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PAPER 2 RADIOLOGY DIAGNOSIS 1943 - January 2025 (Regular)

Complete Long Answers

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QUESTION 1 (Long Answer - 30 Marks)

Enumerate the Posterior Fossa Lesions in Pediatrics. Detail Imaging Findings of Any Three.

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ENUMERATION OF POSTERIOR FOSSA LESIONS IN PEDIATRICS

A. Cerebellar Lesions

1. Medulloblastoma - most common malignant posterior fossa tumor in children
2. Cerebellar Pilocytic Astrocytoma (Juvenile Pilocytic Astrocytoma - JPA)
3. Atypical Teratoid/Rhabdoid Tumor (ATRT)
4. Dysembryoplastic Neuroepithelial Tumor (DNET)
5. Hemangioblastoma (sporadic or Von Hippel-Lindau syndrome)
6. Cerebellar Metastasis

B. Fourth Ventricular Lesions

1. Ependymoma
2. Choroid Plexus Papilloma

C. Brainstem Lesions

1. Diffuse Intrinsic Pontine Glioma (DIPG) - most common brainstem lesion
2. Focal Brainstem Glioma
3. Dorsally Exophytic Brainstem Glioma
4. Cervicomedullary Glioma

D. Cerebellopontine Angle (CPA) Lesions

1. Epidermoid Cyst
2. Arachnoid Cyst
3. Vestibular Schwannoma (Acoustic Neuroma) - rare in children unless NF2
4. Meningioma - rare in children

E. Non-Neoplastic Posterior Fossa Lesions

1. Dandy-Walker Malformation
2. Blake's Pouch Cyst
3. Mega Cisterna Magna
4. Posterior Fossa Arachnoid Cyst
5. Cerebellar Abscess
6. Rhombencephalosynapsis

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DETAILED IMAGING FINDINGS - ANY THREE

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1. MEDULLOBLASTOMA

• Most common pediatric posterior fossa tumor (30-40% of all posterior fossa masses in children)
• Most common malignant primary brain tumor in children
• Peak incidence: 5-9 years; boys > girls (2:1)
• WHO Grade IV embryonal tumor
• CSF dissemination in ~33% at initial diagnosis (drop metastases to spine)
• Associated with Gorlin (basal cell nevus) syndrome and Turcot syndrome

• Arises from the cerebellar vermis in 75% of cases (midline)
• Grows into the 4th ventricle
• In older children/adolescents: may arise from cerebellar hemisphere (desmoplastic variant)

• May show signs of raised intracranial pressure: spread sutures, "beaten copper" pattern
• Usually not diagnostic

• Non-contrast CT: Well-defined, midline, hyperdense mass (due to high nuclear-to-cytoplasmic ratio and dense cellularity) in the posterior fossa/4th ventricle
• Calcifications in ~20% of cases
• Cysts/necrosis in 50-60% of cases
• Surrounding vasogenic edema
• Obstructive hydrocephalus (4th ventricle compression)
• Post-contrast: avid, homogeneous enhancement

• T1WI: Iso- to hypointense relative to gray matter; heterogeneous when cystic
• T2WI: Variable - typically isointense to cerebellar cortex (not as bright as pilocytic astrocytoma due to high cellularity); heterogeneous with cysts
• FLAIR: Iso-hypointense
• DWI (Diffusion Weighted Imaging): Restricted diffusion (low ADC values ~0.6-0.8 × 10⁻³ mm²/s) - KEY DISTINGUISHING FEATURE due to densely packed cells
• Post-contrast T1: Intense, heterogeneous enhancement
• MR Spectroscopy: Elevated choline peak, reduced NAA, and characteristic taurine peak (specific for medulloblastoma)
• Perfusion MRI: Elevated rCBV (relative cerebral blood volume)

• M0: No CSF dissemination
• M1-M4: Increasing CSF/systemic spread
• Spine MRI mandatory to look for "sugar coating" (leptomeningeal seeding)

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2. CEREBELLAR PILOCYTIC ASTROCYTOMA (JPA)

• Most common pediatric brain tumor (overall)
• WHO Grade I tumor (excellent prognosis after surgical resection)
• Peak age: 5-15 years
• 40% involve the cerebellum, 20% brainstem
• Slow-growing, well-circumscribed
• Gorlin syndrome association possible

• Cerebellar hemisphere or vermis
• Occasionally optic chiasm, hypothalamus, brainstem

• Non-contrast CT: Large, well-circumscribed, hypodense cyst in the posterior fossa with a slightly denser mural nodule
• Cyst wall may or may not enhance
• Calcifications in ~10-20%
• Mass effect with hydrocephalus
• Post-contrast: Intense enhancement of the mural nodule (wall nodule); cyst wall may or may not enhance

• T1WI:
  • Cyst: hypointense (CSF-like or slightly hyperintense)
  • Mural nodule: isointense
• T2WI:
  • Cyst: markedly hyperintense to brain (high water content, low cellularity)
  • Mural nodule: hyperintense to cerebellar cortex
  • Flow voids may be seen within the nodule (prominent vascularity)
• FLAIR: Cyst suppresses (like CSF) or shows signal if proteinaceous
• DWI: No restricted diffusion (high ADC values) - differentiates from medulloblastoma
• Post-contrast T1: Intense, avid enhancement of mural nodule; the cyst wall does NOT enhance in classical type
• MR Spectroscopy: Elevated choline, reduced NAA, may show lactate peak; NO taurine peak

• Higher T2 signal, no restricted diffusion, peripheral location, mural nodule pattern

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3. EPENDYMOMA

• Third most common pediatric posterior fossa tumor
• Majority are WHO Grade II (myxopapillary variant Grade I)
• Bimodal age distribution; children < 5 years most commonly affected
• CSF dissemination in ~10-15% at presentation (less than medulloblastoma)
• Poorest prognosis of the "big three" posterior fossa tumors due to surgical inaccessibility

• Arises from ependymal cells lining the floor and lateral walls of the 4th ventricle
• Characteristic extension through the foramen of Luschka (lateral) and foramen of Magendie (inferior) - "plastic" or "toothpaste" tumor
• The plastic extension through foramina is pathognomonic

• Non-contrast CT: Iso- to slightly hyperdense heterogeneous 4th ventricular mass
• Calcifications in up to 50% (coarse, punctate) - KEY FEATURE
• Cysts and necrosis common
• Obstructive hydrocephalus
• Post-contrast: Heterogeneous, moderate enhancement

• T1WI: Iso- to hypointense, heterogeneous
• T2WI: Heterogeneously hyperintense; areas of calcification appear hypointense
• FLAIR: Heterogeneous signal
• DWI: Intermediate ADC values (higher than medulloblastoma, lower than JPA)
• Post-contrast T1: Heterogeneous, moderate enhancement
• Key finding: Extension through the foramen of Luschka into the cerebellopontine angle cisterns and through the foramen of Magendie toward the cervical spinal canal ("plastic ependymoma")
• MR Spectroscopy: Elevated choline, reduced NAA; no taurine peak

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BONUS: 4. BRAINSTEM GLIOMA (DIPG)

• Fourth most common pediatric posterior fossa tumor
• Diffuse Intrinsic Pontine Glioma (DIPG) is the most common subtype
• Most lethal pediatric brain tumor; median survival ~9-11 months
• Peak age: 6-9 years
• Histone H3K27M mutation (new WHO designation: Diffuse Midline Glioma H3K27M-altered)

• Diffuse, infiltrative hypodense expansion of the pons
• Usually crosses the midline
• Basilar artery often engulfed (encasement)
• Enhancement variable (rings or patchy)

• T1WI: Ill-defined, low signal brainstem lesion with pons expansion
• T2WI: High signal infiltrative lesion; "engulfing" the basilar artery
• FLAIR: Hyperintense
• DWI: Variable; restricted diffusion in high-grade areas
• Post-contrast: Heterogeneous enhancement (worse prognosis indicator)
• Characteristic pontine expansion with tumor extending around basilar artery

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QUESTION 2 (Long Answer - 30 Marks)

Describe Types of Esophageal Fistula with Their Radio Imaging Findings

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INTRODUCTION

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EMBRYOLOGY AND CLASSIFICATION

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TYPE I - ESOPHAGEAL ATRESIA WITHOUT FISTULA

• The esophagus ends in a blind upper pouch; there is no connection to the trachea
• The lower esophagus connects to the stomach normally
• Prenatal US: Polyhydramnios, absent or small stomach bubble; dilated proximal esophageal pouch ("blind pouch sign")
• Prenatal MRI: Absent lower esophageal lumen (confirms no fistula)
• Postnatal CXR:
  • Coiled nasogastric/feeding tube in upper esophageal pouch (unable to pass)
  • Gasless abdomen (no air in GI tract as no pathway for swallowed/inspired air)
  • AP and lateral views show the coiled tube in upper mediastinum
• Esophagram/Fluoroscopy: Rarely needed; confirms blind pouch; water-soluble contrast preferred

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TYPE II - ESOPHAGEAL ATRESIA WITH UPPER POUCH FISTULA

• Upper esophagus connects to trachea; lower esophagus has no connection
• CXR:
  • Coiled tube in upper esophagus
  • Gas-filled stomach may be present due to upper fistula
  • Tube tip shows fistulous connection on fluoroscopy

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TYPE III - ESOPHAGEAL ATRESIA WITH DISTAL TRACHEOESOPHAGEAL FISTULA

• Upper esophagus ends in blind pouch (no fistula to trachea)
• Lower esophagus connects to the trachea via a fistula (usually at the level of carina or just above)
• Prenatal US: Polyhydramnios; absent/small stomach (though stomach can be seen as air enters via TEF)
• CXR (Classic Findings):
  • Coiled nasogastric tube in the upper pouch
  • Air-distended stomach and bowel (because inspired air passes through the distal TEF into the GI tract)
  • Upper mediastinal widening (distended upper esophageal pouch)
  • Aspiration pneumonia in upper lobe/right upper lobe (recurrent)
• Fluoroscopy (Contrast Study):
  • Water-soluble contrast (not barium, to avoid aspiration complications)
  • Shows upper esophageal pouch with blind ending
  • Fistula not directly seen (located in lower segment)
• Associated anomalies (VACTERL): Vertebral anomalies, Anal atresia, Cardiac defects, TEF, Esophageal atresia, Renal anomalies, Limb defects - look for these on imaging
  • Echocardiography for cardiac defects
  • Renal US for renal anomalies
  • Spinal X-rays

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TYPE IV - ESOPHAGEAL ATRESIA WITH UPPER AND LOWER FISTULA

• Both upper and lower esophagus connect to the trachea
• CXR:
  • Air-filled GI tract
  • NG tube coils in upper esophagus
  • Most complex form; difficult preoperative diagnosis
• Fluoroscopy/CT Bronchoscopy: Needed to map both fistulas

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TYPE V - H-TYPE (OR N-TYPE) TRACHEOESOPHAGEAL FISTULA WITHOUT ATRESIA

• The esophagus is patent and continuous
• Fistula connects esophagus to trachea in an "H" or "N" configuration
• Usually at cervicothoracic junction (C5-T2)
• Clinically: Recurrent aspiration pneumonia, coughing/choking during feeds, abdominal distension (air enters stomach via fistula during crying/coughing)
• Often diagnosed late (weeks to years)

• Usually normal or shows recurrent aspiration changes (right upper lobe or right lower lobe pneumonia)
• No esophageal atresia; NG tube passes normally to stomach

• Water-soluble contrast esophagram in prone position - best for demonstrating H-type fistula
• The fistula runs obliquely from esophagus (above) to trachea (below) in an anterosuperior direction
• Contrast seen crossing from esophagus to trachea and then into airways
• Thin-barium swallow with video fluoroscopy is preferred by many centers for better detail
• Performed in prone position to fill the esophagus under gravity

• CT esophagram/CT bronchoscopy (MDCT with thin cuts): Excellent for mapping fistula in complex cases
• Multiplanar reconstructions (MPR) demonstrate the course
• Can show associated mediastinal pathology

• Gold standard for confirmation; the fistulous opening seen as a pit in the posterior tracheal wall

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ACQUIRED ESOPHAGEAL FISTULAS

Tracheoesophageal Fistula (Acquired)

• CT Chest with oral contrast: Demonstrates the fistulous tract; oral contrast seen in the trachea/bronchi; CT is investigation of choice for acquired TEF
• Shows mediastinal involvement, tumor extension
• Air in mediastinum, aspiration pneumonia
• Barium swallow: contraindicated in acute settings (risk of aspiration and mediastinitis); water-soluble contrast is used

Esophagobronchial Fistula

• Communication between esophagus and bronchus (usually left main bronchus or right lower lobe bronchus)
• Causes: Carcinoma, lymph node erosion (TB, carcinoma), following pneumonectomy
• Imaging:
  • CXR: aspiration pneumonia, lung abscess, air-fluid levels
  • Barium/water-soluble esophagram: contrast fills the bronchial tree
  • CT: demonstrates fistulous tract clearly

Esophagopleural Fistula

• Communication between esophagus and pleural cavity
• Causes: Spontaneous esophageal perforation (Boerhaave syndrome), post-surgical leak, malignancy, foreign body
• CXR: Hydropneumothorax, pleural effusion, mediastinal shift, subcutaneous emphysema
• CT Chest: Pleural effusion with air-fluid levels, mediastinal air, fistulous tract
• Gastrografin esophagram: Contrast extravasation into pleural space

Esophagoaortic Fistula (Rare, Catastrophic)

• Communication between esophagus and aorta
• Causes: Aortic aneurysm erosion, foreign body (fish/chicken bone), post-surgical, malignancy
• CXR: Mediastinal widening
• CT Angiography: Investigation of choice; shows fistulous tract, pseudoaneurysm
• Presents with "herald bleed" followed by massive hematemesis

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SUMMARY TABLE - TYPES OF TEF

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QUESTION 3 (Short Answer - 10 Marks each)

Part 1: SILICOSIS IN RADIO DIAGNOSIS

Definition

At-Risk Occupations

• Surface and underground mining, tunneling
• Stone cutting, quarrying, stone masonry
• Sandblasting (denim workers - accelerated form)
• Construction (concrete demolition/repair)
• Foundry workers
• Artificial/engineered stone countertop fabrication
• Dental technicians, jewelers (chalk molds)
• Agricultural workers (dust storms)

Types of Silicosis

• Exposure: >10 years to lower concentrations
• Pathological hallmark: silicotic nodule - well-circumscribed lesion with central acellular hyalinized collagen (whorled appearance) surrounded by dust-laden macrophages

• Exposure: 5-10 years to higher concentrations
• Faster progression than classic form
• Radiological features similar to chronic silicosis

• Exposure: Short, massive exposure (months to <5 years)
• Mimics pulmonary alveolar proteinosis
• Most severe form; can be fatal within months

Radiological Features

• Small rounded opacities (nodules), predominantly in the upper and mid-zones of both lungs (upper lobe predominance)
• ILO classification: p, q, or r type rounded opacities (diameter 1-10 mm)
• Bilateral symmetrical distribution
• Hilar lymphadenopathy with characteristic "eggshell calcification" of hilar nodes (calcification at the periphery of the node) - PATHOGNOMONIC of silicosis
• As disease progresses: nodes enlarge, parenchymal nodules coalesce

• Silicotic nodules enlarge and coalesce into masses > 1 cm (ILO category B or C; or lesions > 10 cm)
• "Angel wings" or "butterfly" appearance - bilateral upper/mid-zone opacities migrating toward the hila
• Adjacent emphysema (perifocal or bullous) - the masses "sweep" toward the hila over years
• Traction bronchiectasis

• Bilateral ground-glass opacities and consolidation
• Perihilar distribution
• "Crazy-paving" pattern on CT (interlobular septal thickening + GGO)
• No nodules initially

• Centrilobular and subpleural small rounded nodules, upper lobe predominance
• Interlobular septal thickening
• Hilar and mediastinal lymphadenopathy
• Eggshell calcification of lymph nodes (CT shows this better than CXR)
• Interlobular fissure nodularity

• Large conglomerate masses, upper lobe posterior regions
• Surrounding emphysema
• Displacement of bronchovascular structures
• May develop central necrosis (Caplan syndrome: PMF + rheumatoid arthritis)

• Diffuse GGO
• Bilateral airspace consolidation (perihilar)
• Crazy-paving pattern
• Pleural effusion may occur

Complications (Detectable on Imaging)

• Tuberculosis (silicotuberculosis) - cavitation, upper lobe consolidation
• Cor pulmonale - enlarged right heart, pulmonary arteries
• Spontaneous pneumothorax - bullous disease
• Lung carcinoma (increased risk)
• Progressive respiratory failure

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Part 2: CAUSES OF HILAR ENLARGEMENT AND THEIR DIFFERENTIALS

Normal Hilum

• The hila are formed by the pulmonary arteries, bronchi, pulmonary veins, and lymph nodes
• On CXR: left hilum is usually higher than the right by up to 1-1.5 cm
• Normal hilar density = pulmonary arteries

Classification of Hilar Enlargement

Differentiating Vascular vs. Nodal Enlargement

• Vascular: Smooth contour, follows pulmonary artery branching, associated with RV/PA enlargement, responds to pulmonary artery pressure changes
• Nodal: Lobulated, irregular contour, dense; does NOT taper; may have mediastinal extension

CT/HRCT Role

• CT with contrast is the investigation of choice
• Differentiates vascular from nodal hilar enlargement definitively
• Characterizes node morphology (central necrosis = TB; eggshell calcification = silicosis/histoplasmosis; homogeneous = sarcoidosis/lymphoma)
• Guides biopsy

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QUESTION 4 (Short Answer - 10 Marks each)

Part 1: DESCRIBE TYPES OF BONE METASTASIS WITH THEIR DIFFERENTIALS

Introduction

Most Common Primary Tumors

1. Breast (osteolytic, osteosclerotic, or mixed) - 70-80%
2. Bronchus/Lung - 40-80%
3. Prostate (typically osteosclerotic) - 80-85%
4. Kidney/Renal cell (purely lytic) - 20-35%
5. Thyroid - 50-60%

Distribution

• Axial skeleton > appendicular skeleton (red marrow-containing bones)
• Most common sites: Spine (thoracic > lumbar > cervical), pelvis, ribs, sternum, skull, proximal femur, proximal humerus
• Batson's vertebral venous plexus explains spinal predominance (valveless plexus)
• Prostatic carcinoma: predilection for lumbosacral spine and pelvis

Types of Bone Metastasis

• Plain Radiograph: Geographic area of bone destruction; "punched out" lytic lesion
• Ill-defined margins with permeative pattern in aggressive lesions
• Cortical destruction and breakthrough
• Soft tissue mass extension
• Pathological fracture (vertebra plana, femoral neck fracture)
• No periosteal reaction (typically)
• Vertebral involvement: pedicle destruction ("winking owl" sign on AP view of spine - loss of one pedicle)
• Skull: "Raindrop skull" - multiple lytic lesions (myeloma > metastasis)

• Kidney (nearly always purely lytic; may be expansile, "blow-out" appearance)
• Thyroid (expansile lytic lesions)
• Breast (most common)
• Lung
• Melanoma (hypervascular)

• Plain Radiograph: Increased bone density, ivory-like sclerosis
• Vertebral body: "ivory vertebra" (completely dense vertebra)
• Multiple dense foci in axial skeleton
• No bone expansion typically
• Note: The sclerosis reflects host bone osteoblastic response, NOT tumor bone (unlike osteosarcoma)

• Prostate (most common cause of sclerotic metastases; lumbosacral spine/pelvis)
• Breast (can also be sclerotic, especially post-treatment)
• Carcinoid
• Medulloblastoma
• Hodgkin lymphoma (ivory vertebra)
• Bladder, stomach (rare)

• Prostate carcinoma (metastasis) - most common
• Lymphoma (Hodgkin's)
• Osteoblastoma (rare)
• Tubercular spondylitis (with healing)
• Metastasis (others: bladder, breast, gastric)
• Paget's disease (vertebra also enlarged)

• Areas of both lucency and sclerosis
• Common in breast metastases (mixed appearance)
• Treatment response: lytic lesions may become sclerotic (healing response)

• Less common; arise along diaphyses of long bones
• Primary sources: lung, kidney, breast
• May show saucerization or periosteal reaction (more than medullary type)

Imaging Modalities

• First-line but insensitive (requires 30-50% bone loss for detection)
• Shows lytic, sclerotic, or mixed lesions; cortical destruction; soft tissue mass; periosteal reaction; pathological fracture

• Most cost-effective screening method
• Shows multiple foci of increased uptake (hot spots) - axial skeleton predominance
• "Cold spots" (photopenic) in purely lytic lesions (renal cell carcinoma) or infarcted metastases
• "Superscan": diffuse homogeneous increased uptake, poor visualization of kidneys (extensive bone metastases - prostate/breast)

• Sensitive for cortical destruction, soft tissue mass, epidural extension
• Mediastinal and abdominal staging; guided biopsy
• CT myelogram for cord compression

• Most sensitive modality for bone marrow involvement (before cortical destruction)
• T1WI: Low signal in tumor (replaces normal bright fatty marrow)
• T2WI/STIR: High signal in metastases (edema, tumor)
• STIR sequence: Very sensitive for marrow infiltration
• Whole-body MRI: emerging sensitive screening tool

• Most sensitive and specific overall
• Detects metabolically active metastases
• Particularly useful for lytic lesions (bone scan can miss these)
• Evaluates systemic disease burden simultaneously

Differentials for Bone Metastases

1. Multiple myeloma (raindrop skull; Bence-Jones protein; plasma cell dyscrasia)
2. Lymphoma (Hodgkin's: ivory vertebra; NHL: lytic)
3. Polyostotic fibrous dysplasia (ground glass, shepherd's crook deformity, skin café-au-lait)
4. Brown tumors of hyperparathyroidism (PTH elevated, subperiosteal resorption)
5. Histiocytosis X / Langerhans cell histiocytosis (children; punched-out skull lesions)
6. Paget's disease (bone expansion, coarsened trabecular, "picture frame" vertebra)

1. Primary bone sarcoma (osteosarcoma, Ewing's sarcoma - younger age, periosteal reaction, Codman's triangle)
2. Benign lesions (enchondroma, fibrous dysplasia, bone cyst)
3. Infection/osteomyelitis (periosteal reaction, sequestrum)

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Part 2: RADIOLOGICAL ANATOMY OF THE ORAL CAVITY

Introduction

Subdivisions of the Oral Cavity

1. Lips (upper and lower)
2. Buccal mucosa (inner cheek surface; attached to alveolar ridges)
3. Alveolar ridges (upper and lower; include teeth and adjacent gingiva)
4. Floor of mouth - below the mobile tongue
5. Hard palate - bony roof of mouth (palatine process of maxilla + horizontal plate of palatine bone)
6. Retromolar trigone (RMT) - posterior gingiva behind lower molar teeth, overlying ascending ramus of mandible
7. Anterior 2/3 of the tongue (oral tongue) - mobile portion anterior to the circumvallate papillae

Spaces of the Oral Cavity

• Paired; above the mylohyoid muscle; below the mucous membrane of the floor of mouth
• Contents: sublingual gland, Wharton's duct (submandibular gland duct), hypoglossal nerve (CN XII), lingual nerve, deep part of submandibular gland
• Communicates with submandibular space around the posterior free edge of mylohyoid

• Below the mylohyoid muscle; bounded superiorly by mylohyoid, posteriorly by posterior belly of digastric
• Contents: submandibular gland (superficial lobe), submandibular lymph nodes, facial artery and vein

• Contains: masseter, medial and lateral pterygoid muscles, ramus and posterior body of mandible, inferior alveolar nerve
• Important for spread of oral cavity tumors (especially RMT cancers)

Key Structures and Their Radiological Appearance

Dental Anatomy on Imaging

• Shows all teeth, mandible, and maxilla in one image
• 32 permanent teeth (adult): 4 incisors, 2 canines, 4 premolars, 6 molars (each jaw)
• Shows tooth roots, pulp chambers, periodontal ligament space, alveolar bone
• Used for: dental caries, periapical disease, impacted teeth, jaw lesions, fractures

• Shows individual teeth and supporting bone
• Demonstrates: root morphology, caries, periapical abscess, root resorption

• Identifies impacted teeth, cysts, bone tumors, radiolucencies

Salivary Gland Anatomy on Imaging

• Located lateral to the masseter; divided by CN VII (facial nerve) into superficial and deep lobes
• CT: low-density due to fatty component (distinguishes from other glands)
• Stensen's duct: drains anteriorly into buccal mucosa opposite upper 2nd molar

• In submandibular triangle; Wharton's duct (5 cm long) drains into floor of mouth at sublingual papilla
• Most common site of salivary calculi (80%)

• Smallest major salivary gland; above mylohyoid
• Bartholin's duct (opens into Wharton's duct or directly into floor of mouth)

Clinical Applications of Oral Cavity Radiology

Important Radiological Landmarks

• Mylohyoid line: Oblique internal ridge on medial mandible (mylohyoid muscle attachment) - separates sublingual from submandibular space
• Retromolar trigone: Posterior to lower 3rd molar; RMT cancers spread to masticator space and pterygoid muscles
• Foramen cecum of tongue: Midline depression at junction of anterior 2/3 and posterior 1/3 of tongue
• Valleculae: Recesses between base of tongue and epiglottis (junction of oral cavity/oropharynx)

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SUMMARY