hnbs neuro copy

Question 1

Disk protrusion terminology

Answer 1

Bulge: Broad-based disk bulge. Usually bulging annulus fibrosus. Protrusion: Focal disk bulge. Usually herniated nucleus pulposus.

Question 2

Intervertebral disk high intensity zone (HIZ)

Answer 2

High T2 signal of annulus indicating annular tear.

Question 3

Disk free fragment mimickers

Answer 3

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.

Question 4

Lateral Disks

Answer 4

May cause nerve root impingement causing symptoms of a superior level. Nerve root has already exited central canal.

Question 5

Common causes of Central Canal Stenosis

Answer 5

Facet joint degenerative change (most common). Lligamentum flavum hypertrophy.

Question 6

Most common cause of neuroforaminal stenosis

Answer 6

Facet joint degenerative change with bony encroachment.

Question 7

Lateral recess

Answer 7

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.

Question 8

Spondylolysis identified on axial images

Answer 8

Break in bony ring of the lamina (pars interarticularis) at the mid vertebral body level.

Question 9

Spondylolisthesis occurs from either

Answer 9

Bilateral spondylolysis. Facet joint degenerative change.

Question 10

Distinguishes postop scar from disk material

Answer 10

Scar tissue enhances. Disk material has only minimal peripheral enhancement.

Question 11

Differentiates disk infection fromdegenerative disk disease at MR

Answer 11

Type 2 degenerative disk disease: Low T1 disk and high T2 parallel endplate bands. Disk space infection: High T2 disk.

Question 12

Myelopathy neurologic signs

Answer 12

Ataxia. Bowel and bladder incontinence. Babinski sign.

Question 13

Radiculopathy neurologic signs

Answer 13

Muscle weakness. Decreased reflexes. Dermatomal sensory deficits.

Question 14

Urgency for imaging acute myelopathy

Answer 14

Poor prognosis if left untreated for greater than 24 hours.

Question 15

Common causes of myelopathy

Answer 15

Extramedullary: Epidural mass cord compression. Cervical spine stenosis. Intramedullary: Tumor. Inflammation, Arteriovenous malformation (AVM). Spinal dural arteriovenous fistula (SPAVF).

Question 16

Definition of Intramedullary spinal canal lesion

Answer 16

Usually confined to spinal cord. May be exophytic.

Question 17

Definition of extramedullary spinal canal lesion

Answer 17

Outside of spinal cord. May be intradural or extradural.

Question 18

Intradural intramedullary lesions

Answer 18

Ependymoma. Astrocytoma. Hemangioblastoma. Lipoma/(Epi)dermoid. Syringohydromyelia. Intramedullary AVM. Met/abscess (rare).

Question 19

Intradural extramedullary lesions (includes subarachnoid space)

Answer 19

Meningioma. Schwannoma/neurinoma. Neurofibroma. Hemangiopericytoma. Lipoma/(Epi)dermoid. Arachnoid cyst/adhesion. Drop/leptomeningeal metastasis. Veins (extramedullary AVM).

Question 20

Extradural extramedullary lesions

Answer 20

Degenerative: Herniated disc. Synovial cyst. Osteophyte. Rheumatoid pannus. Nondegenerative: Metastasis. Abscess. Hematoma. Primary tumor expansion or invasion. Epidural lipomatosis

Question 21

Most common intramedullary lesion at MRI

Answer 21

Multiple sclerosis

Question 22

Lupus Erythematosus spinal cord involvement

Answer 22

Areas of high T2 signal with cord swelling. May involve 4 or 5 vertebral segments. Have less well-defined margins than MS plaques.

Question 23

Atlantoaxial instability and rheumatoid arthritis

Answer 23

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.

Question 24

Vertebral body and disc infection findings

Answer 24

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.

Question 25

Vertebral body neoplasm findings

Answer 25

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.

Question 26

Vertebral body osteoporosis findings

Answer 26

Several vertebral bodies with height loss. Anterior weding with posterior elements spared. Normal T1 and T2 unless fracture. Disk spared.

Question 27

TB of the spine, or Pott disease

Answer 27

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.

Question 28

Most common neoplasm of the spine

Answer 28

Metastases

Question 29

Two most common primary intramedullary tumors

Answer 29

Astrocytoma. Ependymoma.

Question 30

Spinal cord astrocytoma and ependymoma shared features

Answer 30

Expansile. Low T1 and high T2 signal with variable enhancement. Increased incidence in neurofibromatosis.

Question 31

Spinal cord Ependymoma features

Answer 31

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.

Question 32

Spinal cord Astrocytoma features

Answer 32

Most (75%) occur in cervical and upper to midthoracic cord. Fusiform cord widening. High T2 signal. Contrast enhancement over several vertebral body segments.

Question 33

Hemangioblastoma features

Answer 33

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).

Question 34

Syrinx

Answer 34

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.

Question 35

Most common intradural tumor in thoracic region

Answer 35

Meningioma

Question 36

Spinal meningioma features

Answer 36

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.

Question 37

Most common intraspinal mass

Answer 37

Schwannoma

Question 38

Spinal schwannoma features

Answer 38

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.

Question 39

Common intrathecal drop metastases

Answer 39

Subarachnoid seeding of primary CNS tumors: Posterior fossa medulloblastomas. Ependymomas. Pineal region neoplasms.

Question 40

Most common spine extradural neoplasm

Answer 40

Metastatses: Breast, Lung, Prostate carcinoma.

Question 41

Very low T1 and T2 marrow signal

Answer 41

Myelofibrosis

Question 42

Spinal AVM features

Answer 42

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.

Question 43

Tethered Cord features

Answer 43

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.

Question 44

Caudal Regression Syndrome

Answer 44

Hypoplastic or absent distal spine and sacrum. Blunted conus.

Question 45

Spinal Arachnoid cysts and epidermoids

Answer 45

Similar to brain arachnoid cysts and epidermoids. Arachnoid cysts follow CSFsignal. Epidermoids restrict diffusion, bright on DWIs.

Question 46

Spinal Epidural Hematoma

Answer 46

Ventral epidural space contains plexus of veins. These can tear in trauma, resulting in epidural hematoma.

Question 47

Nerve Root Avulsion

Answer 47

Most commonly occur in cervical spine. Typically involve roots of brachial plexus and upper extremities. Birth trauma from shoulder traction is common example.

Question 48

Acute versus chronic sinusitis findings

Answer 48

Acute sinusitis: Air-fluid levels and foamy secretions. Typically caused by viral URI. Chronic sinusitis: Mucoperiosteal thickening. Thickening of bony sinus walls.

Question 49

Disease limited to the infundibulum of the maxillary ostium will result in

Answer 49

Isolated obstruction of maxillary sinus.

Question 50

Lesion located at hiatus semilunaris (middle meatus) results in

Answer 50

Obstruction of ipsilateral maxillary sinus, anterior and middle ethmoid air cells, and frontal sinus. Described as ostiomeatal pattern of obstruction.

Question 51

Sphenoid sinusitis is of great clinical concern as it may

Answer 51

Extend intracranially due to presence of valveless veins.

Question 52

Sinus mucous retention cyst versus mucocele

Answer 52

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.

Question 53

Inverting Papilloma

Answer 53

Neoplastic epithelium inverts and grows into underlying mucosa of lateral nasal wall. Surgically resected due to association with squamous cell carcinoma.

Question 54

Juvenile nasopharyngeal angiofibromas

Answer 54

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.

Question 55

Malignancies of paranasal sinuses and nasal cavity.

Answer 55

Squamous cell carcinoma. Lymphoma. Minor salivary tumors.

Question 56

Most common salivary malignancies include

Answer 56

Adenoid cystic carcinoma. Adenocarcinoma. Mucoepidermoid carcinoma.

Question 57

Esthesioneuroblastoma

Answer 57

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.

Question 58

Three most common primary (mets by far more common) skull base malignant tumors

Answer 58

Chordoma (destructive midline mass). Chondrosarcoma. Osteogenic sarcoma (from radiation or Paget s degeneration).

Question 59

Cholesteatoma

Answer 59

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.

Question 60

Opacified petrous apex differential

Answer 60

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.

Question 61

Cholesterol granuloma

Answer 61

Granulation tissue within partially obsructed petrous air cells. Have cholesterol and hemorrhagic component (high T1 and T2 signal).

Question 62

Deep anatomy of the head and neck is subdivided by layers of deep cervical fascia into the following spaces:

Answer 62

(1) Superficial mucosal. (2) Parapharyngeal. (3) Carotid. (4) Parotid. (5) Masticator. (6) Retropharyngeal. (7) Prevertebral.

Question 63

Mucosal head and neck compartment contents

Answer 63

Squamous mucosa. Lymphoid tissue (adenoids, lingual tonsils). Minor salivary glands.

Question 64

Mucosal head and neck compartment pathology

Answer 64

Nasopharyngeal carcinoma. Squamous cell carcinoma. Lymphoma. Minor salivary gland tumors. Juvenile angiofibroma. Rhabdomyosarcoma.

Question 65

Parapharyngeal head and neck compartment contents

Answer 65

Fat. Trigeminal nerve (V3). Internal maxillary artery. Ascending pharyngeal artery.

Question 66

Parapharyngeal head and neck compartment pathology

Answer 66

Minor salivary gland tumor. Lipoma. Cellulitis/abscess. Schwannoma.

Question 67

Parotid head and neck compartment contents

Answer 67

Parotid gland. Intraparotid lymph nodes. Facial nerve (VII). External carotid artery. Retromandibular vein.

Question 68

Parotid head and neck compartment pathology

Answer 68

Salivary gland tumors. Metastatic adenopathy. Lymphoma. Parotid cysts.

Question 69

Carotid head and neck compartment contents

Answer 69

Cranial nerves IX-XII. Sympathetic nerves. Jugular chain nodes. Carotid artery. Jugular vein.

Question 70

Carotid head and neck compartment pathology

Answer 70

Schwannoma. Neurofibroma. Paraganglionoma. Metastatic adenopathy. Lymphoma. Cellulitis/abscess. Meningioma.

Question 71

Masticator head and neck compartment contents

Answer 71

Muscles of mastication. Ramus and body of mandible. Inferior alveolar nerve.

Question 72

Masticator head and neck compartment pathology

Answer 72

Odontogenic abscess. Osteomyelitis. Direct spread of squamous cell carcinoma. Lymphoma. Minor salivary tumor. Sarcoma of muscle or bone.

Question 73

Retropharyngeal head and neck compartment contents

Answer 73

Lymph nodes (lateral and medial retropharyngeal). Fat.

Question 74

Retropharyngeal head and neck compartment pathology

Answer 74

Metastatic adenopathy. Lymphoma.

Question 75

Prevertebral head and neck compartment contents

Answer 75

Cervical vertebrae. Prevertebral muscles. Paraspinal muscles. Phrenic nerve.

Question 76

Prevertebral head and neck compartment pathology

Answer 76

Osseous metastases. Chordoma. Osteomyelitis. Cellulitis. Abscess.

Question 77

Tornwaldt cysts

Answer 77

Benign midline nasopharynx lesion of high T2 signal. Believed to be remnant of notochordal tissue (benign).

Question 78

Most common minor salivary gland malignancy and has propensity for perineural spread

Answer 78

Adenoid cystic carcinoma

Question 79

The parapharyngeal space is surrounded by what spaces

Answer 79

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.

Question 80

Triad of nasopharyngeal malignancy

Answer 80

1) Mucosal mass of lateral nasopharynx (fossa of Rosenmuller). (2) Lateral retropharyngeal nodes. (3) Mastoid opacification (eustachian tube dysfunction)

Question 81

Head and neck paragangliomas

Answer 81

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).

Question 82

Salivary gland tumors

Answer 82

Benign: Pleomorphic adenoma. Warthin tumor. Malignant: Adenocystic carcinoma. Adenocarcinoma. SCC. Mucoepidermoid carcinoma.

Question 83

Head and neck trans-spatial disease categories

Answer 83

Lymphatic masses (lymphangioma). Neural masses (neurofibroma, schwannoma, perineural spread of tumor). Vascular masses (hemangioma).

Question 84

Head and neck diseases that demonstrate perineural spread

Answer 84

Fungal infections. Squamous cell carcinoma. Adenoid cystic carcinoma.

Question 85

This lymph node chain serves as the final common afferent pathway for lymphatic drainage of the entire head and neck.

Answer 85

Internal jugular nodal chain

Question 86

Pathologic size of head and neck lymph nodes

Answer 86

Jugulodigastric and submandibular nodes may normally measure up to 1.5 cm. All other nodes up to 1.0 cm.

Question 87

Common optic nerve sheath complex tumors

Answer 87

Optic nerve glioma. Optic sheath meningioma.

Question 88

Optic nerve glioma

Answer 88

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.

Question 89

Arachnoidal hyperplasia or gliomatosis

Answer 89

Thickening of perioptic meninges associated with optic nerve gliomas. Reflects peritumoral reactive meningeal change.

Question 90

Optic sheath meningiomas

Answer 90

Grow in a linear fashion along optic nerve. Tram track pattern of linear enhancement. May invade through dura. May be extensively calcified.

Question 91

Orbital vascular lesions and age groups

Answer 91

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.

Question 92

Superior ophthalmic vein pathology

Answer 92

Thrombosis often occurs with cavernous sinus thrombosis. Loss of normal flow void. Enlargement occurs with cavernous carotid fistulas.

Question 93

Most common cause of intraorbital mass in an adult

Answer 93

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.

Question 94

3 common adult intraorbital masses

Answer 94

Idiopathic inflammatory pseudotumor. Cavernous hemangioma. Lymphoma.

Question 95

Enlargement of extraocular muscles with sparing of tendinous attachments to the globe

Answer 95

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.

Question 96

Lesions of the lacrimal gland

Answer 96

Inflammatory: Sarcoidosis. Sjogren syndrome. Neoplastic: Salivary gland (mixed-cell tumor or adenoid cystic carcinoma). Lymphoma. Pseudotumor. Dermoid (fat-fluid level).

Question 97

Retinoblastoma features

Answer 97

Most common primary ocular malignancy. Leukocoria. Calcified ocular mass.

Question 98

Thyroglossal duct

Answer 98

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.

Question 99

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.

Answer 99

Second branchial cleft cyst. Anterior to mid sternocleidomastoid muscle. Lateral to internal jugular vein at the level of carotid bifurcation.

Question 100

Lymphangiomas

Answer 100

Congenital malformations of lymphatic channels. Benign and nonencapsulated. Classified as capillary, cavernous, or cystic. Most present at birth or during infancy.

Question 101

Subgaleal hematoma

Answer 101

Soft tissue swelling of the scalp located beneath subcutaneous fibrofatty tissue and above temporalis muscle.

Question 102

Intracranial air, pneumocephalus, may be seen with what fractures

Answer 102

Compound skull fractures. Fractures involving paranasal sinuses.

Question 103

Epidural hematoma generalities

Answer 103

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.

Question 104

Venous epidural hematomas

Answer 104

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.

Question 105

Subdural hematomas

Answer 105

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.

Question 106

Subarachnoid hemorrhage

Answer 106

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.

Question 107

Intraventricular hemorrhage

Answer 107

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.

Question 108

Diffuse axonal injury (DAI)

Answer 108

Widespread disruption of axons due to acceleration or deceleration injury. Small, petechial hemorrhages at gray-white junction of cerebral hemispheres and or corpus callosum.

Question 109

T2 shinethrough

Answer 109

T2 and DW bright and ADC dark.

Question 110

Cortical contusions

Answer 110

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.

Question 111

Traumatic Intracerebral Hematoma

Answer 111

Rupture of small intraparenchymal blood vessels. Tend to have less surrounding edema than cortical contusions. Most are located in the frontotemporal white matter.

Question 112

Traumatic subcortical gray matter injury

Answer 112

Uncommon manifestation of primary intra-axial injury. Multiple petechial hemorrhages primarily affecting basal ganglia and thalamus.

Question 113

Von Hippel-Lindau syndrome imaging manifestations

Answer 113

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.

Question 114

Distinguishing epidermoids from arachnoid cysts on MR imaging.

Answer 114

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.

Question 115

Pachymeningeal versus leptomeningeal enhancement findings unfinished.

Answer 115

Pachymeningeal enhancement is characteristically thick, smooth, and uninterrupted.

Question 116

Rare cystic lesion classically located at the anterior roof of the third ventricle at the foramen of Monro.

Answer 116

Colloid cyst. Generally are hyperdense to brain parenchyma. Do not enhance.

Question 117

Carotid cavernous fistula (CCF)

Answer 117

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.

Question 118

Diffuse cerebral edema CT imaging findings

Answer 118

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.

Question 119

Subfalcial herniation

Answer 119

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.

Question 120

Uncal herniation

Answer 120

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.

Question 121

Transtentorial Herniation

Answer 121

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

Question 122

Leptomeningeal cyst

Answer 122

Known as a growing fracture. Caused by traumatic tear of the dura. Outpouching of arachnoid at site of suture or skull fracture.

Question 123

Duret hemorrhage

Answer 123

Midline hematoma within tegmentum of rostral pons and midbrai. Associated with descending transtentorial herniation. Due to stretching or tearing of penetrating arteries.

Question 124

Nonaccidental trauma head findings

Answer 124

Skull fractures. Subdural hematomas. Diffuse brain swelling.

Question 125

Moya moya disease

Answer 125

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.

Question 126

Differential diagnosis of supratentorial partially cystic, partially solid mass in a child:

Answer 126

Pilocytic astrocytoma. PNET (primitive neuroectodermal tumor). Hemorrhage.

Question 127

Le Fort I

Answer 127

Floating palate. Horizontal fracture through maxillary sinuses, nasal septum, and inferior ptyergoid plates.

Question 128

Le Fort II

Answer 128

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.

Question 129

Le Fort III

Answer 129

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.

Question 130

CT scans done within 6 hours of MCA occlusion will commonly exhibit

Answer 130

Insular ribbon sign: Subtle blurring of gray-white layers of insula. Caused by early edema. Lentiform nucleus edema sign: Hypodense putamen.

Question 131

Ischemic penumbra

Answer 131

ischemic but not infarcted (salvageable) tissue. Peri-infarct tissue.

Question 132

Diffusion-Weighted MR in Acute Ischemia

Answer 132

Brain water diffusion rates fall rapidly during acute ischemia. Bright signal on DWIs.

Question 133

Apparent diffusion coefficient (ADC).

Answer 133

Reflects pure diffusion behavior. Free of underlying T2 contributions (shine through or dark through).

Question 134

Fluid-Attenuated Inversion Recovery (FLAIR) in Ischemia

Answer 134

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.

Question 135

Fogging effect

Answer 135

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.

Question 136

Hemorrhagic Transformation of Infarction

Answer 136

Seen 1 to 2 weeks postinfarction. Hemorrhage of reperfused capillaries. Serpiginous line of petechial blood following gyral contours of infarcted cortex.

Question 137

Time course of CT-detected enhancement of infarcted brain

Answer 137

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.

Question 138

Intravascular MR enhancement of infarcted brain

Answer 138

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.

Question 139

Maximal brain swelling post brain infarction occurs at what days

Answer 139

3 to 7 days postinfarction.

Question 140

Encephalomalacia post brain infarction occurs when

Answer 140

30 to 90 days (1 to 3 months) postinfarction.

Question 141

ACA (anterior cerebral artery) three subgroups:

Answer 141

Medial lenticulostriate branches: Rostral portions of basal ganglia. Pericallosal branches: Corpus callosum. Hemispheric branches: Medial frontal and parietal lobes.

Question 142

Two main branch groups of MCA (middle cerebral artery)

Answer 142

Lateral lenticulostriate branches: Supply most of basal ganglia. Hemispheric branches: Lateral cerebral surface.

Question 143

Major branches of PCA (posterior cerebral artery)

Answer 143

Midbrain and thalamic perforating branches. Posterior choroidal arteries. Cortical branches to medial temporal and occipital lobes.

Question 144

(Deficit/Syndrome : Cerebral artery/branch/side affected), Leg weakness :

Answer 144

ACA/Hemispheric branch/either side

Question 145

(Deficit/Syndrome : Cerebral artery/branch/side affected), Incontinence, akinetic mutism :

Answer 145

ACA/Hemispheric branch/both sides

Question 146

(Deficit/Syndrome : Cerebral artery/branch/side affected), Facial weakness :

Answer 146

ACA/Medial lenticulostriates/either side

Question 147

(Deficit/Syndrome : Cerebral artery/branch/side affected), Dysarthria with or without motor aphasia :

Answer 147

ACA/Medial lenticulostriates/Left

Question 148

(Deficit/Syndrome : Cerebral artery/branch/side affected), Face and arm weakness > leg weakness :

Answer 148

MCA/Hemispheric branch/either side

Question 149

(Deficit/Syndrome : Cerebral artery/branch/side affected), Motor aphasia (anterior lesion) :

Answer 149

MCA/Hemispheric branch/Left

Question 150

(Deficit/Syndrome : Cerebral artery/branch/side affected), Receptive aphasia (posterior lesion) :

Answer 150

MCA/Hemispheric branch/Left

Question 151

(Deficit/Syndrome : Cerebral artery/branch/side affected), Global aphasia :

Answer 151

MCA/Hemispheric branch (total)/Left

Question 152

(Deficit/Syndrome : Cerebral artery/branch/side affected), Neglect syndromes :

Answer 152

MCA/Hemispheric branch/Left

Question 153

(Deficit/Syndrome : Cerebral artery/branch/side affected), Visulospatial dysfunction :

Answer 153

MCA/Hemispheric branch/Right

Question 154

(Deficit/Syndrome : Cerebral artery/branch/side affected), Variable lacunar syndromes :

Answer 154

MCA/Lateral lenticulostriate branches/Either

Question 155

(Deficit/Syndrome : Cerebral artery/branch/side affected), Hemianopsia :

Answer 155

PCA/Hemispheric branch/Either

Question 156

(Deficit/Syndrome : Cerebral artery/branch/side affected), Cortical blindness :

Answer 156

PCA/Hemispheric branch/Both

Question 157

(Deficit/Syndrome : Cerebral artery/branch/side affected), Memory deficits :

Answer 157

PCA/Hemispheric branch/Both

Question 158

(Deficit/Syndrome : Cerebral artery/branch/side affected), Somnolence :

Answer 158

PCA/Thalamoperforators/Either

Question 159

(Deficit/Syndrome : Cerebral artery/branch/side affected), Sensory disturbances :

Answer 159

PCA/Thalamoperforators/Either

Question 160

(Deficit/Syndrome : Cerebral artery/branch/side affected), Ataxia, vertigo, vomiting :

Answer 160

Cerebellar/PICA, AICA, or SCA/ Either

Question 161

(Deficit/Syndrome : Cerebral artery/branch/side affected), Coma if mass effect :

Answer 161

Cerebellar/PICA, AICA, or SCA/ Either

Question 162

(Deficit/Syndrome : Cerebral artery/branch/side affected), +/- brainstem deficits :

Answer 162

Cerebellar/PICA, AICA, or SCA/ Either

Question 163

(Deficit/Syndrome : Cerebral artery/branch/side affected), Man-in-a-barrel syndrome :

Answer 163

Watershed/ACA,MCA,PCA/Either

Question 164

(Deficit/Syndrome : Cerebral artery/branch/side affected), Severe memory problems :

Answer 164

Watershed/ACA,MCA,PCA/Bilateral

Question 165

Order of cerebellar branches going from top to bottom can be remembered using the acronym

Answer 165

SAP: Superior cerebellar artery. Anterior inferior cerebellar artery. Posterior inferior cerebellar artery.

Question 166

SCA territory

Answer 166

Superior vermis. Middle and superior cerebellar peduncles. Superolateral aspects of cerebellar hemispheres.

Question 167

Anterior Inferior Cerebellar Arteries (AICA) arise from

Answer 167

Proximal basilar artery.

Question 168

Posterior Inferior Cerebellar Arteries (PICA) arise from

Answer 168

Distal vertebral artery, 1 to 2 cm below basilar origin.

Question 169

Involvement of the medulla in PICA infarction adds elements of Wallenberg syndrome, which include

Answer 169

Ataxia. Facial numbness. Horner syndrome. Dysphagia. Dysarthria.

Question 170

Lacunes

Answer 170

Small subcortical infarcts. May occur in any territory. Characteristic locations: Lenticular nucleus (37%). Pons (16%). Thalamus (14%). Caudate (10%). Internal capsule/corona radiata (10%).

Question 171

Beginning at the genu and working back, the internal capsule carries somatotopically organized fibers

Answer 171

Corticobulbar fibers. HAL: Head fibers. Arm fibers. Leg fibers.

Question 172

Perivascular spaces

Answer 172

Virchow-Robin spaces. May simulate lacunes. Follow CSF signal. No mass effect. Occur along path of a penetrating vessel.

Question 173

Small-Vessel Ischemic Changes

Answer 173

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.

Question 174

Some cerebral vasculitides

Answer 174

Autoimmune disorders. Drug exposure (heroin, amphetamines). Polyarteritis nodosa. Idiopathic processes (giant cell arteritis).

Question 175

Venous sinus thrombosis predisposing factors include

Answer 175

Hypercoagulable states. Pregnancy. Infection (spread from contiguous scalp, face, middle ear, or sinus). Dehydration. Meningitis. Direct invasion by tumor.

Question 176

Empty delta sign

Answer 176

Filling defect within sagittal sinus on postcontrast CT. Indicates venous sinus thrombosis.

Question 177

Superficial hemosiderosis (or superficial siderosis)

Answer 177

Diffuse hemosiderin deposition on brain surface. Due to large or recurrent subarachnoid hemorrhages.

Question 178

MR oxyhemoglobin per time, RBC, and T1 and T2 signal

Answer 178

Less than 1 day. RBC intact. T1 iso/dark. T2 bright.

Question 179

MR deoxyhemoglobin per time, RBC, and T1 and T2 signal

Answer 179

0-2 days. RBC intact. T1 iso/dark. T2 dark.

Question 180

MR methemoglobin (intracellular) per time, RBC, and T1 and T2 signal

Answer 180

2-14 days. RBC intact. T1 bright. T2 dark.

Question 181

MR methemoglobin (extracellular) per time, RBC, and T1 and T2 signal

Answer 181

10-21 days. RBC lysed. T1 bright. T2 bright.

Question 182

MR hemosiderin/ferritin per time, RBC, and T1 and T2 signal

Answer 182

> 21 days. RBC lysed. T1 dark. T2 dark.

Question 183

Most sensitive areas for detecting SAH

Answer 183

Dependent parts of occipital horns. Interpeduncular fossa.

Question 184

Main finding in patients whose condition continues to deteriorate after the initial SAH

Answer 184

Infarcts from post SAH increased intracranial pressure or arterial vasospasm.

Question 185

Congenital berry aneursym

Answer 185

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.

Question 186

Distal branch cerebral aneurysms are seen in what conditions

Answer 186

Prior trauma. Systemic infection (bacterial endocarditis with mycotic aneurysm).

Question 187

Besides berry aneursyms, list other causes of cerebral aneurysms

Answer 187

Atherosclerosis. Fibromuscular disease. Polycystic kidney disease. Mycotic. Post-traumatic.

Question 188

Main differential considerations for cerebral parenchymal hemorrhage

Answer 188

Hypertensive hemorrhage. Vascular malformations. Drug effects. Amyloid angiopathy. Bloody tumors.

Question 189

Common locations for intracranial hypertensive hemorrhages

Answer 189

Putamen (35% to 50%). Subcortical white matter (30%). Cerebellum (15%). Thalamus (10% to 15%). Pons (5% to 10%).

Question 190

Intracranial hemorrhage cause in young patients, less common than hypertension

Answer 190

Vascular malformations: AVMs. Cavernous malformations. Telangiectasias. Venous malformations.

Question 191

Arteriovenous malformations

Answer 191

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,

Question 192

Cavernous malformations

Answer 192

Thin-walled sinusoidal vessels (neither arteries nor veins). May present with seizures or small parenchymal hemorrhages.

Question 193

Venous malformations

Answer 193

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.

Question 194

Amyloid angiopathy cerebral hemorrhage

Answer 194

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.

Question 195

Hemorrhagic cerebral neoplasm

Answer 195

Primary: Glioblastomas. Metastatses: Bronchogenic carcinoma. Thyroid. Melanoma. Choriocarcinoma. Renal cell carcinoma.

Question 196

Features of Benign Versus Malignant Intracranial Hemorrhage

Answer 196

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.

Question 197

Glial cell intracranial neoplasms (gliomas)

Answer 197

Astrocytoma. Oligodendroglioma. Ependymoma. Choroid plexus tumor.

Question 198

Nerve sheath intracranial neoplasms

Answer 198

Schwannoma, Neurofibroma.

Question 199

Extra-axial tumors

Answer 199

Tumors occuring along brain meninges or within the ventricles. Most nonglial tumors.

Question 200

Significant general midline shift, if shift is greater than

Answer 200

3 mm.

Question 201

Hallmarks of uncal herniation?

Answer 201

Effacement of ambient cistern. Contralateral hydrocephalus. May compromise ipsilateral oculomotor (III) nerve (pupillary dilation).

Question 202

Differentiating a small neoplasm from a small infarct may be very difficult. When can followup imaging be obtained to help distinguish between the two.

Answer 202

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.

Question 203

Extra-axial mass refers to

Answer 203

Everything outside the brain: Arachnoid. Meninges. Dural sinuses. Skull. Ventricles.

Question 204

White matter buckling?

Answer 204

Extra-axial lesions may buckle white matter. Inward compression of white matter (thinning of fronds). Preserved gray-white matter differentiation.

Question 205

Tumors of high cellular density

Answer 205

Usually small cell tumors (high nucleus:cytoplasm ratio, hyperdense and T2 hypointense): Lymphoma. Pineoblastoma. Neuroblastoma. Medulloblastom. Metastases: Melanoma. Lung carcinoma. Colon carcinoma. Breast carcinoma.

Question 206

Some specialized areas of the brain have no blood-brain barrier and will normally enhance

Answer 206

Choroid plexus. Pituitary glands. Pineal glands. Tuber cinereum. Area postrema.

Question 207

Tumor enhancement generally means

Answer 207

Aggressive, high-grade neoplasms tend to have fenestrated capillaries (blood-brain barrier breakdown) allowing for enhancement.

Question 208

Postop granulation tumor versus residual tumor?

Answer 208

Granulation tissue generally forms 72 hours after surgery. Early (less than 72 hours) postop enhancement likely reflects residual tumor rather than granulation tumor.

Question 209

Diffuse white matter radiation injury

Answer 209

Unenhancing geographic white matter T2 hyperintensity conforming to radiation ports. Develops 6 months postradiation therapy.

Question 210

Radiation necrosis

Answer 210

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.

Question 211

Astrocytoma grades and types

Answer 211

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).

Question 212

Female predominant brain tumors

Answer 212

Meningioma (4:1). Neurofibroma. Pineocytoma. Pituitary tumor.

Question 213

Male predominant brain tumors

Answer 213

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.

Question 214

Two neoplasms that may exhibit bihemispheric spread through the corpus callosum.

Answer 214

Glioblastoma multiforme. CNS lymphoma.

Question 215

Intra-axial Lesions With Marked Surrounding Edema

Answer 215

Metastases. Abscess. Glioblastoma multiforme. Radiation necrosis. Hematoma (mild).

Question 216

Hemorrhagic Brain Tumors

Answer 216

Primary: Glioblastoma multiforme (most common overall). Oligodendroglioma. Metastasis: RCC. Thyroid carcinoma. Choriocarcinoma. Melanoma.

Question 217

Cerebral Ring-Enhancing Lesions

Answer 217

MAGIC DR. Metastasis. Abscess. Glioblastoma multiforme. Infarct. Contusion. Demyelinating disease. Resolving hematoma. radiation necrosis.

Question 218

This MR sequence may help distinguish acute infarct from low-grade neoplasm.

Answer 218

DWI. Infarct exhibitis restricted diffusion.

Question 219

Gliomatosis cerebri

Answer 219

Rare neoplastic infiltration of at least three lobes of the brain. Poor prognosis. Diffuse involvement of cerebral white matter with or without a mass.

Question 220

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

Answer 220

Oligodendroglioma.

Question 221

Oligodendroglioma features

Answer 221

Grade II tumor. Commonly located in the frontal lobes. Often extends to cortex and may erode calvarium. 70% calcify.

Question 222

Calcified Glial Tumors in Order of Frequency

Answer 222

Old Elephants Age Gracefully: Oligodendroglioma. Ependymoma. Astrocytoma. Glioblastoma multiforme.

Question 223

CNS lymphoma imaging characteristics

Answer 223

Hyperdense and T1 hypointensity on T2WIs with surrounding vasogenic edema. Subependymal spread is common. Bihemispheric involvement via corpus callosum may be seen.

Question 224

Ganglioglioma and Gangliocytoma

Answer 224

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.

Question 225

Desmoplastic Infantile Ganglioglioma

Answer 225

Rare variant of ganglioglioma seen in the first year of life. Very large heterogeneous mass with intense enhancement.

Question 226

Most common tumor associated with medically refractory partial complex seizures

Answer 226

Dysembryoplastic neuroepithelial tumor. Always involves cortical gray matter. May have “soap bubble” appearance with exophytic extension beyond cortical gray matter margin.

Question 227

Congenital Brain Tumors in Infants Younger Than 60 Days Old

Answer 227

Teratoma (most common): Two thirds are supratentorial. Primitive neuroectodermal tumors: Curvilinear, sparse calcification. Astrocytoma. Choroid plexus papilloma. Ependymoma. Medulloepithelioma. Germinoma. Angioblastic meningioma. Ganglioglioma.

Question 228

Most (80% to 85%) metastatic lesions occur supratentorially, with the exception of ___________, which has a predilection for the posterior fossa.

Answer 228

Renal cell carcinoma.

Question 229

Most Common Intra-axial Metastases to the CNS

Answer 229

Lung. Breast. Melanoma. Colon cancer.

Question 230

Most Common Extra-axial Metastases to the CNS

Answer 230

Breast. Prostate. Lung. Neuroblastoma.

Question 231

Most Common Hemorrhagic Metastases to the CNS

Answer 231

Melanoma. Renal. Thyroid. Choriocarcinoma.

Question 232

Leptomeningeal carcinomatosis

Answer 232

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.

Question 233

Most common primary cerebellar neoplasm in adult population.

Answer 233

Hemangioblastoma.

Question 234

Most reliable way to differentiate a medulloblastoma from an astrocytoma on cross-sectional imaging studies is

Answer 234

Noncontrast CT scan. Astrocytoma will usually be hypodense. Medulloblastoma will almost never be hypodense.

Question 235

Posterior Fossa Masses in Children: Medulloblastoma

Answer 235

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.

Question 236

Posterior Fossa Masses in Children: Pilocytic astrocytoma

Answer 236

Location: Cerebellar vermis. Hemisphere. Cystic with enhancing nodule.

Question 237

Posterior Fossa Masses in Children: Ependymoma

Answer 237

Location: 4th ventricle. Appearance: Foraminal extension. Heterogeneous on CT and MR. Intense but heterogeneous enhancement.

Question 238

Posterior Fossa Masses in Children: Brainstem glioma

Answer 238

Location: Brainstem. Appearance: Expansile brainstem. Isodense to hypodense on CT. Hypointense on T1WIs. Hyperintense on T2WIs.

Question 239

Most common brain tumor seen in neurofibromatosis type 1 (NF1)

Answer 239

Pilocytic astrocytoma.

Question 240

Cystic cerebellar mass with an enhancing mural nodule suggests two possible diagnoses, and the best discriminator between the two is

Answer 240

Age. Pilocytic astrocytoma, peak age of birth to 9 years. Hemangioblastoma, peak age of 35 years.

Question 241

Capillary hemangioblastomas

Answer 241

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.

Question 242

Dysplastic Cerebellar Gangliocytoma (Lhermitte-Duclos Disease)

Answer 242

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.

Question 243

Meningioma

Answer 243

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,

Question 244

Cerebral Intraventricular Masses

Answer 244

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%).

Question 245

Most Common Lateral Ventricle Masses, by Location and Age: 0 - 10 yo, Ventricle Body

Answer 245

PNET (Primitive neuroectodermal tumor). Teratoma. Choroid plexus papilloma.

Question 246

Most Common Lateral Ventricle Masses, by Location and Age: 0 - 40 yo, Ventricle Trigone

Answer 246

Choroid plexus papilloma.

Question 247

Most Common Lateral Ventricle Masses, by Location and Age: 10 - 40 yo, Foramen of Monro

Answer 247

Subependymal giant cell astrocytoma. Pilocytic astrocytoma.

Question 248

Most Common Lateral Ventricle Masses, by Location and Age: 10 - 40 yo, Ventricle Body

Answer 248

Ependymoma. Pilocytic astrocytoma. Central neurocytoma.

Question 249

Most Common Lateral Ventricle Masses, by Location and Age: > 40 yo, Ventricle Body

Answer 249

Subependymoma.

Question 250

Most Common Lateral Ventricle Masses, by Location and Age: > 40 yo, Ventricle Trigone

Answer 250

Meningioma. Metastasis.

Question 251

Choroid Plexus Papilloma

Answer 251

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.

Question 252

Central neurocytoma

Answer 252

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.

Question 253

Subependymoma

Answer 253

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.

Question 254

Subependymal giant cell astrocytoma

Answer 254

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.

Question 255

Colloid cyst

Answer 255

Occurs in anterosuperior portion of third ventricle near foramen of Monro. Can cause acute hydrocephalus. Almost all are hyperdense. Variable T1 and T2 signal.

Question 256

Masses of the Anterosuperior Third Ventricle

Answer 256

Colloid cyst. Meningioma. Choroid plexus papilloma. Hamartoma. Glioma. Vascular lesion. Granulomatous disease.

Question 257

Most common neoplasm of pineal region

Answer 257

Germ cell tumors

Question 258

Calcified pineal mass in a female is more likely to be

Answer 258

Pineocytoma. In a male more likely to be a germinoma.

Question 259

When calcification in the pineal region exceeds ____ in size, a pathologic pineal process should be suspected.

Answer 259

1 cm.

Question 260

Cerebral Germ cell tumors

Answer 260

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.

Question 261

Pineal region masses

Answer 261

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.

Question 262

Pineoblastoma

Answer 262

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.

Question 263

Pineocytoma

Answer 263

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.

Question 264

Pineal cysts

Answer 264

Are common. Signal similar to or slightly higher than CSF, likely due to lack of CSF puslation. No enhancement.

Question 265

Pituitary adenomas

Answer 265

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).

Question 266

Craniopharyngioma

Answer 266

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.

Question 267

Rathke cleft cyst

Answer 267

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.

Question 268

Schwannoma

Answer 268

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.

Question 269

Most helpful imaging feature in distinguishing vestibular schwannomas

Answer 269

Extension of enhancement along course of seventh and eighth nerves.

Question 270

Suprasellar Masses

Answer 270

SATCHMO Sella (pituitary) tumor. Sarcoid. Aneurysm. Arachnoid cyst. Teratoma. Craniopharyngioma. Hypothalamic glioma. Hamartoma of tuber cinereum. Histiocytosis. Meningioma. Optic nerve glioma.

Question 271

Cerebellopontine Masses

Answer 271

AMEN Acoustic (vestibular) schwannoma. Meningioma. Ependymoma. Neuroepithelial cyst (arachnoid, epidermoid).

Question 272

Epidermoid versus Dermoid

Answer 272

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.

Question 273

Intracranial lipomas

Answer 273

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.

Question 274

Arachnoid cysts

Answer 274

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.

Question 275

Hamartoma of tuber cinereum

Answer 275

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.

Question 276

Intracranial tuberculoma

Answer 276

Granuloma with central caseous necrosis. Isodense or slightly hyperdense nodules or small mass lesions.

Question 277

Brain Coccidioidomycosis

Answer 277

Occurs in southwestern United States. Focal parenchymal granulomas are rare. Hydrocephalus is common from complicating meningitis.

Question 278

Brain Blastomycosis

Answer 278

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.

Question 279

Brain Histoplasmosis

Answer 279

Occurs in Midwest and southern United States. Meningitis is most common. Multiple or solitary granulomas may occur.

Question 280

CNS Aspergillosis

Answer 280

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.

Question 281

CNS Mucormycosis

Answer 281

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.

Question 282

CNS Candidiasis

Answer 282

Usually causes meningitis. Granulomas and small abscesses may occur. Meningeal enhancement or multiple small enhancing granulomas or microabscesses are usually seen.

Question 283

Most frequently reported CNS fungal infection.

Answer 283

Cryptococcosis.

Question 284

CNS Cryptococcosis

Answer 284

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.

Question 285

Gelatinous pseudocyst

Answer 285

Cystic lesion usually in basal ganglia. Perivascular spaces filled with cryptococcal organisms. Usually found only in immunocompromised.

Question 286

Cysticercosis

Answer 286

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.

Question 287

Echinococcosis

Answer 287

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.

Question 288

Congenital CNS toxoplasmosis

Answer 288

Atrophy, dilated ventricles, and calcifications. Periventricular white matter, basal ganglia and cerebral hemisphere calcifications. In CMV, calcifications are usually periventricular only.

Question 289

Amebic meningoencephalitis

Answer 289

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.

Question 290

Neurosyphilis

Answer 290

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.

Question 291

CNS Lyme disease

Answer 291

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.

Question 292

Cytomegalovirus, congenital CNS infection

Answer 292

Most common CT findings: Periventricular calcification. No calcifications of basal ganglia or cortices as seen congenital toxoplasmosis.

Question 293

Neonatal herpes simplex encephalitis

Answer 293

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.

Question 294

Adult herpes simplex CNS infection

Answer 294

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).

Question 295

Ramsay Hunt syndrome

Answer 295

Herpes zoster facial neuritis. Ear pain, facial paralysis, vesicular eruption about the ear. MR may reveal increased enhancement of facial nerve.

Question 296

Acute disseminated encephalomyelitis (ADEM)

Answer 296

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.

Question 297

Subacute sclerosing panencephalitis

Answer 297

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.

Question 298

Progressive multifocal leukoencephalopathy (PML)

Answer 298

Demyelinating disease caused by a papova virus. Occurs only in immunosuppressed patients, especially in AIDS.

Question 299

Creutzfeldt-Jakob disease

Answer 299

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.

Question 300

Meningitis forms causing thick meningeal enhancement (pachymeningeal)

Answer 300

Tuberculous meningitis. Fungal meningitis. Racemose cysticercosis. Sarcoidosis.

Question 301

Most common AIDS CNS infections

Answer 301

HIV encephalopathy. Toxoplasmosis. Cryptococcosis. Other fungal infections. CMV and Herpes meningoencephalitis. Mycobacterial infection. PML. Meningovascular syphilis.

Question 302

Most common CNS AIDS tumor

Answer 302

Primary CNS lymphoma.

Question 303

HIV Encephalopathy

Answer 303

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.

Question 304

Most common opportunistic CNS infection in AIDS

Answer 304

Toxoplasmosis.

Question 305

Toxoplasmosis

Answer 305

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.

Question 306

Most common AIDS CNS fungal infection

Answer 306

Cryptococcosis.

Question 307

Progressive multifocal leukoencephalopathy

Answer 307

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.

Question 308

Primary CNS lymphoma

Answer 308

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.

Question 309

Dysmyelination

Answer 309

Inherited disorder (leukodystrophy), affecting formation or maintenance of myelin. Generally encountered within pediatric population.

Question 310

Demyelination

Answer 310

Acquired disorder that affects normal myelin. Generally encountered within adult population.

Question 311

Multiple sclerosis (MS, Primary Demyelination)

Answer 311

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).

Question 312

Involvement of callosal-septal interface is quite specific for

Answer 312

MS.

Question 313

Nonspecific punctuate white matter lesions (small bright lesions on T2WIs) are more prominent in any patient with

Answer 313

Vasculopathy or hypercoagulable state.

Question 314

A classic case presentation is that of a young adult female with prior miscarriages presenting with headaches/migraines and ischemic white matter changes.

Answer 314

Antiphospholipid syndrome (phospholipid antibody syndrome). Hypercoagulable state with white matter and ischemic changes.

Question 315

Ependymitis granularis

Answer 315

Normal anatomic finding. May mimic pathology. High T2 signal at tips of frontal horns. Due to porous ependyma allowing transependymal flow of CSF.

Question 316

Senescent periventricular hyperintensity

Answer 316

Age-related high T2 signal along entire length of lateral ventricles.

Question 317

Prominent perivascular spaces

Answer 317

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.

Question 318

MR sequences that help distinguish perivascular spaces from parenchymal lesions

Answer 318

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.

Question 319

Central pontine myelinolysis (CPM)

Answer 319

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.

Question 320

Posterior reversible encephalopathy syndrome (PRE)

Answer 320

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).

Question 321

Marchiafava-Bignami disease

Answer 321

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

Question 322

Wernicke encephalopathy and Korsakoff syndrome

Answer 322

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.

Question 323

Radiation Leukoencephalitis

Answer 323

Occurs 6 to 9 months after treatment in excess of 40 Gy. Confluent high T2 signal within white matter extending to subcortical U fibers.

Question 324

Radiation Necrosis

Answer 324

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).

Question 325

Metachromatic leukodystrophy: head size, age of onset, white matter involvement, gray matter involvement

Answer 325

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.

Question 326

Adrenoleukodystrophy leukodystrophy: head size, age of onset, white matter involvement, gray matter involvement

Answer 326

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.

Question 327

Leigh disease: head size, age of onset, white matter involvement, gray matter involvement

Answer 327

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.

Question 328

Alexander disease: head size, age of onset, white matter involvement, gray matter involvement

Answer 328

Normal to large head size. Less than 1 yo. Frontal white matter involvement. No gray matter involvement.

Question 329

Canavan disease: head size, age of onset, white matter involvement, gray matter involvement

Answer 329

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).

Question 330

Transependymal flow of CSF

Answer 330

Occurs in acute hydrocephalus. May mimic periventricular white matter disease. Important means of CSF reabsorption during ventricular obstruction.

Question 331

CSF circulation route

Answer 331

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.

Question 332

Will commonly demonstrate supratentorial ventriculomegaly, with a fourth ventricle that appears normal.

Answer 332

Communicating hydrocephalus. Dilated 4th ventricle can be seen in communicating and non-communicating hydrocephalus.

Question 333

Ex Vacuo Ventriculomegaly

Answer 333

Enlarged ventricles due to cerebral atrophy. Prominence of both sulci and ventricles.

Question 334

Normal pressure hydrocephalus

Answer 334

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.

Question 335

Alzheimer disease (AD)

Answer 335

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.

Question 336

Parkinson disease

Answer 336

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).

Question 337

Huntington disease

Answer 337

Progressive hereditary disorder occuring in fourth and fifth decades. Findings: Diffuse cortical atrophy. Caudate nucleus atrophy. Putamen atrophy. Enlargement of frontal horns (heart-shaped).

Question 338

Wilson disease

Answer 338

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.

Question 339

Bilateral lesions of basal ganglia can be seen in a variety of insults

Answer 339

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).

Question 340

Myelination Landmarks by Age 0 days

Answer 340

High T1 signal: Dorsal brainstem. Ventrolateral thalamus. Lentiform nucleus. Central corticospinal tracts. Low T2 signal: Posterior limb internal capsule posterior portion.

Question 341

Myelination Landmarks by Age 3 months

Answer 341

High T1 signal: Anterior limb internal capsule. Cerebellar white matter.

Question 342

Myelination Landmarks by Age 6 months

Answer 342

High T1 signal: Genu of corpus callosum. Low T2 signal: Splenium of corpus callosum.

Question 343

Myelination Landmarks by Age 11 months

Answer 343

Low T2 signal: Anterior limb internal capsule.

Question 344

Myelination Landmarks by Age 18 months

Answer 344

Adult appearance except for terminal myelination zones (periatrial and adjacent to frontal horns)

Question 345

Myelination Landmarks by Age 24 months

Answer 345

Dark white matter on T2 (some minimal high-signal areas may persist peripherally)

Question 346

Pelizaeus-Merzbacher Disease

Answer 346

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.

Question 347

HYPOXIC ISCHEMIC ENCEPHALOPATHY (HIE)

Answer 347

Damage to brain from hypoxia/ischemia occurring in utero or around time of delivery.

Question 348

Hydranencephaly

Answer 348

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.

Question 349

Hypoxic ischemic encephalopathy occuring within 1st trimester

Answer 349

Cortical irregularity and/or hydranencephaly.

Question 350

Hypoxic ischemic encephalopathy occuring at less than 26 weeks of gestation

Answer 350

Periatrial injury. No gliosis. Ex vacuo enlargement.

Question 351

Hypoxic ischemic encephalopathy occuring at greather than 28 weeks

Answer 351

Periatrial gliosis: high T2 signal.

Question 352

Hypoxic ischemic encephalopathy occuring at term

Answer 352

Watershed infarcts. Ulegyria. Variable deep, superficial white matter gliosis and atrophy. Myelination delay. Injury to hippocampus and pons.

Question 353

Periventricular Leukomalacia (PVL)

Answer 353

Occurs in term infants, premature infants greater than 26 weeks of gestation. Periventricular gliosis. Ex vacuo ventriculomegaly. Apposition of sulci to ventricular surface.

Question 354

Gliosis in the periatrial region (seen best on proton-density scans) is caused by injury to the developing brain at what gestational age or older.

Answer 354

28 weeks .

Question 355

Ex vacuo atrial enlargement without gliosis reflects injury prior to what gestational age.

Answer 355

26 weeks.

Question 356

Acute imaging findings of Profound Perinatal Hypoxic Ischemic Injury

Answer 356

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.

Question 357

Subacute imaging findings of Profound Perinatal Hypoxic Ischemic Injury

Answer 357

Deep gray matter: Variable T1 and T2 signal. White matter: High T1 and low T2 perirolandic cortex.

Question 358

Chronic imaging findings of Profound Perinatal Hypoxic Ischemic Injury

Answer 358

Deep gray matter: High T2 signal. White matter: High T2 perirolandic cortex. Thinned gyri, atrophy.

Question 359

Imaging of Profound Postnatal Hypoxic Ischemic Injury

Answer 359

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)

Question 360

Septo-optic dysplasia (SOD)

Answer 360

Congenital disorder with variable hypoplasia of optic nerves and complete or partial absence of septum pellucidum. Squared-off appearance of frontal horns.

Question 361

Alobar holoprosencephaly

Answer 361

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.

Question 362

Semilobar holoprosencephaly

Answer 362

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.

Question 363

Lobar holoprosencephaly

Answer 363

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).

Question 364

Lipomas of corpus callosum

Answer 364

Congenital abnormalities. High T1 signal with fat supression. No mass effect. Vessels course through these lesions. Occur because of persistence of meninx primitiva.

Question 365

Lissencephaly and pachygria/agyria complex

Answer 365

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.

Question 366

Hemimegalencephaly

Answer 366

Asymmetric hemispheric enlarged with polymicrogyric and pachygyric changes. May be associated with neurofibromatosis.

Question 367

Polymicrogyria and pachygria

Answer 367

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.

Question 368

Heterotopic Gray Matter

Answer 368

Islands of gray matter anywhere between ependymal surface and subcortical white matter. May cause seizures.

Question 369

Schizencephaly

Answer 369

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.

Question 370

Distinguishing porencephaly from open lipped schizencephaly

Answer 370

Porencephaly: encephalomalacia that communicates with ventricle. Schizencephalic clefts are lined by gray matter. Porencephalic cysts are lined by a thin layer of white matter.

Question 371

Chiari II malformations

Answer 371

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.

Question 372

Chiari I malformations

Answer 372

Cerebellar tonsillar ectopia (tonsils extend > 5 mm below foramen magnum). Patients may be asymptomatic. May give rise to cervical spinal cord syrinx.

Question 373

Dandy-Walker Malformations

Answer 373

Large posterior fossa with high tentorial insertion. Dilated cystic 4th ventricle fills posterior fossa. Cerebellar vermis and hemispheres may be hypoplastic or absent.

Question 374

Neurofibromatosis type 1 imaging findings (chromosome 17)

Answer 374

Altered signal in white matter and basal ganglia. Dural ectasia. Optic and other gliomas. Sphenoid dysplasia. Thinning long bone cortex (ribbon ribs). Plexiform neurofibromas. Cafe au lait spots. Iris hamartomas (Lisch nodules). Vascular stenoses.

Question 375

Neurofibromatosis type 2 imaging findings (chromosome 22)

Answer 375

Vestibular schwannomas. Meningiomas. Spinal glial tumors. Optic and other gliomas.

Question 376

Tuberous sclerosis

Answer 376

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)

Question 377

Sturge-Weber Syndrome

Answer 377

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.

Question 378

Von Hippel-Lindau Syndrome

Answer 378

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.

Question 379

most common primary petrous apex lesion

Answer 379

cholesterol granuloma (T1 + T2 bright)

Question 380

“smoothly marginated lobulated cystic expansion of the petrous apex”

Answer 380

herniation of Meckel s cave into the superomedial aspect of the petrous apex

Question 381

what s another name for an cholesteatoma in the petrous apex?

Answer 381

basically an epidermoid (T1 dark, T2 bright, restricts diffusion)

Question 382

classic triad of Grandenigo syndrome

Answer 382

otomastoiditis + face pain (trigeminal neuropathy) + lateral rectus palsy (unilateral cross eye)

Question 383

petrous apex/CPA tumor with internal calcs on CT + T2 bright/intense enhancement

Answer 383

endolymphatic sac tumor - very vascular with flow voids and tumor blush on angio

Question 384

most common presenting symptom in glomus jugulare/paraganglioma?

Answer 384

hoarseness from vagal nerve compression

Question 385

large vesitbular aqueduct syndrome is associated with what type of hearing loss?

Answer 385

progressive sensioneural hearing loss (90% association with absence of bony modiolus)

Question 386

who gets labyrinthitis ossificans?

Answer 386

kids (2-18 months) s/p meningitis - also get sensineural hearing loss

Question 387

what s a better term for osteosclerosis

Answer 387

“otospongiosus” b/c bone becomes more lytic, not sclerotic

Question 388

findings in fenestral ostosclerosis

Answer 388

bony resorption anterior the oval window

Question 389

findings in retro-fenestral ostosclerosis

Answer 389

more severe form, demineralization around the cochlea, bilateral/symmetric nearly 100%

Question 390

4 complications of otitis media

Answer 390

1. coalescent mastoiditis 2. facial nerve palsy 3. dural sinus thrombosis 4. meningitis/labrynthitis

Question 391

order of destruction in cholesteatoma

Answer 391

1. the scutum 2. the ossicles (long process of the incus) 3. lateral segment of the semi-circular canal

Question 392

most common type of cholesteatoma

Answer 392

Pars flaccida (the flimsy, whimpy part of the ear drum)

Question 393

potential complication of cholesteatoma

Answer 393

labryrinthine fistula - bony defect between inner ear + tympanic cavity (usually lateral SCC)

Question 394

“noise induced vertigo” or “tulio s phenomenon”

Answer 394

superior semicircular canal dehiscence (aunt minnie)

Question 395

what causes abnormal enhancement of the facial nerve?

Answer 395

1. Bell s Palsy! 2. Lyme 3. Ramsay hunt 4. cancer

Question 396

what kind of trauma involves the facial nerve?

Answer 396

transverse T-bone fracture

Question 397

“osteolysis circumscripta”

Answer 397

Paget skull changes - well-defined large radiolucent region favoring front/occipital bones (inner table > outer)

Question 398

4 skull base Paget related complications

Answer 398

1. deafness! 2. cranial nerve paresis 3. basilar invagination -> hydro -> brainstem compression 4. 2/2 (high gr) osteosarcoma

Question 399

2 most common locations of chordoma

Answer 399

1. sacrum 2. clivus

Question 400

clivus lesions: chordoma vs. chrondrosarcoma

Answer 400

chordoma = midline, chondrosarcoma = lateral to midline (both T2 bright)

Question 401

primary vascular supply of JNA (juvenile nasal angiofibroma)

Answer 401

ascending pharyngeal artery and/or internal maxillary artery

Question 402

origin/location of JNA (juvenile nasal angiofibroma)

Answer 402

centered on the sphenopalantine foramen

Question 403

10% of inverting papillomas harbor a

Answer 403

squamous cell CA

Question 404

“cerebrifom pattern” (sinus lesion)

Answer 404

inverting papilloma

Question 405

class location of inverting papilloma

Answer 405

lateral wall of the nasal cavity - most frequently related to middle turbinate

Question 406

dumbbell shaped lesion with AVID enhancement

Answer 406

esthesioneuroblastoma - waist of dumbbell at cribiform plate

Question 407

demographic of esthesioneuroblastoma

Answer 407

bimodal - 20s and 60s

Question 408

most common location of SNUC vs. squamous

Answer 408

SNUC(sinonasal undifferentiated carcinoma) large! ethmoid > maxillary; Squamous cell: maxillary antrum

Question 409

“male teenager with nose bleeds”

Answer 409

JNA (juvenile nasal angiofibroma)

Question 410

main vascular supply to the posterior nose (for uncontrolled nosebleeds)

Answer 410

sphenopalatine artery (terminal internal maxillary artery) - watch out for anastomosis btw ECA and ophthalmic

Question 411

midline “sack of marbles” in the mouth

Answer 411

floor of mouth dermoid/epidermoid - fluid sack with globules of fat/midline

Question 412

what s another term for ranula

Answer 412

mucous retention cyst

Question 413

from whence do ranula arise?

Answer 413

sublingual gland/space

Question 414

when do you use the term “plunging” for a ranula?

Answer 414

when it s under the mylohyoid muscle

Question 415

“grandma s dentures won t stay in”

Answer 415

torus palatinus - bony exostosis

Question 416

submandibular gland proper name

Answer 416

Wharton s (most common location for stones)

Question 417

most common cause of odontogenic infection

Answer 417

extracted tooth (not an intact one)

Question 418

what muscle separates the sublingual vs. submandibular space (and thus where infections go)?

Answer 418

mylohyoid (below the mylohyoid are the 2nd and 3rd molars - infections go to submandibular space)

Question 419

most common masticator space “mass” in adult

Answer 419

odontogenic abscess

Question 420

most common cause of Ludwig s angina

Answer 420

odontogenic infection

Question 421

floor of mouth cellulitis + gas everywhere!

Answer 421

ludwig s angina

Question 422

3 causes of osteonecrosis of the jaw

Answer 422

1. bisphosphonate treatment 2. prior radiation 3. licking a radium paint brush

Question 423

cancer of the mouth in a younger person

Answer 423

HPV-related SCC

Question 424

“young adult with new level 2 neck mass”

Answer 424

HPV-related SCC - large necrotic level 2a node

Question 425

most common salivary gland tumor

Answer 425

pleomorphic adenoma aka benign mixed tumor

Question 426

2nd most common benign tumor of the parotid

Answer 426

warthins - only occurs in parotid

Question 427

4 things to know about warthins

Answer 427

1. usually cystic 2. male 3. bilateral (15%) 4. smoker 5. takes up pertechnetate

Question 428

most common malignant tumor of the minor salivary glands

Answer 428

mucoepidermoid carcinoma

Question 429

only salivary gland with lymph nodes

Answer 429

parotid (so it s the only one that can get lymphoma)

Question 430

“bilateral parotid lymphoma”

Answer 430

Sjogrens

Question 431

“bilateral mixed solid/cystic parotid lesions + HIV”

Answer 431

benign lymphoepithelial disease, painless

Question 432

what s in the carotid space?

Answer 432

carotid artery, jugular vein, CN 9, 10, 11, and some nodes

Question 433

glomus tympanicum: location

Answer 433

confined to middle ear, “overlying the cochlear promontory”

Question 434

glomus vagale: location

Answer 434

above carotid bifurcation, but below the jugular foramen

Question 435

glomus jugulare: location

Answer 435

skull base (destruction of jugular foramen)

Question 436

carotid body tumor: location

Answer 436

carotid birfucation (splaying of ICA and ECA)

Question 437

what s in the masticator space?

Answer 437

muscle of mastication, angle/ramus of the mandible, inferior aveloar nerve

Question 438

angry masticator space mass in a kid

Answer 438

rhabomyosarcoma (less angry could be chondrosarc from the TMJ)

Question 439

masticator space mass + phleboliths

Answer 439

cavernous hemangiomas (can also have venous/lymphatic malformations)

Question 440

nerve sheath tumor in the masticator space

Answer 440

schwannoma or neurofibroma of V3

Question 441

what s in the paraphyngeal space?

Answer 441

mostly fat, few branches of the trigeminal nerves and pterygoid veins

Question 442

Grisel s syndrome

Answer 442

torticollis with atlanto-axial joint inflammation seen in H&N surgery or retropharyngeal abscess

Question 443

nasopharyngeal SCC demographics

Answer 443

more common in Asians and bimodal - group 1 = 15-30yo/Chinese group 2 = >40yo

Question 444

most common location of nasopharyngeal SCC

Answer 444

Fossa of Rosenmuller (causing unilateral mastoid effusion/blocking eustaschian tube)

Question 445

3 subtypes of laryngeal SCC

Answer 445

1. supraglottic 2. glottic 3. infraglottic 4. “transglottic” (aggressive, crosses laryngeal ventricle, T3)

Question 446

fixation of the cords indicates what T?

Answer 446

at least T3 laryngeal SCC

Question 447

only reliable sign of cricoid invasion in laryngeal SCC

Answer 447

tumor on both sides of cartilage

Question 448

implication of cricoid invasion in laryngeal SCC

Answer 448

contraindication to all types of laryngeal conservation surgery

Question 449

ipsilateral expanded (vocal cord) ventricle

Answer 449

vocal cord paralysis (tumor is contralateral)

Question 450

left-sided vocal cord paralysis should prompt

Answer 450

chest CT - for recurrent laryngeal nerve involvement at the AP window

Question 451

definition: coloboma

Answer 451

focal discontinuity of the globe (usually posterior)

Question 452

when I say “bilateral coloboma”, you say

Answer 452

CHARGE (coloboma, heart, GU, ears)

Question 453

“small eye with increases density of vitreous”

Answer 453

persistent hyperplastic primary vitreous (not calcification, but very dense on CT)

Question 454

Coat s disease

Answer 454

retinal telangiectasia with leaky blood and subretinal exudate (hyperdense back of eye)

Question 455

5 causes of retinal detachment

Answer 455

1. PHPV 2. Coats 3. trauma 4. sickle cell 5. old age

Question 456

who gets optic glioma?

Answer 456

90% < 20 yo; if bilateral = NF-1

Question 457

what s the optic nerve look like in optic glioma?

Answer 457

expansion/enlargement of the entire nerve

Question 458

what s the optic nerve look like in optic nerve sheath meningioma?

Answer 458

“tram-track” calcification, circumferential enhancement around the optic nerve

Question 459

3 syndromes of IgG4

Answer 459

1. orbital pseudotumor 2. Tolosa Hunt (cavernous sinus CN palsies) 3. lymphocytic hypophysitis (pituitary gland)

Question 460

typical findings of orbital pseudotumor

Answer 460

painful, unilateral, lateral rectus, does NOT spare myotendinous insertions (unlike thyroid)

Question 461

who gets lymphocytic hypophysitis

Answer 461

post-partum/3rd trimester woman - enlarged pituitary stalk (looks like adenoma with T2 dark rim)

Question 462

most common benign orbital mass

Answer 462

dermoid - usually superior and lateral, arising from frontozygomatic suture

Question 463

most common extraocular orbital malignancy in kids

Answer 463

rhabomyosarcoma

Question 464

“racoon eyes” on physical exam

Answer 464

metastatic neuroblatoma - periorbital tumor infiltration with proptosis (also, basilar skull fracture)

Question 465

cancer that causes enophlamos

Answer 465

metastatic breast causes a desmoplastic reaction and enophthalmos (primary orbitals cause proptosis)

Question 466

weird associated between Chlamydia psittaci + this orbital tumor

Answer 466

MALT lymphoma of the orbit (enhances homogenously and restricts diffusion)

Question 467

most common intra-ocular lesion in an adult

Answer 467

melanoma “collar button shaped”

Question 468

most common primary malignancy of the globe

Answer 468

retinoblastoma

Question 469

what is trilateral or quadrilateral retinoblastoma?

Answer 469

trilateral = both eyes + pineal gland, quadrilateral = both eyes + pineal + suprasellar

Question 470

most common cause of spontaneous orbital hemorrhage

Answer 470

varix (also distend with provocative maneuvers)

Question 471

2 types of carotid-cavernous fistulae

Answer 471

1. direct = 2/2 trauma 2. indirect = randomly in post-menopausal females

Question 472

most common causes of pulsatile exophtalmos (2)

Answer 472

1. C-C fistula 2. NF-1 from sphenoid wing dysplasia

Question 473

classic findings of C-C fistula

Answer 473

1. prominent superior ophthalmic vein 2. prominent cavernous sinus 3. proptosis

Question 474

most common cause of pre-septal orbital cellulitis

Answer 474

adjacent structures (teeth/face)

Question 475

most common cause of post-septal orbital cellulitis

Answer 475

paranasal sinuses

Question 476

etiology of dacrocystitis

Answer 476

obstructon of lacrimal sac drainage –> bacterial infection (strep + staph)

Question 477

enhancement of the optic nerve WITHOUT enlargement

Answer 477

optic neuritis - usually unilateral and painful

Question 478

order of involvement of extraocular muscles in thyroid orbitopathy

Answer 478

I M SLOw (inferior, medial, superior, lateral, superior Oblique)

Question 479

thyroid orbitopathy vs. pseudotumor: symptoms

Answer 479

thyroid - not painful, pseudotumor is

Question 480

thyroid orbitopathy vs. pseudotumor: tendon involvement?

Answer 480

thyroid - enlargement of only muscle belly, spares tendon; pseudotumor - involves the whole thing

Question 481

Is pars flaccida or pars tensa more superior?

Answer 481

pars flaccida