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753 Cards in this Set

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Patients with Sjogren syndrome are at increased risk for developing what diffuse lung diseases
Lymphocytic interstitial pneumonitis (LIP). Non-Hodgkin pulmonary lymphoma.
Ankylosing spondylitis lung involvement
Young to middle-aged man with spine changes (kyphosis, spinal ankylosis). Increased lung volumes. Upper lobe fibrobullous disease. Simulates postprimary fibrocavitary Tb or mycetoma formation.
These histologic terms provide the most precise method of classifying the idiopathic interstitial pneumonias
UIP. Acute interstitial pneumonia (AIP). COP. Respiratory bronchiolitis-associated interstitial lung disease (RB-ILD). DIP. Nonspecific interstitial pneumonia (NSIP).
Usual Interstitial Pneumonia
Most common of the idiopathic interstitial pneumonias. Most cases are sporadic. 30% of cases associated with collagen vascular or immunologic disorder. Findings: Irregular septal or subpleural thickening. Intralobular lines. Honeycombing. Traction bronchiectasis. Typically most severe in peripheral and basal lungs.
Acute Interstitial Pneumonia
Diffuse ground-glass opacity and consolidation with air bronchograms. Linear opacities, honeycombing, and traction bronchiectasis are uncommon.
Conditions associated with BOOP, organizing pneumonia.
Viral infection (influenza, adenovirus, measles). Toxic fume inhalation (sulfur dioxide, chlorine). Collagen vascular disease (rheumatoid arthritis and SLE). Organ transplantation (bone marrow, lung, and heart-lung). Drug reactions. Chronic aspiration.
Cryptogenic Organizing Pneumonia
Idiopathic form of organizing pneumonia. Most common finding: Patchy consolidation or ground-glass opacity with subpleural or peribronchial distribution. Scattered nodular opacities may be present.
Respiratory Bronchiolitis-Associated Interstitial Lung Disease
Typically young, heavy smokers. Scattered ground-glass opacities. Small centrilobular nodules with upper lobe predominance.
Desquamative Interstitial Pneumonia
95% are cigarette smokers. Cannot be radiologically distinguished from UIP. Bibasilar reticular opacities. Normal or midly decreased lung volumes. May have ground-glass opacities. Honeycombing is rare.
Neurofibromatosis ILD
Generally asymmetric upper lung bullae. Generally symmetric lower lung interstitial fibrosis.
Tuberous Sclerosis (TS) ILD
Indistinguishable from LAM. Symmetric bilateral reticular or reticulonodular opacities. Scattered lung cysts. Normal to increased lung volumes. Pneumothorax is common
Lymphangioleiomyomatosis
Exclusively in women. Lung cysts separated by interlacing bundles of smooth muscle. May obstruct lymphatics causing chylothorax. Poor prognosis.
Alveolar Septal Amyloidosis
Simulates silicosis or lung sarcoidosis. Upper lung reticulonodular opacities.
Chronic Aspiration Pneumonia
Irregular reticular interstitial opacities.
3 major pneumoconioses
Asbestosis. Silicosis. CWP.
Asbestosis
Pleura: Parietal pleural plaques. Pleural effusion. Localized visceral pleural fibrosis. Diffuse pleural fibrosis. Mesothelioma. Lung parenchyma: Interlobular septal thickening. Interstitial fibrosis (asbestosis). Rounded atelectasis. Bronchogenic carcinoma. Lower lung predominance.
Silicosis
Mining, ceramic work, and sandblasting. Upper lobe and parahilar nodules. Nodule calcification may occur. Egg shell calcification of hilar lymph nodes. Silicoproteinosis like alveolar proteinosis has increased susceptibility to TB.
Coal Worker's Pneumoconiosis
Predominantly upper lung reticulonodular or small nodular opacities.
Rare Pneumoconioses
Berylliosis. Aluminum. Hard metal (cobalt, tungsten).
Hypersensitivity Pneumonitis
Inhaled antigenic organic dusts: Farmer's lung (moldy hay). Humidifier lung (thermophilic bacteria). Bird-fancier's lung (avian proteins). Acute and chronic forms. Chronic disease findings: Interlobular and intralobular interstitial thickening. Honeycombing, Traction bronchiectasis. May spare costophrenic angles.
Lung Sarcoidosis staging
0 Normal chest radiograph. 1 Bilateral hilar lymph node enlargement. 2 Bilateral hilar lymph node enlargement and parenchymal disease 3. Parenchymal disease only. 4 Pulmonary fibrosis.
Sarcoidosis ILD
Common findings: Symmetric hilar adenopathy allows distinction from malignancy and TB. Symmetric mid and upper lung reticulonodular opacities. Perilymphatic interstitial nodules, 3 to 10 mm.
Langerhans Cell Histiocytosis of Lung
Very high association with cigarette smoking. Mid and upper lung centrilobular small nodules. In late stages may develop cysts or bullae. Risk of pneumothorax. Nodule-cyst evolution: Nodule to Cavitated nodule to Thick-walled cyst to Thin-walled cyst.
Wegener Granulomatosis
Necrotizing granulomatous vasculitis involving upper and lower respiratory tracts and kidneys. Discrete nodules or masses with central necrosis and cavitation. May mimic Goodpasture syndrome and idiopathic pulmonary hemorrhage. Tracheal or bronchial lesions may be present. c-ANCA positive.
Chronic Eosinophilic Pneumonia
Symptoms and radiographic abnormalities last longer than 1 month. Predilection for women. Responds to corticosteroid therapy, improving within 4 to 7 days. Peripheral, homogeneous, ill-defined areas of consolidation that may parallel the chest wall
Hypereosinophilic syndrome
Male predominance. Blood eosinophilia. Cardiomegaly. Pulmonary edema. Pleural effusions. Pulmonary parenchymal infiltration with eosinophils may produce interstitial or airspace opacities.
Eosinophilic Lung Disease Associated With Autoimmune Diseases
Wegener granulomatosis. Sarcoidosis. Rheumatoid lung disease. Polyarteritis nodosa. Allergic angiitis and granulomatosis.
Eosinophilic Lung Disease of Identifiable Etiology
Drugs (Nitrofurantoin and Penicillins). Parasites (Ascaris lumbricoides, Strongyloides stercoralis).
Pulmonary alveolar proteinosis
Lipoproteinaceous material deposits within alveoli. Predilection for males in their 20s to 40s. Bilateral symmetric perihilar airspace opacification. Crazy paving CT finding: Geographic ground-glass opacities with thickened interlobular and intralobular septa. Prone to superinfection with Nocardia, Aspergillus, Cryptococcus, and atypical mycobacteria.
Alveolar microlithiasis
Deposition of minute calculi within alveolar spaces. Confluent bilateral dense micronodular opacities. So-called black pleura sign. Apical bullous disease is common.
Diffuse pulmonary ossification
Formation of bone within lung parenchyma. Associations: Mitral stenosis. UIP. Amyloidosis.
Tracheocele
Paratracheal air cysts. True diverticula. Occur at weakened posterior membrane of cervical trachea.
Tracheal bronchus
Bronchus suis. Accessory bronchus to all or a portion of right upper lobe. Arises from right lateral tracheal wall within 2 cm of tracheal carina. Associated with congenital tracheal stenosis and aberrant left pulmonary artery.
Primary neoplasms of trachea
Malignant: Squamous cell carcinoma. Adenoid cystic carcinoma (cylindroma). Benign: Chondroma. Fibroma. Squamous cell papilloma. Hemangioma.
Tracheal Narrowing
Saber-sheath trachea. Amyloidosis. Tracheobronchopathia osteochondroplastica. Relapsing polychondritis. Wegener granulomatosis. Tracheal scleroma.
Tracheal dilation
Tracheobronchomegaly (Mounier-Kuhn syndrome). Tracheomalacia. Interstitial pulmonary fibrosis.
Saber-sheath trachea
Coronal diameter is less than two thirds of sagittal diameter. Affects older men with chronic obstructive pulmonary disease (COPD).
Tracheobronchopathia osteochondroplastica
Multiple submucosal osseous and cartilaginous deposits within trachea and central bronchi of elderly men. Spares membranous posterior wall of trachea.
Relapsing polychondritis
Systemic autoimmune disorder. Affects cartilage of earlobes, nose, larynx, tracheobronchial tree, joints, and large elastic arteries. Diffuse smooth wall thickening of the wall of trachea and central bronchi with luminal narrowing.
Tracheobronchomegaly (Mounier-Kuhn syndrome)
Congenital. Associated with Ehlers-Danlos syndrome. Men under age 50. Trachea and central bronchi measure greater than 3.0 cm and 2.5 cm.
Tracheobronchomalacia
Diffuse tracheal and central bronchial dilation. Congenital or acquired (COPD, Chronic bronchitis, Cystic fibrosis, Relapsing polychondritis).
Fallen lung sign
Subtended lung remains collapsed against lateral chest wall. Secondary to bronchial injury. Responds poorly to chest tube evacuation.
Broncholithiasis
Calcified material within bronchus. Usually from eroding calcified lymph nodes (Histoplasmosis or TB).
Asthma
Transient bronchial narrowing. Peribronchial cuffing and tram tracking. Air trapping: Hyperinflation, Flattening or inversion of diaphragm, Attenuation of peripheral vascular markings. Prominence of the retrosternal airspace. Complications: Pneumomediastinum. Pneumothorax, Subpleural blebs from expiratory air dissection.
Chronic bronchitis
Excess production of sputum on most days for at least 3 months in 2 consecutive years. 50% have normal chest radiographs. Some patients show peribronchial cuffing or tram tracks.
Bronchiectasis
Permanent dilation of bronchi. Cylindric bronchiectasis: mild diffuse dilation. Varicose bronchiectasis: cystic dilation interrupted by focal areas of narrowing. Cystic bronchiectasis: localized saccular dilation. Caused by chronic inflammation with cartilage damage and dilation. Localized bronchiectasis is most commonly a result of prior TB. Generalized bronchiectasis is seen in cystic fibrosis. Central bronchiectasis: Allergic bronchopulmonary aspergillosis. Cystic fibrosis. Bronchial atresia. Acquired central bronchial obstruction.
Cystic fibrosis
Production of abnormally thick, tenacious mucus. Recurrent infection commonly with Pseudomonas aeruginosa or Staphylococcus aureus. Severe bronchiectasis. Hyperinflation with predominantly upper lobe bronchiectasis and mucus plugging.
Dysmotile cilia syndrome
May result in Rhinitis. Sinusitis. Bronchiectasis. Dysmotile spermatozoa and sterility. Situs inversus. Dextrocardia.
Kartagener syndrome triad
Sinusitis. Situs inversus.. Bronchiectasis.
Allergic bronchopulmonary aspergillosis
Hypersensitivity reaction to Aspergillus. Asthma, blood eosinophilia, bronchiectasis with mucus plugging, and circulating antibodies to Aspergillus antigen. Proximal upper lobe bronchiectasis with mucoid impaction. Finger in glove appearance.
Emphysema
Permanent enlargement of airspaces distal to terminal bronchiole. Destruction of alveolar walls without obvious fibrosis.
Centrilobular emphysema
Airspace distention in central portion of lobule. Spares distal portions of the lobule. Upper lobe predominance. Associated with cigarette smoking.
Panlobular emphysema
Distention of airspaces throughout lobule. Destruction of central respiratory bronchioles and peripheral alveolar sacs and alveoli. Predilection of lower lobes. Associated with alpha-1 antitrypsin deficiency.
Paraseptal emphysema
Distention of peripheral airspaces adjacent to interlobular septa. Spares centrilobular region. Generally involves subpleural regions of upper lobes.
Paracicatricial or irregular emphysema
Lung destruction associated with fibrosis. No consistent relationship to a given portion of the lobule. Commonly associated with old granulomatous inflammation.
Emphysema findings
Diffuse hyperlucency (panlobular). Flattening and depression of hemidiaphragms. Increased retrosternal airspace (panlobular > centrilobular). Bulla. Enlarged central pulmonary arteries. Right heart enlargement (centrilobular). Loss of pulmonary capillary bed.
Arterial deficiency emphysema versus increased markings emphysema.
Arterial deficiency: Predominantly panlobular emphysema. Hyperinflated lungs with peripheral vascular attenuation and bullae. Pink Puffers. Increased markings: Increased linear parenchymal markings. Small airways thickening of chronic bronchitis. Bullae uncommon. Blue Bloaters.
Bulla defined
Thin-walled cystic space > 1 cm in diameter. Found within lung parenchyma.
Bullae may be seen in diseases that cause chronic upper lobe fibrosis, such as
Sarcoidosis. Pulmonary Langerhans cell histiocytosis. Ankylosing spondylitis.
Primary bullous disease
Isolated bullae without intervening emphysema or interstitial lung disease. Associated with: Marfan or Ehlers-Danlos syndromes. Intravenous drug use. HIV infection. Vanishing lung syndrome.
CT findings and associations of infectious bronchiolitis
Tree-in-bud opacities. Generally due to infection: Viral. Atypical. Mycobacterial.
CT findings of diffuse panbronchiolitis
Tree-in-bud opacities. Bronchial dilation and thickening.
CT findings and associations of Respiratory bronchiolitis–associated interstitial lung disease
Centrilobular and geographic ground-glass opacities. Cigarette smoking.
CT findings and associations of Hypersensitivity pneumonitis (subacute)
Centrilobular ground-glass nodules. Air trapping on expiratory scans. Inhaled organic antigen.
CT findings and associations of Follicular bronchiolitis
Centrilobular ground-glass nodules. Rheumatoid arthritis. Sjögren syndrome.
CT findings and associations of Constrictive bronchiolitis
Mosaic attenuation with air trapping on expiratory scans. Bronchial dilation (late). Transplant patients. Drug reactions. Inhalation injury.
Transudative pleural effusion lab values
Pleural/serum protein ratio less than 0.5. Pleural/serum LDH ratio less than 0.6. Pleural LDH less than 200 IU/L.
Infectious causes of pleural effusion?
Bacterial/mycobacterial. Viral. Fungal. Parasitic.
Cardiovascular causes of pleural effusion?
Heart failure. Pericarditis. Superior vena cava obstruction. Postcardiac surgery. Myocardial infarction. Pulmonary embolism.
Neoplastic causes of pleural effusion?
Bronchogenic carcinoma. Metastases. Lymphoma. Pleural or chest wall neoplasms (mesothelioma).
Immunologic causes of pleural effusion?
Systemic lupus erythematosus. Rheumatoid arthritis. Sarcoidosis (rare). Wegener granulomatosis.
Inhalational cause of pleural effusion?
Asbestosis.
Trauma causes of pleural effusion?
Blunt or penetrating chest trauma.
Abdominal disease causes of pleural effusion?
Cirrhosis (hepatic hydrothorax). Pancreatitis. Subphrenic abscess. Acute pyelonephritis. Ascites (from any cause). Splenic vein thrombosis.
Miscellaneous causes of pleural effusion?
Drugs. Myxedema. Ovarian tumor.
Pleural effusion from congestive heart failure features
Transudative. Bilateral, right larger than left. Isolated right effusion twice as common as isolated left effusion.
Findings on CT that are fairly specific for the presence of an exudative pleural effusion
Thickening and enhancement of parietal pleura. Loculations. Soft tissue lesions along parietal pleura outlined by pleural fluid.
Tumors most commonly associated with pleural effusion are, in order of frequency,
Lung carcinoma. Breast carcinoma. Pelvic tumors (ovarian fibroma = Meigs syndrome). Gastric carcinoma. Lymphoma.
Lung abscess versus empyema?
Empyema: Oval. Oriented longitudinally. Thin. Smooth (split pleura sign). Obtuse chest wall angle. Compresses lung. Requires drainage. Abscess: Round. Thick and irregular wall. Acute chest wall angle. Consumes lung. Antibiotics and postural drainage to treat.
Most common intrathoracic manifestation of rheumatoid arthritis
Pleural effusion.
Most common causes of chylothorax are
Malignancy. Iatrogenic trauma. TB
Left chylothorax versus right chylothorax?
Left chylothorax: Injury to upper duct. Right chylothorax: Injury to lower duct.
Bronchopleural Fistula
Communication between lung and pleural space. If bronchus involved, may result in empyema. If peripheral airspace (bronchiole) involved, may result in intractable pneumothorax.
Primary spontaneous pneumothorax
Often occurs in young or middle-aged men. Predilection of taller individuals. Results from bleb or bulla rupture, usually within upper lungs.
Secondary Spontaneous Pneumothorax
COPD. Asthma. Valsalva (cocaine, marijuana, labor). Sarcoidosis. Langerhans cell histiocytosis. Lymphangioleiomyomatosis. Necrotizing pneumonia. Abscess. Mechanically ventilated patients.
Catamenial pneumothorax
Rare recurrent pneumothoraces. Occurs with menses. Pleural endometrial implants. Treated with OCPs.
Most common cause of tension pneumothorax
Iatragenic trauma in mechanically ventilated patients.
Causes of pleural thickening
Pneumonia. Pulmonary infarct. Trauma. Asbestos exposure (bilateral).
Causes of pleural calcification
Visceral pleura: Hemothorax, Empyema (tuberculosis). Parietal pleura:  Asbestos exposure (bilateral).
Causes of pleural/extrapleural masses
Benign: Fibroma. Lipoma. Neurofibroma. Malignant: Metastases (usually multiple).  Mesothelioma (usually diffuse pleural thickening). Other: Loculated pleural effusion/empyema. Hematoma.
Fluid within calcified pleural layers seen on CT suggests
Active empyema. Most commonly within patients with prior TB.
Fibrothorax
Pleural thickening extending over more than one fourth of the costal pleural surface. Commonly results from resolution of an exudative pleural effusion (including asbestos-related effusions), Empyema, or Hemothorax. Pleurectomy (decortication) may be necessary to restore function.
Malignant pleural disease is most often caused by one of four conditions:
Metastatic adenocarcinoma (lung, breast, ovary, kidney, GI tract). Invasive thymoma or thymic carcinoma. Mesothelioma. Rarely non-Hodgkin lymphoma.
Benign and malignant Asbestos-Related Pleural Diseases
Benign: Pleural plaques. Pleural effusions. Diffuse pleural fibrosis. Malignant: Mesothelioma.
When viewed en face, calcified pleural plaques appear as
Geographic opacities. Llikened to a holly leaf.
Poland syndrome
Autosomal recessive disorder. Unilateral absence of sternocostal head of pectoralis major. Ipsilateral syndactyly. Rib anomalies.
Most common benign neoplasm of chest wall
Lipoma
Most common malignant soft tissue neoplasms of the chest wall in adults.
Fibrosarcomas. Liposarcomas.
A rare malignant neoplasm arising from the chest wall of children and young adults
Askin tumor. Arises from primitive neuroectodermal rests. Very aggressive with a poor prognosis.
Benign chest wall lesions
Abscess. Hematoma. Lipoma. Hemangioma. Desmoid tumor.
Inferior rib notching causes
Coarctation of aorta. Aortic thrombus. Takayasu arteritis. SVC syndrome. Neurofibromatosis.
Suprior rib notching cause
Paralysis.
Benign rib neoplasms, most common first
Osteochondroma. Enchondroma. Osteoblastoma.
Most common primary rib malignancy
Chondrosarcoma.
Rib malignancies
Most common: Myeloma. Metastatic carcinoma. Primary malignancies: Chondrosarcoma. Osteogenic sarcoma. Fibrosarcoma.
Most common metastatic lesions to ribs
Breast cancer. Lung cancer.
Expansile lytic rib metastases are seen most commonly from
Renal cell carcinoma. Thyroid carcinoma.
Sclerotic rib metastases are most commonly seen in
Breast cancer. Prostate cancer.
Pleuropulmonary infections that may traverse the pleural space and produce a chest wall infection include
TB. Actinomycosis. Nocardiosis.
Sprengel deformity
Congenital hypoplastic and elevated scapula.
Klippel-Feil syndrome.
Sprengel deformity (hypoplastic, elevated scapula). Omovertebral bone. Fused cervical vertebrae. Hemivertebrae. Kyphoscoliosis. Rib anomalies.
Erosion of the distal clavicles
Rheumatoid arthritis: Well-defined pointed distal clavicle. Hyperparathyroidism: Irregular and wide distal clavicle.
H-shaped or Lincoln log vertebrae on lateral chest radiographs
Sickle cell anemia.
Rugger jersey appearance to thoracic spine on lateral chest radiographs
Renal osteosclerosis.
Pectus excavatum is commonly associated with congenital connective tissue disorders, such as
Marfan syndrome. Poland syndrome. Osteogenesis imperfecta. Congenital scoliosis.
Pectus carinatum
Outward bowing of sternum. May be congenital or acquired.
Eventration of the diaphragm
Congenital absence or underdevelopment of diaphragmatic musculature. Localized elevation of anteromedial hemidiaphragm in older individuals.
Unilateral diaphragmatic paralysis is usually caused by
Surgical injury or neoplastic involvement of phrenic nerve.
Bilateral Diaphragmatic Elevation that is not effort related may be caused by
Neuromuscular disturbance. Intrathoracic or intra-abdominal disease.
Bochdalek Hernia
Herniation through embryonic pleuroperitoneal canal. Neonates present with large hernias with lung hypoplasia and respiratory distress. Adults present with small hernias, mostly on the left side (liver thought to be protective).
Morgagni Hernia
Parasternal diaphragm defect. Invariably right sided. Asymptomatic cardiophrenic angle mass.
Primary diaphragmatic tumors
Benign: Lipomas. Fibromas. Schwannomas. Neurofibromas. Leiomyomas. Echinococcal cysts and extralobar sequestrations may be found within the diaphragm. Metastatic invasion more common than primary malignancy (Fibrosarcoma): Lower lobe bronchogenic carcinoma. Mesothelioma.
Cystic adenomatoid malformation
Usually seen in infancy. One or several large cysts lined with respiratory epithelium with scattered mucous glands, smooth muscle, and elastic tissue. Round, air-filled masses that compress adjacent lung and mediastinum.
Bronchial atresia presentation
Central bronchial mucocele with peripheral hyperlucency in a young, asymptomatic patient.
Intralobar and extralobar sequestration blood supply and drainage
Intralobar sequestration: Single large artery from infradiaphragmatic aorta. Pulmonary vein drainage. Extralobar sequestration: Small branches systemic arteries and occasionally pulmonary arteries. Systemic venous drainage (inferior vena cava, azygos, or hemiazygos veins).
Hypogenetic lung-scimitar syndrome
Variant of hypoplastic lung with abnormal venous drainage to the IVC just above or below right hemidiaphragm. Small right hemithorax with diaphragmatic elevation or eventration. Dextroposition of heart. Herniation of left lung anteriorly into right hemithorax.
Three radiographic patterns of aspiration pneumonitis
Extensive bilateral airspace opacification. Diffuse but discrete airspace nodular opacities. Irregular parenchymal opacities that are not obviously airspace.
Exogenous lipoid pneumonia
Older patients with swallowing disorders or gastroesophageal reflux. Use mineral oil as a laxative or inhale oily nose drops. Fat density opacity.
Drug that cause drug induced chest diseases
Lupus-like syndrome (procainamide, isoniazid, hydralazine). Nitrofurantoin. Bleomycin. Methotrexate. Amiodarone.
A confident diagnosis of hamartoma can be made when HRCT shows
Nodule less than 2.5 cm with a smooth or lobulated border and containing focal fat. May have popcorn calcification.
Benign neoplasm arising from neural elements in the central airways or lung parenchyma. The skin is the most common site for these tumors.
Granular cell myoblastoma.
Bronchogenic adenocarcinoma features
Most common type of lung cancer (nonsmokers, too). Arise from bronchiolar or alveolar epithelium. Irregular or spiculated appearance. ccur in the lung periphery.
Bronchioloalveolar cell carcinoma (BAC)
Grows along bronchiolar and alveolar walls (lepidic growth). May appear as: Solitary nodule. Focal ground-glass opacity. May mimic pneumonia or bilateral nodular airpsace processes.
Squamous cell carcinoma features
Arises centrally within lobar or segmental bronchi. Central necrosis with cavitation may be seen. Generally presents as hilar mass and atelectasis.
Small cell carcinoma features
Arises centrally within main or lobar bronchi from bronchial neuroendocrine (Kulchitsky) cells. Hematogenous dissemination. Hilar/mediastinal mass.
Large cell bronchogenic carcinoma radiographic feature
Large peripheral mass.
In addition to cigarette smoke, well-recognized risk factors for the development of bronchogenic carcinoma include
Asbestos exposure. Previous Hodgkin lymphoma. Radon exposure. Viral infection. Diffuse interstitial or localized lung fibrosis.
Most common radiographic findings from endobronchial tumor obstruction.
Resorptive atelectasis. Obstructive pneumonitis.
Majority of pancoast tumors, histology type
SCC. Adenocarcinoma.
Pancoast tumor symptoms
Arm pain and muscular atrophy due to brachial plexus involvement. Horner syndrome (ptosis, anhydrosis, miosis) from involvement of sympathetic chain. Shoulder pain from chest wall invasion.
CT angiogram sign and BAC
Filling of airspaces with mucoid material produced by malignant cells creates low-density airspace opacification surrounding enhanced pulmonary arteries.
Typical radiologic findings of lymphangitic carcinomatosis
Linear and reticulonodular opacities. Peribronchial cuffing. Subpleural edema or pleural effusion.
Helps distinguish lymphangitic carcinomatosis due to lung cancer from other metastases
Unilateral or asymmetric involvement of lungs suggests lung cancer rather than an extrapulmonary site.
Two patient groups of small cell lung cancer
Disease limited to one hemithorax (limited disease). Contralateral lung or extrathoracic spread (extensive disease).
Two most common primary tracheal malignancies
SCC > Adenoid cystic carcinoma
Tracheal mass size and malignancy
Masses > 2 cm are likely to be malignant. Less than 2 cm are more likely benign.
Other, less common primary tracheal malignancies
Mucoepidermoid carcinoma. Carcinoid tumor. Adenocarcinoma. Lymphoma. Small cell carcinoma. Leiomyosarcoma. Fibrosarcoma. Chondrosarcoma.
Primary malignant neoplasms of the central bronchi include
Squamous cell carcinoma. Small cell carcinoma. Carcinoid tumor. Bronchial gland tumors (adenoid cystic carcinoma, mucoepidermoid carcinoma).
Carcinoid radiologic features
Prefers right upper and middle lobes. Well-defined smooth or lobulated nodules or masses. Iceberg tumor: small intrabronchial and large extraluminal soft tissue component.
A benign neoplasm comprised of disorganized epithelial and mesenchymal elements normally found in the bronchus or lung.
Pulmonary hamartoma.
A feature that helps distinguish lymphangitic carcinomatosis from interstitial fibrosis,
Thickened septal lines of lymphangiti carcinomatosis do not distort the pulmonary lobule.
Lymphocytic interstitial pneumonitis
Infiltration of pulmonary interstitium by mature lymphocytes. CT findings: Diffuse ground-glass opacity. Poorly defined centrilobular nodules. Thin-walled cysts. Associations: Sjogren syndrome. Hypogammaglobulinemia. Multicentric Castleman disease. AIDS.
Posttransplant lymphoproliferative disorder (PTLD)
Spectrum of entities. Ranging from benign polyclonal lymphoid proliferation to aggressive non-Hodgkin lymphoma.
Pulmonary blastoma
Rare malignant tumor affecting children and young adults. Histology simulates fetal lung at 10 to 16 weeks’ gestation. Tend to be extremely large at presentation.
Lobar pneumonia features
Typical of pneumococcal pulmonary infection. Inflammatory process spreads via pores of Kohn and canals of Lambert to produce nonsegmental consolidation. Air bronchograms are common.
Bronchopneumonia features
Most common pattern of pneumonia. Typical of staphylococcal pneumonia. Inflammation centered around lobular bronchi. Multifocal opacities produce patchwork quilt of scattered normal and diseased lobules. No air bronchograms due to exudate within bronchi.
Interstitial pneumonia features
Viral and mycoplasma infection. Inflammatory thickening of bronchial and bronchiolar walls and pulmonary interstitium. Peribronchial cuffing and reticulonodular opacities.
Pneumatoceles may be distinguished from abscesses by
Thin walls. Rapid change in size. Generally develop during late phase of infection.
Ranke complex
Calcified parenchymal focus (Ghon lesion) and lymph nodel calcification. Primary TB.
Postprimary TB
Reactivation occurs in apical and posterior segments of upper lobes and superior segments of lower lobes. Ill-defined patchy and nodular opacities. Cavitation usually indicates active and transmissible disease.
Rasmussen aneurysm
Erosion of cavitary focus into pulmonary artery branch can produce an aneurysm.
Miliary TB
May complicate primary or reactivation disease. Hematogenous dissemination. Diffuse bilateral 2- to 3-mm pulmonary nodules.
Opportunistic fungal lung pathogens
Aspergillus. Candida. Cryptococcus.
Aspergillus lung involvement
Aspergilloma or mycetoma within preexisting cavities. Semi-invasive (chronic necrotizing) aspergillosis in mildly impaired immunity. Invasive pulmonary aspergillosis in neutropenia. Allergic bronchopulmonary aspergillosis in hyperimmunity.
Pulmonary echinococcal cysts are composed of three layers:
Inside out: Endocyst, produces daughter cyts. Exocyst (chitinous layer), protective membrane. Pericyst, surrounding compressed, fibrotic lung.
CT halo sign
Decreased attenuation surrounding a dense, mass-like opacity. Relatively specific for invasive aspergillosis in a neutropenic patient.
Most common AIDS-defining opportunistic infection.
PCP
Interlobular (Septal) Lines
Thin, short, 1- to 2-cm lines oriented perpendicular to and intersecting costal pleura.
Interlobular (septal) lines DDx:
Interstitial edema.   Lymphangitic carcinomatosis.   Sarcoidosis.   Idiopathic pulmonary fibrosis (IPF) (other forms of usual interstitial pneumonia UIP).
Intralobular lines ILD DDx
IPF (UIP). Asbestosis. Alveolar proteinosis. Hypersensitivity pneumonitis.
Thickened fissures ILD DDx
Pulmonary edema.   Sarcoidosis.   Lymphangitic carcinomatosis.
Peribronchovascular interstitial thickening
Pulmonary edema (smooth).   Sarcoidosis (nodular).   Lymphangitic carcinomatosis (smooth or nodular).
Centrilobular nodules ILD DDx
Hypersensitivity pneumonitis.  Bronchiolitis obliterans with organizing pneumonia (BOOP)/cryptogenic organizing pneumonia (COP).  Respiratory bronchiolitis-associated interstitial lung disease (RB-ILD).
Subpleural lines ILD DDx
Asbestosis.   IPF (UIP).
Parenchymal bands ILD DDx
Asbestosis.   IPF (UIP).   Sarcoidosis.
Honeycombing
IPF (UIP).   Asbestosis.  Hypersensitivity pneumonitis (chronic).  Sarcoidosis.
Thin-walled cysts ILD DDx
Eosinophilic granuloma (EG). Lymphangioleiomyomatosis.  Tuberous sclerosis.  Neurofibromatosis (pneumatocele). (emphysema).
Micronodules, random distribution ILD DDx
Miliary tuberculosis or histoplasmosis.  Hematogenous metastases.  Silicosis/coal worker's pneumoconiosis (CWP).  EG.
Micronodules, perilymphatic distribution ILD DDx
Sarcoidosis.   Lymphangitic carcinomatosis.  Silicosis/CWP.
Ground-glass opacities ILD DDx
Desquamative interstitial pneumonia.  Acute interstitial pneumonia (AIP).  Hypersensitivity pneumonitis. BOOP/COP.  RB-ILD.  Hemorrhage.  Pneumocystis jiroveci pneumonia.  Cytomegalovirus pneumonia.  Alveolar proteinosis.
Traction bronchiectasis ILD DDx
Sarcoidosis.   Silicosis/CWP.
Conglomerate mass ILD DDx
Sarcoidosis.  Silicosis.  CWP.  Radiation fibrosis.
Subpleural Lines
5- to 10-cm-long curvilinear opacities are found within 1 cm of the pleura and parallel the chest wall. Most often seen in patients with asbestosis and, less commonly, IPF.
Parenchymal bands
Nontapering linear opacities, 2 to 5 cm in length. Extend from lung to contact pleural surface. Asbestosis. IPF. Sarcoidosis.
Honeycombing
Small (6 to 10 mm) cystic spaces with thick (1 to 3 mm) walls. usually have shared walls . Usually in posterior subpleural regions. End-stage pulmonary fibrosis: IPF (UIP). Chronic hypersensitivity pneumonitis. Occasionally sarcoidosis.
Thin-walled cysts
Slightly larger in diameter (10 mm) than honeycomb cysts. Uniform in size. Thinner walls. Do not share walls with adjacent cysts. Cysts of LCH and LAM are usually evenly distributed from central to peripheral portions of upper lobes
Micronodules
1- to 3-mm. Sharply marginated. Round opacities seen on HRCT. Represent conglomerates of granulomas or tumor cells within the interstitium.
Ground-Glass or Hazy Increased Density
Granular appearance with maintained visibility of pulmonary vessels. Absence of air bronchograms. Desquamative interstitial pneumonia (DIP). Pneumocystis jiroveci (formerly P carinii) pneumonia. Acute hypersensitivity pneumonitis. Nonspecific interstitial pneumonia (NSIP). Interstitial pulmonary edema.
Traction bronchiectasis
Fibrosis causes traction on the walls of bronchi, resulting in irregular dilation.
ILDs Upper zone distribution
Tuberculosis (postprimary). Chronic fungal infection (Histoplasmosis, Coccidioidomycosis).  Sarcoidosis.  Eosinophilic granuloma.  Silicosis.  Ankylosing spondylitis.  Hypersensitivity pneumonitis (chronic). Radiation fibrosis from treatment of head and neck malignancy.
ILDs Lower zone distribution
Idiopathic pulmonary fibrosis.  Asbestosis.  Rheumatoid lung.  Scleroderma.  Neurofibromatosis.  Dermatomyositis/polymyositis.  Chronic aspiration.
ILDs normal or increased lung volumes
Sarcoidosis.  Eosinophilic granuloma.  Lymphangioleiomyomatosis.  Tuberous sclerosis.  Interstitial disease superimposed on emphysema.
ILDs Honeycombing
Idiopathic pulmonary fibrosis.  Sarcoidosis.  Eosinophilic granuloma.  Rheumatoid lung.  Scleroderma.  Pneumoconiosis.  Hypersensitivity pneumonitis.  Chronic aspiration.  Radiation fibrosis.
ILDs miliary nodules
Tuberculosis.  Fungi (Histoplasmosis, Coccidioidomycosis, Cryptococcosis). Silicosis.  Metastases (Thyroid carcinoma, Renal cell carcinoma, Bronchogenic carcinoma, Melanoma, Choriocarcinoma).  Sarcoidosis.  Eosinophilic granuloma.
Hilar/mediastinal lymph node enlargement
Sarcoidosis.  Lymphangitic carcinomatosis.  Lymphoma.  Hematogenous metastases.  Tuberculosis. Fungal infection.  Silicosis.
ILDs Pleural disease
Asbestosis (plaques).  Lymphangitic carcinomatosis (effusion).  Rheumatoid lung disease (effusion/thickening).  Lymphangioleiomyomatosis (chylous effusion).
Manifestations of Rheumatoid Lung Disease
Pleural effusion. Pleural thickening. Pericarditis. Pericardial effusion. Pulmonary fibrosis (basilar predominance). Necrobiotic nodules (peripheral cavitating nodules, Caplan syndrome). Bronchiolitis obliterans (Hyperinflation) Pulmonary arteritis. Pulmonary arterial hypertension. Right heart enlargement. Pulmonary hemorrhage
Caplan syndrome
Thick walled cavitating lung nodules. Rheumatoid arthritis patients with hypersensitivity to inhaled dust particles (coal, silica, asbestos).
Scleroderma ILD findings
Interlobular septal thickening. Ground-glass opacities. Honeycombing. Lower lung predominance. Patulous esophagus.
Interstitial pulmonary edema CXR findings?
Intrapulmonary vascular shadows. Peribronchial cuffing. Tram tracking.
Kerley A and B lines?
Kerley A lines thickening of central connective tissue septa. Kerley B lines thickening of peripheral interlobular septa.
Alveolar pulmonary edema localized to the right upper lung may be seen in patients with
Severe mitral regurgitation.
Causes of Pulmonary Venous Hypertension and Pulmonary Edema
LV failure. Mitral valve disease (Mitral stenosis, Mitral insufficiency). LA myxoma. Cor triatriatum. Obstruction of central pulmonary veins (fibrosing mediastinitis, pulmonary vein stenosis, pulmonary venous thrombosis). Obstruction of intrapulmonary veins (pulmonary venoocclusive disease).
Radiographic findings of pulmonary venous hypertension are
Enlargement of pulmonary veins (progressive dilation of horizontally oriented pulmonary veins). Redistribution of pulmonary blood flow to upper lungs.
ARDS
Respiratory failure due to increased capillary permeability edema. Associated with increased lung stiffness (noncompliance).
Common causes of ARDS
Shock. Severe trauma. Burns. Sepsis. Narcotic overdose. Pancreatitis.
ARDS radiographic findings
Patchy peripheral airspace opacities (12-24 hrs). Confluent bilateral airspace opacities with air bronchograms (days). Coarse reticulonodular pattern (week) that may resolve.
Causes of neurogenic pulmonary edema
Head trauma. Seizure. Increased intracranial pressure.
Hemorrhage or hemorrhagic edema of the lung can result from
Trauma. Bleeding diathesis. Infections (invasive aspergillosis, mucormycosis, Pseudomonas, influenza). Drugs (penicillamine). Pulmonary embolism. Fat embolism. ARDS. Autoimmune diseases (Goodpasture syndrome, idiopathic pulmonary hemorrhage, Wegener granulomatosis, systemic lupus erythematosus, rheumatoid arthritis, and polyarteritis nodosa).
Goodpasture syndrome
Damage to alveolar and renal glomerular basement membranes by cytotoxic antibody.
Idiopathic Pulmonary Hemorrhage
Indistinguishable from Goodpasture syndrome. Pulmonary hemorrhage and anemia in patient with normal renal function and urinalysis. No antiglomerular basement membrane antibodies.
Vasculitides that can cause pulmonary hemorrhage
Wegener granulomatosis. Systemic lupus erythematosus. Rheumatoid arthritis. Polyarteritis nodosa.
D-dimer
Sensitive, but not specific marker of venous thrombosis.
Most common radiographic findings in PE without infarction are
Localized peripheral oligemia with or without distended proximal vessels (Westermark sign). Peripheral airspace opacification. Linear atelectasis.
Radiographic features that suggest infarction in PE
Small pleural effusion and pleura-based wedge-shaped opacity (Hampton hump).
Nonthrombotic pulmonary embolism causes
Air embolism. Macroscopic fat embolism. Methylmethacrlate embolization from vertebroplasty. Radioactive seed embolization from prostate brachytherapy.
PAH is defined as a systolic pressure in the pulmonary artery exceeding
30 mm Hg.
Typical radiographic findings of PAH are
Enlarged main and hilar pulmonary arteries that taper rapidly toward lung periphery. RV enlargement.
PAH measurements of proximal interlobar pulmonary artery (CXR) and main pulmonary artery (CT)
Interlobar pulmonary artery > 16 mm. Main pulmonary artery > 28.6 mm.
In addition to PAH, enlargement of the central pulmonary arteries may be seen in
High cardiac output (anemia, thyrotoxicosis). Left-to-right shunts (ASD, VSD, PDA, PAPVR).
Shunt vascularity on chest radiographs
Enlargement of both central and peripheral pulmonary arteries.
Disorders of the pulmonary arteries that produce PAH include
Chronic PEs. Vasculitis. Pulmonary arteriopathy resulting from long-standing increased pulmonary blood flow from left-to-right shunt.
Multiple pulmonary nodules of similar size and appearance are almost always
Metastases. Granulomas.
Pulmonary nodule is defined as
Round or oval opacity 4 to 30 mm in diameter.
Pulmonary mass is defined as
Round opacity greater than 3 cm.
Differential in a patient under the age of 35, particularly a nonsmoker without a history of malignancy,
Granuloma. Hamartoma, Inflammatory lesion.
An SPN in a patient over 35 years of age should never be followed radiographically without tissue confirmation unless the lesion contains
Benign pattern of calcification. Presence of intralesional fat.
Studies have shown that bronchogenic carcinoma has a doubling time of
Between 1 month and 2 years.
Presence of small satellite nodules around the periphery of a dominant pulmonary nodule is strongly suggestive of
Benign disease, particularly granulomatous infection.
Presence of a halo of ground-glass opacity encircling an SPN in an immunocompromised, neutropenic patient should suggest the diagnosis of
Invasive pulmonary aspergillosis.
Comet tail of bronchi and vessels entering the hilar aspect of the mass, and associated with lobar volume loss is characteristic of
Round atelectasis.
Complete or central calcification within an SPN is specific for
Healed granuloma from tuberculosis or histoplasmosis.
Concentric or laminated calcification of an SPN
Granuloma and allows confident exclusion of neoplasm.
Popcorn calcification within a pulmonary nodule is diagnostic of
Pulmonary hamartoma.
Fat within an SPN is diagnostic of a
Pulmonary hamartoma.
Enhancement of malignant SPNs
15 H.
Most common thoracic inlet masses?
Thyroid masses. Lymphomatous nodes. Lymphangiomas.
Intrathoracic thyroid goiter CT findings?
Well-defined margins. Continuity of mass with cervical thyroid. Coarse calcifications. Cystic or necrotic areas. Baseline high CT attenuation (intrinsic iodine content). Intense enhancement (>25 H).
Lymphangioma?
Tumor of dilated lymphatic channels. Cystic or cavernous form (cystic hygroma) is commonly discovered in infancy and is often associated with : Turner syndrome and trisomies 13, 18, and 21.
Anterior mediastinal masses?
Thymic neoplasms. Lymphoma. Germ cell neoplasms. Primary mesenchymal tumors.
Thymoma versus thymic carcinoma
Thymomas may be encapsulated (noninvasive) or invasive. Thymic carcinomas, epithelial component shows signs of frank malignancy.
Thymoma-associated autoimmune diseases
Myasthenia gravis. Pure red cell aplasia. Graves disease. Sjogren syndrome. Hypogammaglobulinemia.
Thymic cysts
Congenital: Remnants of thymopharyngeal duct. Contain thin or gelatinous fluid. Acquired: Postinflammatory. Associations: AIDS, Prior radiation or surgery, Autoimmune conditions (Sjögren syndrome, Myasthenia gravis, Aplastic anemia).
Thymic masses
Thymoma. Thymic cyst. Thymolipoma. Thymic hyperplasia. Thymic neuroendocrine tumors. Thymic carcinoma. Thymic lymphoma.
Germ cell neoplasms
Teratoma (benign and malignant). Seminoma. Embryonal cell carcinoma. Endodermal sinus tumor. Choriocarcinoma.
Mesenchymal anterior mediastinal tumors
Lipoma. Hemangioma. Leiomyoma. Liposarcoma. Angiosarcoma.
_________ is the most frequent site of a localized nodal mass in patients with Hodgkin disease.
Anterior mediastinum.
A key in distinguishing primary from metastatic mediastinal germ cell neoplasm is the presence of
Retroperitoneal lymph node involvement in metastatic gonadal tumors.
Benign and malignant teratoma features on CT
Benign: round or oval and smooth in contour. Malignant: irregular, lobulated, or ill-defined margin.
Middle mediastinal masses
Foregut and mesothelial cysts. Tracheal and central bronchial neoplasms. Diaphragmatic hernias. Vascular lesions.
Differential for central calcification of mediastinal/hilar lymph nodes on CT?
Mycobacteria. Fungus.
Differential for peripheral (eggshell)l calcification of mediastinal/hilar lymph nodes on CT?
Silicosis. Sarcoidosis.
Differential for hypervascular mediastinal/hilar lymph nodes on CT?
Carcinoid tumor/small cell carcinoma. Kaposi sarcoma. Metastases (RCC. Thyroid carcinoma). Castleman disease.
Differential for necrotic mediastinal/hilar lymph nodes on CT?
Mycobacteria. Fungus. Metastases (SCC. Seminoma. Lymphoma).
Differences in lymph nodes of sarcoidosis and lymphoma/metastases?
Sarcoidosis: Lobular lymph nodes that do not coalesce. Lymphoma/mets: May form conglomerate enlarged nodal masses.
Castleman disease also known as
Angiofollicular lymph node hyperplasia.
Pericardial cysts most commonly arise in the
Anterior cardiophrenic angles. Right-sided lesions being twice as common as left-sided lesions.
Three groups of neurogenic tumors of the posterior mediastinum.
Intercostal nerves: Neurofibroma. Schwannoma. Sympathetic ganglia: Ganglioneuroma. Ganglioneuroblastoma. Neuroblastoma. Paraganglionic cells: Chemodectoma. Pheochromocytoma.
Most common posterior mediastinal neurogenic tumors in children
Neuroblastoma. Ganglioneuroma.
Most common posterior mediastinal neurogenic tumors in adults
Neurofibroma. Schwannoma.
Multiple lesions in the mediastinum, particularly bilateral apicoposterior masses, are virtually diagnostic of
Neurofibromatosis.
Posterior mediastinal masses
Esophageal lesions. Foregut cysts. Vertebral lesion. Lateral thoracic meningocele. Pancreatic pseudocyst.
Causes of chronic sclerosing (fibrosing) mediastinitis
Histoplasmosis (most common). TB. Radiation therapy. Drugs (methysergide). Idiopathic (autoimmune).
SVC syndrome manifestations
Headache. Epistaxis. Cyanosis. Jugular venous distention. Edema.
Ludwig angina describes
Substernal chest pain caused by intramediastinal extension of infection.
Causes of unilateral pulmonary artery enlargement incluce
Poststenotic dilation from valvular or postvalvular pulmonic stenosis. Pulmonary artery aneurysms. Distension of pulmonary artery by thrombus or tumor.
Rare vasculitides that may present with pulmonary artery aneurysms
Behçet disease and Hughes-Stovins syndrome
Sarcoidosis 1-2-3 sign
1: Right paratracheal. 2. Right hilar. 3. Left hilar lymph node enlargement
Coronary calcification is detected at angiography in ____% of patients with 50% diameter stenosis.
75%
A_____% diameter narrowing is the physiologic point at which flow is restricted enough to result in ischemia under stress conditions.
50% diameter narrowing. Roughly predicts a 75% cross-sectional area reduction.
Cardiac MR uses?
Define location and size of previous myocardial infarctions. Demonstrate complications of previous infarctions. Establish presence of viable myocardium for possible revascularization. Differentiate acute versus chronic myocardial infarction. Evaluate regional myocardial wall motion and systolic wall thickening. Demonstrate global myocardial function with right ventricular and left ventricular ejection fractions. Demonstrate regional myocardial perfusion. Evaluate papillary muscle and valvular abnormalities.
Myocardial rupture (may occur ______ days after infarction.
3 to 14 days.
Dressler syndrome
Onset is typically 1 week to 3 months postinjury. Fever, chest pain, pericarditis, pericardial effusion, and pleuritis, with pleural effusion usually more prominent on the left. Dressler syndrome responds well to anti-inflammatory medications.
Hibernating myocardium versus stunned myocardium?
Hibernating: High-grade stenosis resulting in chronically ischemic myocardium. May act like postinfarction scar. Improved function with revascularization. At risk for acute infarction. Stunned myocardium: Postischemic, dysfunctional myocardium without complete necrosis. Potentially salvageable.
Causes of dilated cardiomyopathies
Ischemic cardiomyopathy (most common cause): Chronic ischemia. Prior infarction. Anomalous coronary arteries. Long-term sequelae of myocarditis: Coxsackie virus. Toxins: Ethanol, Adriamycin, Doxorubicin. Metabolic conditions: Mucolipidosis. Mucopolysaccharidosis. Glycogen storage disease. Nutritional deficiencies: Thiamin. Selenium). Infants of diabetic mothers. Muscular dystrophies.
Ventricular Wall. Ventricular Cavity. Contractility. Compliance features of dilated cardiomyopathy?
LV thin. LV dilated. Decreased contractility. Normal to decreased compliance.
Ventricular Wall. Ventricular Cavity. Contractility. Compliance features of hypertrophic cardiomyopathy?
LV thick. LV normal to decreased. Increased contractility. Decreased compliance.
Ventricular Wall. Ventricular Cavity. Contractility. Compliance features of restrivice cardiomyopathy?
Normal LV wall. Normal LV cavity. Normal to decreased contractility. Severely decreased compliance.
Ventricular Wall. Ventricular Cavity. Contractility. Compliance features of Uhl anomaly?
RV thin. RV dilated. Decreased contractility. Normal to decreased compliance.
Hypertrophic cardiomyopathies are divided into two basic types:
Concentric hypertrophy: may be diffuse, midventricular, or apical in distribution. Asymmetrical septal hypertrophy (ASH), also known as idiopathic hypertrophic subaortic stenosis (IHSS).
Hypertrophic cardiomyopathy causes?
May be familial (60%). Autosomal dominant with variable penetrance. Associated with neurofibromatosis and Noonan syndrome. Secondary to pressure overload.
Features of ASH (asymmetric septal hypertrophy)?
Hypertrophy of the interventricular septum (>12 to 13 mm). Abnormal ratio of thickness of interventricular septum to left ventricular posterior wall (>1.3:1). Narrowing of left ventricular outflow tract during systole.
Restrictive cardiomyopathy causes
Infiltrative disorders: Amyloid. Glycogen storage disease. Mucopolysaccharidosis. Hemochromatosis. Sarcoidosis. Myocardial tumor infiltration.
What other disease should be ruled out when considering restrictive cardiomyopathy?
Constrictive pericarditis.
MR finding in restrictive cardiomyopathy caused by amyloidosis or sarcoidosis?
high signal in the myocardium on T2WIs.
Defined as right ventricular failure secondary to pulmonary parenchymal or pulmonary arterial disease.
Cor pulmonale.
Etiologies of cor pulmonale include
destructive pulmonary disease (pulmonary fibrosis and chronic obstructive pulmonary disease). hypoxic pulmonary vasoconstriction resulting from chronic bronchitis, asthma, CNS hypoxia, upper airway obstruction. Acute and chronic pulmonary embolism. Idiopathic pulmonary hypertension. Extrapulmonary diseases affecting pulmonary mechanics such as chest deformities, morbid obesity (pickwickian syndrome), neuromuscular diseases.
Uhl anomaly
Acquired disorder in infants or adults. Also called arrhythmogenic right ventricular dysplasia. Dilation of RV with marked thinning of anterior right ventricular wall. MR may show fatty infiltration of anterior RV free wall. Premature death from early congestive failure or arrhythmias.
Enlargement of pulmonary outflow tract causes
Left-to-right shunts. Poststenotic dilation secondary to pulmonary stenosis. Pulmonary arterial hypertension. Marfan syndrome. Takayasu arteritis. Idiopathic dilation of pulmonary artery.
Differential diagnosis for pulmonary arterial hypertension includes
Long-standing pulmonary venous hypertension (mitral stenosis). Eisenmenger physiology (long-standing left-to-right shunts). Pulmonary emboli. Vasculitides (rheumatoid arthritis or polyarteritis nodosa). Primary pulmonary hypertension.
Increased pulmonary blood flow is caused by
Left-to-right shunts. High output states: Volume loading. Pregnancy. Peripheral shunt lesions (arteriovenous malformations). Hyperthyroidism. Anemia. Leukemia.
Decreased pulmonary blood flow with a small heart is caused by
Chronic obstructive pulmonary disease. Hypovolemia. Malnourishment. Addison disease.
Mitral stenosis in the adult is usually caused by
Rheumatic heart disease.
Causes of Pulmonary Venous Hypertension
Left ventricular failure. Mitral stenosis. Mitral regurgitation. Aortic stenosis. Aortic regurgitation. Pulmonary veno-occlusive disease. Congenital heart disease.
Left atrial enlargement, left ventricular enlargement, and bulging of the atrial septum to the right.
Mitral regurgitation.
Cardiac thrombus features
Intra-atrial thrombi are usually associated with atrial fibrillation, often secondary to rheumatic heart disease. Commonly occurs along posterior wall of LA. Left ventricular thrombi are usually secondary to recent infarction or ventricular aneurysm. Clots typically have low MR GRE signal, whereas tumors have intermediate signal. Clots will not enhance.
Intracardiac lipomas or lipomatous hypertrophy features
High T1 signal and fat suppression. Second most common benign cardiac tumor.
Atrial myxoma features
50% of primary cardiac tumors. Most common primary benign cardiac tumor. Most (75% to 80%) are in LA. May mimic rheumatic valvular disease clinically.
Benign cardiac tumors
Atrial myxoma. Lipoma. Rhabdomyoma (50% to 85% of tuberous sclerosis). Fibromas (12% may calcify). Rare teratoma.
Metastatic cardiac tumor features
10 to 20 times more common than primary cardiac tumors. Breast. Lung. Melanoma. Lymphoma.
Primary malignant cardiac tumors
Angiosarcoma (most common). Rhabdosarcoma. Liposarcoma. Other sarcomas.
Constrictive pericardial disease features
Fibrous or calcific thickening of pericardium. Compromises ventricular filling through restriction of cardiac motion. Most common cause is postpericardiotomy. Other causes: Coxsackie B. Tuberculosis. Chronic renal failure. Rheumatoid arthritis. Neoplastic involvement. Radiation pericarditis.
Differential diagnosis for a cardiophrenic angle mass includes
Pericardial cyst. Fat pad. Lipoma. Enlarged lymph nodes. Diaphragmatic hernia. Ventricular aneurysm.
Congenital absence of pericardium features
Complete left-sided absence (55%). Foraminal defects (35%). Total absence (10%). M > F. Complete absence: Heart is shifted toward the left, with prominent bulge of right ventricular outflow tract, main pulmonary artery, and left atrial appendage. Partial absence of the pericardium risks strangulation of cardiac structures. Surgical closure of partial defects is usually recommended.
Noninfectious causes of miliary pattern
Pneumoconioises (silicosis). Eosinophilic granuloma. Sarcoidosis. Metastases (Thyroid. Melanoma.)
Minimal pleural effusion volume visible on frontal, lateral, and decubitus chest radiographs
Frontal (200 mL). Lateral (75 mL). Decubitus (5 mL)
Which junction line, anterior or posterior, extends above the clavicles
Posterior junction line.
Define pulmonary cavity
Refers to a lucency located wtihin a nodule, mass, or focus of consolidation.
Order of the left lower lobe basilar segments (from lateral to medial) on a frontal radiograph
Anteromedial, Lateral, Posterior (ALP).
DDx of subcarinal mass on radiograph
Lymph node enlargement. Bronchogenic cyst. Left atrial enlargement.
Classic primary TB chest radiograph findings
Parenchymal consolidation with mediastinal and hilar lymph node enlargement.
Ranke complex
Combination of calcified lung nodule and calcified lymph nodes.
Ghon lesion
Lung nodule that is a residum of primary TB. Usually is calcified.
At what pulmonary venous wedge pressures do Kerley lines, effusions, and airspace opacities occur?
Normal 12 mm Hg. Kerley lines 17 mm Hg. Effusion 20 mm Hg. Airspace opacity 25 mm Hg.
Complications of bronchiectasis
Recurrent infections. Hemoptysis. Mucoid impaction. Atelectasis.
Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease)
Telangiectasias. AVMs. Aneurysms in multiple organ systems (Pulmonary. GI. Cutaneous. CNS)
Parenchymal findings associated with acute PE
Wedge-shaped peripheral foci of consolidation. Linear bands.
Focal areas of chronic consolidation may be seen in
Lipoid pneumonia. Bronchoalveolar cell carcinoma. Lymphoma.
Diffuse chronic consolidation can be seen in
Bronchoalveolar cell carcinoma. Alveolar proteinosis. Sarcoid. Lipoid pneumonia.
Kartagener's syndrome (dyskinetic cilia syndrome) triad
Situs invertus. Bronchiectasis. Sinusitis.
Wegener's granulomatosis lung findings
Multiple lung nodules or masses. Cavitation occurs 50%. Local or diffuse consolidation due to hemorrhage.
Help distinguish LCH from LAM
LCH: Usually associated with nodules and variable appearing cysts. Spares costophrenic angles.
PCP findings
Extensive ground glass opacities in a patchy or geographic pattern. 1/3 have upper lobe predominant cysts of varying sizes and wall thicknesses
Bronchopleural fistula, postpneumonectomy should be considered if
Pneumonectomy space fails to fill with fluid. Abrupt decrease in air-fluid level in the pneumonectomy space. New collection of air in previously opacified pneumectomy space. Contralateral mediastinal shift.
Superior sulcus tumor symptoms
Shoulder pain. Horner's syndrome (ptosis, miosis, anhidrosis). Weakness and atrophy of hand muscles.
Deems a superior sulcus tumor unresectable
Any involvement of vertebral body, brachial plexus, subclavian artery.
Satellite nodules
Smaller nodules adjacent to a lung mass. Suggests an infectious etiology.
Mediastinal lipomatosis causes
Cushing's syndrome. Steroid therapy. Obesity.
Rounded atelectasis
Form of peripheral lobar atelectasis that develops with pleural disease (commonly asbestosis). Volume loss. Comet tail (whorled bronchovascular structures).
Diameter of ascending aorta aneurysm
4 cm. 6 cm significant risk of rupture.
Bulla versus bleb
Bulla, sharply demarcated area of emphysema greater than 1 cm. Bleb, gas-containing space within visceral pleura.
Chest radiograph finding in healed varicella pneumonia
Diffuse discrete pulmonary calcifications.
Nodal status and stage in NSCLC
N0, No metastatic lymph nodes. N1, Metastatic ipsilateral hilar lymph nodes. N2, Metastatic ipsilateral mediastinal and subcarinal lymph nodes. N3, Metastatic contralateral mediastinal or hilar lymph nodes.
Causes of SVC syndrome
Neoplastic: Lung cancer (especially small cell carcinoma). Lymphoma. Metastatic carcinoma. Benign: Long-term IV devices (catheters. pacemakers). Fibrosing mediastinitis (Histoplasmosis).
Neoplastic and nonneoplastic causes of hypertrophic pulmonary osteoarthropathy
90% Malignant lung neoplasms. Nonneoplastic: Cystic fibrosis. IPF. Localized fibrous lesions of the pleura
Epicardial fat pad sign
Double lucency sign. Displacement (>4 mm) of anterior and posterior (epicardial) pericardial fat by pericardial fluid.
What obvious structures should be avoided while planning a TTNB (transthoracic needle biopsy)
Interlobar fissures. Pulmonary vessels. Bullae. Areas of severe emphysema.
Peripheral consolidation (photographic negative of pulmonary edema)
Chronic eosinophilic pneumonia.
Sloughed lung within a cavity
Pulmonary gangrene. Closely associated with Klebsiella.
Mosaic lung attenuation causes
Small airways disease. Chronic pulmonary embolism.
Distinguishes small airways disease of chronic PE in setting of mosaic attenuation
Expiratory images demonstrate air-trapping in small airways disease.
Congenital tracheobronchomegaly
Mounier-Kuhn syndrome.
Allergic bronchopulmonary aspergillosis radiographic findings
Central bronchiectasis. Mucous plugging (finger-in-glove). Atelectasis. Patchy migratory foci of consolidation.
Pulmonary alveolar proteinosis susceptible infections
Nocardia. Aspergillus. Mucormycetes.
Localized fibrous tumor of the pleura enhancement pattern
Intense and homogeneous contrast enhancement.
Calcified fine lung nodules differential
Healed varicella. Healed histoplasmosis. Silicosis. Calcified metastases.
CT findings of Swyer-James syndrome
Areas of decreased lung attenuation with associated reducting in number and size of vessels. Bronchiectasis. Air trapping on expiratory images.
Cardiac bronchus
Blind-ending diverticulum arising from medial wall of bronchus intermedius. Rarely presents with recurrent infections, hemoptysis, cough, and or dyspnea.
Bronchiolitis obliterans organizing pneumonia CT findings
Patchy bilateral airspace consolidation with peripheral, subpleural distribution. Poorly defined lung nodules in a peribronchiolar distribution.
Triad of pulmonary veno-occlusive disease
Severe pulmonary artery hypertension. Evidence of pulmonary edema. Normal wedge pressure.
Water lily sign
Echinococcus cysts: Endocyst ruptures its contents within the ectocyst, floating on top of debris, like a water lily.
Differential diagnosis for wall-to-wall heart?
Tricuspid regurgitation. Pericardial effusion. Dilated cardiomyopathy.
Common predisposing factors for aortic dissection
Hypertension. Annuloaortic ectasia: Marfan or Ehlers-Danlos syndrome. Bicuspid aortic valve. Aortic aneurysm. Arteritis.
Anatomic structure separating Type A from Type B (Stanford) aortic dissections
Left subclavian artery. Distal type B. Proximal type A.
Chest bone findings associated with Marfan syndrome
Pectus excavatum. Scoliosis.
Pectus excavatum associations
Marfan syndrome. Ehlers-Danlos syndrome. Mitral valve prolapse. Homocystinuria. Hunter-Hurler syndromes.
4 life threatening complications of type A aortic dissection
Coronary artery dissection (myocardial infarction). Carotid artery dissection (stroke). Pericardial hemorrhage (tamponade). Aortic valve rupture (aortic regurgitation).
Helps distinguish ventricle true aneurysms from pseudoaneurysms
Pseudoaneurysm: Inferoposterior location. Narrow neck (less than 50%). Aneurysm: Anteroapical location. Wide neck.
Which aberrant subclavian artery (right or left) is a vascular ring
Right aortic arch with aberrant left subclavian artery. Left-sided ligamentum arteriosum completes the ring.
Causes of SVC syndrome
Neoplastic: Bronchogenic carcinoma. Metastases. Lymphoma. Infectious: Fungal infection (histoplasmosis, fibrosing mediastinitis).
Persistent left superior vena cava associations
ASD. Tetralogy of Fallot. P(T)APVR.
Tetralogy of Fallot. 4 primary lesions
Overriding aorta. VSD. Pulmonar infundibular stenosis. Right ventricular hypertrophy.
Thoracic vessels. Takayasu arteritis involvement
Aorta. Right common carotid.Subclavian arteries. Pulmonary arteries.
Causes of constritive pericarditis
Cardiac surgery. Radiation therapy. Uremic pericarditis. Viral pericarditis (coxsackie). Tuberculous pericarditis.
Treatment of intramural hematoma of aorta
Similar to aorta dissections: type A (surgically) type B (medically).
Sinus of valsalva aneurysm versus aortic root dilation
Sinus of valsalva aneurysm is focal dilation of one sinus of Valsalva, not entire root.
TAPVR types
Type I: Supracardiac drainage. Snowman heart. Type II: Cardiac. Coronary sinus or right atrium drainage. Type III: Infracardiac. Portal vein, hepatic vein, or ductus venosus drainage (pulmonary edema due to obstruction).
Aortic pseudoaneurysm causes
Atherosclerosis (penetrating ulcer). Infection. Trauma. Iatrogenic.
Mirror-image right aortic arch congential heart disease associations
Tetralogy of Fallot. Truncus arteriosus.
4 components of scimitar syndrome
Right lung hypoplasia. Hypoplastic right pulmonary artery. Right lower lobe systemic arterial supply. PAPVR from right lung.
Partial congenital absence of the pericardium findings:
Leftward deviation of the heart without deviation of mediastinum. Prominent left atrial appendage. Lung located between aorta and pulmonary artery confirms diagnosis.
Heterotaxy syndrome associated with interruption of IVC with Azygous continuation
Bilateral left-sidedness/polysplenia syndrome.
Features that suggest a primary malignant cardiac tumor
Invasiveness. Extension outside of heart. Involvement of more than one chamber. Central necrosis or cavitation. Large pericardial effusion.
Pulmonary sling aberrant course
Left pulmonary artery arises from right pulmonary artery and courses between esophagus and trachea.
question
answer
Disk protrusion terminology
Bulge: Broad-based disk bulge. Usually bulging annulus fibrosus. Protrusion: Focal disk bulge. Usually herniated nucleus pulposus.
Intervertebral disk high intensity zone (HIZ)
High T2 signal of annulus indicating annular tear.
Disk free fragment mimickers
Conjoined root: Normal variant of two roots exiting thecal sac together. Same density of thecal sac. Tarlov cyst: Normal variant of dilated nerve root sleeve. Same density of thecal sac.
Lateral Disks
May cause nerve root impingement causing symptoms of a superior level. Nerve root has already exited central canal.
Common causes of Central Canal Stenosis
Facet joint degenerative change (most common). Lligamentum flavum hypertrophy.
Most common cause of neuroforaminal stenosis
Facet joint degenerative change with bony encroachment.
Lateral recess
Lumbar spine bony canals where nerve roots lie after exiting thecal sac and before entering neuroforamen. Hypertrophy of superior articular facet is most common cause of encroachment.
Spondylolysis identified on axial images
Break in bony ring of the lamina (pars interarticularis) at the mid vertebral body level.
Spondylolisthesis occurs from either
Bilateral spondylolysis. Facet joint degenerative change.
Distinguishes postop scar from disk material
Scar tissue enhances. Disk material has only minimal peripheral enhancement.
Differentiates disk infection fromdegenerative disk disease at MR
Type 2 degenerative disk disease: Low T1 disk and high T2 parallel endplate bands. Disk space infection: High T2 disk.
Myelopathy neurologic signs
Ataxia. Bowel and bladder incontinence. Babinski sign.
Radiculopathy neurologic signs
Muscle weakness. Decreased reflexes. Dermatomal sensory deficits.
Urgency for imaging acute myelopathy
Poor prognosis if left untreated for greater than 24 hours.
Common causes of myelopathy
Extramedullary: Epidural mass cord compression. Cervical spine stenosis. Intramedullary: Tumor. Inflammation, Arteriovenous malformation (AVM). Spinal dural arteriovenous fistula (SPAVF).
Definition of Intramedullary spinal canal lesion
Usually confined to spinal cord. May be exophytic.
Definition of extramedullary spinal canal lesion
Outside of spinal cord. May be intradural or extradural.
Intradural intramedullary lesions
Ependymoma. Astrocytoma. Hemangioblastoma. Lipoma/(Epi)dermoid. Syringohydromyelia. Intramedullary AVM. Met/abscess (rare).
Intradural extramedullary lesions (includes subarachnoid space)
Meningioma. Schwannoma/neurinoma. Neurofibroma. Hemangiopericytoma. Lipoma/(Epi)dermoid. Arachnoid cyst/adhesion. Drop/leptomeningeal metastasis. Veins (extramedullary AVM).
Extradural extramedullary lesions
Degenerative: Herniated disc. Synovial cyst. Osteophyte. Rheumatoid pannus. Nondegenerative: Metastasis. Abscess. Hematoma. Primary tumor expansion or invasion. Epidural lipomatosis
Most common intramedullary lesion at MRI
Multiple sclerosis
Lupus Erythematosus spinal cord involvement
Areas of high T2 signal with cord swelling. May involve 4 or 5 vertebral segments. Have less well-defined margins than MS plaques.
Atlantoaxial instability and rheumatoid arthritis
Inflammatory changes (pannus) destroy transverse ligament of C1. Dens may slide posteriorly and intermittently compress cord causing myelomalacia. 5% of RA patients frank atlantoaxial instability.
Vertebral body and disc infection findings
Adjacent vertebral bodies and disc usually involved. Destruction greatest at endplates. Posterior elements usually spared. Low T1 and high T2 marrow signal with normal diffusion. If pyogenic disk enhances, granulation tissue extends above and below affected vertebrae.
Vertebral body neoplasm findings
Isolated or noncontiguous involvement. Pedicles typically affected. Low T1 and high T2 signal with restricted diffusion. Disk typically spared (except prostate cancer). Enhancement may obscure metastases within fatty marrow.
Vertebral body osteoporosis findings
Several vertebral bodies with height loss. Anterior weding with posterior elements spared. Normal T1 and T2 unless fracture. Disk spared.
TB of the spine, or Pott disease
Causes slow collapse of one or more vertebral bodies. Gibbus deformity, acute kyphosis. Infection spreads underneath longitudinal ligaments. Can lead to cord compression. May spare disks.
Most common neoplasm of the spine
Metastases
Two most common primary intramedullary tumors
Astrocytoma. Ependymoma.
Spinal cord astrocytoma and ependymoma shared features
Expansile. Low T1 and high T2 signal with variable enhancement. Increased incidence in neurofibromatosis.
Spinal cord Ependymoma features
Most common spinal cord tumor in adults. Divided into cellular (intramedullary) and myxopapillary (filum terminale) types. Peak incidence inf ourth decade. Male predominance. These slow-growing neoplasms arise from ependymal cells lining the central canal of the cord or cell rests along the filum. Expansile. Low T1 and high T2 signal with variable enhancement. Increased incidence in neurofibromatosis.
Spinal cord Astrocytoma features
Most (75%) occur in cervical and upper to midthoracic cord. Fusiform cord widening. High T2 signal. Contrast enhancement over several vertebral body segments.
Hemangioblastoma features
Occur in spinal cord and posterior fossa. High association with Von Hippel-Lindau syndrome. Densely enhancing nidus with related cyst and or cord expansion. May be extramedullary and multiple. May be mistaken for arteriovenous malformation (AVM).
Syrinx
Shorter term for syringohydromyelia. Hydromyelia, dilation of central canal and lined by ependyma. Syringomyelia, cavity outside central canal lined by glial cells. Suspect tumor as a cause of unexplained syrinx.
Most common intradural tumor in thoracic region
Meningioma
Spinal meningioma features
Most (80%) occur in women. Average age of 45. Multiple meningiomas suspicious for neurofibromatosis. Usually extramedullary/intradural. Can have extradural component. Dense calcification can occur. Dense homogenous enhancement. Broad dural tails.
Most common intraspinal mass
Schwannoma
Spinal schwannoma features
Neuroforaminal extension and expansion are common in cervical and thoracic spine with intra and extraspinal components, dumbbell shape. In lumbar spine, tend to remain within dural sac.
Common intrathecal drop metastases
Subarachnoid seeding of primary CNS tumors: Posterior fossa medulloblastomas. Ependymomas. Pineal region neoplasms.
Most common spine extradural neoplasm
Metastatses: Breast, Lung, Prostate carcinoma.
Very low T1 and T2 marrow signal
Myelofibrosis
Spinal AVM features
May be intramedullary or extramedullary. Intramedullary AVMs have a nidus of abnormal vessels that may cause hemorrhage or ischemia. Extramedullary AVMs generally are arteriovenous fistulas. Spinal dural arteriovenous fistulas (SDAVFs) cause symptoms through venous hypertension and congestion of the cord with edema.
Tethered Cord features
Low-lying conus medullaris. In a newborn conus normally at L2. Typically ascends one to two vertebral segments as child grows. May form a taut mass in posterior lumbar canal, obscuring conus/cauda junction.
Caudal Regression Syndrome
Hypoplastic or absent distal spine and sacrum. Blunted conus.
Spinal Arachnoid cysts and epidermoids
Similar to brain arachnoid cysts and epidermoids. Arachnoid cysts follow CSFsignal. Epidermoids restrict diffusion, bright on DWIs.
Spinal Epidural Hematoma
Ventral epidural space contains plexus of veins. These can tear in trauma, resulting in epidural hematoma.
Nerve Root Avulsion
Most commonly occur in cervical spine. Typically involve roots of brachial plexus and upper extremities. Birth trauma from shoulder traction is common example.
Acute versus chronic sinusitis findings
Acute sinusitis: Air-fluid levels and foamy secretions. Typically caused by viral URI. Chronic sinusitis: Mucoperiosteal thickening. Thickening of bony sinus walls.
Disease limited to the infundibulum of the maxillary ostium will result in
Isolated obstruction of maxillary sinus.
Lesion located at hiatus semilunaris (middle meatus) results in
Obstruction of ipsilateral maxillary sinus, anterior and middle ethmoid air cells, and frontal sinus. Described as ostiomeatal pattern of obstruction.
Sphenoid sinusitis is of great clinical concern as it may
Extend intracranially due to presence of valveless veins.
Sinus mucous retention cyst versus mucocele
Mucous retention cyst: Obstructed mucous glands within mucosal lining. Usually round. 1 to several cm in diameter. Mucocele: Entire sinus is obstructed. Expansion of sinus. Sinus wall bony thinning and remodeling. Mass may be present obstrucing draining ostium.
Inverting Papilloma
Neoplastic epithelium inverts and grows into underlying mucosa of lateral nasal wall. Surgically resected due to association with squamous cell carcinoma.
Juvenile nasopharyngeal angiofibromas
Male adolescents with epistaxis. Benign tumor but can be locally aggressive. Fills nasopharynx and bows posterior wall of maxillary sinus forward. Retromaxillary pterygopalatine fossa location is a hallmark feature. Avidly enhance.
Malignancies of paranasal sinuses and nasal cavity.
Squamous cell carcinoma. Lymphoma. Minor salivary tumors.
Most common salivary malignancies include
Adenoid cystic carcinoma. Adenocarcinoma. Mucoepidermoid carcinoma.
Esthesioneuroblastoma
Arises from neurosensory receptor cells of olfactory nerve and mucosa. Occurs anywhere from cribriform plate to turbinates. Often quite destructive by time of diagnosis. Usually found high within nasal vault.
Three most common primary (mets by far more common) skull base malignant tumors
Chordoma (destructive midline mass). Chondrosarcoma. Osteogenic sarcoma (from radiation or Paget's degeneration).
Cholesteatoma
Soft tissue mass (epidermoid cyst of desquamating stratified squamous epithelium) within middle ear cavity. Typically associated with bone erosion. Superior tympanic membrane (pars flaccida) is the most common site. CT images extent of disease.
Opacified petrous apex differential
Retained fluid secretions: Dark T1, bright T2, no enhancement. Petrous apicitis: Dark T1, bright T2, and ring enhancement. Nonaerated petrous apex: Bone marrow, bright T1, dark T2, and no enhancement. Cholesterol granuloma: Hemorrhagic component, bright T1 and T2.
Cholesterol granuloma
Granulation tissue within partially obsructed petrous air cells. Have cholesterol and hemorrhagic component (high T1 and T2 signal).
Deep anatomy of the head and neck is subdivided by layers of deep cervical fascia into the following spaces:
(1) Superficial mucosal. (2) Parapharyngeal. (3) Carotid. (4) Parotid. (5) Masticator. (6) Retropharyngeal. (7) Prevertebral.
Mucosal head and neck compartment contents
Squamous mucosa. Lymphoid tissue (adenoids, lingual tonsils). Minor salivary glands.
Mucosal head and neck compartment pathology
Nasopharyngeal carcinoma. Squamous cell carcinoma. Lymphoma. Minor salivary gland tumors. Juvenile angiofibroma. Rhabdomyosarcoma.
Parapharyngeal head and neck compartment contents
Fat. Trigeminal nerve (V3). Internal maxillary artery. Ascending pharyngeal artery.
Parapharyngeal head and neck compartment pathology
Minor salivary gland tumor. Lipoma. Cellulitis/abscess. Schwannoma.
Parotid head and neck compartment contents
Parotid gland. Intraparotid lymph nodes. Facial nerve (VII). External carotid artery. Retromandibular vein.
Parotid head and neck compartment pathology
Salivary gland tumors. Metastatic adenopathy. Lymphoma. Parotid cysts.
Carotid head and neck compartment contents
Cranial nerves IX–XII. Sympathetic nerves. Jugular chain nodes. Carotid artery. Jugular vein.
Carotid head and neck compartment pathology
Schwannoma. Neurofibroma. Paraganglionoma. Metastatic adenopathy. Lymphoma. Cellulitis/abscess. Meningioma.
Masticator head and neck compartment contents
Muscles of mastication. Ramus and body of mandible. Inferior alveolar nerve.
Masticator head and neck compartment pathology
Odontogenic abscess. Osteomyelitis. Direct spread of squamous cell carcinoma. Lymphoma. Minor salivary tumor. Sarcoma of muscle or bone.
Retropharyngeal head and neck compartment contents
Lymph nodes (lateral and medial retropharyngeal). Fat.
Retropharyngeal head and neck compartment pathology
Metastatic adenopathy. Lymphoma.
Prevertebral head and neck compartment contents
Cervical vertebrae. Prevertebral muscles. Paraspinal muscles. Phrenic nerve.
Prevertebral head and neck compartment pathology
Osseous metastases. Chordoma. Osteomyelitis. Cellulitis. Abscess.
Tornwaldt cysts
Benign midline nasopharynx lesion of high T2 signal. Believed to be remnant of notochordal tissue (benign).
Most common minor salivary gland malignancy and has propensity for perineural spread
Adenoid cystic carcinoma
The parapharyngeal space is surrounded by what spaces
the carotid space posteriorly, the parotid space laterally, the masticator space anteriorly, and the superficial mucosal space medially. Therefore, the parapharyngeal space will be compressed on its medial surface by masses originating from the mucosal surface, displaced anteriorly by carotid sheath masses, displaced medially by parotid masses, and displaced posteriorly and medially by masses within the masticator space.
Triad of nasopharyngeal malignancy
1) Mucosal mass of lateral nasopharynx (fossa of Rosenmuller). (2) Lateral retropharyngeal nodes. (3) Mastoid opacification (eustachian tube dysfunction)
Head and neck paragangliomas
Vascular tumors arising from neural crest cell derivatives. Names given according to location: Carotid body tumor (at carotid bifurcation). Glomus vagale tumor (vagus nerve). Glomus jugulare tumor (jugular ganglion of vagus nerve). Glomus tympanicum tumor (Arnold and Jacobson nerves of middle ear).
Salivary gland tumors
Benign: Pleomorphic adenoma. Warthin tumor. Malignant: Adenocystic carcinoma. Adenocarcinoma. SCC. Mucoepidermoid carcinoma.
Head and neck trans-spatial disease categories
Lymphatic masses (lymphangioma). Neural masses (neurofibroma, schwannoma, perineural spread of tumor). Vascular masses (hemangioma).
Head and neck diseases that demonstrate perineural spread
Fungal infections. Squamous cell carcinoma. Adenoid cystic carcinoma.
This lymph node chain serves as the final common afferent pathway for lymphatic drainage of the entire head and neck.
Internal jugular nodal chain
Pathologic size of head and neck lymph nodes
Jugulodigastric and submandibular nodes may normally measure up to 1.5 cm. All other nodes up to 1.0 cm.
Common optic nerve sheath complex tumors
Optic nerve glioma. Optic sheath meningioma.
Optic nerve glioma
Low grade pilocytic astrocytoma. Most common tumor of optic nerve. Typically occurs during first decade of life. High association with neurofibromatosis type 1. Enlarged sheath complex may be tubular, fusiform, or eccentric with kinking. Rarely calcify.
Arachnoidal hyperplasia or gliomatosis
Thickening of perioptic meninges associated with optic nerve gliomas. Reflects peritumoral reactive meningeal change.
Optic sheath meningiomas
Grow in a linear fashion along optic nerve. Tram track pattern of linear enhancement. May invade through dura. May be extensively calcified.
Orbital vascular lesions and age groups
Capillary hemangiomas, infants (younger than 1 year). Diagnosed within first weeks of life. Lymphangiomas, older group of children (3 to 15 years). Propensity to bleed. Often contain blood degradation products. Cavernous hemangiomas, adults. Sharply circumscribed and round. Venous varix, generally in adults. Dilated vein. Changes with Valsalva maneuver.
Superior ophthalmic vein pathology
Thrombosis often occurs with cavernous sinus thrombosis. Loss of normal flow void. Enlargement occurs with cavernous carotid fistulas.
Most common cause of intraorbital mass in an adult
Idiopathic inflammatory pseudotumor. Inflammatory lymphocytic infiltrate. Involves tendinous attachments to the globe. Often rapidly develops presenting with painful proptosis, chemosis, and ophthalmoplegia.Lymphoma tends to present with painless proptosis.
3 common adult intraorbital masses
Idiopathic inflammatory pseudotumor. Cavernous hemangioma. Lymphoma.
Enlargement of extraocular muscles with sparing of tendinous attachments to the globe
Thyroid ophthalmopathy (Graves disease). Causes unilateral or bilateral proptosis in adults. Muscles involved, in decreasing order: I'M SLow. Inferior rectus. Medial rectus. Superior rectus. Lateral retus.
Lesions of the lacrimal gland
Inflammatory: Sarcoidosis. Sjogren syndrome. Neoplastic: Salivary gland (mixed-cell tumor or adenoid cystic carcinoma). Lymphoma. Pseudotumor. Dermoid (fat-fluid level).
Retinoblastoma features
Most common primary ocular malignancy. Leukocoria. Calcified ocular mass.
Thyroglossal duct
Epithelium-lined tract along which primordial thyroid gland migrates. Extends from foramen cecum (tongue base) to anterior of thyrohyoid membrane and strap muscles to ends at thyroid isthmus. Normally involutes by 8 to 10 weeks of gestation. May give rise to cyst, sinus tract, or ectopic thyroid tissue.
The usual clinical presentation is that of a painless neck mass along the anterior border of the sternocleidomastoid muscle, presenting during the first to third decade.
Second branchial cleft cyst. Anterior to mid sternocleidomastoid muscle. Lateral to internal jugular vein at the level of carotid bifurcation.
Lymphangiomas
Congenital malformations of lymphatic channels. Benign and nonencapsulated. Classified as capillary, cavernous, or cystic. Most present at birth or during infancy.
Subgaleal hematoma
Soft tissue swelling of the scalp located beneath subcutaneous fibrofatty tissue and above temporalis muscle.
Intracranial air, pneumocephalus, may be seen with what fractures
Compound skull fractures. Fractures involving paranasal sinuses.
Epidural hematoma generalities
Usually arterial in origin. Often result from skull fracture disrupting middle meningeal artery.Strips dura from inner table of the skull. Forms an ovoid mass. Generally does not cross suture lines.
Venous epidural hematomas
Less common than arterial epidurals. Tend to occur at the vertex, posterior fossa, or anterior aspect of middle cranial fossa. Usually result from disrupted dural venous sinuses. Vertex epidurals can cross sagittal suture.
Subdural hematomas
Typically result from tearing of cortical veins that traverse the subdural space. Will not cross falx cerebri or tentorium. Can cross sutural margins. Frequently layer along hemispheric convexity from anterior falx to posterior falx. Crescent-shaped in axial plane. Biconvex in coronal plane.
Subarachnoid hemorrhage
Result from disruption of small subarachnoid vessels, aneurysm, or direct extension by a contusion or hematoma. Hyperdense linear areas within cisterns and sulci. May lead to subsequent hydrocephalus by impaired CSF resorption at the arachnoid villi.
Intraventricular hemorrhage
May result from tearing of subependymal veins, direct extension of parenchymal hematoma, retrograde flow of subarachnoid hemorrhage. Risk of hydrocephalus by obstruction of the aqueduct or arachnoid villi. Hyperdense material layering within ventricular system.
Diffuse axonal injury (DAI)
Widespread disruption of axons due to acceleration or deceleration injury. Small, petechial hemorrhages at gray-white junction of cerebral hemispheres and or corpus callosum.
T2 shinethrough
T2 and DW bright and ADC dark.
Cortical contusions
Focal brain injury involving superficial gray matter. Occur near bony protuberances: Temporal lobes above petrous bone or posterior to greater sphenoid wing. Frontal lobes above cribriform plate, planum sphenoidale, and lesser sphenoid wing.
Traumatic Intracerebral Hematoma
Rupture of small intraparenchymal blood vessels. Tend to have less surrounding edema than cortical contusions. Most are located in the frontotemporal white matter.
Traumatic subcortical gray matter injury
Uncommon manifestation of primary intra-axial injury. Multiple petechial hemorrhages primarily affecting basal ganglia and thalamus.
Von Hippel-Lindau syndrome imaging manifestations
Visceral: Renal cell carcinomas. Pheochromocytomas. Pancreatic islet cell tumors. Pancreatic, hepatic, renal, and splenic cysts. CNS: Retinal capillary hemangiomas. Spinal cord and posterior fossa hemangioblastomas. Endolymphatic sac adenocarcinomas.
Distinguishing epidermoids from arachnoid cysts on MR imaging.
Both follow CSF T1 and T2 signal. Epidermoids restrict diffusion, are bright at DWI. Arachnoid cysts do not restrict diffusion. Epidermoids are composed of epithelial cells that grow in layers. Arachnoid cysts contains CSF.
Pachymeningeal versus leptomeningeal enhancement findings unfinished.
Pachymeningeal enhancement is characteristically thick, smooth, and uninterrupted.
Rare cystic lesion classically located at the anterior roof of the third ventricle at the foramen of Monro.
Colloid cyst. Generally are hyperdense to brain parenchyma. Do not enhance.
Carotid cavernous fistula (CCF)
Communication between cavernous portion of internal carotid artery and surrounding venous plexus. Typically follows a full-thickness arterial injury. Results in venous engorgement of cavernous sinus, ipsilateral superior ophthalmic vein, inferior petrosal sinus.
Diffuse cerebral edema CT imaging findings
Decreased cerebral density. Loss of gray-white differentiation. Usually spares cerebellum and brainstem, which appear relatively hyperdense.. Falx and cerebral vessels may appear dense, mimicking acute subarachnoid hemorrhage.
Subfalcial herniation
Most common form of brain herniation. Cingulate gyrus is displaced across midline under the falx. May compress adjacent lateral ventricle. May enlarge contralateral ventricle (obstruction of the foramen of Monro). Both anterior cerebral arteries may be displaced to contralateral side.
Uncal herniation
Medially displaced medial temporal lobe over free margin of tentorium. Focal effacement of ambient cistern and lateral suprasellar cistern. Rarely compresses contralateral cerebral peduncle (Kernohan's notch) against tentorial margin.
Transtentorial Herniation
Descending transtentorial herniation: Effacement of suprasellar and perimesencephalic cisterns. Pineal calcification is displaced inferiorly. Ascending transtentorial herniation: May involve vermis and parts of cerebellar hemispheres. Large posterior fossa hematomas
Leptomeningeal cyst
Known as a growing fracture. Caused by traumatic tear of the dura. Outpouching of arachnoid at site of suture or skull fracture.
Duret hemorrhage
Midline hematoma within tegmentum of rostral pons and midbrai. Associated with descending transtentorial herniation. Due to stretching or tearing of penetrating arteries.
Nonaccidental trauma head findings
Skull fractures. Subdural hematomas. Diffuse brain swelling.
Moya moya disease
Rare leptomeningeal vascular collaterals that form due to stenosis or occlusion of Circle of Willis arteries. Puff of smoke appearance at angiography. Associations: Sickle cell disease. Neurofibromatosis type I. Down's syndrome. Fibromuscular dysplasia.
Differential diagnosis of supratentorial partially cystic, partially solid mass in a child:
Pilocytic astrocytoma. PNET (primitive neuroectodermal tumor). Hemorrhage.
Le Fort I
Floating palate. Horizontal fracture through maxillary sinuses, nasal septum, and inferior ptyergoid plates.
Le Fort II
Pyramidal fracture through bridge of nose, medial orbits, lateral and posterior maxillary walls, nasal septum, inferior orbital rim (infraorbital nerve injury), and midportion of ptyergoid plates.
Le Fort III
Craniofacial dysjunction. Horizontal fracture through orbits. Begins near nasofrontal suture and extends posteriorly through nasal septum, medial and lateral orbit walls, zygomatic arch, and base (superior aspect) of pterygoid plates.
CT scans done within 6 hours of MCA occlusion will commonly exhibit
Insular ribbon sign: Subtle blurring of gray-white layers of insula. Caused by early edema. Lentiform nucleus edema sign: Hypodense putamen.
Ischemic penumbra
ischemic but not infarcted (salvageable) tissue. Peri-infarct tissue.
Diffusion-Weighted MR in Acute Ischemia
Brain water diffusion rates fall rapidly during acute ischemia. Bright signal on DWIs.
Apparent diffusion coefficient (ADC).
Reflects pure diffusion behavior. Free of underlying T2 contributions (shine through or dark through).
Fluid-Attenuated Inversion Recovery (FLAIR) in Ischemia
Suppresses free water CSF signal but allows T2 weighting of parenchyma. Increases conspicuity of T2 changes in ischemia. May help detect small cortical lesions and acute subarachnoid hemorrhage.
Fogging effect
CT finding occuring during 2nd week after infarction. Cerebral edema and mass effect subside while proteins accumulate from cell lysis. Injurred brain morphology and density appear normal at CT.
Hemorrhagic Transformation of Infarction
Seen 1 to 2 weeks postinfarction. Hemorrhage of reperfused capillaries. Serpiginous line of petechial blood following gyral contours of infarcted cortex.
Time course of CT-detected enhancement of infarcted brain
Begins at about 1 week. Peaks at 7 to 14 days. Often assumes a gyral pattern. As gliosis ensues and blood-brain barrier is repaired, enhancement fades and resolves by 3 months.
Intravascular MR enhancement of infarcted brain
Commonly seen in infarct during the first week. May be due to slow flow or vasodilation in arteries and veins. May be detected within minutes of vessel occlusion. Seen in a majority of cortical infarcts at 1 to 3 days. Resolves by 10 days.
Maximal brain swelling post brain infarction occurs at what days
3 to 7 days postinfarction.
Encephalomalacia post brain infarction occurs when
30 to 90 days (1 to 3 months) postinfarction.
ACA (anterior cerebral artery) three subgroups:
Medial lenticulostriate branches: Rostral portions of basal ganglia. Pericallosal branches: Corpus callosum. Hemispheric branches: Medial frontal and parietal lobes.
Two main branch groups of MCA (middle cerebral artery)
Lateral lenticulostriate branches: Supply most of basal ganglia. Hemispheric branches: Lateral cerebral surface.
Major branches of PCA (posterior cerebral artery)
Midbrain and thalamic perforating branches. Posterior choroidal arteries. Cortical branches to medial temporal and occipital lobes.
(Deficit/Syndrome : Cerebral artery/branch/side affected), Leg weakness :
ACA/Hemispheric branch/either side
(Deficit/Syndrome : Cerebral artery/branch/side affected), Incontinence, akinetic mutism :
ACA/Hemispheric branch/both sides
(Deficit/Syndrome : Cerebral artery/branch/side affected), Facial weakness :
ACA/Medial lenticulostriates/either side
(Deficit/Syndrome : Cerebral artery/branch/side affected), Dysarthria with or without motor aphasia :
ACA/Medial lenticulostriates/Left
(Deficit/Syndrome : Cerebral artery/branch/side affected), Face and arm weakness > leg weakness :
MCA/Hemispheric branch/either side
(Deficit/Syndrome : Cerebral artery/branch/side affected), Motor aphasia (anterior lesion) :
MCA/Hemispheric branch/Left
(Deficit/Syndrome : Cerebral artery/branch/side affected), Receptive aphasia (posterior lesion) :
MCA/Hemispheric branch/Left
(Deficit/Syndrome : Cerebral artery/branch/side affected), Global aphasia :
MCA/Hemispheric branch (total)/Left
(Deficit/Syndrome : Cerebral artery/branch/side affected), Neglect syndromes :
MCA/Hemispheric branch/Left
(Deficit/Syndrome : Cerebral artery/branch/side affected), Visulospatial dysfunction :
MCA/Hemispheric branch/Right
(Deficit/Syndrome : Cerebral artery/branch/side affected), Variable lacunar syndromes :
MCA/Lateral lenticulostriate branches/Either
(Deficit/Syndrome : Cerebral artery/branch/side affected), Hemianopsia :
PCA/Hemispheric branch/Either
(Deficit/Syndrome : Cerebral artery/branch/side affected), Cortical blindness :
PCA/Hemispheric branch/Both
(Deficit/Syndrome : Cerebral artery/branch/side affected), Memory deficits :
PCA/Hemispheric branch/Both
(Deficit/Syndrome : Cerebral artery/branch/side affected), Somnolence :
PCA/Thalamoperforators/Either
(Deficit/Syndrome : Cerebral artery/branch/side affected), Sensory disturbances :
PCA/Thalamoperforators/Either
(Deficit/Syndrome : Cerebral artery/branch/side affected), Ataxia, vertigo, vomiting :
Cerebellar/PICA, AICA, or SCA/ Either
(Deficit/Syndrome : Cerebral artery/branch/side affected), Coma if mass effect :
Cerebellar/PICA, AICA, or SCA/ Either
(Deficit/Syndrome : Cerebral artery/branch/side affected), ± brainstem deficits :
Cerebellar/PICA, AICA, or SCA/ Either
(Deficit/Syndrome : Cerebral artery/branch/side affected), Man-in-a-barrel syndrome :
Watershed/ACA,MCA,PCA/Either
(Deficit/Syndrome : Cerebral artery/branch/side affected), Severe memory problems :
Watershed/ACA,MCA,PCA/Bilateral
Order of cerebellar branches going from top to bottom can be remembered using the acronym
SAP: Superior cerebellar artery. Anterior inferior cerebellar artery. Posterior inferior cerebellar artery.
SCA territory
Superior vermis. Middle and superior cerebellar peduncles. Superolateral aspects of cerebellar hemispheres.
Anterior Inferior Cerebellar Arteries (AICA) arise from
Proximal basilar artery.
Posterior Inferior Cerebellar Arteries (PICA) arise from
Distal vertebral artery, 1 to 2 cm below basilar origin.
Involvement of the medulla in PICA infarction adds elements of Wallenberg syndrome, which include
Ataxia. Facial numbness. Horner syndrome. Dysphagia. Dysarthria.
Lacunes
Small subcortical infarcts. May occur in any territory. Characteristic locations: Lenticular nucleus (37%). Pons (16%). Thalamus (14%). Caudate (10%). Internal capsule/corona radiata (10%).
Beginning at the genu and working back, the internal capsule carries somatotopically organized fibers
Corticobulbar fibers. HAL: Head fibers. Arm fibers. Leg fibers.
Perivascular spaces
Virchow-Robin spaces. May simulate lacunes. Follow CSF signal. No mass effect. Occur along path of a penetrating vessel.
Small-Vessel Ischemic Changes
Small foci of T2 hyperintensity scattered throughout brains of older patients. May or may not have clinical symptoms. Commonly associated with patchy or diffuse T2 hyperintensity in the centrum semiovale.
Some cerebral vasculitides
Autoimmune disorders. Drug exposure (heroin, amphetamines). Polyarteritis nodosa. Idiopathic processes (giant cell arteritis).
Venous sinus thrombosis predisposing factors include
Hypercoagulable states. Pregnancy. Infection (spread from contiguous scalp, face, middle ear, or sinus). Dehydration. Meningitis. Direct invasion by tumor.
Empty delta sign
Filling defect within sagittal sinus on postcontrast CT. Indicates venous sinus thrombosis.
Superficial hemosiderosis (or superficial siderosis)
Diffuse hemosiderin deposition on brain surface. Due to large or recurrent subarachnoid hemorrhages.
MR oxyhemoglobin per time, RBC, and T1 and T2 signal
Less than 1 day. RBC intact. T1 iso/dark. T2 bright.
MR deoxyhemoglobin per time, RBC, and T1 and T2 signal
0-2 days. RBC intact. T1 iso/dark. T2 dark.
MR methemoglobin (intracellular) per time, RBC, and T1 and T2 signal
2-14 days. RBC intact. T1 bright. T2 dark.
MR methemoglobin (extracellular) per time, RBC, and T1 and T2 signal
10-21 days. RBC lysed. T1 bright. T2 bright.
MR hemosiderin/ferritin per time, RBC, and T1 and T2 signal
> 21 days. RBC lysed. T1 dark. T2 dark.
Most sensitive areas for detecting SAH
Dependent parts of occipital horns. Interpeduncular fossa.
Main finding in patients whose condition continues to deteriorate after the initial SAH
Infarcts from post SAH increased intracranial pressure or arterial vasospasm.
Congenital berry aneursym
May be due to congenital absence of arterial media. Those larger than 3 to 5 mm are at increased risk for rupture. Often occur near branch points of circle of Willis.
Distal branch cerebral aneurysms are seen in what conditions
Prior trauma. Systemic infection (bacterial endocarditis with mycotic aneurysm).
Besides berry aneursyms, list other causes of cerebral aneurysms
Atherosclerosis. Fibromuscular disease. Polycystic kidney disease. Mycotic. Post-traumatic.
Main differential considerations for cerebral parenchymal hemorrhage
Hypertensive hemorrhage. Vascular malformations. Drug effects. Amyloid angiopathy. Bloody tumors.
Common locations for intracranial hypertensive hemorrhages
Putamen (35% to 50%). Subcortical white matter (30%). Cerebellum (15%). Thalamus (10% to 15%). Pons (5% to 10%).
Intracranial hemorrhage cause in young patients, less common than hypertension
Vascular malformations: AVMs. Cavernous malformations. Telangiectasias. Venous malformations.
Arteriovenous malformations
Most common type of brain vascular malformation. Abnormal tangle of arteries directly connected to veins without intervening capillaries. Most present with hemorrhage or seizures. 2% to 3% annual risk of bleeding,
Cavernous malformations
Thin-walled sinusoidal vessels (neither arteries nor veins). May present with seizures or small parenchymal hemorrhages.
Venous malformations
Anomalous veins that drain normal brain. Occur in 1% to 2% of patients. Enlarged enhancing stellate venous complex that extends to ventricular or cortical surface.
Amyloid angiopathy cerebral hemorrhage
Can cause intracranial, frequently lobar, hemorrhage. Amyloid deposits within media and adventitia of medium size and small cortical arteries. Not associated with systemic vascular amyloidosis. Affects elderly.
Hemorrhagic cerebral neoplasm
Primary: Glioblastomas. Metastatses: Bronchogenic carcinoma. Thyroid. Melanoma. Choriocarcinoma. Renal cell carcinoma.
Features of Benign Versus Malignant Intracranial Hemorrhage
Benign: Complete hemosiderin rim. Mild edema. Minimal acute enhancement (unless AVM). Blood products evolve from periphery to center. Malignant: Delayed or incomplete hemosiderin ring. Moderate surrounding edema. Moderate to severe acute enhancement. Irregular or complex blood product evolution.
Glial cell intracranial neoplasms (gliomas)
Astrocytoma. Oligodendroglioma. Ependymoma. Choroid plexus tumor.
Nerve sheath intracranial neoplasms
Schwannoma, Neurofibroma.
Extra-axial tumors
Tumors occuring along brain meninges or within the ventricles. Most nonglial tumors.
Significant general midline shift, if shift is greater than
3 mm.
Hallmarks of uncal herniation?
Effacement of ambient cistern. Contralateral hydrocephalus. May compromise ipsilateral oculomotor (III) nerve (pupillary dilation).
Differentiating a small neoplasm from a small infarct may be very difficult. When can followup imaging be obtained to help distinguish between the two.
Virtually all infarcts will be smaller in size by 3 weeks. If lesion is same size or larger at 3 weeks, a neoplasm should be favored.
Extra-axial mass refers to
Everything outside the brain: Arachnoid. Meninges. Dural sinuses. Skull. Ventricles.
White matter buckling?
Extra-axial lesions may buckle white matter. Inward compression of white matter (thinning of fronds). Preserved gray-white matter differentiation.
Tumors of high cellular density
Usually small cell tumors (high nucleus:cytoplasm ratio, hyperdense and T2 hypointense): Lymphoma. Pineoblastoma. Neuroblastoma. Medulloblastom. Metastases: Melanoma. Lung carcinoma. Colon carcinoma. Breast carcinoma.
Some specialized areas of the brain have no blood-brain barrier and will normally enhance
Choroid plexus. Pituitary glands. Pineal glands. Tuber cinereum. Area postrema.
Tumor enhancement generally means
Aggressive, high-grade neoplasms tend to have fenestrated capillaries (blood-brain barrier breakdown) allowing for enhancement.
Postop granulation tumor versus residual tumor?
Granulation tissue generally forms 72 hours after surgery. Early (less than 72 hours) postop enhancement likely reflects residual tumor rather than granulation tumor.
Diffuse white matter radiation injury
Unenhancing geographic white matter T2 hyperintensity conforming to radiation ports. Develops 6 months postradiation therapy.
Radiation necrosis
Indistinguishable from recurrent tumor on conventional imaging. May demonstrate mass effect and enhancement. Radiation necrosis may have elevated lactate peak (necrosis) on MRS. Recurrent tumor may have elevated choline peak and depressed n-acetyl aspartate (NAA) peak.
Astrocytoma grades and types
Grade I (pilocytic astrocytoma, subependymal giant cell astrocytoma). Grade II (lack necrosis and endothelial proliferation). Grade III (anaplastic astrocytoma). Grade IV (necrosis and endothelial proliferation, Glioblastoma multiforme).
Female predominant brain tumors
Meningioma (4:1). Neurofibroma. Pineocytoma. Pituitary tumor.
Male predominant brain tumors
Pineal germinoma (10:1). Pineal parenchymal tumor (4-7:1). Medulloblastoma (3:1). Glioblastoma multiforme (3:2). Choroid plexus papilloma (2:1). CNS lymphoma. Hamartoma of tuber cinereum.
Two neoplasms that may exhibit bihemispheric spread through the corpus callosum.
Glioblastoma multiforme. CNS lymphoma.
Intra-axial Lesions With Marked Surrounding Edema
Metastases. Abscess. Glioblastoma multiforme. Radiation necrosis. Hematoma (mild).
Hemorrhagic Brain Tumors
Primary: Glioblastoma multiforme (most common overall). Oligodendroglioma. Metastasis: RCC. Thyroid carcinoma. Choriocarcinoma. Melanoma.
Cerebral Ring-Enhancing Lesions
MAGIC DR. Metastasis. Abscess. Glioblastoma multiforme. Infarct. Contusion. Demyelinating disease. Resolving hematoma. radiation necrosis.
This MR sequence may help distinguish acute infarct from low-grade neoplasm.
DWI. Infarct exhibitis restricted diffusion.
Gliomatosis cerebri
Rare neoplastic infiltration of at least three lobes of the brain. Poor prognosis. Diffuse involvement of cerebral white matter with or without a mass.
In an adult with a heterogeneous calcified mass within the periphery of a frontal lobe with calvarial erosion and relative absence of edema should suggest the diagnosis of
Oligodendroglioma.
Oligodendroglioma features
Grade II tumor. Commonly located in the frontal lobes. Often extends to cortex and may erode calvarium. 70% calcify.
Calcified Glial Tumors in Order of Frequency
Old Elephants Age Gracefully: Oligodendroglioma. Ependymoma. Astrocytoma. Glioblastoma multiforme.
CNS lymphoma imaging characteristics
Hyperdense and T1 hypointensity on T2WIs with surrounding vasogenic edema. Subependymal spread is common. Bihemispheric involvement via corpus callosum may be seen.
Ganglioglioma and Gangliocytoma
Ganglioglioma contains glial cells and differentiated neurons. Most common tumor seen with chronic temporal lobe epilepsy. Gangliocytoma and ganglioneuroma are pure neuronal tumors without glial components. Floor of third ventricle is the most common location for gangliocytoma.
Desmoplastic Infantile Ganglioglioma
Rare variant of ganglioglioma seen in the first year of life. Very large heterogeneous mass with intense enhancement.
Most common tumor associated with medically refractory partial complex seizures
Dysembryoplastic neuroepithelial tumor. Always involves cortical gray matter. May have “soap bubble” appearance with exophytic extension beyond cortical gray matter margin.
Congenital Brain Tumors in Infants Younger Than 60 Days Old
Teratoma (most common): Two thirds are supratentorial. Primitive neuroectodermal tumors: Curvilinear, sparse calcification. Astrocytoma. Choroid plexus papilloma. Ependymoma. Medulloepithelioma. Germinoma. Angioblastic meningioma. Ganglioglioma.
Most (80% to 85%) metastatic lesions occur supratentorially, with the exception of ___________, which has a predilection for the posterior fossa.
Renal cell carcinoma.
Most Common Intra-axial Metastases to the CNS
Lung. Breast. Melanoma. Colon cancer.
Most Common Extra-axial Metastases to the CNS
Breast. Prostate. Lung. Neuroblastoma.
Most Common Hemorrhagic Metastases to the CNS
Melanoma. Renal. Thyroid. Choriocarcinoma.
Leptomeningeal carcinomatosis
Malignant invasion of leptomeninges. May mimic meningitis. Commonly involves basal cisterns. May present with cranial nerve palsies. Common malignancies: Breast. Lung. Lymphoma. Leukemia. Primary CNS malignancies.
Most common primary cerebellar neoplasm in adult population.
Hemangioblastoma.
Most reliable way to differentiate a medulloblastoma from an astrocytoma on cross-sectional imaging studies is
Noncontrast CT scan. Astrocytoma will usually be hypodense. Medulloblastoma will almost never be hypodense.
Posterior Fossa Masses in Children: Medulloblastoma
Most common pediatric CNS malignancy. Majority (85%) arise from cerebellar vermis. Commonly extends into fourth ventricle causing hydrocephalus. Highly malignant neoplasm (WHO grade IV). Hyperdense on CT. Hypointense on T1WIs. Variable on T2WIs.
Posterior Fossa Masses in Children: Pilocytic astrocytoma
Location: Cerebellar vermis. Hemisphere. Cystic with enhancing nodule.
Posterior Fossa Masses in Children: Ependymoma
Location: 4th ventricle. Appearance: Foraminal extension. Heterogeneous on CT and MR. Intense but heterogeneous enhancement.
Posterior Fossa Masses in Children: Brainstem glioma
Location: Brainstem. Appearance: Expansile brainstem. Isodense to hypodense on CT. Hypointense on T1WIs. Hyperintense on T2WIs.
Most common brain tumor seen in neurofibromatosis type 1 (NF1)
Pilocytic astrocytoma.
Cystic cerebellar mass with an enhancing mural nodule suggests two possible diagnoses, and the best discriminator between the two is
Age. Pilocytic astrocytoma, peak age of birth to 9 years. Hemangioblastoma, peak age of 35 years.
Capillary hemangioblastomas
Benign neoplasms of endothelial origin. Most common primary cerebellar neoplasm in adults. 4% to 20% occur as part of von Hippel-Lindau syndrome. Occur most often in cerebellar hemispheres and spinal cord. Well-defined cystic mass with an intensely enhancing mural nodule.
Dysplastic Cerebellar Gangliocytoma (Lhermitte-Duclos Disease)
Likely a hamartoma. Half of patients have Cowden disease (phacomatosis, colonic polyps, cutaneous tumors, meningioma, glioma, thyroid, breast neoplasms). CT often is normal. Striated cerebellar mass on T1and T2 WIs.
Meningioma
Most common extra-axial neoplasm of adults. Peak age of 50 to 60 years. Occur more commonly within women. Multiple tumors are associated with neurofibromatosis. Common locations: Parasagittal or convexity locations (50%). Sphenoid wing (20%). Olfactory groove/planum sphenoidale (10%). Parasellar region (10%). Hyerdense, hyperenhancing mass with variable surrounding edema. Calcification occurs in 10% to 20% of cases. Angiographically, early dense tumor blush that persists well into venous phase,
Cerebral Intraventricular Masses
Choroid plexus papilloma (24%). Choroid plexus carcinoma (2%). Ependymoma (18%). Subependymoma (11%). Central neurocytoma (10%). Subependymal giant cell astrocytoma (6%). All other astrocytomas (9%). Meningioma (6%). Colloid cyst (4%). Metastasis (2%).
Most Common Lateral Ventricle Masses, by Location and Age: 0 - 10 yo, Ventricle Body
PNET (Primitive neuroectodermal tumor). Teratoma. Choroid plexus papilloma.
Most Common Lateral Ventricle Masses, by Location and Age: 0 - 40 yo, Ventricle Trigone
Choroid plexus papilloma.
Most Common Lateral Ventricle Masses, by Location and Age: 10 - 40 yo, Foramen of Monro
Subependymal giant cell astrocytoma. Pilocytic astrocytoma.
Most Common Lateral Ventricle Masses, by Location and Age: 10 - 40 yo, Ventricle Body
Ependymoma. Pilocytic astrocytoma. Central neurocytoma.
Most Common Lateral Ventricle Masses, by Location and Age: > 40 yo, Ventricle Body
Subependymoma.
Most Common Lateral Ventricle Masses, by Location and Age: > 40 yo, Ventricle Trigone
Meningioma. Metastasis.
Choroid Plexus Papilloma
Most commonly occurs in lateral ventricle, especially in children. Increased intracranial pressure and hydrocephalus due to: Increased tumor production of CSF. Impaired CSF resorption (tumoral hemorrhage). CSF obstruction (mass effect). WHO grade I. May engulf glomus of choroid plexus. Choroid plexus calcification in first decade of life suggests choroid plexus papilloma.
Central neurocytoma
Arises from septum pellucidum or ventricular wall. 50% occur in lateral ventricle near foramen of Monro. May be bilateral. Most patients (75%) are between 20 and 40 years. Well-circumscribed lobulated mass within lateral or third ventricles. Hyperdense at CT. Cystic elements (Swiss cheese) and calcification are common.
Subependymoma
WHO grade I. Most are asymptomatic. Well-circumscribed lobulated intraventricular mass. Isodense to hypodense at CT. Frequent calcification (33%) and cystic degeneration (20%). Low T1 and high T2 signal. Hypointensity on T1WIs and hyperintensity on T2WIs are seen on MR. Enhancement not as diffuse as in central neurocytoma.
Subependymal giant cell astrocytoma
Seen in 10% of patients with tuberous sclerosis (look for subependymal and cortical hamartomas). WHO grade I. Commonly calcifies. and slow-growing, with calcification a common feature. Almost always produces some degree of hydrocephalus.
Colloid cyst
Occurs in anterosuperior portion of third ventricle near foramen of Monro. Can cause acute hydrocephalus. Almost all are hyperdense. Variable T1 and T2 signal.
Masses of the Anterosuperior Third Ventricle
Colloid cyst. Meningioma. Choroid plexus papilloma. Hamartoma. Glioma. Vascular lesion. Granulomatous disease.
Most common neoplasm of pineal region
Germ cell tumors
Calcified pineal mass in a female is more likely to be
Pineocytoma. In a male more likely to be a germinoma.
When calcification in the pineal region exceeds ____ in size, a pathologic pineal process should be suspected.
1 cm.
Cerebral Germ cell tumors
Well-defined, usually midline masses. 65% occur in pineal region (male more than female). 60% of all pineal masses. 35% are suprasellar (male = female). Germinoma is by far the most common. Commonly seen in children and young adults.
Pineal region masses
Germ Cell Tumors (60%): Germinoma. Teratoma. Embryonal carcinoma. Endodermal sinus tumor. Choriocarcinoma. Pineal Parenchymal Tumors (14%): Pineocytoma. Pineoblastoma. Other: Pineal cyst, glioma, tentorial meningioma, vein of galen malformation, arachnoid cyst, lipoma.
Pineoblastoma
Similar to medulloblastoma, part of PNET spectrum. Majority occur in young children. Well-circumscribed, often lobular. Local invasion and frequent calcification. WHO grade IV. Rarely may occur with bilateral retinoblastomas, the so-called trilateral retinoblastoma.
Pineocytoma
Most commonly seen in adults (women more than men). Usually well demarcated, noninvasive, and slow growing. Often calcified. Rarely metastasizes. At imaging, can't be differentiated from pineal germinoma or pineoblastoma.
Pineal cysts
Are common. Signal similar to or slightly higher than CSF, likely due to lack of CSF puslation. No enhancement.
Pituitary adenomas
Most common sellar masses. Microadenomas (10 mm or smaller). Macroadenomas (>10 mm). 75% are hormonally active, most of which are microadenomas. Lateral gland generally contains prolactin and growth hormone secreting adenomas. Central gland generally contains ACTH, TSH, FSH secreting adenomas. Microadenomas best detected on coronal T1WIs: Focal hypointensity (on noncontrast studies).
Craniopharyngioma
Arise from squamous epithelial remnants of anterior lobe of pituitary gland. Commonly are symptomatic due to large size. Most common suprasellar mass in children. Peak incidence between 5 and 10 years of age and 50 and 60 years. Solid and cystic components are typical. Large cystlike sellar/suprasellar mass with enhancing rim and some calcification. T1 (liquid crystal) and T2 hyperintense cyst.
Rathke cleft cyst
Arise from squamous epithelial remnants of anterior lobe of pituitary gland. Usually asymptomatic. Cyst may contain mucus, serous fluid, or cellular debris. Variable signal intensities. May mimic craniopharyngioma.
Schwannoma
Arises from Schwann cells. Commonly affects vestibulocochlear (VIII) and trigeminal (V) nerves. Cystic degeneration is common, especially in larger lesions. T1 hypointense to gray matter and T2 hyperintense to gray matter. Intense enhancement.
Most helpful imaging feature in distinguishing vestibular schwannomas
Extension of enhancement along course of seventh and eighth nerves.
Suprasellar Masses
SATCHMO Sella (pituitary) tumor. Sarcoid. Aneurysm. Arachnoid cyst. Teratoma. Craniopharyngioma. Hypothalamic glioma. Hamartoma of tuber cinereum. Histiocytosis. Meningioma. Optic nerve glioma.
Cerebellopontine Masses
AMEN Acoustic (vestibular) schwannoma. Meningioma. Ependymoma. Neuroepithelial cyst (arachnoid, epidermoid).
Epidermoid versus Dermoid
Epidermoid: Common. 40 to 50 yo. Ectoderm. Off midline (cerebellopontine cistern, parasellar, posterior fossa). Follows CSF, except hyperintense on DWI. Lobulated with peripheral enhancement. Dermoid: Uncommon. 20 to 30 yo. Ectoderm and mesoderm. Midline (pericerebellar, suprasellar). Typical fat attenuation or signal.
Intracranial lipomas
Occur within all age groups. Most common locations: Interhemispheric falx (often associated with agenesis of corpus callosum). Quadrigeminal plate. Suprasellar regions. Chemical shift artifact or fat suppression. Presence of flow void or traversing cranial nerve favors lipoma and excludes dermoid.
Arachnoid cysts
Are intra-arachnoidal. 50% occur in middle cranial fossa. Other sites: Frontal convexity. Suprasellar and quadrigeminal cisterns. Posterior fossa. Follow CSF signal and density. May remodel adjacent bone. Do not restrict diffusion. Enlarged cisterna magna fills immediately at cisternography; whereas, arachnoid cyst may not fill or slowly fill.
Hamartoma of tuber cinereum
Rare congenital hamartoma. More common in boys. Precocious puberty, gelastic seizures, developmental delay, and hyperactivity. Well-circumscribed, round or oval mass centered at the tuber cinereum (base of infundibulum). Does not calcify or hemorrhage. Stalk connecting mass with tuber cinereum or mamillary bodies cinches diagnosis.
Intracranial tuberculoma
Granuloma with central caseous necrosis. Isodense or slightly hyperdense nodules or small mass lesions.
Brain Coccidioidomycosis
Occurs in southwestern United States. Focal parenchymal granulomas are rare. Hydrocephalus is common from complicating meningitis.
Brain Blastomycosis
Occurs in Ohio and Mississippi River valleys. Frequently presents with meningitis with parenchymal abscesses and granulomas less likely. Epidural granulomas and abscesses also occur usually from direct extension from bone infection.
Brain Histoplasmosis
Occurs in Midwest and southern United States. Meningitis is most common. Multiple or solitary granulomas may occur.
CNS Aspergillosis
Parenchymal disease usually takes the form of an abscess. Granulomas are unusual. Abscesses are often multiple with irregular ring enhancement. Subcortical or cortical infarcts and hemorrhage from blood vessel invasion may occur.
CNS Mucormycosis
Invades brain usually by direct extension from sinuses, nose, or oral cavity. Almost all patients are diabetic or immunocompromised. Tends to invade blood vessels. Lesions are often in the base of the brain, adjacent to diseased sinuses. Infarcts, intra-axial or extra-axial hemorrhage, and meningeal enhancement can be seen with CT or MR.
CNS Candidiasis
Usually causes meningitis. Granulomas and small abscesses may occur. Meningeal enhancement or multiple small enhancing granulomas or microabscesses are usually seen.
Most frequently reported CNS fungal infection.
Cryptococcosis.
CNS Cryptococcosis
50% occur in immunocompetent patients. Common infection in patients with AIDS. Usually presents as meningitis. Granulomas can occur and are usually multiple. Abscesses are less common. CT scans can be normal. Cryptococcomas are small, usually multiple, solid-enhancing, peripheral parenchymal nodules. Gelatinous pseudocysts can be seen.
Gelatinous pseudocyst
Cystic lesion usually in basal ganglia. Perivascular spaces filled with cryptococcal organisms. Usually found only in immunocompromised.
Cysticercosis
Caused by larvae of pork tapeworm Taenia solium. Ingested eggs hatch in intestine and larvae are hematogenously distributed, forming cysticerci. 3 stages of CNS disease: Early phase, edema and/or nodular enhancement. Later, peripheral viable cysts. Scolex may be seen as small mural nodule. Late phase, peripheral calcifications without edema or enhancement.
Echinococcosis
Caused by dog tapeworm. More commonly involves liver and lungs, but brain can rarely be involved. Cysts are usually solitary, unilocular, large, round, and smoothly marginated. Most often supratentorial, in the middle cerebral artery territory.
Congenital CNS toxoplasmosis
Atrophy, dilated ventricles, and calcifications. Periventricular white matter, basal ganglia and cerebral hemisphere calcifications. In CMV, calcifications are usually periventricular only.
Amebic meningoencephalitis
Amebae enter nasal cavity of patients swimming in infested water. Direct extension through cribriform plate to the brain. Severe meningoencephalitis results and is usually fatal. Early in infection, meninges and gray matter may enhance. Later, diffuse cerebral edema ensues.
Neurosyphilis
Symptomatic patients may have aseptic meningitis, tabes dorsalis, general paresis, or meningovascular disease. Imaging is usually normal in tabes dorsalis, rarely gummas are found: small enhancing nodules on brain surface with adjacent meningeal enhancement. Meningovascular syphilis thickening of meninges and medium to large vessel arteritis.
CNS Lyme disease
2 Forms. Cranial neuritis: Thick, enhancing nerves. CNs III to VIII may be involved (CN VII most common). Parenchymal form: Multiple small white matter lesions. Similar to multiple sclerosis. Lesions may have nodular or ring enhancement. Meninges may enhance.
Cytomegalovirus, congenital CNS infection
Most common CT findings: Periventricular calcification. No calcifications of basal ganglia or cortices as seen congenital toxoplasmosis.
Neonatal herpes simplex encephalitis
Early in course: Diffuse brain swelling or bilateral patchy areas of decreased density (hypoechoic, too) in cerebral white matter and cortex. Sparing of basal ganglia, thalami, and posterior fossa structures. Multicystic encephalomalacia is the end result.
Adult herpes simplex CNS infection
May cause encephalitis or cranial neuritis. 70% mortality rate in untreated patients. Ill-defined hypodensities within one or both temporal lobes. Virus is usually latent within gasserian ganglion. Frontal lobes may be involved. Insular cortex is often involved, but adjacent putamen is spared. Usually swelling with mass effect. Streaky enhancement is variable. The CT findings are not usually seen before the fifth day of symptoms. Increased FLAIR and T2 signal within temporal and/or frontal lobe(s) with sparing of putamen. Middle cerebral artery infarct (often involves putamen, unlike herpes).
Ramsay Hunt syndrome
Herpes zoster facial neuritis. Ear pain, facial paralysis, vesicular eruption about the ear. MR may reveal increased enhancement of facial nerve.
Acute disseminated encephalomyelitis (ADEM)
May occur after viral infection, following a vaccination, or spontaneously. When treated early with steroids, most patients make a full recovery. Increased T2 and FLAIR signal within white matter of brainstem, cerebellum, and basal ganglia. Optic neuritis is also common.
Subacute sclerosing panencephalitis
caused by variant of measles virus. Occurs in children and young adults who had measles before age 2, after a 6- to 10-year asymptomatic period. Causes progressive dementia, seizures, and paralysis, leading to death. Initially may have focal lesions in gray matter and subcortical white matter. Later, periventricular white matter lesions may enhance. Late stages usually is profound cortical atrophy.
Progressive multifocal leukoencephalopathy (PML)
Demyelinating disease caused by a papova virus. Occurs only in immunosuppressed patients, especially in AIDS.
Creutzfeldt-Jakob disease
Caused by a prion. Rapidly progressive dementia, ataxia, and myoclonus, leading to death. Early stage, high DWI signal within cerebral cortex and basal ganglia. Later stage, atrophy and increased T2 and FLAIR signal within cortex and basal ganglia.
Meningitis forms causing thick meningeal enhancement (pachymeningeal)
Tuberculous meningitis. Fungal meningitis. Racemose cysticercosis. Sarcoidosis.
Most common AIDS CNS infections
HIV encephalopathy. Toxoplasmosis. Cryptococcosis. Other fungal infections. CMV and Herpes meningoencephalitis. Mycobacterial infection. PML. Meningovascular syphilis.
Most common CNS AIDS tumor
Primary CNS lymphoma.
HIV Encephalopathy
Diffuse atrophy is most common manifestation. White matter lesions are seen with AIDS dementia complex. Diffuse pattern of increased T2 signal in deep white matter or multiple small punctate white matter lesions.
Most common opportunistic CNS infection in AIDS
Toxoplasmosis.
Toxoplasmosis
Multiple high T2 signal and enhancing mass lesions (1-4 cm) with surrounding vasogenic edema. Larger lesions usually exhibit ring enhancement. Unlike bacterial abscesses, toxoplasmosis lesions are not high in signal on DWI. Preferred sites: Basal ganglia. White matter. Cortex. Main differential consideration is primary CNS lymphoma.
Most common AIDS CNS fungal infection
Cryptococcosis.
Progressive multifocal leukoencephalopathy
Infection of immunosuppressed patients (AIDS, transplants, leukemics) caused by reactivation of JC virus. Progressive course to death within months. In non-AIDS patients, has a predilection for occipital lobes. In AIDS patients, any part of brain may be involved. High T2 and low T1 lesions within subcortical and deep white matter. Mass effect and contrast enhancement are almost always absent.
Primary CNS lymphoma
Most common intracranial tumor in AIDS. Solitary or multiple enhancing mass lesions, centrally located within deep white matter or basal ganglia. Lesions usually are T2 isointense to white matter with homogeneous enhancement. Toxoplasmosis lesions usually are T2 hypointense.
Dysmyelination
Inherited disorder (leukodystrophy), affecting formation or maintenance of myelin. Generally encountered within pediatric population.
Demyelination
Acquired disorder that affects normal myelin. Generally encountered within adult population.
Multiple sclerosis (MS, Primary Demyelination)
Multiple CNS lesions separated in time and space. Typical lesions are high T2 signal and round or ovoid in a periventricular (perpendicular to ventricle) or subcortical location. Enhancement reflects new lesions. Dark T1 lesions are due to acutal neuronal tissue loss. Other sites affected: Cerebellar and cerebral peduncles. Corpus callosum. Medulla. Spinal cord. Conglomerate large lesions may be mistake for a neoplasm (tumefactive).
Involvement of callosal-septal interface is quite specific for
MS.
Nonspecific punctuate white matter lesions (small bright lesions on T2WIs) are more prominent in any patient with
Vasculopathy or hypercoagulable state.
A classic case presentation is that of a young adult female with prior miscarriages presenting with headaches/migraines and ischemic white matter changes.
Antiphospholipid syndrome (phospholipid antibody syndrome). Hypercoagulable state with white matter and ischemic changes.
Ependymitis granularis
Normal anatomic finding. May mimic pathology. High T2 signal at tips of frontal horns. Due to porous ependyma allowing transependymal flow of CSF.
Senescent periventricular hyperintensity
Age-related high T2 signal along entire length of lateral ventricles.
Prominent perivascular spaces
CSF-filled perivascular clefts. Also called Virchow-Robin spaces. Punctate foci of high T2 signal. Typically within centrum semiovale and lower basal ganglia at the level of the anterior commissure, where lenticulostriate arteries enter the brain.
MR sequences that help distinguish perivascular spaces from parenchymal lesions
Proton-density and FLAIR sequences. PD: CSF has similar signal intensity as white matter. Perivascular space is isointense to brain. Ischemic lesions are bright due to gliosis. FLAIR: Parenchymal lesions with gliosis have abnormal signal.
Central pontine myelinolysis (CPM)
Demyelination of central pons. Due to electrolyte abnormalities, particularly hyponatremia, that are rapidly corrected. Oligodendroglial cells are most susceptible: Central pons. Thalamus. Globus pallidus. Putamen. Lateral geniculate body.
Posterior reversible encephalopathy syndrome (PRE)
Symmetric subcortical and cortical vasogenic edema within parietooccipital lobes. Temporary failure of autoregulation of cerebral arteries. Associations: Cyclosporin A or tacrolimus (FK506). Acute renal failure/uremia. Hemolytic uremic syndrome. Eclampsia. Thrombotic thrombocytopenia purpura. Chemotherapy (interferon).
Marchiafava-Bignami disease
Rare demyelination seen frequently in alcoholics. Involves central fibers (medial zone) of corpus callosum. Anterior and posterior commissures. Centrum semiovale. Mddle cerebral peduncles. Felt to reflect a form of osmotic demyelination
Wernicke encephalopathy and Korsakoff syndrome
Metabolic disorders caused by thiamine (B1 vitamin) deficiency: alcoholics, hematologic malignancies, hyperemesis gravidarum. Wernicke encephalopathy clinical triad of acute ocular movement abnormalities, ataxia, and confusion. If longterm memory and learning problems result then Korsakoff syndrome. Early stage may reveal T2 hyperintensity or contrast enhancement of mamillary bodies, basal ganglia, thalamus, brainstem, and periaqueductal involvement. Chronic stage may show mamillary body and tegmentum atrophy and dilation of third ventricle.
Radiation Leukoencephalitis
Occurs 6 to 9 months after treatment in excess of 40 Gy. Confluent high T2 signal within white matter extending to subcortical U fibers.
Radiation Necrosis
Commonly occurs 6 to 24 months postradiation. Enhancing lesion with mass effect and ring enhancement. Or multiple foci of enhancement, Mimicks recurrent neoplasm. MR spectroscopy (MRS): Elevated lactate and lipids (0.9 to 1.3 ppm). Reduced other major metabolites (choline, creatine, and N-acetylaspartate).
Metachromatic leukodystrophy: head size, age of onset, white matter involvement, gray matter involvement
Normal head size. Infantile form 1-2 yo. Juvenile form 5-7 yo. Diffuse white matter involvement. No gray matter invovlement. Most common Leukodystrophy. Deficiency of the enzyme arylsulfatase A.
Adrenoleukodystrophy leukodystrophy: head size, age of onset, white matter involvement, gray matter involvement
Normal head size. 5-10 yo. Symmetric occiptal and splenium of corpus callossom white matter invovlement. No gray matter involvement. Sex-linked recessive condition (peroxisomal enzyme deficiency) occurring only in boys.
Leigh disease: head size, age of onset, white matter involvement, gray matter involvement
Normal head size. Less than 5 yo. Focal areas of subcortical white matter. Basal ganglia and periaquaductal gray matter involvement. Also called subacute necrotizing encephalomyelopathy. Mitochondrial enzyme defect.
Alexander disease: head size, age of onset, white matter involvement, gray matter involvement
Normal to large head size. Less than 1 yo. Frontal white matter involvement. No gray matter involvement.
Canavan disease: head size, age of onset, white matter involvement, gray matter involvement
Normal to large head size. less than 1 yo. Diffuse white matter involvement. Vacuolization of cortical gray matter. deficiency of aspartoacylase, leads to the buildup of NAA (MRS).
Transependymal flow of CSF
Occurs in acute hydrocephalus. May mimic periventricular white matter disease. Important means of CSF reabsorption during ventricular obstruction.
CSF circulation route
Produced mainly by choroid plexus of lateral, third, and fourth ventricles. Flows from lateral ventricles through foramina of Monro to third ventricle through cerebral aqueduct to fourth ventricle through lateral and medial fourth foramina (Luschka and Magendie) to basilar cisterns and over hemisphere surfaces. Principal site of absorption is into venous circulation through arachnoid villi.
Will commonly demonstrate supratentorial ventriculomegaly, with a fourth ventricle that appears normal.
Communicating hydrocephalus. Dilated 4th ventricle can be seen in communicating and non-communicating hydrocephalus.
Ex Vacuo Ventriculomegaly
Enlarged ventricles due to cerebral atrophy. Prominence of both sulci and ventricles.
Normal pressure hydrocephalus
Chronic, low-level form of hydrocephalus. Clinical triad: Dementia, gait disturbance, and urinary incontinence. CSF pressure is within normal limits. Slight gradient exists between ventricular system and subarachnoid space due to incomplete subarachnoid CSF block. Commonly results from prior subarachnoid hemorrhage or meningitis. Diffuse ventriculomegaly out of proportion to sulcal prominence. Early entry of radiotracer into lateral ventricles, with persistence at 24 and 48 hours. Delay ascent to parasagittal region.
Alzheimer disease (AD)
Most common cause of dementia. Prefential atrophy of: Hippocampal formation. Temporal lobes. Parietotemporal cortices. Enlargement of temporal horns, suprasellar cisterns, and sylvian fissures may distinguish from age-related atrophy.
Parkinson disease
Most common basal ganglia disorder. Deficiency of dopamine specifically within pars compacta of the substantia nigra. MR imaging is relatively insensitive but is useful in excluded other causes of movement disorders (stroke).
Huntington disease
Progressive hereditary disorder occuring in fourth and fifth decades. Findings: Diffuse cortical atrophy. Caudate nucleus atrophy. Putamen atrophy. Enlargement of frontal horns (heart-shaped).
Wilson disease
Hepatolenticular degeneration. Inborn error of copper metabolism. Hepatic cirrhosis and degenerative changes of basal ganglia. Diffuse atrophy with signal abnormalities involving deep gray matter nuclei and deep white matter.
Bilateral lesions of basal ganglia can be seen in a variety of insults
Carbon monoxide exposure (globus pallidus). Methanol toxicity (putaminal). Metabolic conditions (Wilson disease). Hallervorden-Spatz disease (iron deposition within globus pallidus). Mitochondrial disorders (Leigh disease and Kearns-Sayre syndrome).
Myelination Landmarks by Age 0 days
High T1 signal: Dorsal brainstem. Ventrolateral thalamus. Lentiform nucleus. Central corticospinal tracts. Low T2 signal: Posterior limb internal capsule posterior portion.
Myelination Landmarks by Age 3 months
High T1 signal: Anterior limb internal capsule. Cerebellar white matter.
Myelination Landmarks by Age 6 months
High T1 signal: Genu of corpus callosum. Low T2 signal: Splenium of corpus callosum.
Myelination Landmarks by Age 11 months
Low T2 signal: Anterior limb internal capsule.
Myelination Landmarks by Age 18 months
Adult appearance except for terminal myelination zones (periatrial and adjacent to frontal horns)
Myelination Landmarks by Age 24 months
Dark white matter on T2 (some minimal high-signal areas may persist peripherally)
Pelizaeus-Merzbacher Disease
Rare X-linked leukodystrophy. Arrest of myelin development, usually in neonatal period. Shows lack only of myelin formation, rather than myelin formation followed by destruction.
HYPOXIC ISCHEMIC ENCEPHALOPATHY (HIE)
Damage to brain from hypoxia/ischemia occurring in utero or around time of delivery.
Hydranencephaly
Ischemic infarction of both cerebral hemispheres. Early compromise of both carotid arteries with preservation of posterior circulation. Mimics severe hydrocephalus (thin rind of cortical gray matter). Complete infarction of supratentorial cerebral tissues with preservation of thalami and cerebellum.
Hypoxic ischemic encephalopathy occuring within 1st trimester
Cortical irregularity and/or hydranencephaly.
Hypoxic ischemic encephalopathy occuring at less than 26 weeks of gestation
Periatrial injury. No gliosis. Ex vacuo enlargement.
Hypoxic ischemic encephalopathy occuring at greather than 28 weeks
Periatrial gliosis: high T2 signal.
Hypoxic ischemic encephalopathy occuring at term
Watershed infarcts. Ulegyria. Variable deep, superficial white matter gliosis and atrophy. Myelination delay. Injury to hippocampus and pons.
Periventricular Leukomalacia (PVL)
Occurs in term infants, premature infants greater than 26 weeks of gestation. Periventricular gliosis. Ex vacuo ventriculomegaly. Apposition of sulci to ventricular surface.
Gliosis in the periatrial region (seen best on proton-density scans) is caused by injury to the developing brain at ______ gestational age or older.
28 weeks .
Ex vacuo atrial enlargement without gliosis reflects injury prior to _______ gestational age.
26 weeks.
Acute imaging findings of Profound Perinatal Hypoxic Ischemic Injury
Deep gray matter: Isodense to white matter. Mottled high T1 and low T1 signal. White matter: Normal. May see blurred gray-white junction on protein density images.
Subacute imaging findings of Profound Perinatal Hypoxic Ischemic Injury
Deep gray matter: Variable T1 and T2 signal. White matter: High T1 and low T2 perirolandic cortex.
Chronic imaging findings of Profound Perinatal Hypoxic Ischemic Injury
Deep gray matter: High T2 signal. White matter: High T2 perirolandic cortex. Thinned gyri, atrophy.
Imaging of Profound Postnatal Hypoxic Ischemic Injury
Deep gray (Damage to corpus striatum: high signal on T2WIs Relative sparing of thalami) Cortex (Majority of cortex injured: high signal on T2WIs Relative sparing of perirolandic cortex Thinned gyri)
Septo-optic dysplasia (SOD)
Congenital disorder with variable hypoplasia of optic nerves and complete or partial absence of septum pellucidum. Squared-off appearance of frontal horns.
Alobar holoprosencephaly
Poor prognosis. Anterior rind of brain tissue and monoventricle communicating with dorsal cyst. Fused thalami. Absent septum pellucidum, corpus callosum, and falx. Upside-down U-shaped mantle of brain tissue. Ends of U are hippocampal ridges.
Semilobar holoprosencephaly
Partial fusion of hemispheres. Absent or dysgenic corpus callosum and septum pellucidum. High association with migration anomalies. Posterior portion of interhemispheric fissure and falx are usually formed.
Lobar holoprosencephaly
Partial absence of frontal interhemispheric fissure. Absent septum pellucidum and relatively normal brain overlap with SOD. Body and splenium of corpus callosum are usually present with genu and rostrum absent (dysgenic corpus callosum).
Lipomas of corpus callosum
Congenital abnormalities. High T1 signal with fat supression. No mass effect. Vessels course through these lesions. Occur because of persistence of meninx primitiva.
Lissencephaly and pachygria/agyria complex
Synonyms meaning absence of gyri. Smooth hourglass brain. Thick, multilayered cortex. Classic pattern: Arrested neuronal migration with only four cortical layers. Premature infant's brain can be a mimic.
Hemimegalencephaly
Asymmetric hemispheric enlarged with polymicrogyric and pachygyric changes. May be associated with neurofibromatosis.
Polymicrogyria and pachygria
Pachygyria is a incomplete lissencephaly. Broad, thick gyri with shallow sulci. Normal interdigitating fingers of subcortical white matter are absent. Polymicrogyria is a cortical dysplasia. Thick mantle of gray matter with multiple small gyri. Normal interdigitating fingers of subcortical white matter are absent. Underlying white matter gliosis in polymicrogyria can sometimes help differentiate it from pachygyria.
Heterotopic Gray Matter
Islands of gray matter anywhere between ependymal surface and subcortical white matter. May cause seizures.
Schizencephaly
Abnormal neuronal migration resulting in gray matter-lined clefts that invaginate brain. Extend from ventricular ependymal surface to pial cortical surface. Polymicrogyric clefts do not extend to ventricle. Open lip or closed lip (apposed walls) forms.
Distinguishing porencephaly from open lipped schizencephaly
Porencephaly: encephalomalacia that communicates with ventricle. Schizencephalic clefts are lined by gray matter. Porencephalic cysts are lined by a thin layer of white matter.
Chiari II malformations
Small posterior fossa: Cerebellum is squeezed up against tentorium, down through foramen magnum (tonsillar herniation), and forward around brainstem. Pons and medulla are squeezed inferiorly with cervicomedullary kink. Cord syrinx is present. Nearly all have hydrocephalus. Most have partial or complete agenesis of corpus callosum. Most present with myelomeningocele.
Chiari I malformations
Cerebellar tonsillar ectopia (tonsils extend > 5 mm below foramen magnum). Patients may be asymptomatic. May give rise to cervical spinal cord syrinx.
Dandy-Walker Malformations
Large posterior fossa with high tentorial insertion. Dilated cystic 4th ventricle fills posterior fossa. Cerebellar vermis and hemispheres may be hypoplastic or absent.
Neurofibromatosis type 1 imaging findings (chromosome 17)
Altered signal in white matter and basal ganglia. Dural ectasia. Optic and other gliomas. Sphenoid dysplasia. Thinning long bone cortex (ribbon ribs). Plexiform neurofibromas. Café au lait spots. Iris hamartomas (Lisch nodules). Vascular stenoses.
Neurofibromatosis type 2 imaging findings (chromosome 22)
Vestibular schwannomas. Meningiomas. Spinal glial tumors. Optic and other gliomas.
Tuberous sclerosis
Skin lesions: Adenoma sebaceum. Ash-leaf spots. Brain lesions: Subependymal hamartomas. Cortical tubers. Subependymal giant cell astrocytomas located at foramina of Monro (May lead to hydrocephalus)
Sturge-Weber Syndrome
Skin and meningeal angiomatous lesions. Port-wine nevus: skin angioma in ophthalmic division of trigeminal nerve. Pial angiomas may result in chronic ischemia, gliosis, and gyral cortical calcifications. Enlargement of deep and subependymal veins may mimic arteriovenous malformations.
Von Hippel-Lindau Syndrome
Inherited disorder consisting of retinal angiomas and cerebellar and spinal hemangioblastomas. Cerebellar hemangioblastomas: well-circumscribed cystic lesion with enhancing mural nodule. Prone to sudden spontaneous hemorrhage. Other associations: renal cell carcinoma, liver and kidney angiomas.