Clinical Radiology xxx (2015) e1ee10

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Pictorial Review

Patterns of spread of head and neck adenoid cystic carcinoma F.M. Singh a, b, *, S.Y. Mak a, S.C. Bonington a a b

The Christie NHS Foundation Trust, Manchester, UK North Western Deanery School of Radiology, Manchester, UK

art icl e i nformat ion Article history: Received 2 September 2014 Received in revised form 14 January 2015 Accepted 23 January 2015

We present a review of head and neck adenoid cystic carcinoma (ACC). Imaging features of the primary tumour, patterns of locoregional spread, and distant metastasis with emphasis on perineural extension and imaging pitfalls are discussed with illustrated examples. Ó 2015 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.

Introduction Adenoid cystic carcinoma (ACC) was first described by three French authors, Robin, Lorain and Laboulbene in the 1850s. They used the term “tumeur heteradenique” and noted that it was able to spread along nerves.1 ACC accounts for 1% of all head and neck malignancy and arises in secretory glands,2 most commonly the major and minor salivary glands of the head and neck. ACC arises most frequently (60%) in the minor salivary glands distributed throughout the head and neck mucosa, the most common locations being the palate, tongue, paranasal sinuses, and nasal cavity.3e6 The parotid gland is the most common single site of origin (25%).5 It has also been reported to arise from the external auditory canal,7 lacrimal gland,8,9 and orbit.10 Although primary ACC arises most commonly within the head and neck, it has rarely been described in the trachea and central airways, breast, female reproductive tract, thymus, prostate, oesophagus, and skin.11 * Guarantor and correspondent: F. M. Singh, Wrightington Wigan and Leigh NHS Foundation Trust, Radiology Department, Royal Albert Edward Infirmary, Wigan Lane, Wigan WN1 2NN, UK. Tel.: þ1942 778627; fax: þ1942 822402. E-mail address: fi[email protected] (F.M. Singh).

Characteristically, ACC has a slow but relentless growth rate with overall treatment failure, locoregional recurrence, and distant metastatic rates of 62%, 51%, and 38%, respectively.12 Recurrence typically occurs late, with diseasespecific survival of 89% at 5 years and 40% at 15 years.13 Metastases are rare at presentation but occur in over 50% of patients over the course of the disease.5,14,15 Perineural invasion is defined as tumour cell invasion in, around, and through the nerves.16 Some authors use the terms perineural invasion and spread interchangeably, and others refer to invasion as the microscopic process and spread as the macroscopic result seen on imaging such as MRI.17 Perineural invasion is common in head and neck ACC, seen in over 50% of cases on histopathological examination.18,19 Some studies have shown perineural spread to be under-reported on imaging and detection of its extent is variable when comparing MRI to histology as the reference standard. It ranges from 10 to 100% and appears to depend, at least in part, on whether the actual preoperative report was used or whether the preoperative images were later reported by a head and neck imaging specialist.19e22 Tumour reaches distant locations by travelling along the neural sheath in the absence of lymphatic or vascular

http://dx.doi.org/10.1016/j.crad.2015.01.013 0009-9260/Ó 2015 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.

Please cite this article in press as: Singh FM, et al., Patterns of spread of head and neck adenoid cystic carcinoma, Clinical Radiology (2015), http://dx.doi.org/10.1016/j.crad.2015.01.013

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invasion. This is thought to be facilitated by the expression of neural adhesion molecules.16,23,24 Extension most frequently occurs centripetally, towards the central nervous system, but can also occur peripherally. Perineural spread is also seen in other malignancies such as squamous cell carcinoma20,25,26 and melanoma, particularly the desmoplastic subtype.14,23,27 The radiologist plays a crucial role in detecting perineural spread as it is frequently asymptomatic.17,25 The mainstay of treatment is surgery and postoperative radiotherapy.28 Perineural invasion of major nerves, positive margins at surgery, and solid histological subtype are associated with treatment failure.13

Imaging the primary tumour MRI is the optimum imaging technique due to its high soft-tissue contrast, although it is not specific for distinguishing ACC from other head and neck primary tumours14,29 (Fig. 1).

Suggested MRI sequences Routine use of intravenous gadolinium and fatsuppression sequences aids detection of locoregional spread. Axial and coronal planes are most useful for assessing skull base involvement. Unenhanced T1-weighted (T1W) images are important for assessing fat planes and fatcontaining structures such as the pterygopalatine fossa and bone marrow for low signal tumour infiltration.14,30 Our regional guidelines recommend the routine use of thin-section axial T1 and T2, coronal T2 STIR (short tau

inversion recovery), and axial and coronal T1 postgadolinium with fat saturation with additional sagittal sequences for midline disease.

Imaging features of primary acc Primary ACC tumour can have a variable appearance at MRI and CT. It can present as a well-defined mass or an illdefined mass with diffuse infiltration of surrounding structures.31 The latter has a tendency to invade fat and bone with a permeative pattern rather than present as an expanding mass14 (Fig. 2). ACC typically enhances homogeneously, although heterogeneous enhancement and necrosis can also be a feature of this tumour.31 Three histological subtypes have been described: cribriform, solid, and tubular.3,5 The more cellular, solid form has lower signal on T2W imaging and carries a worse prognosis.29 Although ultrasound is frequently used in the initial detection of ACC within the major salivary glands, there are no specific ultrasound features to distinguish ACC from other head and neck tumours (Fig. 3).

Patterns of perineural extension The trigeminal (V) and facial (VII) nerves are commonly involved due to their distribution at sites where primary head and neck ACC frequently arises. The maxillary (V2) and mandibular (V3) branches of the trigeminal nerve are most frequently involved in perineural spread and allow a route of tumour infiltration into the

Figure 1 Coronal MRI images of a patient with primary ACC of the hard palate. (a) T1W and (b) STIR images from the same examination demonstrate a well-defined mass within the right hard palate, which has low signal on T1W and intermediate to high signal on STIR images (arrows). Please cite this article in press as: Singh FM, et al., Patterns of spread of head and neck adenoid cystic carcinoma, Clinical Radiology (2015), http://dx.doi.org/10.1016/j.crad.2015.01.013

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Figure 2 Axial MRI images in a patient with recurrent ACC of the left maxillary sinus. (a) T1W image shows a low signal mass in the left retromolar trigone, which is obliterating the parapharyngeal fat (long arrow) and invading the mandible with low signal marrow replacement (short arrow). (b) T1W post-gadolinium fat-suppressed image showing enhancement of the mass with invasion into the tongue base (short arrow) and extension along the buccal mucosa (long arrow).

pterygopalatine fossa (PPF), Meckel’s cave, and the cavernous sinus (Table 1).23,32 The PPF is a major crossroads for tumour extension, linking the orbital apex, inferior orbital fissure, cavernous sinus via the foramen rotundum, vidian canal, infratemporal fossa via the pterygomaxillary fissure, greater and lesser palatine canals, and the sphenopalatine foramen.33,34 Primary head and neck ACC most frequently arises in the palate, from which sensory fibres of the greater and lesser palatine nerves can act as a conduit for spread into the PPF.23,32,34 The facial nerve is frequently involved in ACC of the parotid gland due to centripetal extension from the intraparotid segment through the stylomastoid foramen, into the petrous portion of the nerve and beyond.23

Figure 3 Colour Doppler ultrasound of the left submandibular salivary gland showing an ill-defined region of hypoechogenicity with internal vascular flow later proven to be a primary ACC. These appearances are not specific for ACC.

Table 1 Sites of perineural spread of primary adenoid cystic carcinoma. Primary tumour location

Potential local sites of perineural spread

Palate

Greater and lesser palatine nerves (branches of maxillary nerve, V2) and on to pterygopalatine fossa (PPF) and foramen rotundum. Infraorbital nerve (branch of maxillary nerve, V2) and on to PPF and foramen rotundum. Inferior alveolar and lingual nerves (branches of mandibular nerve, V3) and on to foramen ovale. Facial nerve (stylomastoid foramen, petrous portion, internal auditory canal) and auriculotemporal branch of V3.

Nasal cavity and maxillary sinus Retromolar trigone and tongue Parotid gland

Figure 4 Coronal CT image showing an enlarged right infraorbital canal (long arrow) due to tumour infiltration of the infraorbital nerve, a branch of the maxillary division (V2) of the trigeminal nerve. Note the normal left infraorbital canal (short arrow).

Please cite this article in press as: Singh FM, et al., Patterns of spread of head and neck adenoid cystic carcinoma, Clinical Radiology (2015), http://dx.doi.org/10.1016/j.crad.2015.01.013

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Figure 5 (a) Axial T1W post-gadolinium fat-suppressed MRI image of a patient with ACC of the left paranasal sinuses. Enhancing tumour is seen in the left cavernous sinus with anterior extension into the left orbit involving the lateral rectus muscle (short arrow). Tumour extends along the meninges into the temporal lobe (long arrow). (b) Axial T1W post-gadolinium fat-suppressed MRI image of a different patient with primary ACC of the parotid. The lumen of the left internal carotid artery contains enhancing tumourethrombus (long solid arrow). Normal intraluminal low signal is seen in the right internal carotid artery (short solid arrow). Tumour infiltration is also seen in the mandibular branch of the left trigeminal nerve, V3 (long dashed arrow), with associated enhancement of the left temporalis muscle secondary to denervation (short dashed arrow).

There are several interconnections where perineural spread can occur between the trigeminal and facial nerves such as the vidian nerve, greater superficial petrosal nerve (GSPN) and auriculotemporal nerve. The GSPN leaves the geniculate ganglion of the facial nerve, courses anteriorly into the foramen lacerum, joins the deep petrosal nerve and enters the vidian canal as the vidian nerve.32,35 The auriculotemporal nerve is formed by two roots arising from V3, which encircle the middle meningeal artery and enter the parotid substance to join the facial nerve.23,36

Imaging features of local invasion and perineural spread MRI is more sensitive for detecting perineural spread when compared to CT.19,37 Sensitivity values of 95e100% have been reported,19,20 although this drops to 63% for complete accurate mapping of the extent of disease.20 CT is complementary to MRI for assessing local bone changes such as widening of the skull base foramen (Fig. 4).

Figure 6 Coronal T1W post-gadolinium fat-suppressed MRI images of a patient with recurrent parotid ACC. (a) There is enlargement and enhancement of the left maxillary branch of the trigeminal nerve (V2) within the foramen rotundum (long arrow) and the vidian nerve within the vidian canal (short arrow). (b) Gross enlargement and enhancement of the left mandibular branch of the trigeminal nerve (V3) with widening of the foramen ovale (long arrow). Note the normal contralateral side (short arrow).

Please cite this article in press as: Singh FM, et al., Patterns of spread of head and neck adenoid cystic carcinoma, Clinical Radiology (2015), http://dx.doi.org/10.1016/j.crad.2015.01.013

Figure 7 (aeb) T1W post-gadolinium fat-suppressed MRI images of the same examination as Fig. 6. (a) Coronal image showing nodular enhancement of the mastoid segment of the left facial nerve (arrow) indicating tumour infiltration. Further tumour is seen in the left brainstem with adjacent meningeal enhancement. (b) Axial image showing the enlarged and enhancing left facial nerve within the mastoid bone (long arrow). Note the normal right facial nerve is just visible (short arrow). (c) T1W post-gadolinium fat-suppressed MRI image of a different patient showing normal native enhancement in the tympanic segments of the facial nerves bilaterally (arrows).

ACC infiltrates into surrounding structures such as muscle, blood vessels, the meninges, and brain (Fig. 5) as well as its classical tendency to extend along nerves. The key features of perineural extension are as listed in Box 1.

Box 1. Imaging features of perineural tumour spread.  Enlargement/erosion of foramen (Figs. 4 and 6).  Nerve enlargement/enhancement (Figs. 6e10)  Obliteration of the fat plane around the nerves including PPF (Figs. 11 and 12).  Enlargement and convexity of lateral cavernous sinus wall (Fig. 10).  Soft-tissue replacement of cerebrospinal fluid-filled Meckels cave (Fig. 10).  Muscular denervation: firstly oedema and enhancement, then atrophy (Figs. 5 and 12).

Muscular denervation Muscle denervation caused by nerve damage is a secondary sign of perineural spread. In the acute and subacute stages there is contrast enhancement and T2W and STIR hyperintensity secondary to muscular oedema.14,17,25,38 This can last up to a year. The chronic appearance is that of fatty replacement of muscle and muscular atrophy. Although CT can detect the chronic changes of denervation, MRI is required to detect the acute and subacute changes.39,40

Imaging pitfalls There are several conditions that may mimic tumour in the head and neck. These include infection, inflammation, trauma, vascular lesions, and haematoma (Fig. 13; Box 2).

Figure 8 (a) Axial T1W image of a patient with left parotid ACC showing enlargement of the left auriculotemporal nerve posterior to the mandibular ramus (long arrow) indicating tumour involvement. Note the two rootlets of the normal right auriculotemporal nerve are visible (short arrow). (b) Axial T1W post-gadolinium fat-suppressed MRI image of a different patient showing enlargement and enhancement of the right greater superficial petrosal nerve (GSPN) within the petrous temporal bone (arrow) coursing anterior and parallel to the carotid canal. Please cite this article in press as: Singh FM, et al., Patterns of spread of head and neck adenoid cystic carcinoma, Clinical Radiology (2015), http://dx.doi.org/10.1016/j.crad.2015.01.013

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Figure 9 T1W post-gadolinium fat-suppressed MRI images of the same patient as Fig. 8 with recurrent ACC of the hard and soft palate. (a) Axial image showing enlargement and enhancement of the left oculomotor nerve (long arrow) as it travels anteriorly to the cavernous sinus. Enhancing tissue is also seen in the left orbital apex and adjacent brain parenchyma indicating tumour infiltration (short arrow). (b) Coronal image showing tumour infiltration of the left oculomotor (short solid arrow), trigeminal (long solid arrow) and abducens nerves (short dashed arrow) and cranial nerves IX, X and XI entering the jugular foramen (long dashed arrow). Enhancing tumour is seen extending along the adjacent meninges (arrowheads).

There are segments of normal cranial nerves V and VII that can display enhancement on MRI in the absence of disease. This native enhancement is seen in some portions of the normal facial nerve: the proximal greater superficial petrosal nerve, the geniculate ganglion, and the tympanic and mastoid segments.20 This complicates the detection of perineural spread. Only enlargement of the facial nerve can be used as a reliable indicator of tumour at these locations, thus avoiding false positives due to native enhancement. The perineural venous plexus surrounding the trigeminal ganglion and proximal branches (V1, V2 and V3) can have a variable appearance. In some normal individuals, there is asymmetry in the venous plexus enhancement and

the nerve may not be visible at all as a separate structure. It is also suggested that occasionally the trigeminal ganglion itself and V2 and V3 can enhance independently of their venous plexus as a normal variant, although it is unclear whether this enhancement is real or apparent.41 There are several non-neoplastic aetiologies that disrupt the bloodebrain barrier causing segmental nerve enhancement. Inflammation, ischaemia, infarction, trauma, and demyelination can give false positives at MRI and should be considered.23 MRI may underestimate the extent of perineural spread due to microscopic foci of perineural tumour infiltration, which are below the resolution of MRI.14,20,22 A further

Figure 10 (a) Axial T1W post-gadolinium fat-suppressed MRI image showing enlargement and enhancement of the left cavernous sinus (long arrow) extending anteriorly through the left superior orbital fissure into the orbital apex (short arrow) indicating tumour infiltration. (b) Coronal T1W post-gadolinium fat-saturated MRI image of the same patient showing the normal, non-enhancing cerebrospinal fluid-filled Meckel’s cave on the right (short arrow). This is obliterated on the left with enlargement and enhancement of the trigeminal ganglion (long arrow). The left cavernous sinus is expanded with tumour. Please cite this article in press as: Singh FM, et al., Patterns of spread of head and neck adenoid cystic carcinoma, Clinical Radiology (2015), http://dx.doi.org/10.1016/j.crad.2015.01.013

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Figure 11 (a) Axial T1W MRI image of a patient with nasopharyngeal ACC. There is low-signal tumour invading the right pterygopalatine fossa (long solid arrow). The normal high-signal fat-filled pterygopalatine fossa is seen on the contralateral side (short solid arrow). Low-signal tumour infiltration is also seen in the right parapharyngeal fat (long dashed arrow) and the clivus and foramen lacerum (short dashed arrow).

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Figure 13 Coronal T1W post-gadolinium fat-suppressed MRI image showing an asymmetrical prominent pterygoid venous plexus within the left infratemporal fossa, which may mimic tumour infiltration.

Figure 12 (a) Coronal T1W post-gadolinium fat-suppressed MRI image of a patient with maxillary ACC showing tumour infiltration of the mandibular branch of the right trigeminal nerve (V3) as it travels through the foramen ovale (long arrow). Note the normal contralateral nerve with minimal enhancement of the perineural vascular plexus within the left foramen ovale (short arrow). The right pterygoid muscles enhance diffusely and avidly due to acute denervation (dashed arrow). (bec) Coronal T1W post-gadolinium fat-suppressed MRI images of a patient with ACC of the left paranasal sinuses. (b) There is gross tumour infiltration of the left foramen ovale (arrow) with obliteration of Meckel’s cave. (c) Volume loss and low signal fat replacement is seen in the left masseter muscle (white arrow) due to chronic denervation. The left pterygoid muscles are enhancing but reduced in volume in keeping with subacute denervation (black arrow). Please cite this article in press as: Singh FM, et al., Patterns of spread of head and neck adenoid cystic carcinoma, Clinical Radiology (2015), http://dx.doi.org/10.1016/j.crad.2015.01.013

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Box 2. Imaging pitfalls of perineural spread.  Non-neoplastic nerve enhancement mimicking perineural tumour spread secondary to: - Normal native nerve enhancement (Figs. 7 and 12) - Pathological enhancement (e.g., inflammation)  Skip lesions and resurfacing phenomenon due to foci of tumour below the resolution of the MRI scan.  Muscular enhancement and oedema due to denervation mimicking tumour infiltration (Fig. 12)

cause for MRI false negatives is the so-called “resurfacing phenomenon” whereby visible tumour resurfaces distal to a canal or foramen but is not visible within the bony confines due to nerve and tumour compression.14,20,42 The term “skip lesion” has been used to describe a macroscopically discontinuous tumour that can only be seen microscopically as continuous perineural invasion.23 Acute and subacute muscle denervation cause muscular enhancement and frequently a visible degree of increase in muscle bulk is seen due to oedema. These appearances can

cause confusion and mimic tumour infiltration. The chronic appearance is that of fatty atrophy.39,40

Distant metastases Metastases are rare at presentation but occur in over 50% of patients over the course of the disease (Figs. 14 and 15).5,14,15 Haematogenous metastases to lung and bone occur frequently3,12 and lymphatic spread to local lymph nodes is rare.5,6,43 PET-CT is used for detecting metastases when radical surgery is being considered. ACC has variable 2-[18F]-fluoro2-deoxy-D-glucose (FDG) uptake, but tends to be lower than other head and neck tumours.44 Perineural spread can be seen at PET-CT as linear or focal FDG uptake at expected sites of cranial nerve distribution such as the foramen ovale and Meckel’s cave.45

Conclusion Local invasion and perineural spread of head and neck ACC worsen prognosis and can alter the surgical options and

Figure 14 (a) Axial contrast-enhanced CT image through the upper abdomen showing multiple hypodense liver metastases (long arrows) and a solitary hypodense renal metastasis (short arrow) in a patient with nasopharyngeal ACC. (b) Axial contrast-enhanced CT image showing multiple lung metastases in a patient with submandibular salivary gland ACC. (c) Sagittal CT image of another patient with ACC showing widespread sclerotic bone metastases. Please cite this article in press as: Singh FM, et al., Patterns of spread of head and neck adenoid cystic carcinoma, Clinical Radiology (2015), http://dx.doi.org/10.1016/j.crad.2015.01.013

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Figure 15 FDG PET-CT images of a patient who had undergone left neck dissection 10 years prior for primary left submandibular ACC. (a) FDG PET MIP (maximum intensity projection) image shows left sternocleidomastoid muscle infiltration (long arrow) and bilateral lung metastases (short arrow). (b) Fused axial FDG PET-CT image at the level of the thyroid cartilage lamina showing FGD-avid tumour infiltration of the left strap muscles (arrow).

treatment regime. Detection on imaging is vital to allow the patient to undergo appropriate treatment. Perineural spread is frequently asymptomatic and under-reported by radiologists. Vigilant review of the cranial nerve pathways on imaging and good knowledge of skull base anatomy are essential.

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Patterns of spread of head and neck adenoid cystic carcinoma.

We present a review of head and neck adenoid cystic carcinoma (ACC). Imaging features of the primary tumour, patterns of locoregional spread, and dist...
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