Imaging of the neck part ii

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IMAGING OF THE NECK DR/ Wafik Ebrahim, MD Assistant Professor of Rradiodiagnosis Faculty of Medicine Alazhar University

Transcript of Imaging of the neck part ii

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IMAGING OF THE NECK

DR/ Wafik Ebrahim, MDAssistant Professor of Rradiodiagnosis

Faculty of MedicineAlazhar University

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Imaging modalities: CT MRI US: Plain X ray and conventional studies. Isotope scan. Angiography.

Multiplanner capability allows good anatomical description. Vascularity of lesion. Consistency of the lesion.

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CT scan: IV contrast is important for better

cracterization of the mass. Start from superior orbital rim to apex of

the lung. Extension to carina may be accomplished according to suspected disease.

To avoid artifacts of dental filling, planes are parallel to skull base down to alveolar ridge then parallel to body of mandible.

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MRI: Use dedicated surface colis better than

cervical coil for better resolution. T1 in the 3 planes followed by T2 in planes

best depict the lesion. 4-6mm thickness with 1-2mm gap. IV contrast is not routine due to inherent

tissue characterization of MRI. If IV contrast is used, fat sat sequences

are added.

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Neck triangles :

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Lymph nodes: Enlarged lymph node is the most

common neck mass in adults. About 300 nodes are located in the head

and neck. They are divided in groups described by the anatomist Rouviere.

20-40 years—lymphoma>40 years----metastasis

6. Submental 1. Occipital7. Sublingual 2. Mastoid

8. Retropharyngeal 3. Parotid

9. Anterior cervical 4. Facial

10. Lateral cervical. 5. Submandibular

The first 6 form lymphoid collar at junction between head and neck

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Lymph nodes groups:

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Lymph nodes: NORMAL nodes are oval with fatty sinus. Size criteria for benign nodes:

< 1.5cm for IJC near angle of mouth.< 0.8cm for retropharyngeal nodes.< 1cm for the rest of groups.

Pathological signs: Central necrosis (DD fatty hilum “peripheral

fat density”)Matting.Infiltrated surrounding fat planes.

We consider the short axis

of nodes.

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Lymph nodes stations:

IA & IB submental and

submandibular

II IJC posterior to PB

digastric:A: around IJV (any

direction)

B: posterior to IJV with

fat planes separation III: Between hyoid bone and inferior cricoid margin

V: PCS: SAC:A: skull base to cricoid.B: cricoid to clavicle.

IV cricoid to clavicle

VI: visceral s. nodes (hyoid to manubr)

VII: Super. Mediast.

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LN: Other groups include:

Parotid group: Retropharyngeal group.Facial group:

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LN

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PMS: Anatomy

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Pharyngeal mucosal space (PMS) Psudomass:

Asymmetry of fossa of Rosenmuller (lateral pharyngeal recesses) may result from inflammatory debris or asymmetry in the amount of lymphoid tissue thereby giving the impression of a mass.

A mass is ruled out when: 1. The adjoining soft tissue planes in the PPS and

RPS are maintained.2. The nasopharyngeal mucosa is clinically intact.3. The collapsed recess opens when rescanning

by CT scan is used during the Valvalva maneuver.

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Adenoid hypertrophy: It represents normal immunolgical

activity that starts at age of 2-3 years and regresses during adolescence.

Absence of adenoid tissue in young children should alert for immune disease.

Smoking can produce adenoid hypertrophy in adults.

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Adenoid: Hypertrophied

adenoid should be confined to mucosal space with intact underlying fascia.

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Thornwaldt cyst:

CT: Hypodense lesion:CECT: May be wall enhancement. •MRI:

• TI: intermediate to high according to protein contents.

• T2: High signal• +C: may be wallenhancement.

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Tonsillar abscess:

Cellulitis versus abscess: As a rule in cervical infection: Thickening of overlying skin or mucosa, smudging of the fat planes (or linear opacities), thickening of adjacent muscles, and enhancement of fascial planes WITHOUT fluid collection denote cellulitis but if WITH fluid seen it means abscess. LOOK CAREFULLY TO FAT PLANES BY ADUSTING WINDOW AND LEVEL.

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Tonsillar abscess:

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Tonsillar abscess: DD:

Tonsillar retntion cyst. Lymphoid hyperplasia.Retropharyngeal abscess.Benign mixed tumor of salivary gland.Tonsillar SCCA.NHL.

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Retention cyst:

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Retention cyst:

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Benign mixed tumors of minor salivary gland tumors (BMT):

NO invasion of surrounding structures

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MST

CT:Isodense mass lesion.Minimally enhancing.Necrosis and calcifications may be seen.Bone remodeling (benign longstanding

feature).

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BMTPEARL

SHAPED

NO PALATE DESTRUCTION

RIGHT MASTOIDITIS NO muscle

invasion

T1: isointense to muscleT2: variable mostly hyperIf calcified, foci of low signal. T1+C: intense enhancement

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BMT: Age: 30-60 years. But may be any age

even in neonate. DD:

Thyroglossal duct cyst in foramen coecom.Retention cyst. SCCA.Malignant salivary gland tumor (poorly

defined).

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Minor salivary gland malignancy: Rare aggressive tumor (1/10 of minor

salivary glandstumors. Occurs in adults.

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Minor salivary gland malignancy: Pathology: adenoid cystic carcinoma

and mucoepidermoid carcinoma. Rarely complicates pleomorphic

adenoma. Treatment is wide surgical excision.

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Minor salivary gland malignancy:

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Minor salivary gland malignancy: MRI:

T1 WI: Isoointense mass.T2: Variable signal.

Low signal (more cellular poorer prognosis).High signal (less cellular better prognosis).

T1+C enhancing with infiltrating margin. Add fat sat sequence for better assessment of

perineural spread).

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Minor salivary gland malignancy:

T1+C T2

PPS

RPS:LN

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Minor salivary gland malignancy:

Perineural spread CN V3 through F. Ovale

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Minor salivary gland malignancy: DD:

Benign mixed salivary gland tumors (well defined and regular non-invasive margin).

SCCA (usually with malignant adenopathy).Lymphoma (usually with associated non-

necrotic nodes).

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Squamous cell carcinoma “SCCA” Nasopharynx SCCA arising from nasopharynx has

three histological subtypes:1. Keratinizing SCCA (WHO type 1).2. Non-Keratinizing SCCA (WHO type 2).3. Undifferentiated SCCA (WHO type 3).

Size: Usually multiple CMs when discovered.

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SCCA Nasopharynx: Spread

Anterior: Nasal cavity then ptrygopalatine fossa

Anteroinferior to levator velli paltini ms with eustachian T. dysfunction

Lateral to PPS then to MS

(then foramen ovale up)

Posterior to RPS to PVS

and spineInferior to oropharynx

Superior to skull base

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SCCA Nasopharynx: Spread Lymphatic spread: usually seen at

presentation: retropharyngeal nodes, jagular nodes and spinal accsssory nodes.

Blood spread (10% at time of presentation): to bone > lung > liver. )

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SCCA: Imaging: CT scan: Isodense

poorly enhancing masslook also at bone

window to assess skull base.

Show the mass and extension.

Look at skull base foramina

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MRI: Low T1 signal and internediate to high T2 signal with intense postcontrast enhancement.

Add fat sat. for Better depiction of bone marrow invasion.Better evaluation of perineural spread.

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SCCA: Imaging: NSCCA starts usually in the fossa of

Rusenmuller and has same signal and density to normal mucosa. First signs are:Asymmetry of nasopharyngeal mucosa (regarding

cautions said before), attention is applied to:○ Fat stripe between levator and tensor velli palatine

muscles. Obliteration mass. ○ Middle ear collection warning sign.○ Associated lymphadenopathy especially

retropharyngeal nodes.

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SCCA: Imaging: Fat stripe between levator and tensor velli

palatine muscles. Obliteration mass.

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Staging:

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DD Benign mixed tumor (non invasive). Malignant salivary tumor (may be

indistinguishable). . NHL.

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Squampos cell carcinoma Oropharynx: Location:

Lingual tonsils (posterior to circumvillate papillae). The mass is more invasive with difficult early detection because it has same density and signal like the lymphoid tissue of normal lingual tonsils.

Palatine tonsils and facuial arches.

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Lingual tonsil SCCA spread pattern: Anterior: root of tongue, subliungal space (neurovascular bundle) and floor of mouth.

Posterolateral: palatine tonsils and tonsillar pillars.

Inferior to supraglottic larynx and preepiglottic

fossa .

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Lingual tonsils SCCA :

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MRI

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Palatine tonsils SCCA: Tonsils > Anterior pillar } posterior pillar. Asymmetry of tonsils may be seen

normally however mass is suspected when there is obliteration of fat planes in PPS and / or associated lymph node enlargement.

Mass may spread to PPS, masticator space (foramen ovale) or carotid space.

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Palatine tonsils SCCA:

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Palatine tonsils SCCA:

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Non-Hodjkin lymphoma:

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NHL

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Non-Hodjkin lymphoma:

Benign mixed salivary tumor

was suspected

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Parotid space: Anatomic considerations:

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Parotid space :

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Parotid space: Acute parotitis Bacterial:

Suppurative infection abscess.Usually unilateral.

Viral:75% bilateral though one is earlier involve.May be associated other sialadenitis.

Calcular induced:Stone impacted in the duct. Unilateral

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Acute parotitis: imaging : CT: Cuts taken parallel to mandible to avoid artifacts of

dental filling. Enlarged ill-defined hyper dense gland with

smudging of adjacent fat planes. Cystic changes denote abscess formation. search for a stone in the duct.

MRI:Diffuse gland enlargement: Liquefaction means abscess.

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Acute parotitis: imaging :

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Acute parotitis: imaging :

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Sjogren disease:

Bilateral parotid enlargement with multiple intraglandular cysts and occasional calcifications.

Diffuse disease is usual but sometimes single localized disease: DD from tumor.

Age: 50-70 YJuvenile type < 20 Y mostly cures at puberty.

Higher incidence in females.

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Sjogren disease: Stages:

Early: the glands may look normal.Intermediate: Multiple small intraparotid

cysts.Late: gland destruction with variable sized

cysts. At any stage there may be solid masses

related to lymphocytes aggregations. Calcifications are common.

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Sjogren disease:

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Benign mixed tumors: Parotid

Small lesion: is sharply demarcated ovoid intraparotid mass with homogeneous enhancement.

Large mass >2cm is lobulated heterogeneously enhancing.

Deep lobe mass is pear shaped pushing PPS medially. .

Usually unilateral mass.Age> 40 years.

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Benign mixed tumors: Parotid

Facial nerve palsy is rare.

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Warthin Tumor:

Sharply marginated mass mostly in parotid tail.

Parenchymal inhomogeneity is a rule with cystic components. Cyst with solid nodule is also seen.

Multicentericity and bilaterality: 20%.

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Warthin Tumor:Inhomogeneity

is a ruleCyst with solid

nodule

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Malignant tumors: Mucoepidermoid carcinoma:

Low grade: well circumscribed mass lesion.High grade: infiltrative heterogeneous mass.

Adenoid cystic carcinoma: Low grade: well circumscribed mass lesion.High grade: infiltrative heterogeneous mass.

Lymphoma: may be primary or secondary with associated multiple bilateral lymph nodes enlargement.

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Mucoepidermoid carcnoma

Adenoid cystic carcinoma

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Carotid space:

SHN IHN

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CS: Pathology: Arterial disease:

Thrombosis, dissection aneurysm or pseudoaneurysm.

Venous disease:Thrombosis or thrombophlibitis.

Benign tumors:Glomus jagulare and glomus vegale paragangliomas.Carotid body paraganglioma.CN 9-11 Schowanoma and neurofibroma.Jugular foramen meningioma.

Malignant tumorsSpreading SCCA or lymphoma.

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CS

Kissing ICAs Ectatic ,medially migrating ICA (RPS)

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IJV thrombosis

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Paragangliomas (glomus tumors): They are neoplasms of neural crest cell origin

that arise within the adventitial layer of blood vessels at multiple sites in the head and neck.

They include the middle ear (glomus tyrnpanicum, parapharyngeal space (glomus jugulare) and larynx.

The two most common paragangliomas to present as a neck massCarotid body tumor (carotid bifurcation)Glomus vagale (along the nodosa ganglion of the

vagus nerve).

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Paragangliomas The constant features:

CT: intense progressive enhancement.MRI: pepper (flow void blood vessels) and

salt (foci of hemorrhage) appearance on T1 WI.

Mass in the neck showing signal void blood vessel signal should alert for paraganglioma (considering anatomical location).

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Paragangliomas: Carotid body tumor arise juxtahyoid and

splays the ICA and ECA.

Multiplicity is common (10-30%)

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Paragangliomas: Glomus vagale arises in the SHN and

displaces ICA anteromedially and IJV posterolaterally.

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Neurogenic tumors: Vagal Neurofibroma and Schwanomas:

without history of neurofibromatosis they could not be differentiated.

They have same location like glomus vagale displacing the ICA anteromedially and the IJV posteromedially.

They show any pattern of enhancement from non to avid enhancement.

DD from paraganglioma by absence of flow void and pattern of enhancement.

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Vagal Schwanoma

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Vagal neurofibroma

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Masticator space :

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Benign masticator space hypertrophy:

Smooth enlargement of the muscles of mastication.

May be up to 3 times volume increase.

May be bilateral with asymmetry.

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Motor denervation: Denervation of muscles supplied by

mandibular division of trigeminal nerve (only motor branch).

The involved muscles are:Muscles of mastication:

○ Masseter, Ptrygoid, Temporalis muscles.Others supplied by V3 nerve:

○ Mylohyoid and anterior belly of digastric muscle.

○ Tensor veli palatini and tensor tympani.

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Motor denervation: stages Acute stage: (<1 month):

Muscle enlargement with edema and enhancement.

Subacute stage: (<12- 20 months);Fatty replacement with starting atrophy. Enhancement may be noted.

Chronic: (>12-20 months):Fatty replacement with volume loss.

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Motor denervation

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Motor denervation

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Masticator space infection: Mostly secondary to molar tooth

infection. Same like all infections in head and

neck:CellulitisAbscess formation.

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Masticator space infection:

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Mandibular nerve schwanoma:

May involve the mandibular nerve through its course from Meckel’s cave and downward.

May involve mandibular nerve branch including inferior alveolar and mental nerves.

It widens the foramen if it is site of involvement.

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Schwanoma: Imaging CT:

Isodense ovoid smooth mass lesion with occasional cystic changes.

Mild to moderate homogeneous or heterogeneous enhancement (due to cystic changes).

Muscle denervation changes may be noted.

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Scwanoma: CT

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Schwanoma: MRI:

T1: isointense mass. Hypointense cystic areas may be seen. Nemorrhagic bright foci may be also noted.

T2: Iso to hyperintense. Cystic changes may be also senen.

T1+C: variable enhancement.

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MRI

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Chondrosarcoma: Malignant tumor of cartilage. Soft tissue mass in masticator space close to

mandible with bone erosion and variable calcification pattern.

CT: Soft tissue density with calcification:

○ Low grade crescents and rings.○ High grade amorphous or no calcifications.

Heterogeneous peripheral enhancement.

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CT

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MRI T1:

Homogeneous intermediate signal. Cartilage matrix or calcifications make it heterogeneous.

Bone marrow infiltration (best seen on T1). T2:

High signal is characteristic. Calcifications make it heterogeneous.

T1+C: enhancement increases with grade.

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MRI

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Mandibular nerve perineural infiltration: Can occur at any point from mental

foramen to root entery zone of CN V on lateral pons.

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Perineural spread: CT:

Widened neural foramen of nerve bony canal.Nerve thickening and enhancement.

MRI:Nerve thickening with low T1 signal, high T2 signal

and intense postcontrast enhancement. Infiltration of masticator space with involvement of

the fat planes especially the perineural fat. Infiltration of fat planes below foramen ovale.Evidence of denervation of the muscles in the

space.

Be aware from enhancing vasa vasorum and ptrygoid plexus of veins. Here, enhancement around dark nerve.

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Retropharyngeal space:

SHN IHN

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RPS

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Non-abscess fluid: May be reactive to nearby pathology:

IJV thrombosis.Longus colli tendinosis.Neck surgery.

Early infection pre-abscess. General principle:

Smooth expansion of the space without enhancement.

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DD from RPS abscess:

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Abscess formation (RPS): < 6years or immunocompromised. Like abscess elsewhere. Tense fluid collection distending the

space with variable enhancement.

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RPS: Lymphadenopathy: Benign: smooth homogeneous < 0.8cm. Malignant: oval to round mass with

occasional enhancement and possible necrosis.

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VISCRAL SPACE:

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Hashimoto thyroiditis: Chronic autoimmune-mediated lymphocytic

inflammation of thyroid gland. Non-specific enlargement of the gland without

calcification or necrosis. CT scan:

Diffuse non-specific enlargement. Hypodensity is typical finding.

MRI: Non-specific finding with high signal during T2WI.

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US Real time:

Early Stages: Non-specific: ○ Enlarged Heterogeneous Hypoechoic gland.○ Hypoechoic foci may be seen (micronodulation).

Late: small hypoechoic heterogenous fibrotic gland. Uncommon: focal disease within normal gland. Color Doppler:

Early: increased vascularity.Late: absent blood flow signal.

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Multinodular goiter: Enlarged gland with multiple nodules. The gland is well marginated. Calcification, necrosis, cystic degeneration

and hemorrhage may be seen. US shows cystic and solid nodules

Hemorrhage may be seen as high echogenecities CT shows cystic and solid nodules with Ca.

Hemorrhage may be seen as high densities .

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Thyroid adenoma: Thyroid adenoma: (true neoplasm with

complete capsule): Single well defined intrathyroid mass within normal gland.

Adenomatous polyp: adenomatous hyperplasia with incomplete capsule: less distinct and may be multiple.

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Malignant thyroid mass: Types:

Differentiated carcinoma:○ Papillary (70%).○ Follicular and carcinoma (10%).

Aggressive tumors:○ Medullary carcinoma (5%).○ Anaplastic carcinoma (5%).

Others including lymphoma and metastasis (10%).

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Thyroid malignancy: Unfortunately the appearance of thyroid

malignancy is usually non-specific. Nodules with irregular margin or mass invading

surrounding structures should alert for malignancy.

60% of malignant nodules have irregular border and also 45% of benign nodules have irregular border.

Calcifications:Microcalcifications malignancyEgg shell calcifications benignity.

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Thyroid malignancy: Role of imaging:

Evaluation of thyroid capsule integrity.Detection of infiltration of surrounding

structures. Identification of malignant lymph nodes.

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Differentiated carcinoma: Invasive mass with

thyroid capsular invasion and metastatic lymph nodes.

Hypoechoic mostly solid tumor but cystic changes are seen in follicular type

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Malignant thyroid:

Medullary carcinoma Anaplastic carcinoma

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Parathyroid gland: Adenoma

It is well defined small mass in expected location. Associated hyperparathyroidism.

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Posterior cervical space:

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Spinal accessory schwanoma:

Oblong well defined mass along the course of spinal accessory nerve.