Soft tissue swelling of larynx, sloughing of arytenoids with subluxation, fragmentation, sclerosis, collapse of thyroid cartilage, gas bubbles around cartilage. May have superinfection. Tx total laryngectomy.
(Spindle cell sarcoma). Characteristics of SCC and sarcoma. Rare outside larynx. Prognosis similar to SCC.
Difficult to distinguish between benign chondroma from malignant chondrosarcoma. May affect cricoid or vocal cord. Popcorn-like whorls of calcium.