NASOPHARYNGEAL CARCINOMA

STAGING BY COMPUTED TOMOGRAPHY AND

MAGNETIC RESONANCE IMAGING

Thesis

Submitted to the Faculty of Medicine

Alexandria University

In partial fulfillment of the requirements for the degree of

Master of Radiodiagnosis

By

Islam Mohamed El Gezeiry

MBBCh, University of Alexandria

Faculty of Medicine

Alexandria University

2014

NASOPHARYNGEAL CARCINOMA

STAGING BY COMPUTED TOMOGRAPHY AND

MAGNETIC RESONANCE IMAGING

Presented by

Islam Mohamed El Gezeiry

For the Degree of

Master of Radiodiagnosis

Examiners Committee:

Approved

Prof. Dr. Shadia Abou Seif Helmy

Professor of Radiodiagnosis

Faculty of Medicine

University of Alexandria

Prof. Dr. Mahmoud Lotfy El-Sheikh

Professor of Radiodiagnosis

Faculty of Medicine

University of Alexandria

....

Prof. Dr. Ahmed Abdel Khalek Abdel Razek

Professor of Radiodiagnosis

Faculty of Medicine

University of Mansoura

Date: / /

SUPERVISORS

Prof. Dr. Shadia Abou Seif Helmy

Professor of Radiodiagnosis

Faculty of Medicine

University of Alexandria

Prof. Dr. Mohamed Basiouny Atalla

Professor of Otorhinolaryngology

Faculty of Medicine

University of Alexandria

.

Ass. Prof. Dr. Mohamed Eid Ibrahim

Assistant Professor of Radiodiagnosis

Faculty of Medicine

University of Alexandria

ACKNOLEDGEMENT

Praise to Allah, the Most Gracious and the Most Merciful

Who Guides me to the right way

First and foremost, my thanks are directed to Professor Dr.

Shadia Abou Seif Helmy, Professor of Radiodiagnosis, Faculty of

Medicine, University of Alexandria, for her unlimited help and

continuous insistence on perfection, without her constant supervision, this

thesis could not have achieved its present form.

Many thanks and appreciation to Ass. Prof. Dr. Mohamed Eid

Ibrahim, Assistant Professor in Radiodiagnosis, Faculty of Medicine,

University of Alexandria, for his supervision and encouragement and for

his kindness throughout the work.

I am greatly indebted to Prof. Dr. Mohamed Basiouny Atalla,

Professor of Otorhinolaryngology, Faculty of Medicine, University of

Alexandria, for fruitful suggestions and wise guidance created this thesis.

Last but not the least, special thanks to my parents and my wife

for their continuous encouragement and kind support during the progress

of this work, to whom I owe a lot of things more than I can count.

CONTENTS

LIST OF ABBREVIATIONS -------------------- I

LIST OF TABLES---------------------------------- II

LIST OF FIGURES-------------------------------- III

INTRODUCTION----------------------------------- 1

AIM OF THE WORK------------------------------ 34

PATIENTS AND METHODS--------------------- 35

RESULTS--------------------------------------------- 38

DISCUSSION---------------------------------------- 69

SUMMARY------------------------------------------ 84

CONCLUSION-------------------------------------- 87

REFERENCES-------------------------------------- 88

ARABIC SUMMARY-----------------------------

Abbreviations

i

ABBREVIATIONS

NPC Nasopharyngeal Carcinoma

EBV Epstein-Barr virus

PPS Parapharyngeal space

PMS Pharyngeal mucosal space

MS Masticator space

PS Parotid space

CS Carotid space

BS Buccal space

RPS Retropharyngeal space

DS Danger space

PVS Perivertebral space

LRP Lateral retropharyngeal

LN Lymph nodes

WHO World Health Organization

AJCC American Joint Committee on Cancer

CN Cranial nerve

RT Radiotherapy

IMRT Intensity Modulated Radiotherapy

CRT Combined chemotherapy and radiotherapy

RPLN Retropharyngeal lymph nodes

PPF Pterygopalatine fossa

PNS Perineural spread

ii

LIST OF TABLES

Table Page

(1) Distribution of studied cases according to demographic data

38

(2) Distribution of studied cases according to side involved 38

(3) Distribution of studied cases according to neck spaces involved

38

(4) Distribution of studied cases according to extension pattern

39

(5) Distribution of studied cases according to paranasal sinus involvement

39

(6) Distribution of studied cases according to pterygopalatine fossa involvement

40

(7) Distribution of studied cases according to skull base bone involvement pattern

40

(8) Distribution of studied cases according to foramina 40

(9) Distribution of studied cases according to perineural spread

41

(10) Distribution of studied cases according to lymph nodal involvement

41

(11) Distribution of studied cases with cervical nodal metastases according to criteria of involvement

41

(12) Distribution of studied cases according to primary tumor T-stage

42

(13) Distribution of studied cases according to lymph nodes involvement N-stage

42

(14) Distribution of studied cases according to TNM stage 42

iii

LIST OF FIGURES

Figure Page

(1) Graphic of the nasopharyngeal mucosal space seen from

behind.

3

(2) A graphic of skull base from below shows spaces of

suprahyoid neck relationships to skull base with emphasis on

the pharyngeal mucosal space.

4

(3) Axial graphic of the nasopharyngeal mucosal space. 4

(4) Mid-line sagittal graphic of the nasopharynx. 5

(5) Lateral radiograph of the nasopharynx showing enlarged

adenoids.

5

(6) A graphic showing the lateral wall structures of the

nasopharynx.

6

(7) Spaces related to the nasopharynx. 8

(8) A graphic of the neck as seen from left anterior view showing specific

margins of the levels of the imaging-based classification for the lymph

nodes of the neck

10

(9) A lateral radiograph of mildly enlarged adenoid. 12

(10) The superior end of the para-pharyngeal space just before it

abuts the skull base.

13

(11) Axial T2w image at the level of the opening of the Eustachian

tube.

15

(12) Axial T1w image of the pharyngeal mucosal space at the

level of the Eustachian tube opening.

15

(13) Sagittal T1w image of the pharynx. 16

(14) Coronal enhanced fat-saturated T1 MR image. 16

(15) Coronal enhanced fat-saturated T1w MR Image. 17

iv

Figure Page

(16) Axial T2w image of the nasopharynx with demonstration of

the related spaces.

17

(17) Shaded triangular area corresponding to the supraclavicular

fossa used in staging carcinoma of the nasopharynx.

22

(18) (Right)Axial T2wI MR shows large right NP mass.

(Left) Axial bone CT showing enlarged right foramen ovale.

24

(19) Patient presenting with a left nasopharyngeal tumor. 25

(20) Axial TSE T2-weighted image showing left nasopharyngeal

tumor extending to the pterygo-palatine fossa.

26

(21) Contrast-enhanced SE T1-weighted MR images with fat

saturation illustrating different pathways of extension in a

patient suffering nasopharyngeal tumor.

27

(22) Contrast-enhanced T1-weighted MR images in a patient

presenting with direct lateral extension through the

pharyngobasilar fascia to the prestyloid compartment of the

parapharyngeal space, and the infratemporal fossa, with

infiltration of the pterygoid muscles.

28

(23) Spread of an advanced nasopharyngeal tumor. 29

(24) (a) Non-enhanced T1-weighted MR image without fat

saturation of a nasopharyngeal tumor infiltrating the clivus

bone marrow.

(b) Enhanced T1-weighted image with fat saturation, the

tumor extends laterally to the jugular foramen and the

hypoglossal canal.

29

v

Figure Page

(25) Patient presenting with a nasopharyngeal tumor (a) revealed

a serous otitis. (b) Posterior spread to the retropharyngeal

space and parapharyngeal space. (c) A left retropharyngeal

node and inferior extension to the oropharynx.

30

(26) (a) CT images illustrate a nasopharyngeal tumor extending to

the foramen lacerum.

(b) Note the enlargement of the foramen lacerum.

31

(27) (a) CT depicts small skull base erosions.

(b) MRI non-enhanced T1-weighted sequence without fat

saturation shows infiltration of sphenoid bone marrow.

31

Introduction

1

INTRODUCTION

Epidemiology (1)

Nasopharyngeal carcinoma (NPC) is a rare malignancy in most

parts of the world, with an incidence well under 1 per 100,000 person-

years. Populations with elevated rates include the natives of Southeast

Asia, the natives of the Arctic region, and the Arabs of North Africa

and parts of the Middle East. (1)

Sex and Age Distributions:

In almost all populations, the incidence of NPC is 2- to 3- folds

higher in males than in females. (1)

In most low-risk populations, NPC incidence increases

monotonically with increasing age. In contrast, in high-risk groups, the

incidence peaks around ages 50 to 59 years and declines thereafter.

Risk factors:

1. Epstein-Barr virus:

Primary EBV infection is typically subclinical; the virus is

associated with later development of several malignancies,

including NPC. (2)

NPC patients were found to express antibodies

against EBV. Antibody against EBV capsid antigen is now

established as the basis of a screening test for NPC in high-risk

populations. (3-8)

Introduction

2

2. Salt-Preserved Fish and Other Foods:

NPC risk is also elevated in association with salt preserved

fish and other preserved food items, including meats, eggs, fruits,

and vegetables (excluding type I NPC). (9)

3. Tobacco, and Other Smoke:

The majority of case-control studies examining cigarette

smoking and risk of NPC in a variety of populations reported an

increased risk of 2- to 6-fold. In one U.S. study, an estimated two

thirds of type I NPC was attributable to smoking, but risk of type II

or III NPC was not associated with smoking. (10-20)

4. Occupational Exposures:

Occupational exposure to fumes, smokes, dusts, or

chemicals overall was associated with a 2- to 6-folds higher risk of

NPC in some studies. (15, 18, 21, 22)

5. Other Exposures:

Most studies investigating prior chronic ear, nose, throat, and

lower respiratory tract conditions found that they approximately

doubled the risk of NPC. (11-13)

6. Familial Clustering:

Familial aggregation of NPC has been widely documented in

high-incidence, intermediate-incidence, and low-incidence

populations. (23-39)

Introduction

3

ANATOMY OF THE NASOPHARYNX AND

RELATED SPACES (40-42)

The nasopharynx extends from the base of the skull to the lower

border of the soft palate. The rigid pharyngobasilar fascia keeps it from

collapsing at the back and sides. At the front the upper part communicates

with the nose through the choanae, while below this the soft palate forms

its anterior wall. The space between the lower border of the soft palate

and the posterior pharyngeal wall through which the nasopharynx joins

the oral part of the pharynx is the oropharyngeal isthmus. The soft palate

becomes a mobile floor, like a trap door, when elevated during

swallowing to meet the posterior wall, so closing the isthmus. (43)

The nasopharynx communicates anteriorly with the posterior nasal

choanal openings and downward with the oropharynx. (Fig. 1)

Fig. 1 Graphic of the nasopharyngeal mucosal space/surface seen from behind shows

communication of the nasopharyngeal mucosal space anteriorly with the posterior

nasal choanal openings. (41)

The roof and posterior margins are formed by the sphenoid bone,

the clivus and the insertion of the prevertebral muscles into the skull base.

Introduction

4

Fig. 2 A graphic of skull base from below shows spaces of suprahyoid neck

relationships to skull base with emphasis on the pharyngeal mucosal space. Notice the

pharyngeal mucosal space abuts a broad area of the sphenoid and occipital bones. The

foramen lacerum, the cartilaginous floor to the anteromedial horizontal petrous

internal carotid artery canal, is within this abutment area. Malignant tumors of the

nasopharyngeal mucosal space can access the intracranial compartment via the

foramen lacerum. (41)

Fig. 3 Axial graphic of the nasopharyngeal mucosal space (in blue) shows the

superior pharyngeal constrictor and levator veli palatine muscles are within the space.

The middle layer of the deep cervical fascia provides a deep margin to the space. The

retropharyngeal space is behind and the parapharyngeal space is lateral to the

pharyngeal mucosal space. (41)

Introduction

5

This roof shows downward slopping and is formed, cranially-to-

caudally, by the basisphenoid, the basiocciput, and the anterior aspect of

the first two cervical vertebrae. On this wall a prominence produced by a

mass of lymphoid tissue, more prominent in childhood, is known as

pharyngeal tonsils (adenoids). (40)

(Fig. 4 & Fig. 5)

Fig. 4 Mid-line sagittal graphic of the nasopharynx.

Fig. 5 Lateral radiograph of the nasopharynx showing enlarged adenoids. (44)

Prominent adenoids

Introduction

6

The lateral margins are made up by the pharyngeal constrictors and

the torus tubaris, in the center of which is the opening of the Eustachian

tube. (Fig. 4 & Fig. 6) The Eustachian tube enters the nasopharynx

through the sinus of Morgagni, a defect in the anterior portion of the

pharyngobasilar fascia, which is above the superior pharyngeal

constrictor muscle and along the upper posterior border of the medial

pterygoid plate. The levator veli palatini muscle also enters through the

sinus of Morgagni.

Fig. 6 A graphic showing the lateral wall structures of the nasopharynx. (45)

Behind the ostium of the Eustachian tube is a deep recess, the

pharyngeal recess (fossa of Rosenmller). The fossa of Rosenmller is

the most common site of origin in nasopharyngeal carcinoma (NPC).

The inverted J-shape of the torus tubaris explains why the fossa of

Rosenmller appears posterior (on axial images) and superior (on coronal

images) to the Eustachian tube orifice.

Introduction

7

The inferior margin of the nasopharynx is the level of the hard

palate and Passavants muscle. This muscle is composed of fibers that

arise laterally from the palatopharyngeus muscle and the lateral aspect of

the posterior border of the hard palate. The fibers encircle the pharynx

inside the superior constrictor muscle.

The lateral nasopharyngeal walls are supported by the margins of

the superior constrictor muscle and the pharyngobasilar fascia.

Spaces related to the nasopharynx

In the suprahyoid neck, three layers of deep cervical fascia are

detected. These fascias are: (41)

1- Superficial layer (investing fascia)

2- Middle layer (buccopharyngeal fascia)

3- Deep layer (prevertebral fascia)

Spaces related to the nasopharynx are defined by these three layers

of deep cervical fascia. (Fig. 7)

Introduction

8

Fig. 7 (PPS) parapharyngeal space, (PMS) pharyngeal mucosal space, (MS)

masticator space, (PS) parotid space, (CS) carotid space, (BS) buccal space, (RPS)

retropharyngeal space, (DS) danger space, (PVS) perivertebral space. (41)

1. Parapharyngeal space (41)

A slit-like space lateral to the nasopharynx extending down from

the base of the skull. Potential space filled with loose connective tissue.

The space is pyramidal in shape with apex directed towards the lesser

cornu of the hyoid bone and the base towards the skull base. It extends

from skull base to mid-oropharynx. It is lined medially by the superior

constrictor muscles of the pharynx, tensor and levator veli palatini

muscles. Laterally is lined by the mandible, the deep part of the parotid

gland, and medial pterygoid muscle. Anteriorly lying is the buccinator

muscle, the pterygoid, and the mandible. Posteriorly is the carotid sheath.

The parapharyngeal space contains fat, ascending pharyngeal and internal

maxillary arteries, pharyngeal venous plexus, and branches of the

mandibular nerve.

Introduction

9

2. Retropharyngeal space and the prevertebral spaces (41)

Lie between the nasopharynx and the vertebral bodies. The

retropharyngeal space extends as a potential space from the skull base to

about the level of T4 vertebral body and it serves as a conduit through

which infections spread from the neck to the mediastinum. It contains fat

and lymph nodes (lateral nodes of Rouvier and medial nodes).

3. Nasopharyngeal masticator space (41)

Lies lateral to the nasopharynx behind the posterior wall of the

maxilla and extends from the base of the skull to the hyoid bone. It

contains medial and lateral pterygoid muscles. No fascia defines this

space which was previously named as infratemporal fossa. This term was

used to describe the area between the pterygopalatine fossa and

zygomatic arch. Medial to this, the roof is formed by the inferior surface

of the middle cranial fossa and is pierced by the foramen ovale and

foramen spinosum.

Lymphatic drainage of the nasopharynx

Lymphatic drainage is abundant in the nasopharynx, as evidenced

by the high rate of nodal metastases found by the time of diagnosis of

nasopharyngeal carcinomas. Three main groups of submucosal collecting

pathways drain the pharynx, the superior, the middle, and the inferior

pathways. The superior pathway drains the oropharynx, soft palate,

Eustachian tube, fossa of Rosenmller, tympanic cavity, and nasal fossae.

(45)

Introduction

10

Fig. 8 A graphic of the neck as seen from left anterior view. Drawing shows specific

margins of the levels of the imaging-based classification for the lymph nodes of the

neck. Note that the line of separation between levels I and II is the posterior margin of

the submandibular gland. Separation between levels II and III and level V is the

posterior edge of the sternocleidomastoid muscle. The line of separation between

levels IV and V is the oblique line extending from the posterior edge of the

sternocleidomastoid muscle to the posterior edge of the anterior scalene muscle.

Posterior edge of internal jugular vein separates level IIA and IIB nodes. Carotid

arteries separate levels III and IV from level VI. Top of manubrium separates levels

VI and VII. (46, 47)

Within the retropharyngeal space there are lateral retropharyngeal

(LRP) lymph nodes of Rouvire. These nodes are the first nodes in the

lymphatic drainage of the nasopharynx and maybe identified as discrete

3-5 mm nodules. (48)

Introduction

11

The adenoids, or pharyngeal tonsils, are lymphatic tissue located in

the midline roof of the nasopharynx. Prominent adenoids are typically

present in children, and of such adenoids are not identified, the patient is

either in an immune deficiency state or has immune deficiency syndrome.

The maximal size of the adenoids occurs at about 5 years of age, around

the time of puberty, gradual adenoidal involution normally begins. The

majority of individuals have lost most this adenoidal tissues by 30 years

of age. (49-51)

Introduction

12

RADIOLOGICAL ANATOMY OF THE

NASOPHARYNX (41, 52)

Plain X-ray film (48)

Fig. 9 A lateral radiograph of mildly enlarged adenoid. (48)

Conventional radiographs are used to evaluate patients with stridor,

suspected retropharyngeal abscess or adenoid hypertrophy.

Lateral soft tissue neck radiography may be helpful in making the

diagnosis of nasopharyngeal masses. Perform the study during inspiration

with neck held in normal extension. (53)

The posterior wall of the pharynx forms a soft-tissue shadow

curving posteroinferiorly below the body of the sphenoid and anterior to

the cervical vertebrae. This shadow thins as it passes down anterior to the

upper cervical vertebrae, measuring 3mm anterior to C4. Below this the

wall is thicker but should not exceed the AP diameter of the cervical

Introduction

13

vertebrae. In children, lymphoid tissue results in a relatively thicker

posterior wall, measuring up to 5 mm anterior to C4 and up to 12 mm

anterior to C6 (Fig. 9). (48)

Widening of the soft tissues observed between the radiolucent

airway and the spine is pathologic until otherwise proven.

CT anatomy of the nasopharynx (41)

Axial contrast enhanced CT (CECT) of the nasopharynx:

Fig. 10 The superior end of the parapharyngeal space just before it abuts the skull

base, Notice the 4 major spaces surrounding the parapharyngeal space, the pharyngeal

mucosal, masticator, parotid and carotid spaces. (41)

CT evaluation of the nasopharynx is achieved with axial images

with the patient lying supine. The head should be aligned carefully with

the cranio-caudal axis, usually with the hard palate perpendicular to the

table top and a scan plane parallel to the inferior orbital meatal plane.

Poor positioning may result in an appearance that either simulates

pathology or occasionally make pathology difficult to see. (54)

Introduction

14

At CT the tissue density of the fascia itself is inseparable from that

of the adjacent musculature. The normal fat content of surrounding

spaces compounded by associated muscle atrophy in the elderly patients

will produce low density regions permitting a CT identification of the

fascial planes. (48)

The fat content of the paranasopharyngeal space allows one to

easily identify it as a low density tissue plane lying between the pterygoid

and pharyngeal musculature. Inferiorly the buccopharyngeal fascia is

continuous with the covering of the nasopharynx and esophagus. The

infratemporal fossa lies lateral to the paranasopharyngeal space. The

infratemporal fossa is bounded laterally by the zygomatic arch. Within

this space is most of the mandible, pterygoid, masseter, and parts of the

temporalis muscle and deep lobe of the parotid gland. (42, 55)

Other spaces defined by these fascial planes are important because

their contents determine the cell of origin of some tumors. A potential

space, the retropharyngeal space, exists between the pharyngobasilar

fascia and the prevertebral fascia. This space contains the chains of lymph

nodes lying to either side of the midline posteriorly. (42)

Laterally the carotid sheath forms a posterolateral boundary to the

retropharyngeal space. Within the carotid sheath lie the carotid vessels,

sympathetic chains, and the vagus and proximal parts of XI and XII

cranial nerves together with major deep lymphatic chains intimately

associated with the jugular vein. (42)

Introduction

15

Normal MRI anatomy of the nasopharynx (41)

The routine MR examination after obtaining scout images, sagittal,

axial and coronal T1-weighted images, and axial T2-weighted images,

with post-contrast (gadolinium-DTPA) injection T1-weighted images are

obtained. Comparison of the pre- and post-contrast images is made to

determine the areas of enhancement and to differentiate these areas from

fat.

Axial T2w Image of the nasopharyngeal mucosal space: (41)

Fig. 11 Axial T2w image at the level of the opening of the Eustachian tube

Axial T1w image of the nasopharyngeal mucosal space: (49)

Fig. 12 Axial T1w image of the pharyngeal mucosal space at the level of the

Eustachian tube opening.

Introduction

16

Sagittal T1w image of the pharynx:

Fig. 13 Sagittal T1w image of the pharynx (48)

Coronal T1w images of the nasopharynx: (41)

Fig. 14 Coronal enhanced fat-saturated T1 MR image shows the pharyngeal mucosal

space surface enhances.

1. Soft palate 2. Adenoids 3. Middle turbinate 4. Inferior turbinate 5. Hard palate 6. Intrinsic muscle of

tongue

7. Genioglossus 8. Mandible 9. Myelohyoid muscle 10. Hyoid bone 11. Epiglottis 12. Vocal cord 13. Thyroid cartilage 14. Nasopharynx 15. Oropharynx 16. Corniculate cartilage 17. Arytenoid cartilage 18. Cricoid cartilage

1

2

Introduction

17

Fig. 15 Coronal enhanced fat-saturated T1w MR image reveals the enhancing sheet of

mucosa with the torus tubarius (cartilaginous Eustachian tube) and lateral pharyngeal

recess.

Fig. 16 Axial T2w image of the nasopharynx with demonstration of the related

spaces. (41)

The superficial nasopharyngeal landmarks and deep fascial planes

of the nasopharynx are normally bilaterally symmetrical. The most

prominent of these is the torus tubaris, the cartilaginous part of the

Eustachian tube, usually seen on MR as a medium- to high-intensity

protuberance projecting into the aerated nasopharyngeal cavity. (42)

Introduction

18

In the mid- to upper nasopharynx, the tensor veli palatini and

levator veli palatini muscle bundles are routinely shown by MR as they

descend from their origin at the base of the skull to their insertion in the

soft palate. At the transition from the nasopharynx to the oropharynx, the

soft palate, tensor and levator palate, and pharyngeal constrictor muscles

blend together, producing a low-intensity signal which surrounds the

airway. (42)

Although the tonsils may normally be quite large, they should not

cause a mass effect involving the airway or deep soft tissue planes. A U-

shaped ring of high-intensity tissue near the base of the tongue,

corresponding to the lingual tonsil, is also routinely demonstrated on long

TR sequences. (56)

Below the nasopharyngeal mucosa and pharyngobasilar fascia,

symmetrical fatty parapharyngeal spaces extend bilaterally from the base

of the skull to the oropharynx. (42)

Introduction

19

PATHOLOGY OF THE NASOPHARYNGEAL

CARCINOMA

Normal histology of the nasopharynx

The anterior and cranial portions of the nasopharynx are lined by

respiratory mucosa with ciliated columnar epithelium with goblet cells

and foci of metaplastic squamous epithelium. Squamous mucosa

predominates in the lower nasopharynx adjacent to the oropharynx. Small

seromucinous glands and aggregates of lymphoid tissue are present in the

submucosa throughout the nasopharynx as a normal finding without

qualifying as chronic inflammation. (57)

Pathology of nasopharyngeal carcinoma (NPC)

Three subtypes of NPC are recognized in the World Health Organization

(WHO) classification 2005: (58-60)

1. Keratinizing squamous cell carcinoma (type I)

2. Non-keratinizing carcinoma:

a) undifferentiated (type II)

b) differentiated (type III)

3. Basaloid squamous cell carcinoma

Most cases in childhood and adolescence are type III, with a few

type II cases. Type II and III are associated with elevated Epstein-Barr

virus titers, but type I is not. Types II and III may be accompanied by an

inflammatory infiltrate of lymphocytes, plasma cells, and eosinophils,

which are abundant, giving rise to the term lymphoepithelioma. (61, 62)

Introduction

20

Staging

The tumor, node, metastasis (TNM) classification of the American

Joint Committee on Cancer is usually used to determine the tumor staging

This latest TNM classification (AJCC 7th

ed.) takes into account Hos

modifications for NPC which utilizes the prognostic importance of

affected nodes extending into the lower cervical and supraclavicular

areas. (63)

Definition of TNM

Primary Tumor (T)

TX Primary tumor cannot be assessed

T0 No evidence of primary tumor

Tis Carcinoma in situ

T1 Tumor confined to the nasopharynx, or tumor extends to oropharynx

and/or nasal cavity without parapharyngeal extension*

T2 Tumor with parapharyngeal extension*

T3 Tumor involves bony structures of skull base and/or paranasal

sinuses

T4 Tumor with intracranial extension and/or involvement of cranial

nerves, hypopharynx, orbit, or with extension to the infratemporal

fossa/masticator space

*Note: Parapharyngeal extension denotes posterolateral infiltration of tumor.

Introduction

21

Regional Lymph Nodes (N)

The distribution and the prognostic impact of regional lymph nodes

spread from nasopharynx cancer, particularly of the undifferentiated type,

are different from those of other head and neck mucosal cancers and

justify the use of a different N classification scheme.

NX Regional lymph nodes cannot be assessed

N0 No regional lymph node metastasis

N1 Unilateral metastasis in cervical lymph node(s), 6 cm or less

in greatest dimension, above the supraclavicular fossa,

and/or unilateral or bilateral, retropharyngeal lymph nodes,

6 cm or less, in greatest dimension*

N2 Bilateral metastasis in cervical lymph node(s), 6 cm or less

in greatest dimension, above the supraclavicular fossa*

N3 Metastasis in a lymph node(s)* >6 cm and/or to

supraclavicular fossa*

N3a Greater than 6 cm in dimension

N3b Extension to the supraclavicular fossa**

*Note: Midline nodes are considered ipsilateral nodes.

**Note: Supraclavicular zone or fossa is relevant to the staging of

nasopharyngeal carcinoma and is the triangular region originally

described by Ho. It is defined by three points (Fig. 17):

1. The superior margin of the sternal end of the clavicle.

2. The superior margin of the lateral end of the clavicle.

3. The point where the neck meets the shoulder.

Note that this would include caudal portions of levels IV and VB. All

cases with lymph nodes (whole or part) in the fossa are considered N3b.

Introduction

22

Fig. 17 Shaded triangular area corresponding to the supraclavicular fossa used in

staging carcinoma of the nasopharynx. (64)

Distant Metastasis (M)

M0 No distant metastasis

M1 Distant metastasis

Stage grouping

Stage 0 Tis N0 M0

Stage I T1 N0 M0

Stage II T1

T2

T2

N1

N0

N1

M0

M0

M0

Stage III T1

T2

T3

T3

T3

N2

N2

N0

N1

N2

M0

M0

M0

M0

M0

Stage IVA T4

T4

T4

N0

N1

N2

M0

M0

M0

Stage IVB Any T N3 M0

Stage IVC Any T Any N M1

Introduction

23

Presentation (41)

Early stage NPC is difficult to diagnose clinically because of its

hidden localization in the nasopharynx, and most patients present with

advanced stage of the disease.

Asymmetric neck swelling due to lymphadenopathy.

Nasal symptoms: Epistaxis, bloody, rhinorhea, nasal

obstruction.

Ear symptoms: infection (Recurrent otitis media), deafness,

and tinnitus.

Ophthalmic symptoms: Diplopia, visual loss, squint, Ptosis.

Headache.

Blood in saliva.

Facial numbness.

Cranial nerve palsies; CN 9-12.

Introduction

24

IMAGING OF THE NASOPHARYNGEAL

CARCINOMA

Fig. 18 (Right) Axial T2w MR image shows large right NP mass, extending into

pterygoid muscle (arrow), & posterior to surround ICA (open arrow). Mastoid fluid

(curved arrow) due to Eustachian tube obstruction. (Left) Axial bone CT image

showing enlarged right foramen ovale (arrow) from perineural V3 NPC spread with

adjacent skull base destruction (open arrows). (Curved arrow) normal foramen ovale.

(41)

Aggressive mass centered in lateral pharyngeal recess of the

nasopharynx (fossa of Rosenmller) with deep extension and cervical

adenopathy. It arises from the lateral nasopharynx + posterolateral nasal

cavity. It is usually several centimeters when diagnosed. (41)

Morphology:

Poorly marginated nasopharyngeal mucosal space mass with deep

extension and invasion. (41)

Introduction

25

Extension patterns of the nasopharyngeal carcinoma: (65, 66)

As explained, nasopharyngeal tumors spread along well-defined routes.

1. Anterior spread

Nasopharyngeal tumors often spread to the nasal fossa, which is

not separated from the nasopharynx by any anatomic barrier (Fig. 19).

From the nasal fossa, the tumor may easily infiltrate the pterygopalatine

fossa through the sphenopalatine foramen (Fig. 20). The earliest sign of

involvement of the pterygopalatine fossa is replacement of its normal fat

content by tumoral tissue (Fig. 21). (66)

Fig. 19 Patient presenting with a left nasopharyngeal tumor (anterior arrow), showing

intermediate signal intensity on T2-weighted MR image. Note the anterior extension

to the left choana (arrowhead). Associated serous otitis (posterior arrow). (66)

Introduction

26

Fig. 20 Axial TSE T2-weighted image showing left nasopharyngeal tumor extending

to the pterygopalatine fossa (arrow) (66)

Once tumor gains access to the pterygopalatine fossa, it can spread

into (Fig. 21): (66)

o The foramen rotundum along the maxillary nerve (V2)

o The inferior orbital fissure and further the orbital apex, from where

the tumor can extend intracranially through the superior orbital

fissure.

o The infratemporal fossa, where the masticator muscles are at risk

of invasion. Erosion of the pterygoid process may occur. Perineural

extension along the mandibular nerve (V3) into the foramen ovale

and the endocranium is also possible (Fig. 22)

o The vidian canal along the pterygoidien nerve and further to the

petrous apex.

Introduction

27

Fig. 21 Contrast-enhanced SE T1-weighted MR images with fat saturation illustrating

different pathways of extension in a patient suffering nasopharyngeal tumor. (a)

Extension through the sinus of Morgagni, weakest point of the pharyngobasilar fascia

(arrow). (b) Extension into the pterygopalatine fossa (arrow), neural crossroad within

the skull base. (c) From the pterygopalatine fossa, the tumor extends to the inferior

orbital fissure (arrow). (d) Extension to the infratemporal fossa (arrow) and to the

pterygoid canal with perineural spread along the vidian nerve (arrowhead). (e)

Perineural spread along the mandibular nerve (V3) extending to the foramen ovale

(arrow) and the cavernous sinus (arrowhead) (66)

Introduction

28

2. Lateral spread

Lateral extension to the parapharyngeal spaces can occur directly

through the pharyngobasilar fascia (Fig. 22), or indirectly through the

sinus of Morgagni, the fascias point of weakness. Further lateral spread

involves the infratemporal fossa and the masticator space infiltrating the

pterygoid muscles. From the masticator space, perineural extension along

the mandibular nerve (V3) may occur, leading to infiltration of the

foramen ovale and the cavernous sinus (Fig. 23). (66)

Fig. 22 Contrast-enhanced T1-weighted MR images in a patient presenting with direct

lateral extension through the pharyngobasilar fascia to the prestyloid compartment of

the parapharyngeal space (a, arrow), and the infratemporal fossa, with infiltration of

the pterygoid muscles (b, arrow) (66)

3. Posterior spread

Nasopharyngeal tumors can extend posteriorly to the

retropharyngeal space and the prevertebral muscles (Fig. 23). Destruction

of vertebral bodies is occasionally seen in very advanced tumors.

Posterolateral extension may involve the jugular foramen and the

hypoglossal canal (Fig. 24), with possible but rare spread to the posterior

fossa. This posterior extension may result in hypoglossal nerve (XII)

palsy. (66)

Introduction

29

Fig. 23 Spread of an advanced nasopharyngeal tumor. (a) Posterior extension to the

retropharyngeal space and prevertebral muscles (arrow). (b) Lateral extension to the

retrostyloid compartment of the parapharyngeal space, with encasement and

narrowing of the internal carotid artery (arrow). (c) Extension to the infratemporal

fossa (arrow) with intracranial spread into the cavernous sinus through the foramen

ovale (arrowhead). (66)

Fig. 24 Non-enhanced T1-weighted MR image of a nasopharyngeal tumor extending

posteriorly, infiltrating the clivus bone marrow (a, arrowhead), well identified on this

sequence by signal loss within the normally hyperintense bone marrow. (b) On the

enhanced T1-weighted fat saturation image, the tumor is seen to extend laterally to the

jugular foramen (anterior arrow) and the hypoglossal canal (XII) (posterior arrow). (66)

Introduction

30

4. Inferior spread

Some nasopharyngeal tumors present with submucosal spread into

the oropharynx, involving the tonsillar fossa (Fig. 24). This extension

may take place submucosally and thus escape detection by endoscopy,

although not detection by imaging. (66)

Fig. 25 Patient presenting with a nasopharyngeal tumor, clinically revealed by a

serous otitis (a, arrowhead) without lateral extension but a posterior spread to the

retropharyngeal space (arrow) and posterior parapharyngeal space (b, arrow). (c) A

left retropharyngeal node (arrow). Note the inferior extension to the oropharynx

(arrowhead). (66)

5. Superior spread

Nasopharyngeal tumor can spread through the foramen lacerum,

even if it is contained by the pharyngobasilar fascia. If the tumor extends

to the tough fibrous cartilage which closes the foramen lacerum,

intracranial extension may occur (Fig. 26).

Superior spread with erosion of the clivus and the sphenoid sinus is

also possible leading to intracranial extension (Fig. 27). (66)

Introduction

31

Fig. 26 (a) Coronal reconstruction of contrast enhanced CT image illustrating a

nasopharyngeal tumor extending to the foramen lacerum. (b) Coronal bone window

CT image. Note the enlargement of the foramen lacerum. (66)

Fig. 27 Patient presenting with a nasopharyngeal tumor showing direct superior

extension and infiltration of the sphenoid bone. (a) CT depicts small skull base clival

erosions, (b) whereas MRI, in particular the non-enhanced T1-weighted sequence

without fat saturation, shows a much more important infiltration of sphenoid bone

marrow. (66)

Intracranial extension of nasopharyngeal tumors is possible via

different pathways such as the foramen lacerum, the foramen ovale and

erosion of the skull base. Many studies have illustrated the good

sensitivity of MRI to detect such extension, which is usually perineural.

The frequency of intracranial abnormalities on MRI is 30%. (67)

Nasopharyngeal tumors with intracranial extension are classified as T4

tumors according to the TNM staging system. (67, 68)

Intracranial spread is

usually extra-axial, resulting in involvement of the cavernous and

temporal meninges. (66)

Introduction

32

Staging and Treatment: (69)

Taking into account the various TNM features, NPC patients are

then staged accordingly from Stage 0 to Stage IV. Several features of

note are:

a) T3 disease indicates a patient is at least Stage III

b) T4 disease places the patient at Stage IV

c) N3 disease (i.e. single node >6 cm in size; supraclavicular

nodes) indicates a patient is at least Stage IVb

d) M1 disease places the patient at stage IVc.

Correct staging enables the clinician to determine which treatment

modality is best for the patient. A detailed discussion of the treatment

options is beyond the scope of this paper. In brief, radiotherapy (RT) is

the mainstay of treatment for NPC, as the differentiated and

undifferentiated non-keratinizing squamous cell carcinomas (formerly

named type II and III) are very radiosensitive. (70, 71)

Conventional

external beam RT was the traditional method of treatment. However, the

tumor could not be maximally irradiated without damaging adjacent

structures such as the parotid glands. With the advent of conformal

techniques, and in particular, intensity-modulated radiotherapy(IMRT),

doses of up to 70 Grays may be delivered with relative sparing of the

adjacent soft tissues. Limitations still remain with very large tumors, for

example, T4 tumors, where NPC may be so close to vital structures such

as the optic chiasm that the latter cannot be spared if the full RT dose

were to be administered.

Combined chemotherapy using platinum-based drugs and

radiotherapy (CRT) is given for patients with T3 disease and nodal

Introduction

33

disease >N1. Patients with T4 and N3 disease may receive neoadjuvant

chemotherapy with platinum-based combination chemotherapy followed

by definitive RT with concurrent chemotherapy. (71)

Patients with T1/T2

N1 disease are also treated with CRT although this is a controversial topic

and beyond the scope of this article.

Aim of the work

34

AIM OF THE WORK

The aim of this work is to describe the role of state of the art cross

sectional imaging computed tomography and magnetic resonance

imaging (CT & MRI) in the staging of nasopharyngeal carcinoma.

Patients and methods

35

PATIENTS AND METHODS

This study included 20 patients presenting with pathologically

proven nasopharyngeal carcinoma referred to the Radiodiagnosis

Department at the Alexandria Main University Hospital.

All the studied patients were subjected to the following:

1. Complete history taking.

2. Thorough clinical ENT examination.

3. The medical ethics were considered. The patient was aware of the

examination, patient's approval was obtained.

4. Multi-detector Computed Tomography examination especially bone

algorithm as well as post contrast sequences.

Patients lying supine were instructed to take shallow breaths and

refrain from swallowing during scanning. MDCT was performed on a 16-

MDCT scanner (Philips MX16, Philips Healthcare) with tube voltage,

120 kV; effective tube current, 150 mAs; collimation, 0.75 mm; table

feed, 12 mm/rotation; and rotation time, 0.5 second. The effective

radiation dose for a typical scanning range of 250 mm was 3.6 mSv for

men and 4.1 mSv for women. A non-ionic contrast agent ULTRAVIST,

Bayer (each ml of injection contains 769 mg iopromide, equivalent to 370

mg iodine) was injected at a flow rate of 1 ml/sec. for 50 seconds then a

waiting time for 50 seconds then inject 50 ml at 2.5 ml/sec. and start scan

at the end of injection. The scanning range started from top of the frontal

sinus base to the tracheal bifurcation. Data set was reconstructed using a

standard soft-tissue (B 40) convolution kernel with a slice thickness of 1

mm (0.7-mm reconstruction increment). For the assessment of bone and

Patients and methods

36

cartilage, additional data set was reconstructed using a sharp (bone)

convolution kernel (B 70).

5. MRI examination:

a. Axial: T1, T2 and T2 Fat Saturation images.

b. Coronal: T1 and T2 Fat Saturation images.

c. Sagittal: T2w images.

d. Post-Contrast T1w Fat Saturation images in 3 planes.

MR imaging was performed with a 1.5 Tesla whole-body MR imaging

system (Philips Achieva 1.5T, the Netherlands), by using a 4-channel

phased array head and neck coil. The following parameters were used:

Pre-contrast axial and coronal T1-images were obtained with SE

450/15, 90, 2 excitations, a 22-cm field of view (FOV), a 256 256

matrix, a 3-mm-thick section and a 0.9-mm gap.

Axial and sagittal T2-images were obtained with SE 4500/88, 180,

3 excitations, a 22-cm field of view (FOV), a 256 256 matrix, a 3-

mm-thick section and a 0.9-mm gap.

Axial and coronal fat-suppressed T2-weighted sequence obtained

with SE 2500 ms/100 ms; echo-train length, 15; 22-cm field of

view (FOV), a 256 256 matrix, 4-mm-thick section, with no

intersection gap; and 256 256 matrix size.

Post-contrast medium (Dotarem ,Guerbet (0.1 mmol/kg)) Axial,

coronal, and sagittal T1w scan with fat suppression images were

obtained with SE 500/22 ms, 2 excitations, a 22-cm field of view

(FOV), a 256 256 matrix, 3-mm section thickness and 0.5-mm

gap.

Patients and methods

37

6. Endoscopic examination and biopsy from the suspected area with

routine histopathologic examination.

7. Correlation with pathological data.

Results

38

RESULTS

Table (1): Distribution of studied cases according to demographic

data (n=20)

No. %

Age (years)

20 >30 3(15%) 15.0

30 >40 3(15%) 15.0

40 >50 6(30%) 30.0

50 >60 3(15%) 15.0

60 >70 5(25%) 25.0

Sex

Male 12(60%) 60.0

Female 8(40%) 40.0

Table (2): Distribution of studied cases according to side (n=20)

No. %

Side

Right 8(40%) 40.0

Left 11(55%) 55.0

Diffuse 1(5%) 5.0

Table (3): Distribution of studied cases according to neck spaces

involvement (n=20)

No.

% CT MRI

Space

Retropharyngeal space (RPLN) 4(20%) 8(40%) 40.0

Carotid sheath 1(5%) 1(5%) 5.0

Parapharyngeal space 7(35%) 8(40%) 40.0

Masticator space 3(15%) 3(15%) 15.0

Results

39

Table (4): Distribution of studied cases according to extension

pattern (n=20)

Extension No.

% CT MRI

Anteriorly

Nasal choana 8(40%) 8(40%) 40.0

Inferiorly

Oropharynx 5(25%) 7(35%) 35.0

Superiorly

Intracranial extension 7(35%) 8(40%) 40.0

Perineural spread 6(30%) 10(50%) 50.0

Posteriorly

Retropharyngeal space (RPLN) 4(20%) 8(40%) 30.0

Posterolaterally

Carotid sheath 1(5%) 1(5%) 5.0

Laterally

Parapharyngeal space 7(35%) 8(40%) 40.0

Masticator space 3(15%) 3(15%) 15.0

Table (5): Distribution of studied cases according to paranasal

sinuses involvement (n=20)

No. of cases

% CT MRI

Paranasal sinus involvement 4 6 30.0

Sphenoid sinus 4(20%) 6(30%) 30.0

Maxillary antrum 1(5%) 1(5%) 5.0

Results

40

Table (6): Distribution of studied cases according to

pterygopalatine fossa involvement (n=20)

No.

% CT MRI

Pterygopalatine fossa 7(35%) 9(45%) 45.0

Right 2(10%) 3(15%) 15.0

Left 5(25%) 6(30%) 30.0

Table (7): Distribution of studied cases according to skull base bone

involvement pattern (n=20)

No. of cases

% CT MRI

Bone 18 17

Lytic 7(40%) 8(40%) 40.0

Sclerotic 5(25%) 3(15%) 25.0

Mixed sclerosis and erosion 6(30%) 6(30%) 30.0

Table (8): Distribution of studied cases according to neural

foraminal involvement (n=20)

No. %

Foramina 17(85%) 85.0

Ovale 8(40%) 40.0

Lacerum 9(45%) 45.0

Jugular 1(5%) 5.0

Sphenopalatine 1(5%) 5.0

Rotundum 1(5%) 5.0

Results

41

Table (9): Distribution of studied cases according to perineural

spread (n=20)

No.

% CT MRI

Perineural spread

Along V3

Along V2

Along vidian nerve

Facial nerve(VII)

8(40%)

5(25%)

2(10%)

3(5%)

0(0%)

11(55%)

6(30%)

3(15%)

4(5%)

1(5%)

50.0

30.0

15.0

20.0

5.0

Table (10): Distribution of studied cases according to lymph nodal

involvement (n=20)

No.

% CT MRI

Supraclavicular lymph nodes 5(25%) 5(25%) 25.0

Retropharyngeal lymph nodes (RPLN) 4(20%) 8(40%) 60.0

Cervical lymph nodes 14(70%) 14(70%) 70.0

Parotid LN 3(15%) 3(15%) 15.0

Table (11): Distribution of studied cases with cervical lymph nodal

metastases according to criteria of involvement (n=20)

No. %

CT MRI

Size enlargement 16 16 80.0

Necrosis 5 5 25.0

Extra-capsular extension 3 3 15.0

Results

42

Table (12): Distribution of studied cases according to primary tumor

T-stage (n=20)

No. %

Primary tumor

T1 0(0%) 0.0

T2 0(0%) 0.0

T3 5(25%) 25.0

T4 15(75%) 75.0

Table (13): Distribution of studied cases according to lymph nodes

involvement N-stage (n=0)

No. %

Lymph nodes

N0 4(20%) 20.0

N1 8(40%) 40.0

N2 3(15%) 15.0

N3a 0(0%) 0.0

N3b 5(25%) 25.0

Table (14): Distribution of studied cases according to TNM stage

(n=20)

No. %

TNM Stage

I 0(0%) 0.0

II 0(0%) 0.0

III 3(15%) 15.0

IVa 11(55%) 55.0

IVb 3(15%) 15.0

IVc 3(15%) 15.0

Results

43

Case 1:

(A) (B)

(C) (D)

Results

44

(E) (F)

(G) (H)

Results

45

Fig. 28 Case 1: 28 years old male patient with right side

nasopharyngeal carcinoma.

(A and B) Axial T2w and T2w fat suppression images: A right

nasopharyngeal iso-intense heterogeneous mass (white arrow)

obliterating the parapharyngeal space fat and the levator veli palatini

muscle, and crossing the midline along the posterior pharyngeal wall.

(C and D) Pre- and post-contrast axial T1w images: The mass

lesion fills anteriorly the scaphoid fossa (white block arrow) of the

pterygoid process. Moderate post-contrast enhancement of the mass is

noted (D image).

(E and F) Axial CT bone window and MR T1w post-contrast

images: In the (E) image (orange curved arrow) represents the tumor

entering through the sphenopalatine foramen into the pterygopalatine

fossa (red arrow head), and hence reaching into the vidian canal (black

arrow). In the (F image) the moderately enhancing tumor filling the

pterygopalatine fossa (red arrow head) and reaching the vidian canal

(black arrow).

(G and H) Pre- and post-contrast sagittal T1w images: The lesion

extends anteriorly to the ipsilateral choana, and inferiorly reaches the

junction of the naso- and oro-pharynx (yellow arrow).

Results

46

Case 2:

(A) (B)

(C) (D)

Results

47

(E)

Fig. 29 Case 2: 50 years old female patient with left sided

nasopharyngeal carcinoma.

(A) Axial CT bone window image: showing lytic lesion eroding the

clivus (red arrow) and bony borders of the vidian canal (black arrow) and

foramen rotundum (white arrow).

(B) Axial T2w image: showing intermediate signal mass lesion with

extension to the left sphenoidal sinus which showed retained secretions

(blue star), near total encasement of the petrous segment of the internal

carotid artery (yellow arrow).

(C) Axial T1w image: showing a nasopharyngeal carcinoma of the

pterygopalatine fossa invasion (green arrow).

Results

48

(D) Post-contrast sagittal T1w fat saturation image: showing

posterior invasion of the clivus with intracranial extension effacing the

pre-pontine cistern (blue arrow).

(E) Enhanced coronal T1w fat saturation image: The

nasopharyngeal mass reaches the cavernous sinus through the vidian

canal and the foramen rotundum (vidian and maxillary (V2) nerves

Perineural spread) with encasement of the internal carotid artery (red

arrow head) and enhancement of the maxillary nerve (yellow arrow

head).

Results

49

Case 3:

(A) (B)

(C) (D)

Results

50

(E)

Fig. 30 Case 3: a 30 years old female patient with left sided

nasopharyngeal carcinoma.

(A) Axial CT bone window image: It shows widening of the petro-

clival fissure (black arrow) and the foramen lacerum (white arrow).

(B) Axial T1w image: a mucosal based mass lesion obliterating the left

fossa of Rosenmller showing T1 intermediate signal.

(C) Post-contrast axial 3D GRE T1w image: The moderately

enhancing tumor reaches along the lateral wall of the nasopharynx to the

pterygopalatine fossa (red arrow head) then along the vidian canal

representing perineural spread along the vidian nerve (red arrow).

(D) Post-contrast axial T1w fat saturation image: (yellow arrow)

Left sided level II enlarged metastatic lymph node with foci of necrosis

showing post-contrast enhancement.

Results

51

(E) Post-contrast sagittal T1w fat saturation image: Superior

extension of the tumor to the floor of the sphenoid sinus with minimal

intra-sinus extension (green arrow).

Results

52

Case 4:

(A) (B)

(C) (D)

Results

53

(E)

Fig. 31 Case 4: a 40 years old male patient with left sided

nasopharyngeal carcinoma.

(A) Axial T1w image: A mass lesion is noted growing and expanding

the left lateral nasopharyngeal recess (Fossa of Rosenmller), showing

intermediate to low T1 signal (white arrow).

(B) Axial 3D GRE T1w image: The nasopharyngeal carcinoma grows

anteriorly to reach the pterygopalatine fossa (yellow arrow) and laterally

to reach the widened foramen ovale (red arrow) and grows along the

mandibular division of the trigeminal nerve V3 (perineural spread) in the

foramen ovale to reach intracranial cavity.

(C and D) Axial T2w and post-contrast T1w fat saturation

images: demonstrates the intracranial extra-axial left temporal

component of the nasopharyngeal carcinoma (blue arrow). Involvement

Results

54

of the cavernous sinus with total encasement of the still patent internal

carotid artery (black arrow).

(E) Post-contrast coronal T1w fat saturation image: The

nasopharyngeal lesion (white arrow) extends superiorly through the

widened foramen ovale (orange arrow) into the intracranial extra-axial

temporal mass lesion (green arrow).

Results

55

Case 5:

(A) (B)

(C) (D)

Results

56

(E)

Fig. 32 Case 5: a 48 years old male patient with left sided

nasopharyngeal carcinoma.

(A) Sagittal reconstruction bone window CT image: Sclerosis and

infiltration of the bone marrow of the clivus (black arrow).

(B) Axial T1w image: Perineural spread along the mandibular division

of the left trigeminal nerve (V3), through the foramen ovale (yellow

arrow) and infiltration of the clival bone marrow (black arrow).

(C) Axial T2w image: An intracranial extra-axial temporal component

(green arrow), reaching the cavernous sinus encasing the patent internal

carotid artery siphon (blue arrow).

(D) Post-contrast coronal T1w fat saturation image: Shows the

nasopharyngeal lesion with perineural spread along the V3 division of the

mandibular nerve through the foramen ovale (yellow arrow) widening the

Results

57

foramen and extending superiorly to an extra-axial temporal mass (green

arrow) reaching the region of the trigeminal ganglion.

(E) Post-contrast sagittal T1w image: shows infiltration of the clival

bone marrow with post-contrast enhancement (black arrow).

Results

58

Case 6:

(A) (B)

(C) (D)

Results

59

Fig. 33 Case 6: a 65 years old male patient with right side

nasopharyngeal carcinoma.

(A and B) Axial T2w and post-contrast T1w fat saturation

images: A right-sided nasopharyngeal carcinoma (black arrow) with

anterior extension to the pterygoid plates and scaphoid fossa (yellow

arrow).

(C) Axial Diffusion weighted image: Restricted diffusion of right

nasopharyngeal mass (white arrow)

(D) Axial T2w image: bilateral jugular chain lymph nodes (red arrows)

with necrosis in the left one.

Results

60

Case 7:

(A) (B)

(C) (D)

Results

61

(E) (F)

Fig. 34 Case 7: a 38 years old male patient with diffuse bilateral

nasopharyngeal carcinoma.

(A) Sagittal reconstruction CT bone window image: shows full

thickness moth eaten erosion of the clivus (white arrows).

(B) Contrast-enhanced axial CT image: shows a nasopharyngeal

heterogeneously enhancing mass lesion obliterating fossae of

Rosenmller bilaterally and filling the nasopharyngeal cavity (red

arrows).

(C) Axial T2w image: shows anterior extension of the hyperintense

nasopharyngeal lesion through both choanae into nasal cavities (orange

arrows)

(D and E) Axial T2w and Diffusion weighted images: show

enlarged hyperintense right sided retropharyngeal lymph node which

showed restricted diffusion (green arrows).

Results

62

(F) Post-contrast sagittal T1w image: shows the enhancing pre-clival

nasopharyngeal mass (blue arrow) infiltrating into the clivus (red arrow)

with pre-pontine enhancing component (yellow arrow).

Results

63

Case 8:

(A) (B)

(C) (D)

Results

64

(E)

Fig. 35 Case 8: A 62 years old female patient of left sided

nasopharyngeal carcinoma

(A) Axial T2w image: shows a left sided iso-intense nasopharyngeal

mass lesion obliterating the left fossa of Rosenmller (orange arrow).

(B) Post-contrast axial T1w fat saturation image: shows superior

extension of the moderately enhancing tumor with total encasement of the

internal carotid artery (blue arrow).

(C) Post-contrast axial T1w fat saturation image: shows inferior

extension of the enhancing nasopharyngeal tumor along the lateral

pharyngeal wall reaching the oropharynx (red arrow).

(D and E) Pre-contrast sagittal T1w and post-contrast T1w fat

saturation images: shows hypo-intense infiltration of the tumor in the

bone marrow of the clivus with post contrast enhancement (yellow

arrow).

Results

65

Case 9:

(A) (B)

(C) (D)

Results

66

Fig. 36 Case 9: A 50 years old male patient with left sided

nasopharyngeal carcinoma.

(A) Axial T2w image: shows a left sided isointense nasopharyngeal

mass lesion (white arrow) with anterior extension through the left choana

into the left nasal cavity (red arrow).

(B) Axial T1w image: The hypointense nasopharyngeal mass extends

anteriorly to the pterygopalatine fossa with obliteration of the

pterygopalatine fossa fat signal (orange arrow).

(C) Post-contrast sagittal T1w image: shows moderately enhancing

nasopharyngeal lesion (green arrow) with superior extension infiltrating

the clival marrow (yellow arrow) and the sphenoid sinus (blue arrow).

(D) Axial T2w image: shows a left sided lateral retropharyngeal

enlarged lymph node showing hyper-intense signal (red arrow).

Results

67

Case 10

(A) (B)

(C) (D)

Results

68

Fig. 37 Case 10: A 65 years old male patient of right sided

nasopharyngeal carcinoma.

(A and B) Axial T2w and post-contrast T1w images: show a right

sided nasopharyngeal mass lesion showing T2 iso-intensity with

moderate post-contrast enhancement which infiltrates the levator veli

palatini and medial pterygoid muscles with obliteration of the

parapharyngeal fat (white arrow). The tumor infiltrates posteriorly the

anterior surface of the right prevertebral muscle (yellow arrow).

(C) Post-contrast axial T1w image: shows enhancing intracranial

extra-axial temporal component (red arrow).

(D) Post-contrast coronal T1w fat saturation image: The

moderately enhancing nasopharyngeal lesion (blue arrow) extends

superiorly through the right foramen ovale (black arrow) with intracranial

extra-axial component reaching the cavernous sinus and encasing the

internal carotid artery (red arrow).

Discussion

69

DISCUSSION

Nasopharyngeal carcinoma (NPC) is a rare malignancy in most parts

of the world, with an incidence well under 1 per 100,000 person-years.

Populations with elevated rates include the natives of Southeast Asia, the

natives of the Arctic region, and the Arabs of North Africa and parts of the

Middle East. (1)

The present study included 20 patients with pathologically proven

NPC as 12 (60%) males and 8 (40%) females with a mean age of 45.9 years.

Parkin DM et al (2002) stated that in almost all populations surveyed,

the incidence of NPC is 2- to 3-folds higher in males than in females. (72)

In

our study, male to female ratio was of about 1.5 folds higher in males than in

females.

In most low-risk populations, NPC incidence increases monotonically

with increasing age. (73-75)

In the contrary, in high-risk groups, the incidence

peaks around ages 50 to 59 years and declines thereafter. (76, 77)

In our study,

patients age ranged from 24 to 65 years with bimodal peaks of 6 and 5 cases

for the 5th

and 7th

decades of life respectively.

Of the studied NPC cases, 8 cases (40%) were seen on the right side,

11 cases (55%) on the left side, and 1 case (5%) diffusely infiltrating both

sides and crossing the midline.

Discussion

70

Since NPC is diagnosed by endoscopy, the foremost role of CT or

MRI is to determine the extent of primary tumor and the presence of

metastatic adenopathy. (78)

Accurate assessment of the disease extent facilitates appropriate

treatment planning and prognosis. (79)

NPC is generally iso-dense to muscle on non-enhanced CT. It is

usually hypo- to iso-intense and relatively hyper-intense to muscles on T1-

weighted and T2-weighted MR images, respectively. Mild to moderate

tumor enhancement is evident following intravenous contrast injection on

both CT and MRI.

Ng SH et al (1997) stated that CT and MRI findings were essentially

in agreement in patients whose disease was limited to the nasopharyngeal

cavity, but not those with tumor spreading beyond the boundaries of the

nasopharynx. (80)

The pharyngobasilar fascia, the medial border of the parapharyngeal

space, is normally seen on MRI and not on CT. Involvement of the

parapharyngeal space denotes at least T2 stage of the tumor. (81-84)

In NPC,

parapharyngeal space involvement can be assessed directly by MRI, which

shows tumor displacement or infiltration of the pharyngobasilar fascia or

extension through the sinus of Morgagni. (81, 85)

In contrast, involvement of

the parapharyngeal space by CT is inferred indirectly by an abnormal soft

tissue deforming the parapharyngeal fibro-fatty tissue plane or by outward

bulging of an imaginary line between the medial pterygoid plate and the

lateral border of the carotid artery. (84, 86)

Discussion

71

In our study the involvement of the parapharyngeal space was

demonstrated in 7 cases by CT and in 8 cases by MRI. King AD et al (2000)

found that CT scanning suggested the presence of parapharyngeal tumor

extension more frequently than MRI because of its inability to distinguish

the primary tumor from lateral retropharyngeal nodes, and direct tumor

invasion of the parapharyngeal region from tumor compression. (87)

Xie C et

al (2004) in a study on 69 patients found that there was no difference

between CT and MRI in demonstrating the invasion of the parapharyngeal

space. (88)

Further laterally, the tumor may spread into the masticator space.

Anatomic masticator space involvement affects the overall survival and local

relapse-free survival of patients with NPC. The frequency of masticator

space involvement in NPC is 19.7% as declared by Abdel Khalek Abdel

Razek A. et al (2012). (89)

Infiltration of the medial and lateral pterygoid

muscles, infratemporal fat, and temporalis muscle is found when tumors

extend laterally from the parapharyngeal space, pterygoid base, or the

pterygo-maxillary fissure. (66, 90)

When the muscles of mastication (notably

the medial and lateral pterygoid muscles) are involved, the patient often

complains of trismus (Chong VF 1997). (91)

The mandibular nerve within the

masticator space may also be infiltrated, resulting in denervation atrophy of

the muscles of mastication. MRI features of denervation atrophy of these

muscles appear as T2 hyperintensity with asymmetrically reduced bulk of

the muscle of the affected side compared to the normal side (Chong VF et al

2008). (92)

In our study, the masticator space was involved in 3 cases (15%) and

it was as well seen in both CT and MRI. 2 cases showed involvement of the

Discussion

72

pterygoid fossa and the pterygo-maxillary fissure, and in the third one

showed denervation changes involving the ipsilateral masticator muscles,

sequel to mandibular nerve affection in the masticator space.

Further posterolateral spread may also involve the carotid space and

encase the carotid artery. (93)

Carotid artery encasement is defined as tumor

tissue surrounding >270o of the vessel circumference.

(69) This becomes

important in the follow-up setting, where surgical resection (e.g.

nasopharyngectomy or lymph node dissection) may be contemplated. The

patient is deemed inoperable if this is present, as the surgeon cannot remove

all the tumor tissue. Other potential issues that may result from encasement

include vascular invasion and potential carotid artery blow-outs post-

radiotherapy. Different criteria for detecting carotid artery involvement on

CT are suggested, and accordingly differs the sensitivity and accuracy in

detecting the vascular encasement. The use of loss of the fat plane between

the tumor and the carotid artery leads to very high false positive rates but

with a sensitivity of 100%. (94-96)

Others, suggest the use of tumor in contact

with one-half of the circumference of the artery and loss of the tissue planes,

with a much less false positive rates. (95, 97)

Other imaging characteristics are

carotid artery deformation, compression and segmental obliteration of the

fat.

Kraus DH et al (1992) declared that MRI was superior to CT in

determining carotid artery involvement. (82)

Yousem DM et al (1995), in a

study of carotid artery encasement, sensitivity of MRI was 100% and

specificity 88%. (98)

Sarvanan K et al (2002) studied encasement of >270

degrees and loss of fat planes. Sensitivity reached 75% and specificity

100%. (99)

Discussion

73

In our study we depicted only 1 case (5%) of carotid space

involvement by total encasement of the still patent carotid artery by NPC,

and that was seen by CT and by MRI as well.

In patients with NPC, paranasal sinuses involvement denotes a tumor

of at least stage T3. Paranasal sinus opacity is a common finding seen on

CT; it is occasionally difficult to differentiate whether it represents tumor

invasion or sinonasal secretions. On MRI, hydrated secretions within the

obstructed paranasal sinuses are of increased signal on T2-weighted images.

Thus, high-signal secretions can be differentiated from an intermediate

signal-intensity tumor. (82)

Desiccated or mixed sinonasal secretions may

exhibit signal characteristics similar to those of tumor on both T1- and T2-

weighted images; contrast-enhanced MRI is then helpful because tumor

within the sinus enhances whereas sinonasal secretions do not enhance and

are surrounded by a rim of strongly enhancing sinus mucosa. (100, 101)

In late

involvement of the sinuses, erosion of the sinus walls is a straightforward

exercise except in early cases. CT is superior to MRI in visualizing erosions

of paranasal sinuses floor. (53, 102)

In our study, we found that paranasal sinuses involvement was

demonstrated in the sphenoid sinus in 6 cases while in CT 4 cases showed

invasion of the sinus floor as erosions and the other 2 cases were equivocal

regarding the discrimination of the paranasal sinus secretions from tumor

tissue infiltration. The remaining 2 cases were only discriminated as

sphenoid sinus involvement in the enhanced MRI series. The maxillary sinus

involvement could be seen equally in CT and MRI in one case. In

agreement, Chong VF et al (1998) and Ng SH et al (1997) stated that

enhanced MRI excels on CT in detection and discrimination of involvement

Discussion

74

of NPC in the sphenoid and ethmoidal sinuses from inflammatory paranasal

secretions, and that both CT and MRI are equal in the detection and

discrimination of the tumor involvement of the maxillary sinus from

inflammatory secretions. (53, 80)

The significance of pterygopalatine fossa (PPF) involvement by

NPC is that once the tumor gains access to the pterygopalatine fossa, it gains

a route of spread to the orbit, infratemporal fossa, nasal cavity, and middle

cranial fossa. Earliest indication of tumor infiltration of the pterygopalatine

fossa is the replacement of the normal fat content. Widening of the fossa and

erosion of the bony margins are late signs. As expected, bony abnormality is

best seen on CT. However, direct visualization of tumor or replacement of

fat is more elegantly demonstrated on T1-weighted MRI. (103)

In our study, Pterygopalatine fossa invasion was demonstrated in 9

cases by MRI and by CT in 7 cases only and 2 cases were seen by MRI only

as obliteration of fossa fat signal by the tumor. This agrees with Tomura N.

et al (1999) where CT didnt depict the abnormalities in the pterygopalatine

fossa in five patients (17%) of a total of 30 patients with pterygopalatine

fossa involvement, while unenhanced T1w MR images depicted the tumoral

invasion in all patients. (104)

In agreement, also Chong VF et al (1995 and

1997) stated that direct visualization of fat replacement by the tumor is

better seen on T1w images. (103, 105)

Detection of skull base bone involvement is based on either direct

visualization of tumor infiltration or detection of the reaction of bone to the

malignant process. MRI can identify early involvement of bone marrow. CT,

which depends mainly on bone destruction, provides detailed bone

Discussion

75

morphology. Both cortical and trabecular bone components are well defined

by CT. Based on the balance between the osteoclastic and osteoblastic

processes, the radiologic appearance of a bone involvement may be lytic,

sclerotic (blastic), or mixed. (106)

Rapidly growing aggressive metastases tend

to be lytic, whereas sclerosis is considered to indicate a slower tumor growth

rate. Sclerosis may also be a sign of repair after treatment. (107-109)

CT is not

sensitive for assessment of malignant marrow infiltration. (106, 110)

In NPC with skull base invasion, CT can directly determine the extent

of cortical bone destruction and/or remodeling by cancer. (82, 85, 86, 111, 112)

On

the other hand, MRI can show tumor involvement of the skull base as a

lesion with different signal intensities encroaching on the signal-void bone

cortex or replacing the marrow. (82, 85)

Contrast-enhanced fat-suppressed MRI

provides a better delineation of tumor extension into the clivus and allows

discrimination of tumor invasion from edema of the marrow. (113)

The clivus,

pterygoid bones, body of the sphenoid and apices of the petrous temporal

bones are most commonly invaded. (114)

In our study skull base bony involvement was seen in 18 cases (90%)

by CT and in 17 cases (85%) by MRI. In 53 patients with NPC studied by

Olmi P et al, CT showed skull base erosion in 12 patients and MRI in 8. (112)

Ng SH et al (1997) stated that skull base destruction was revealed in 27 of

67 cases (40.3 %) on CT and in 40 cases (59.7 %) on MRI, and that there

was no case in which the skull-base invasion was not visible on MRI, while

there were 13 cases (19.4 %) in which it was detected only by MRI. (80)

CT demonstrated lytic bone invasion in 7 cases, while 8 cases were

seen by MRI. MRI, mainly the enhanced T1w fat suppressed images,

Discussion

76

excelled over CT and demonstrated 1 case of lytic infiltration of the skull

base bone that couldnt be seen by CT. In contrast, CT better demonstrated

sclerotic bone involvement in 5 cases but 3 cases were seen only by MRI.

We acknowledge that bone window CT excels over MRI in visualizing tiny

bony erosions by the tumor without involvement of the bone marrow. In

mixed sclerotic and erosive invasion of the bone, both CT and MRI

demonstrated 6 cases as well. To be noted that bone sclerosis alone, can be

either bone infiltration by osteoblastic tumor, or remodeling activity due to

nearby tumor.

The skull base foramina and fissures which include the foramen

rotundum (V2 nerve), the vidian canal (vidian nerve), the foramen ovale (V3

nerve), and foramen lacerum should be examined. The foramen ovale and

lacerum are common routes of tumor extension into the intracranial cavity.

(114) Lederman M (1961) stated that foramen lacerum is the most frequently

invaded foramen due to its close proximity to the lateral pharyngeal recess.

(115) While the skull base foramina present an unobstructed route for tumor

spread, direct invasion of the bone bordering these foramina is also a

common finding. The skull base foramina are best assessed on coronal

images. Less common findings include inferior spread of tumor to involve

the hypoglossal nerve canal (XII nerve) and jugular foramen (IX-XI nerves).

(114)

Nerves are resistant to tumor, and perineural tumor spread (PNS) is

an insidious and often asymptomatic process by which NPC can invade

upward and backward through the skull base to the cavernous sinus and

middle cranial fossa and invade CN II to VI (upper CN palsy). Cranial

nerves involvement indicates a tumor T-stage of T4. It may also involve the

Discussion

77

carotid space, where it may compress or invade CN XII as it exits through

the hypoglossal canal, CN IX to XI as they emerge from the jugular

foramen. (116, 117)

CN involvement on MRI is seen when there is asymmetric

enlargement, asymmetric enhancement on gadolinium-enhanced T1-

weighted images, obliteration of perineural fat planes, denervation changes

in end organs supplied by the nerves, and at last widening of foramina and

foraminal wall affection. (118, 119)

Skip lesions may also be noted. (120)

Widening of a foramen or fissure that an involved nerve normally

traverses is an indirect sign of perineural spread, and this is best appreciated

on CT scan using bone algorithm. Features such as obliteration of juxta-

foraminal fat pads and fat planes along the path of a CN are seen well on

both modalities. Expansion of the cavernous sinus and soft tissue

enhancement of Meckels cave, which is normally fluid filled, are other

indicators of PNS on CT and MRI. (118)

In our study, skull base foraminal involvement was seen by bone

algorithm CT and the enhanced MR T1w fat saturated images as well in 17

cases (85%). The foramen ovale was involved in 8 cases (40%), foramen

lacerum in 9 cases (45%), jugular foramen in 1 case (5%), sphenopalatine

foramen in 1 case (5%), and foramen rotundum in 1 case (5%). Of these 17

cases, only 11 (55%) cases showed perineural spread as demonstrated by

MRI, and 3 cases of perineural spread were missed by CT. Perineural spread

was seen along the mandibular nerve (CN V3) in 6 cases by MRI and of

these cases, one case was missed by CT. Maxillary (CN V2) was involved in

3 cases by MRI, one of them was missed by CT. The vidian nerve

Discussion

78

involvement was demonstrated in 4 cases by MRI, while CT missed one

case. The facial nerve (CN VII) was involved in 1 case by MRI and was

missed in CT. Thus we declare that CT and MRI, especially the 3D gradient-

echo T1w post-contrast series, were as well in depicting the involvement of

the bony foramina, and MRI excelled over CT in detecting perineural

spread. In agreement, King AD et al (1999) acknowledged that perineural

spread would be underestimated unless enhanced fat saturated images are

obtained. (121)

Maxillary and mandibular nerve involvement is best seen on

coronal T1-weighted contrast-enhanced MRI with fat saturation. (118)

MRI is

generally more sensitive than CT in detecting all features of perineural

spread except for enlargement and destruction of bony foraminal boundaries.

Also Caldemeyer KS et al (1998), Liao XB et al (2008); Ng SH et al (2009),

Sakata K et al (1999) agreed in that MRI was superior in identifying

perineural spread. (122-125)

Intracranial extension occurs either from direct extension or through

skull base foramina (direct invasion, or perineural spread). Intracranial

extension denotes T4, stage IV tumors. Features denoting intracranial

extension include cavernous sinus involvement, meningeal involvement

(especially if seen as nodular enhancing masses), and less frequently masses

within the middle and/or posterior cranial fossa, respectively according to

the frequency of involvement. (69, 79)

Anterior cranial fossa invasion by NPC

is rarely seen. To be noted that posterior cranial fossa is seen more readily

with MRI due to its pluri-directional scanning and does not show beam-

hardening artifact from the dense bone of the skull base. (80)

In our study, intracranial extension was detected by CT in 7 cases

(35%) and by MRI in 8 cases (40%). MRI excelled over CT in detection of

Discussion

79

intracranial extension in one case, where minor meningeal involvement was

seen in contrast enhanced T1w MR images. All of the studies we could

reach highlighted the superiority of MRI over CT, revealing intracranial

invasion, especially in conjunction with the contrast-enhanced fat-

suppression technique. (69, 78, 82, 85, 113, 123, 126-129)

Nasopharyngeal carcinoma tumor may infiltrate submucosally

inferiorly to involve the oropharynx or even the hypopharynx. On imaging,

oropharyngeal extension is readily noted on coronal or sagittal MR

imaging as tumor that has extended inferiorly past the plane of palate. On

axial sections, the oropharynx is considered involved when tumor is seen

inferior to the C1/C2 junction. (66, 120)

In our study, MRI excelled over CT in detection of oropharyngeal

infiltration by NPC. Oropharyngeal carcinoma involvement was seen in 7

cases (35%) by CT. By MRI, 2 cases of these 7 cases seen by CT were

interpreted to be retropharyngeal lymph nodal involvement rather than true

oropharyngeal tumoral involvement. MRI detected 7 cases (35%) of

oropharyngeal infiltration by the nasopharyngeal carcinoma. Soft palate was

involved in 2 case, 3 cases showed creeping on the posterior and lateral

walls of the naso- and oro-pharynx, and 2 cases showed palatine tonsils and

pillars involvement. Retropharyngeal lymph nodal involvement in the

retropharyngeal space can be misinterpreted by CT as oropharyngeal

posterior and/or lateral walls involvement as described formerly. In

agreement, Ng SH (1997) in a study, Of 18 patients, in whom CT suggested

oropharyngeal involvement, seven actually had retropharyngeal adenopathy

disclosed by MRI, with subsequent down-staging of the cases. (80)

Although

MR was better in the assessment of the oropharynx, the exam can be non-

Discussion

80

diagnostic secondary to excessive swallowing artifact, which is not

uncommon if the patient has pooling of saliva and a large tumor. (130)

On the

other side, MRI avoids CTs dental amalgam artifact. (131)

Lymphadenopathy has very important prognostic implications. Up to

60-90% of NPC patients will have nodal metastases at presentation

(Glastonbury, 2007; Goh and Lim, 2009). (69, 132)

Positive neck nodal disease

in NPC is associated with an increased risk of local recurrence and distant

metastases (Goh and Lim, 2009). (69)

The presence of a single nodal

metastasis reduces the patients survival rate by 50%. Bilateral

lymphadenopathy further reduces the survival rate by another 50%. Patients

with nodes showing necrosis and extra-nodal spread and fixation have a very

poor prognosis with a further 50% decreased 5-years survival rate. (130, 133, 134)

NPC generally follows a very orderly pathway of nodal spread,

beginning with the lateral retropharyngeal lymph nodes (RPLN) - located

medial to the carotid artery - before involving the nodal groups along the

internal jugular chain (levels II to IV), spinal accessory chain (Va and Vb),

as well as supraclavicular nodes (Glastonbury C, 2007; King AD et al,

2004). (132, 135)

Nodal disease in the submandibular and parotid/periparotid

regions is a rare occurrence (Chong & Fan, 2000; King & Bhatia, 2010) (114,

136) Although the RPLN are generally considered the first echelon of

metastatic spread, studies have shown that this is not true in all cases and

that RPLN may be bypassed allowing direct spread to level IIa and IIb

nodes, which are the most common site for non-retropharyngeal nodal

involvement (Liu et al, 2006; Mao et al, 2008; Ng et al, 2004; Wang et al,

2009; King et al, 2000 and 2004). (135, 137-141)

As medial retropharyngeal

nodes are usually not visible, any medial retropharyngeal nodes detected on

Discussion

81

MRI are highly suspicious of metastatic involvement (Wang et al, 2009).

(142) In addition, Ng SH et al also reported skip metastases in the lower neck

lymph nodes and the supraclavicular fossa, and distant metastases to thoracic

and abdominal nodes. (137)

Several criteria are used in the evaluation of lymph nodes. Size is the

most commonly used. The measurements are taken using the shortest trans-

axial diameter and are considered suspicious when the shortest axis is >5

mm for RPLN, >1.5 cm for levels I and II, and >1 cm for levels IV-VII (Goh

and Lim, 2009; King and Bhatia, 2010). (69, 114)

A cluster of 3 or more lymph nodes borderline in size, rounded nodes

with loss of the fatty hilum, and necrosis are also suggestive of metastatic

disease (King and Bhatia, 2010). (114)

However, nodes may still be of normal

size and harbor malignant cells. The ratio of the longest longitudinal to axial

dimensions has also been proposed; if the ratio is less than 2, this

suggests metastatic carcinoma. Normal nodes should have a ratio greater

than 2. (69)

If identified, necrosis is considered 100% specific. However, due to

resolution restrictions, necrosis can only be reliably identified in tumor foci

greater than 3 mm, of which approximately one-third reportedly have nodal

necrosis (Goh and Lim, 2009; Som and Brandwein, 2003; Yousem et al,

1992). (69, 143, 144)

Necrosis or cystic change is hypo-intense on T1-weighted

images with rim enhancement after contrast injection, and hyper-intense on

T2-weighted images. In CT images, necrosis is seen as a focal area of hypo-

attenuation with or without post-contrast rim enhancement. (110)