PET-CT in Clinical Adult Oncology-V. Head and Neck and Neuro Oncology

Abstract

PET-CT is an advanced imaging modality with many oncologic applications, including staging, assessment of response to therapy, restaging, and longitudinal surveillance for recurrence. The goal of this series of six review articles is to provide practical information to providers and imaging professionals regarding the best use of PET-CT for specific oncologic indications, and the potential pitfalls and nuances that characterize these applications. In addition, key tumor-specific clinical information and representative PET-CT images are provided to outline the role that PET-CT plays in the management of oncology patients. Hundreds of different types of tumors exist, both pediatric and adult. A discussion of the role of FDG PET for all of these is beyond the scope of this review. Rather, this series of articles focuses on the most common adult malignancies that may be encountered in clinical practice. It also focuses on FDA-approved and clinically available radiopharmaceuticals, rather than research tracers or those requiring a local cyclotron. The fifth review article in this series focuses on PET-CT imaging in head and neck tumors, as well as brain tumors. Common normal variants, key anatomic features, and benign mimics of these tumors are reviewed. The goal of this review article is to provide the imaging professional with guidance in the interpretation of PET-CT for the more common head and neck malignancies and neuro oncology, and to inform the referring providers so that they can have realistic expectations of the value and limitations of PET-CT for the specific type of tumor being addressed.

Keywords: CNS lymphoma; FDG; PET; brain tumors; cervical esophageal cancer; encephalitis; head and neck cancer; leptomeningeal carcinomatosis; meningioma; salivary tumors; squamous cell carcinoma.

Figure 1

Inflammatory conditions of the head and neck that mimic tumor on FDG PET-CT. (a) Periodontal abscess, shown by a hypermetabolic inflammatory mass (white arrowhead) on the lingual side of an erosive osseous lesion of a tooth socket (white arrow); (b,c) right maxillary sinusitis, likely chronic because of neo osteogenesis (b, white arrowhead) with associated hypermetabolic lymphoid tissue in the base of the tongue (c, white arrow) and prominent hypermetabolic right cervical lymph nodes (c, white arrowheads).

Figure 2

Squamous cell carcinoma of the central base of tongue with extension into the oral tongue (solid white arrowhead) with bilateral hypermetabolic lymph nodes. The left level 2A node (solid white arrow) is clearly large and heterogeneously enhancing, consistent with tumor involvement. The right sided node (dashed arrow) is smaller but similarly hypermetabolic, and was benign at biopsy. There is considerable overlap in metabolic activity between benign/reactive and malignant nodes.

Figure 3

Complete metabolic and anatomic resolution of nasopharyngeal carcinoma. (a,b) Pre-treatment FDG PET-CT demonstrates hypermetabolic right nasopharyngeal mass (a, white arrow) and right pathologic cervical lymph nodes (b, white arrowheads); (c,d) post-treatment FDG PET-CT demonstrates complete anatomic and metabolic resolution of all sites of tumor.

Figure 4

Incomplete response to treatment. Axial fused FDG PET-CT images before (a) and after (b) chemoradiation therapy demonstrate a right base of tongue squamous cell carcinoma (arrow) and ipsilateral right cervical pathological lymph node (arrowhead) with decreased, but still pathologic in both size and activity, after therapy.

Figure 5

Early post-treatment inflammatory change. (a) Axial fused PET CT images prior to therapy demonstrate a hypermetabolic, enlarged pathologic cervical node (white arrowhead): (b) On the first post-treatment FDG PET-CT scan, the node has decreased in size and activity following but is still evident (white arrowhead) and has surrounding inflammatory changes and fat stranding; (c) Follow-up FDG PET-CT scan 3 months later shows complete resolution of the node and inflammatory stranding.

Figure 6

Muscle paralysis with contralateral increased metabolic activity in two patients. (a) Paralysis of the left vocal cord, which is patulous and low in metabolic activity (white arrow). There is compensatory contralateral increased activity in the right vocal cord and cricoarytenoid muscle (white arrowhead); (b) shown is a paralysis of the left hypoglossal nerve (CN 12) with low attenuation and hypometabolism of the left tongue musculature (white arrow), as well as compensatory increased activity in the right side of the tongue. Note area of recurrent tumor in the left neck (white arrowhead) along the expected course of CN 12.

Figure 7

Trans-spatial recurrent tumor on FDG PET-CT (white arrows) in a patient who has undergone prior laryngectomy and left radical neck dissection.

Figure 8

Perineural spread of tumor. (a) Hypermetabolic infiltrative tumor in the right parotid (white arrowhead, poorly differentiated carcinoma); (b–e) hypermetabolic tumor (white arrow) along the distribution of the right auriculotemporal nerve (branch of the mandibular nerve, V3); (f) extension of metabolically active tumor into the right foramen ovale (white arrow).

Figure 9

FDG PET-CT findings of perineural spread of tumor. (a) Small mildly hypermetabolic adenoid cystic carcinoma of the left sublingual gland (white arrow); (b–e) spread along the mylohyoid nerve, inferior alveolar nerve, and mandibular nerve (white arrowheads); (f) spread of tumor into the trigeminal cistern (Meckel’s cave) and into the middle cranial fossa, which is difficult to appreciate on FDG PET-CT (white arrowheads); (g) tumor is better defined by contrast-enhanced axial T1 with fat saturation MRI extending from the trigeminal cistern into the middle cranial fossa (g, white arrows).

Figure 10

Tumor invading the superior pterygopalatine fossa. (a) FDG PET-CT axial image shows hypermetabolic tumor in the pterygopalatine fossa, which is widened (white arrowheads). The tumor also invades the central skull base and nasopharyngeal soft tissues (white arrows). (b) The tumor extends intracranially into the cavernous sinus (white arrowhead), around the intracranial carotid artery, and enters the inferior orbital fissure (white arrow).

Figure 11

Squamous cell carcinoma of the oral tongue on FDG PET-CT. (a) Hypermetabolic tumor involves the left oral tongue (white arrowhead). (a,b) There is spread to the left floor of mouth musculature shown on both axial (b) and sagittal (c) imaging (white arrowheads). (b) There is also a left level 2A hypermetabolic cervical lymph node consistent with nodal spread of disease.

Figure 12

Squamous cell carcinoma of the oral cavity with bony involvement. (a) Soft tissue window FDG PET-CT demonstrates a hypermetabolic lesion of the left mandibular alveolar mucosa (white arrow). (b) Bone windows demonstrate destruction of the adjacent cortical bone at the mental foramen, consistent with bony involvement (white arrowhead).

Figure 13

Right tonsillar oropharyngeal squamous cell carcinoma. (a) A right palatine tonsillar hypermetabolic squamous cell carcinoma (white arrows). (b) There is an enlarged hypermetabolic right level 2 cervical lymph node consistent with tumor involvement ((b), white arrowhead).

Figure 14

Bilateral oral cavity squamous cell carcinoma of the tongue. (a) Right oral tongue squamous cell carcinoma (white arrow) and left glossotonsillar primary with spread into the oral tongue (white arrow); (b) There is spread to rounded hypermetabolic right anterior submandibular and bilateral level 2A cervical nodes (white arrowheads).

Figure 15

Hypopharyngeal squamous cell carcinoma. (a) Hypermetabolic tumor extends superiorly to the left superior aryepiglottic fold (white arrowhead). (b) The lesion is centered around the left pyriform sinus (white arrowhead) with involvement of a left level 2A hypermetabolic lymph node (white arrow). (c) Inferiorly, the tumor extends to the junction of the hypopharynx and cervical esophagus (white arrowhead) along the lateral wall of the hypopharynx at the level of the cricoid.

Figure 16

Cervical esophageal squamous cell carcinoma. (a,b) Axial and (c) sagittal FDG PET-CT images demonstrate a hypermetabolic cervical esophageal circumferential mass (white arrowheads) with adjacent hypermetabolic lymph nodes (white arrows).

Figure 17

Squamous cell carcinoma of the false cords. (a) A large tumor shown in axial (a), sagittal (b) and coronal (c) FDG PET-CT images (white arrows) involves the left false cord and extends across the anterior midline to involve and anterior aspect of the right false cord. The mass effaces the left pyriform sinus and extends to the base of the epiglottis.

Figure 18

Squamous cell carcinoma of the epiglottis shown on axial FDG PET-CT images. (a–c) A large hypermetabolic mass involves the entire epiglottis (white arrowheads); (b) The tumor fills the preepiglottic space (c), white arrowhead); (d) There is mild metabolic activity and thickening of the false cords (white arrow) that may be related to either tumor involvement or inflammation/edema; (e) The true cords are unremarkable.

Figure 19

Squamous cell carcinoma of the glottis (true cord). A hypermetabolic tumor of the true cords is shown on axial FDG PET-CT images. (a) The lesion involves the anterior commissure (white arrow); (b,c) The tumor involves the entire right true cord white arrowheads).

Figure 20

Squamous cell carcinoma of the subglottic larynx. Contrast-enhanced axial CT (a) and axial FDG PET-CT (b) images show a hypermetabolic soft tissue mass involving the anterior aspect of the subglottic larynx with anterior cricoid destruction (white arrowheads).

Figure 21

Sinonasal squamous cell carcinoma of the anterior nasal septum. (a) Axial FDG PET-CT image demonstrates a hypermetabolic tumor of the anteroinferior nasal septum (white arrowhead). (b) Sagittal FDG PET-CT image demonstrates that there is spread throughout the entire nose (white arrowheads).

Figure 22

Sinonasal undifferentiated carcinoma (SNUC). (a) An intensely hypermetabolic primary tumor in the right maxillary sinus on FDG PET-CT shows extension anteriorly into the pre-maxillary soft tissues (white arrow). (b) There are multiple pleural metastases ((b), white arrowheads) with a malignant right pleural effusion.

Figure 23

Esthesioneuroblastoma of the ethmoid sinus. (a,b) Mildly hypermetabolic tumor fills the ethmoid sinuses on axial FDG PET-CT images (white arrows); (c,d) The tumor extends through the cribriform plate into the anterior cranial fossa/brain (white arrowheads). Without contrast CT, the intracranial extension would be difficult to appreciate on FDG PET.

Figure 24

Non-Hodgkin lymphoma of the right parotid gland. On this axial FDG PET-CT image, diffuse large B-cell lymphoma completely fills the superficial (white arrow) and deep (white arrowhead) lobes of the right parotid gland.

Figure 25

Pleomorphic adenomas, small and large. (a) A small left parotid pleomorphic adenoma is strongly hypermetabolic (white arrow). (b,c) A large pleomorphic adenoma of the left parotid is low in metabolic activity on FDG PET-CT (white arrowheads), (b), but is typically bright on T2 MRI (white arrowheads), (c).

Figure 26

Carcinoma ex-pleomorphic adenoma (CXPA) of the lacrimal gland. (a) CXPA of the left lacrimal gland is mildly hypermetabolic (white arrows). (b) Tumor extends intraorbitally along the lateral orbital wall with medial displacement of the orbital contents.

Figure 27

Warthin tumor (papillary cystadenoma lymphomatosum). On axial FDG PET_CT, a Warthin tumor of the right parotid is a hypermetabolic nodule (white arrow).

Figure 28

Mucoepidermoid carcinoma (MEC). (a) Initial coronal FDG PET-CT image shows a hypermetabolic tumor in the right parotid gland (white arrow) with spread to an adjacent cervical lymph node (white dashed arrow). (b) Seven years after initial right neck dissection, there is recurrence in the deep lobe of the right parotid (white arrowhead). (c) Also 7 years after initial treatment, there are widespread systemic metastases to the bones (white arrowhead), liver (white dashed arrow) and left pleura (white arrow).

Figure 29

Adenoid cystic carcinomas (ACC). (a) ACC of the buccal surface is mildly hypermetabolic on FDG PET-CT (white arrowhead). (b,c) ACC of the trachea is also relatively mild in metabolic activity (white arrows).

Figure 30

Hypermetabolic thyroid nodule (incidentaloma). A hypermetabolic 1.4 cm nodule on FDG PET-CT ((a), white arrow) is lower in attenuation than surrounding thyroid tissue on CT ((b), white arrowheads). The American Thyroid Association recommends FNA for hypermetabolic thyroid nodules > 1 cm in diameter.

Figure 31

Recurrent differentiated thyroid cancer. Coronal (a) FDG PET, (b) fused FDG PET-CT, and (c) CT demonstrate a small hypermetabolic site of recurrent thyroid cancer along the left aspect of the trachea (white arrows) in a patient with a rising thyroglobulin following surgery and ¹³¹I NaI ablation for well-differentiated papillary thyroid cancer.

Figure 32

Anaplastic thyroid cancer. (a,b) At initial diagnosis, tumor is localized to the lower neck, as shown by (a) FDG PET MIP (black arrow) and (b) FDG PET-CT axial image (white arrow); 6 months later (c,d), after treatment for anaplastic thyroid cancer, the primary tumor has become smaller and partially cystic ((c), white arrows) but portions remain metabolically active. However, there is now widespread metastatic disease as shown by FDG PET MIP (d).

Figure 33

Recurrent medullary thyroid cancer. (a,b) FDG PET-CT axial images demonstrate a mild-moderately hypermetabolic mass (white arrowheads) in the left thyroid bed in a patient with a rising serum calcitonin level 5 years following total thyroidectomy for medullary thyroid cancer.

Figure 34

Limbic encephalitis. Patient presented with diplopia, dizziness, headaches, behavioral and memory disturbances. (a–c) Sagittal FDG PET-CT images show increased metabolic throughout the entirety of the hippocampus (white arrows). (d–f) Axial FDG PET-CT images show increased metabolic activity throughout the entire left hippocampus (white arrows). There is also decreased metabolic activity in the anterior left temporal lobe (white arrowhead). Limbic encephalitis can either be autoimmune or paraneoplastic in etiology.

Figure 35

Anti-NMDAR encephalitis. The patient presented with seizures and psychiatric disturbances. Anti-NDMAR Ab titers: serum 1:40, CSF 1:120. MRI imaging was unremarkable. Whole-body FDG PET-CT imaging was negative for sites of tumor involvement, so that the etiology was likely autoimmune. (a–c) Axial FDG PET images demonstrate scattered cortical areas of increased metabolic activity (black arrows) with global decreased metabolic activity within the posterior cerebrum (black arrowheads). (d–f) Fused axial FDG PET-CT images demonstrate similar findings to non-fused imaging, with scattered cortical areas of hypermetabolism (white arrows) and global decreased metabolic activity in the posterior cerebrum (white arrowheads). Anti-NMDAR encephalitis can be either paraneoplastic or autoimmune in etiology.

Figure 36

Mental status changes in a patient being treated for an underlying malignancy, proving to be herpes simplex encephalitis (HSE) at biopsy. (a–c) Increased metabolic activity in the left temporal lobe is typical for acute phase of HSE (black arrowheads). (d–f) Repeat PET-CT 6 months following recovery of HSE shows resultant decreased metabolic activity due to neuronal damage (black arrowheads). Viral encephalitis can mimic either paraneoplastic encephalitis or primary brain tumor on FDG PET.

Figure 37

Subacute stroke with subacute increased uptake of FDG may mimic brain tumor. (a) Acute stroke with hypoattenuation in the right temporal lobe on con-contrast-enhanced CT (white arrowheads). (b) Acute stroke on contrast-enhanced CT with decreased vascularity in area of right temporal lobe infarction (white arrowheads). (c) T2 MRI in acute stroke showing increased signal in right temporal lobe due to edema (white arrowheads). (d) Diffusion weighted MRI (DWI) image shows increased signal in area of the right temporal stroke in the same patient (white arrowheads). (e) Apparent diffusion coefficient (ADC) MRI map shows a corresponding area of decreased signal in the right temporal lobe in the same patient (white arrowheads). (f,g) FDG PET-CT scan in a subacute stroke (2 weeks after presentation, performed because of co-existing vulvar carcinoma) shows increased metabolic activity coinciding with the region of CT high-attenuation pseudolaminar necrosis in the right temporal lobe (white arrowheads).

Figure 38

Active seizure on FDG PET-CT in a patient with paraneoplastic hypercalcemia. (a) The MIP image of an FDG PET-CT demonstrates right hemispheric hypermetabolism (white arrows) in a patient with an active seizure (the patient was sedated for the exam). (b) An axial PET-CT image demonstrates right hemispheric heterogeneous activity due to the seizure activity (white arrows). Active seizure activity may mimic a tumor, and MRI and conventional imaging are critical in making the correct diagnosis.

Figure 39

Pituitary macroadenoma. (a) Coronal Gd+ T1 MRI and (b) coronal FDG PET-CT images demonstrate a sellar-suprasellar hypermetabolic and Gd-enhancing mass (white arrow), unchanged over several years. (c) Axial Gd+ T1 MRI and (d) axial FDG PET-CT images demonstrate a sellar-suprasellar hypermetabolic and Gd-enhancing mass (white arrow). The patient had a corresponding stable subtle bitemporal hemianopia due to optic chiasm mass effect.

Figure 40

High-grade glioma with low FDG uptake. (a,b) FDG PET-CT scan shows very low uptake in the enhancing mass, which was a high-grade glioma by biopsy. (c,d) Gd-enhanced T1 fat saturation axial MRI shows an enhancing mass adjacent to the posterior horn of the left lateral ventricle (white arrows). The patient was on high-dose steroids, although it was not clear whether this was the cause of the low metabolic activity in the tumor.

Figure 41

Diffuse large B-cell lymphoma. (a–d) Findings on MRI in an immunocompromised patient raise the question of infection (such as toxoplasmosis) versus CNS tumor, particularly lymphoma. (a,b) Multiple lesions are peripherally hypermetabolic on axial FDG PET-CT (white arrows) and were biopsy-proven to be DLBCL (c,d) Gd-enhanced fat saturation axial T1 MRI images show multiple ring-enhancing lesions (white arrows).

Figure 42

Primary CNS lymphoma. (a) Enhancing lesion in the right frontal lobe on axial contrast-enhanced Gad+ T1FS MRI, with surrounding edema and mass effect (arrowhead); (b) The lesion shows intense activity on axial fused FDG PET-CT (arrowhead). This was a biopsy-proven primary CNS lymphoma.

Figure 43

Brain metastases, isometabolic to normal brain cortex (melanoma). (a–e) Incremental axial FDG PET-CT images demonstrate some hypometabolism in areas of edema (white arrowhead) but multiple melanoma metastases to the brain are not resolved as having metabolic activity greater than that of normal brain parenchyma; (f–j) Incremental axial Gd-enhanced T1 MRI images demonstrate multiple enhancing brain nodules which were due to metastatic melanoma (white arrows).

Figure 44

Hypermetabolic brain metastases (breast cancer). (a–c) There are multiple intensely hypermetabolic nodules in the brain on axial fused FDG PET-CT images (white arrowheads). These were breast cancer metastases.

Figure 45

Hypothalamic metastasis from melanoma. (a–c) Sagittal, coronal and axial FDG PET-CT images demonstrate intensely hypermetabolic hypothalamic mass (white arrows). (d,e) Sagittal and coronal Gd-enhanced T1 MRI and (f) axial T2 MRI demonstrate a corresponding enhancing hypothalamic mass, proven at biopsy to be a melanoma metastasis. Although rare, metastases to the hypothalamic–hypophyseal axis do occur and have been described with melanoma [137,138].

Figure 46

Leptomeningeal carcinomatosis (breast cancer). (a) Sagittal FDG PET-CT shows hypermetabolism within the spinal canal due to leptomeningeal disease (white arrowheads); (b–d) Axial FDG PET-CT images show intense focal areas of increased metabolic activity are noted over the convexities of the brain (white arrows). (e–g) Axial Gd+ FST1 MRI images show intense enhancement at the sites of increased metabolic activity (white arrows) over the convexities, confirming leptomeningeal carcinomatosis.

Figure 47

Recurrent high-grade glioma following surgery and radiation. (a) T1 non-contrast-enhanced MRI demonstrates a high signal area (white arrow) that does not enhance and is consistent with a region of gliosis. (b) Gd enhanced T1 MRI shows enhancement of a nodular region anterior to the region of gliosis, at the margin of the resection cavity (white arrowhead). (c) Axial FDG PET image shows that the enhancing region on MRI demonstrates prominent metabolic activity, consistent with recurrent glioma (black arrowhead).

Figure 48

Radiation necrosis. (a) Axial Gd enhanced fat suppression T1 MRI shows a region of enhancement in the posterior right temporal lobe in a patient with a high-grade glioma 8 weeks following radiation treatment (white arrow). (b) The region shows low activity on axial FDG PET (black arrow), consistent with radiation necrosis. (c) Fused axial PET-MRI images help localize the region of interest precisely (white arrow).

Figure 49

Meningioma. (a) Axial fused FDG PET-CT image demonstrates a right posterior fossa hypometabolic enhancing mass with broad-based abutment of the basion (white arrowhead). (b) Axial PET only image demonstrates hypometabolism of the mass (white arrowhead), compared to adjacent normal cerebellum, an indicator that this is a lower grade meningioma. (c) Axial contrast-enhanced CT confirms the enhancing mass, typical in appearance for a meningioma (white arrowhead).

Figure 50

Meningioma on ⁶⁸Ga DOTATATE (NETSPOT^®) PET-CT. An axial NETSPOT^® PET-CT performed with contrast-enhanced CT demonstrates a strongly PET-positive mass in the medial middle cranial fossa, corresponding to a contrast enhancing soft tissue mass with broad-based abutment of the sphenoid bone, typical in appearance for a meningioma.

Figure 51

Meningioma on ⁶⁴Cu DOTATATE (Detectnet^®) PET-CT. (a) An axial Gd+ fat saturation T1 MRI image shows bilateral enhancing masses in the cavernous sinuses (white arrowheads). (b) ⁶⁴Cu DOTATATE (Detectnet^®) PET-CT demonstrates concordant increased uptake in the meningioma in the bilateral cavernous sinus (white arrowhead).

Figure 52

Meningioma on ¹⁸F fluciclovine (Axumin^®) PET-CT. (a) An Axumin^® PET-CT performed for evaluation of biochemically recurrent prostate cancer, incidentally noted to have an intensely PET-positive right frontal dural-based mass (white arrowhead). (b) This mass showed homogenous enhancement on Gd+ T1 MRI, arising from the dura, typical in appearance for a meningioma (white arrowhead).