Disk protrusion terminology

Intervertebral disk high intensity zone (HIZ)

Disk free fragment mimickers

Lateral Disks
Common causes of Central Canal Stenosis
Most common cause of neuroforaminal stenosis

Lateral recess
Spondylolysis identified on axial images
Spondylolisthesis occurs from either
Distinguishes postop scar from disk material
Differentiates disk infection fromdegenerative disk disease at
MR
Myelopathy neurologic signs
Radiculopathy neurologic signs
Urgency for imaging acute myelopathy

Common causes of myelopathy

Definition of Intramedullary spinal canal lesion
Definition of extramedullary spinal canal lesion

Intradural intramedullary lesions

Intradural extramedullary lesions (includes subarachnoid

space)

Extradural extramedullary lesions

Most common intramedullary lesion at MRI

Lupus Erythematosus spinal cord involvement

Atlantoaxial instability and rheumatoid arthritis

Vertebral body and disc infection findings

Vertebral body neoplasm findings

Vertebral body osteoporosis findings

TB of the spine, or Pott disease

Most common neoplasm of the spine
Two most common primary intramedullary tumors
Spinal cord astrocytoma and ependymoma shared features

Spinal cord Ependymoma features

Spinal cord Astrocytoma features

Hemangioblastoma features

Syrinx
Most common intradural tumor in thoracic region

Spinal meningioma features

Most common intraspinal mass

Spinal schwannoma features

Common intrathecal drop metastases
Most common spine extradural neoplasm
Very low T1 and T2 marrow signal

Spinal AVM features

Tethered Cord features

Caudal Regression Syndrome
Spinal Arachnoid cysts and epidermoids
Spinal Epidural Hematoma

Nerve Root Avulsion

Acute versus chronic sinusitis findings

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

Lesion located at hiatus semilunaris (middle meatus) results in

Sphenoid sinusitis is of great clinical concern as it may

Sinus mucous retention cyst versus mucocele

Inverting Papilloma

Juvenile nasopharyngeal angiofibromas

Malignancies of paranasal sinuses and nasal cavity.
Most common salivary malignancies include

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

Cholesteatoma

Opacified petrous apex differential

Cholesterol granuloma
Deep anatomy of the head and neck is subdivided by layers of
deep cervical fascia into the following spaces:
Mucosal head and neck compartment contents

Mucosal head and neck compartment pathology

Parapharyngeal head and neck compartment contents
Parapharyngeal head and neck compartment pathology
Parotid head and neck compartment contents
Parotid head and neck compartment pathology

Carotid head and neck compartment contents

Carotid head and neck compartment pathology
Masticator head and neck compartment contents

Masticator head and neck compartment pathology

Retropharyngeal head and neck compartment contents
Retropharyngeal head and neck compartment pathology
Prevertebral head and neck compartment contents
Prevertebral head and neck compartment pathology
Tornwaldt cysts
Most common minor salivary gland malignancy and has
propensity for perineural spread

The parapharyngeal space is surrounded by what spaces

Triad of nasopharyngeal malignancy

Head and neck paragangliomas

Salivary gland tumors

Head and neck trans-spatial disease categories

Head and neck diseases that demonstrate perineural spread

This lymph node chain serves as the final common afferent

pathway for lymphatic drainage of the entire head and neck.
Pathologic size of head and neck lymph nodes
Common optic nerve sheath complex tumors

Optic nerve glioma

Arachnoidal hyperplasia or gliomatosis

Optic sheath meningiomas

Orbital vascular lesions and age groups

Superior ophthalmic vein pathology

Most common cause of intraorbital mass in an adult

3 common adult intraorbital masses

Enlargement of extraocular muscles with sparing of tendinous

attachments to the globe

Lesions of the lacrimal gland

Retinoblastoma features

Thyroglossal duct

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.

Lymphangiomas
Subgaleal hematoma
Intracranial air, pneumocephalus, may be seen with what
fractures

Epidural hematoma generalities

Venous epidural hematomas

Subdural hematomas

Subarachnoid hemorrhage

Intraventricular hemorrhage

Diffuse axonal injury (DAI)

T2 shinethrough

Cortical contusions

Traumatic Intracerebral Hematoma

Traumatic subcortical gray matter injury

Von Hippel-Lindau syndrome imaging manifestations

Distinguishing epidermoids from arachnoid cysts on MR

imaging.
Pachymeningeal versus leptomeningeal enhancement findings
unfinished.
Rare cystic lesion classically located at the anterior roof of the
third ventricle at the foramen of Monro.

Carotid cavernous fistula (CCF)

Diffuse cerebral edema CT imaging findings

Subfalcial herniation

Uncal herniation

Transtentorial Herniation
Leptomeningeal cyst

Duret hemorrhage
Nonaccidental trauma head findings

Moya moya disease

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

Le Fort II

Le Fort III
CT scans done within 6 hours of MCA occlusion will commonly
exhibit
Ischemic penumbra
Diffusion-Weighted MR in Acute Ischemia
Apparent diffusion coefficient (ADC).

Fluid-Attenuated Inversion Recovery (FLAIR) in Ischemia

Fogging effect

Hemorrhagic Transformation of Infarction

Time course of CT-detected enhancement of infarcted brain

Intravascular MR enhancement of infarcted brain

Maximal brain swelling post brain infarction occurs at what
days
Encephalomalacia post brain infarction occurs when

ACA (anterior cerebral artery) three subgroups:

Two main branch groups of MCA (middle cerebral artery)
Major branches of PCA (posterior cerebral artery)
(Deficit/Syndrome : Cerebral artery/branch/side affected), Leg
weakness :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Incontinence, akinetic mutism :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Facial weakness :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Dysarthria with or without motor aphasia :
(Deficit/Syndrome : Cerebral artery/branch/side affected), Face
and arm weakness > leg weakness :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Motor aphasia (anterior lesion) :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Receptive aphasia (posterior lesion) :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Global aphasia :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Neglect syndromes :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Visulospatial dysfunction :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Variable lacunar syndromes :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Hemianopsia :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Cortical blindness :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Memory deficits :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Somnolence :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Sensory disturbances :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Ataxia, vertigo, vomiting :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Coma if mass effect :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
brainstem deficits :

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

Man-in-a-barrel syndrome :
(Deficit/Syndrome : Cerebral artery/branch/side affected),
Severe memory problems :
Order of cerebellar branches going from top to bottom can be
remembered using the acronym
SCA territory
Anterior Inferior Cerebellar Arteries (AICA) arise from
Posterior Inferior Cerebellar Arteries (PICA) arise from
Involvement of the medulla in PICA infarction adds elements of
Wallenberg syndrome, which include

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

Small-Vessel Ischemic Changes

Some cerebral vasculitides

Venous sinus thrombosis predisposing factors include

Empty delta sign
Superficial hemosiderosis (or superficial siderosis)
MR oxyhemoglobin per time, RBC, and T1 and T2 signal
MR deoxyhemoglobin per time, RBC, and T1 and T2 signal
MR methemoglobin (intracellular) per time, RBC, and T1 and
T2 signal
MR methemoglobin (extracellular) per time, RBC, and T1 and
T2 signal
MR hemosiderin/ferritin per time, RBC, and T1 and T2 signal
Most sensitive areas for detecting SAH
Main finding in patients whose condition continues to
deteriorate after the initial SAH

Congenital berry aneursym

Distal branch cerebral aneurysms are seen in what conditions
Besides berry aneursyms, list other causes of cerebral
aneurysms
Main differential considerations for cerebral parenchymal
hemorrhage
Common locations for intracranial hypertensive hemorrhages
Intracranial hemorrhage cause in young patients, less common
than hypertension

Arteriovenous malformations
Cavernous malformations

Venous malformations

Amyloid angiopathy cerebral hemorrhage

Hemorrhagic cerebral neoplasm

Features of Benign Versus Malignant Intracranial Hemorrhage

Glial cell intracranial neoplasms (gliomas)
Nerve sheath intracranial neoplasms
Extra-axial tumors
Significant general midline shift, if shift is greater than
Hallmarks of uncal herniation?
Differentiating a small neoplasm from a small infarct may be
very difficult. When can followup imaging be obtained to help
distinguish between the two.

Extra-axial mass refers to

White matter buckling?

Tumors of high cellular density

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

Tumor enhancement generally means

Postop granulation tumor versus residual tumor?

Diffuse white matter radiation injury

Radiation necrosis

Astrocytoma grades and types

Female predominant brain tumors

Male predominant brain tumors

Two neoplasms that may exhibit bihemispheric spread through
the corpus callosum.
Intra-axial Lesions With Marked Surrounding Edema

Hemorrhagic Brain Tumors

Cerebral Ring-Enhancing Lesions

This MR sequence may help distinguish acute infarct from lowgrade neoplasm.

Gliomatosis cerebri
In an adult with a heterogeneous calcified mass within the
periphery of a frontal lobe with calvarial erosion and relative
absence of edema should suggest the diagnosis of
Oligodendroglioma features
Calcified Glial Tumors in Order of Frequency

CNS lymphoma imaging characteristics

Ganglioglioma and Gangliocytoma

Desmoplastic Infantile Ganglioglioma
Most common tumor associated with medically refractory
partial complex seizures

Congenital Brain Tumors in Infants Younger Than 60 Days Old

Most (80% to 85%) metastatic lesions occur supratentorially,
with the exception of ___________, which has a predilection for
the posterior fossa.
Most Common Intra-axial Metastases to the CNS
Most Common Extra-axial Metastases to the CNS
Most Common Hemorrhagic Metastases to the CNS

Leptomeningeal carcinomatosis
Most common primary cerebellar neoplasm in adult
population.

Most reliable way to differentiate a medulloblastoma from an

astrocytoma on cross-sectional imaging studies is

Posterior Fossa Masses in Children: Medulloblastoma

Posterior Fossa Masses in Children: Pilocytic astrocytoma

Posterior Fossa Masses in Children: Ependymoma

Posterior Fossa Masses in Children: Brainstem glioma

Most common brain tumor seen in neurofibromatosis type 1
(NF1)
Cystic cerebellar mass with an enhancing mural nodule
suggests two possible diagnoses, and the best discriminator
between the two is

Capillary hemangioblastomas

Dysplastic Cerebellar Gangliocytoma (Lhermitte-Duclos

Disease)

Meningioma

Cerebral Intraventricular Masses

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

Most Common Lateral Ventricle Masses, by Location and Age:

0 - 40 yo, Ventricle Trigone
Most Common Lateral Ventricle Masses, by Location and Age:
10 - 40 yo, Foramen of Monro
Most Common Lateral Ventricle Masses, by Location and Age:
10 - 40 yo, Ventricle Body
Most Common Lateral Ventricle Masses, by Location and Age:
> 40 yo, Ventricle Body
Most Common Lateral Ventricle Masses, by Location and Age:
> 40 yo, Ventricle Trigone

Choroid Plexus Papilloma

Central neurocytoma

Subependymoma

Subependymal giant cell astrocytoma

Colloid cyst
Masses of the Anterosuperior Third Ventricle
Most common neoplasm of pineal region
Calcified pineal mass in a female is more likely to be
When calcification in the pineal region exceeds ____ in size, a
pathologic pineal process should be suspected.

Cerebral Germ cell tumors

Pineal region masses

Pineoblastoma

Pineocytoma
Pineal cysts

Pituitary adenomas

Craniopharyngioma

Rathke cleft cyst

Schwannoma
Most helpful imaging feature in distinguishing vestibular
schwannomas

Suprasellar Masses

Cerebellopontine Masses

Epidermoid versus Dermoid

Intracranial lipomas

Arachnoid cysts

Hamartoma of tuber cinereum

Intracranial tuberculoma

Brain Coccidioidomycosis

Brain Blastomycosis
Brain Histoplasmosis

CNS Aspergillosis

CNS Mucormycosis

CNS Candidiasis
Most frequently reported CNS fungal infection.

CNS Cryptococcosis

Gelatinous pseudocyst

Cysticercosis

Echinococcosis

Congenital CNS toxoplasmosis

Amebic meningoencephalitis

Neurosyphilis

CNS Lyme disease

Cytomegalovirus, congenital CNS infection

Neonatal herpes simplex encephalitis

Adult herpes simplex CNS infection

Ramsay Hunt syndrome

Acute disseminated encephalomyelitis (ADEM)

Subacute sclerosing panencephalitis

Progressive multifocal leukoencephalopathy (PML)

Creutzfeldt-Jakob disease
Meningitis forms causing thick meningeal enhancement
(pachymeningeal)

Most common AIDS CNS infections

Most common CNS AIDS tumor

HIV Encephalopathy
Most common opportunistic CNS infection in AIDS

Toxoplasmosis
Most common AIDS CNS fungal infection

Progressive multifocal leukoencephalopathy

Primary CNS lymphoma

Dysmyelination
Demyelination

Multiple sclerosis (MS, Primary Demyelination)

Involvement of callosal-septal interface is quite specific for
Nonspecific punctuate white matter lesions (small bright
lesions on T2WIs) are more prominent in any patient with

A classic case presentation is that of a young adult female

with prior miscarriages presenting with headaches/migraines
and ischemic white matter changes.

Ependymitis granularis
Senescent periventricular hyperintensity

Prominent perivascular spaces

MR sequences that help distinguish perivascular spaces from

parenchymal lesions

Central pontine myelinolysis (CPM)

Posterior reversible encephalopathy syndrome (PRE)

Marchiafava-Bignami disease

Wernicke encephalopathy and Korsakoff syndrome

Radiation Leukoencephalitis

Radiation Necrosis

Metachromatic leukodystrophy: head size, age of onset, white

matter involvement, gray matter involvement

Adrenoleukodystrophy leukodystrophy: head size, age of

onset, white matter involvement, gray matter involvement

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

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

Transependymal flow of CSF

CSF circulation route

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

Normal pressure hydrocephalus

Alzheimer disease (AD)

Parkinson disease

Huntington disease

Wilson disease

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

insults

Myelination Landmarks by Age 0 days

Myelination Landmarks by Age 3 months
Myelination Landmarks by Age 6 months
Myelination Landmarks by Age 11 months
Myelination Landmarks by Age 18 months
Myelination Landmarks by Age 24 months

Pelizaeus-Merzbacher Disease
HYPOXIC ISCHEMIC ENCEPHALOPATHY (HIE)

Hydranencephaly
Hypoxic ischemic encephalopathy occuring within 1st
trimester

Hypoxic ischemic encephalopathy occuring at less than 26

weeks of gestation
Hypoxic ischemic encephalopathy occuring at greather than
28 weeks

Hypoxic ischemic encephalopathy occuring at term

Periventricular Leukomalacia (PVL)

Gliosis in the periatrial region (seen best on proton-density
scans) is caused by injury to the developing brain at ______
gestational age or older.
Ex vacuo atrial enlargement without gliosis reflects injury prior
to _______ gestational age.
Acute imaging findings of Profound Perinatal Hypoxic Ischemic
Injury
Subacute imaging findings of Profound Perinatal Hypoxic
Ischemic Injury
Chronic imaging findings of Profound Perinatal Hypoxic
Ischemic Injury

Imaging of Profound Postnatal Hypoxic Ischemic Injury

Septo-optic dysplasia (SOD)

Alobar holoprosencephaly

Semilobar holoprosencephaly

Lobar holoprosencephaly

Lipomas of corpus callosum

Lissencephaly and pachygria/agyria complex

Hemimegalencephaly

Polymicrogyria and pachygria

Heterotopic Gray Matter

Schizencephaly

Distinguishing porencephaly from open lipped schizencephaly

Chiari II malformations

Chiari I malformations

Dandy-Walker Malformations

Neurofibromatosis type 1 imaging findings (chromosome 17)

Neurofibromatosis type 2 imaging findings (chromosome 22)

Tuberous sclerosis

Sturge-Weber Syndrome

Von Hippel-Lindau Syndrome

Bulge: Broad-based disk bulge. Usually bulging annulus fibrosus. Protrusion:

Focal disk bulge. Usually herniated nucleus pulposus.
High T2 signal of annulus indicating annular tear.
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.
May cause nerve root impingement causing symptoms of a superior level.
Nerve root has already exited central canal.
Facet joint degenerative change (most common). Lligamentum flavum
hypertrophy.
Facet joint degenerative change with bony encroachment.
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.
Break in bony ring of the lamina (pars interarticularis) at the mid vertebral
body level.
Bilateral spondylolysis. Facet joint degenerative change.
Scar tissue enhances. Disk material has only minimal peripheral
enhancement.
Type 2 degenerative disk disease: Low T1 disk and high T2 parallel endplate
bands. Disk space infection: High T2 disk.
Ataxia. Bowel and bladder incontinence. Babinski sign.
Muscle weakness. Decreased reflexes. Dermatomal sensory deficits.
Poor prognosis if left untreated for greater than 24 hours.
Extramedullary: Epidural mass cord compression. Cervical spine stenosis.
Intramedullary: Tumor. Inflammation, Arteriovenous malformation (AVM).
Spinal dural arteriovenous fistula (SPAVF).
Usually confined to spinal cord. May be exophytic.
Outside of spinal cord. May be intradural or extradural.
Ependymoma. Astrocytoma. Hemangioblastoma. Lipoma/(Epi)dermoid.
Syringohydromyelia. Intramedullary AVM. Met/abscess (rare).
Meningioma. Schwannoma/neurinoma. Neurofibroma. Hemangiopericytoma.
Lipoma/(Epi)dermoid. Arachnoid cyst/adhesion. Drop/leptomeningeal
metastasis. Veins (extramedullary AVM).
Degenerative: Herniated disc. Synovial cyst. Osteophyte. Rheumatoid
pannus. Nondegenerative: Metastasis. Abscess. Hematoma. Primary tumor
expansion or invasion. Epidural lipomatosis
Multiple sclerosis
Areas of high T2 signal with cord swelling. May involve 4 or 5 vertebral
segments. Have less well-defined margins than MS plaques.

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.
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.
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.
Several vertebral bodies with height loss. Anterior weding with posterior
elements spared. Normal T1 and T2 unless fracture. Disk spared.
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.
Metastases
Astrocytoma. Ependymoma.
Expansile. Low T1 and high T2 signal with variable enhancement. Increased
incidence in neurofibromatosis.

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.
Most (75%) occur in cervical and upper to midthoracic cord. Fusiform cord
widening. High T2 signal. Contrast enhancement over several vertebral body
segments.
Occur in spinal cord and posterior fossa. High association with Von HippelLindau syndrome. Densely enhancing nidus with related cyst and or cord
expansion. May be extramedullary and multiple. May be mistaken for
arteriovenous malformation (AVM).
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.
Meningioma

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.
Schwannoma
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.
Subarachnoid seeding of primary CNS tumors: Posterior fossa
medulloblastomas. Ependymomas. Pineal region neoplasms.
Metastatses: Breast, Lung, Prostate carcinoma.
Myelofibrosis
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.
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.
Hypoplastic or absent distal spine and sacrum. Blunted conus.
Similar to brain arachnoid cysts and epidermoids. Arachnoid cysts follow
CSFsignal. Epidermoids restrict diffusion, bright on DWIs.
Ventral epidural space contains plexus of veins. These can tear in trauma,
resulting in epidural hematoma.
Most commonly occur in cervical spine. Typically involve roots of brachial
plexus and upper extremities. Birth trauma from shoulder traction is
common example.
Acute sinusitis: Air-fluid levels and foamy secretions. Typically caused by viral
URI. Chronic sinusitis: Mucoperiosteal thickening. Thickening of bony sinus
walls.
Isolated obstruction of maxillary sinus.
Obstruction of ipsilateral maxillary sinus, anterior and middle ethmoid air
cells, and frontal sinus. Described as ostiomeatal pattern of obstruction.
Extend intracranially due to presence of valveless veins.
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.

Neoplastic epithelium inverts and grows into underlying mucosa of lateral

nasal wall. Surgically resected due to association with squamous cell
carcinoma.
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.
Squamous cell carcinoma. Lymphoma. Minor salivary tumors.
Adenoid cystic carcinoma. Adenocarcinoma. Mucoepidermoid carcinoma.
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.
Chordoma (destructive midline mass). Chondrosarcoma. Osteogenic sarcoma
(from radiation or Paget's degeneration).
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.
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.
Granulation tissue within partially obsructed petrous air cells. Have
cholesterol and hemorrhagic component (high T1 and T2 signal).
(1) Superficial mucosal. (2) Parapharyngeal. (3) Carotid. (4) Parotid. (5)
Masticator. (6) Retropharyngeal. (7) Prevertebral.
Squamous mucosa. Lymphoid tissue (adenoids, lingual tonsils). Minor
salivary glands.
Nasopharyngeal carcinoma. Squamous cell carcinoma. Lymphoma. Minor
salivary gland tumors. Juvenile angiofibroma. Rhabdomyosarcoma.
Fat. Trigeminal nerve (V3). Internal maxillary artery. Ascending pharyngeal
artery.
Minor salivary gland tumor. Lipoma. Cellulitis/abscess. Schwannoma.
Parotid gland. Intraparotid lymph nodes. Facial nerve (VII). External carotid
artery. Retromandibular vein.
Salivary gland tumors. Metastatic adenopathy. Lymphoma. Parotid cysts.

Cranial nerves IXXII. Sympathetic nerves. Jugular chain nodes. Carotid

artery. Jugular vein.
Schwannoma. Neurofibroma. Paraganglionoma. Metastatic adenopathy.
Lymphoma. Cellulitis/abscess. Meningioma.
Muscles of mastication. Ramus and body of mandible. Inferior alveolar nerve.
Odontogenic abscess. Osteomyelitis. Direct spread of squamous cell
carcinoma. Lymphoma. Minor salivary tumor. Sarcoma of muscle or bone.
Lymph nodes (lateral and medial retropharyngeal). Fat.
Metastatic adenopathy. Lymphoma.
Cervical vertebrae. Prevertebral muscles. Paraspinal muscles. Phrenic nerve.
Osseous metastases. Chordoma. Osteomyelitis. Cellulitis. Abscess.
Benign midline nasopharynx lesion of high T2 signal. Believed to be remnant
of notochordal tissue (benign).
Adenoid cystic carcinoma

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.
1) Mucosal mass of lateral nasopharynx (fossa of Rosenmuller). (2) Lateral
retropharyngeal nodes. (3) Mastoid opacification (eustachian tube
dysfunction)
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).
Benign: Pleomorphic adenoma. Warthin tumor. Malignant: Adenocystic
carcinoma. Adenocarcinoma. SCC. Mucoepidermoid carcinoma.
Lymphatic masses (lymphangioma). Neural masses (neurofibroma,
schwannoma, perineural spread of tumor). Vascular masses (hemangioma).
Fungal infections. Squamous cell carcinoma. Adenoid cystic carcinoma.

Internal jugular nodal chain

Jugulodigastric and submandibular nodes may normally measure up to 1.5
cm. All other nodes up to 1.0 cm.
Optic nerve glioma. Optic sheath meningioma.
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.
Thickening of perioptic meninges associated with optic nerve gliomas.
Reflects peritumoral reactive meningeal change.
Grow in a linear fashion along optic nerve. Tram track pattern of linear
enhancement. May invade through dura. May be extensively calcified.
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.
Thrombosis often occurs with cavernous sinus thrombosis. Loss of normal
flow void. Enlargement occurs with cavernous carotid fistulas.
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.
Idiopathic inflammatory pseudotumor. Cavernous hemangioma. Lymphoma.
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.
Inflammatory: Sarcoidosis. Sjogren syndrome. Neoplastic: Salivary gland
(mixed-cell tumor or adenoid cystic carcinoma). Lymphoma. Pseudotumor.
Dermoid (fat-fluid level).
Most common primary ocular malignancy. Leukocoria. Calcified ocular mass.
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.

Second branchial cleft cyst. Anterior to mid sternocleidomastoid muscle.

Lateral to internal jugular vein at the level of carotid bifurcation.
Congenital malformations of lymphatic channels. Benign and
nonencapsulated. Classified as capillary, cavernous, or cystic. Most present
at birth or during infancy.
Soft tissue swelling of the scalp located beneath subcutaneous fibrofatty
tissue and above temporalis muscle.
Compound skull fractures. Fractures involving paranasal sinuses.
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.
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.
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.
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.
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.
Widespread disruption of axons due to acceleration or deceleration injury.
Small, petechial hemorrhages at gray-white junction of cerebral hemispheres
and or corpus callosum.
T2 and DW bright and ADC dark.
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.
Rupture of small intraparenchymal blood vessels. Tend to have less
surrounding edema than cortical contusions. Most are located in the
frontotemporal white matter.

Uncommon manifestation of primary intra-axial injury. Multiple petechial

hemorrhages primarily affecting basal ganglia and thalamus.
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.
Both follow CSF T1 and T2 signal. Epidermoids restrict diffusion, are bright
at DWI. Arachnoid cysts do not restrict diffusion. Epidermoids are composed
of epithelial cells that grow in layers. Arachnoid cysts contains CSF.
Pachymeningeal enhancement is characteristically thick, smooth, and
uninterrupted.
Colloid cyst. Generally are hyperdense to brain parenchyma. Do not
enhance.
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.
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.
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.
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.
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
Known as a growing fracture. Caused by traumatic tear of the dura.
Outpouching of arachnoid at site of suture or skull fracture.
Midline hematoma within tegmentum of rostral pons and midbrai. Associated
with descending transtentorial herniation. Due to stretching or tearing of
penetrating arteries.
Skull fractures. Subdural hematomas. Diffuse brain swelling.

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.
Pilocytic astrocytoma. PNET (primitive neuroectodermal tumor). Hemorrhage.
Floating palate. Horizontal fracture through maxillary sinuses, nasal septum,
and inferior ptyergoid plates.
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.
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.
Insular ribbon sign: Subtle blurring of gray-white layers of insula. Caused by
early edema. Lentiform nucleus edema sign: Hypodense putamen.
ischemic but not infarcted (salvageable) tissue. Peri-infarct tissue.
Brain water diffusion rates fall rapidly during acute ischemia. Bright signal on
DWIs.
Reflects pure diffusion behavior. Free of underlying T2 contributions (shine
through or dark through).
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.
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.
Seen 1 to 2 weeks postinfarction. Hemorrhage of reperfused capillaries.
Serpiginous line of petechial blood following gyral contours of infarcted
cortex.
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.
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.
3 to 7 days postinfarction.
30 to 90 days (1 to 3 months) postinfarction.

Medial lenticulostriate branches: Rostral portions of basal ganglia.

Pericallosal branches: Corpus callosum. Hemispheric branches: Medial
frontal and parietal lobes.
Lateral lenticulostriate branches: Supply most of basal ganglia. Hemispheric
branches: Lateral cerebral surface.
Midbrain and thalamic perforating branches. Posterior choroidal arteries.
Cortical branches to medial temporal and occipital lobes.
ACA/Hemispheric branch/either side
ACA/Hemispheric branch/both sides
ACA/Medial lenticulostriates/either side
ACA/Medial lenticulostriates/Left
MCA/Hemispheric branch/either side
MCA/Hemispheric branch/Left
MCA/Hemispheric branch/Left
MCA/Hemispheric branch (total)/Left
MCA/Hemispheric branch/Left
MCA/Hemispheric branch/Right
MCA/Lateral lenticulostriate branches/Either
PCA/Hemispheric branch/Either
PCA/Hemispheric branch/Both
PCA/Hemispheric branch/Both
PCA/Thalamoperforators/Either
PCA/Thalamoperforators/Either
Cerebellar/PICA, AICA, or SCA/ Either
Cerebellar/PICA, AICA, or SCA/ Either
Cerebellar/PICA, AICA, or SCA/ Either

Watershed/ACA,MCA,PCA/Either
Watershed/ACA,MCA,PCA/Bilateral
SAP: Superior cerebellar artery. Anterior inferior cerebellar artery. Posterior
inferior cerebellar artery.
Superior vermis. Middle and superior cerebellar peduncles. Superolateral
aspects of cerebellar hemispheres.
Proximal basilar artery.
Distal vertebral artery, 1 to 2 cm below basilar origin.
Ataxia. Facial numbness. Horner syndrome. Dysphagia. Dysarthria.
Small subcortical infarcts. May occur in any territory. Characteristic locations:
Lenticular nucleus (37%). Pons (16%). Thalamus (14%). Caudate (10%).
Internal capsule/corona radiata (10%).
Corticobulbar fibers. HAL: Head fibers. Arm fibers. Leg fibers.
Virchow-Robin spaces. May simulate lacunes. Follow CSF signal. No mass
effect. Occur along path of a penetrating vessel.
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.
Autoimmune disorders. Drug exposure (heroin, amphetamines). Polyarteritis
nodosa. Idiopathic processes (giant cell arteritis).
Hypercoagulable states. Pregnancy. Infection (spread from contiguous scalp,
face, middle ear, or sinus). Dehydration. Meningitis. Direct invasion by
tumor.
Filling defect within sagittal sinus on postcontrast CT. Indicates venous sinus
thrombosis.
Diffuse hemosiderin deposition on brain surface. Due to large or recurrent
subarachnoid hemorrhages.
Less than 1 day. RBC intact. T1 iso/dark. T2 bright.
0-2 days. RBC intact. T1 iso/dark. T2 dark.
2-14 days. RBC intact. T1 bright. T2 dark.
10-21 days. RBC lysed. T1 bright. T2 bright.
> 21 days. RBC lysed. T1 dark. T2 dark.
Dependent parts of occipital horns. Interpeduncular fossa.
Infarcts from post SAH increased intracranial pressure or arterial vasospasm.

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.
Prior trauma. Systemic infection (bacterial endocarditis with mycotic
aneurysm).
Atherosclerosis. Fibromuscular disease. Polycystic kidney disease. Mycotic.
Post-traumatic.
Hypertensive hemorrhage. Vascular malformations. Drug effects. Amyloid
angiopathy. Bloody tumors.
Putamen (35% to 50%). Subcortical white matter (30%). Cerebellum (15%).
Thalamus (10% to 15%). Pons (5% to 10%).
Vascular malformations: AVMs. Cavernous malformations. Telangiectasias.
Venous malformations.
Most common type of brain vascular malformation. Abnormal tangle of
arteries directly connected to veins without intervening capillaries. Most
present with hemorrhage or seizures. 2% to 3% annual risk of bleeding,
Thin-walled sinusoidal vessels (neither arteries nor veins). May present with
seizures or small parenchymal hemorrhages.
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.
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.
Primary: Glioblastomas. Metastatses: Bronchogenic carcinoma. Thyroid.
Melanoma. Choriocarcinoma. Renal cell carcinoma.
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.
Astrocytoma. Oligodendroglioma. Ependymoma. Choroid plexus tumor.
Schwannoma, Neurofibroma.
Tumors occuring along brain meninges or within the ventricles. Most nonglial
tumors.
3 mm.
Effacement of ambient cistern. Contralateral hydrocephalus. May
compromise ipsilateral oculomotor (III) nerve (pupillary dilation).
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.

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

Ventricles.
Extra-axial lesions may buckle white matter. Inward compression of white
matter (thinning of fronds). Preserved gray-white matter differentiation.
Usually small cell tumors (high nucleus:cytoplasm ratio, hyperdense and T2
hypointense): Lymphoma. Pineoblastoma. Neuroblastoma. Medulloblastom.
Metastases: Melanoma. Lung carcinoma. Colon carcinoma. Breast carcinoma.
Choroid plexus. Pituitary glands. Pineal glands. Tuber cinereum. Area
postrema.
Aggressive, high-grade neoplasms tend to have fenestrated capillaries
(blood-brain barrier breakdown) allowing for enhancement.
Granulation tissue generally forms 72 hours after surgery. Early (less than
72 hours) postop enhancement likely reflects residual tumor rather than
granulation tumor.
Unenhancing geographic white matter T2 hyperintensity conforming to
radiation ports. Develops 6 months postradiation therapy.
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.
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).
Meningioma (4:1). Neurofibroma. Pineocytoma. Pituitary tumor.
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.
Glioblastoma multiforme. CNS lymphoma.
Metastases. Abscess. Glioblastoma multiforme. Radiation necrosis.
Hematoma (mild).
Primary: Glioblastoma multiforme (most common overall).
Oligodendroglioma. Metastasis: RCC. Thyroid carcinoma. Choriocarcinoma.
Melanoma.
MAGIC DR. Metastasis. Abscess. Glioblastoma multiforme. Infarct. Contusion.
Demyelinating disease. Resolving hematoma. radiation necrosis.

DWI. Infarct exhibitis restricted diffusion.

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

Oligodendroglioma.
Grade II tumor. Commonly located in the frontal lobes. Often extends to
cortex and may erode calvarium. 70% calcify.
Old Elephants Age Gracefully: Oligodendroglioma. Ependymoma.
Astrocytoma. Glioblastoma multiforme.
Hyperdense and T1 hypointensity on T2WIs with surrounding vasogenic
edema. Subependymal spread is common. Bihemispheric involvement via
corpus callosum may be seen.
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.
Rare variant of ganglioglioma seen in the first year of life. Very large
heterogeneous mass with intense enhancement.
Dysembryoplastic neuroepithelial tumor. Always involves cortical gray
matter. May have soap bubble appearance with exophytic extension
beyond cortical gray matter margin.
Teratoma (most common): Two thirds are supratentorial. Primitive
neuroectodermal tumors: Curvilinear, sparse calcification. Astrocytoma.
Choroid plexus papilloma. Ependymoma. Medulloepithelioma. Germinoma.
Angioblastic meningioma. Ganglioglioma.

Renal cell carcinoma.

Lung. Breast. Melanoma. Colon cancer.
Breast. Prostate. Lung. Neuroblastoma.
Melanoma. Renal. Thyroid. Choriocarcinoma.
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.
Hemangioblastoma.

Noncontrast CT scan. Astrocytoma will usually be hypodense.

Medulloblastoma will almost never be hypodense.
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.
Location: Cerebellar vermis. Hemisphere. Cystic with enhancing nodule.
Location: 4th ventricle. Appearance: Foraminal extension. Heterogeneous on
CT and MR. Intense but heterogeneous enhancement.
Location: Brainstem. Appearance: Expansile brainstem. Isodense to
hypodense on CT. Hypointense on T1WIs. Hyperintense on T2WIs.
Pilocytic astrocytoma.
Age. Pilocytic astrocytoma, peak age of birth to 9 years. Hemangioblastoma,
peak age of 35 years.
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.
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.

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

Choroid plexus papilloma.

Subependymal giant cell astrocytoma. Pilocytic astrocytoma.
Ependymoma. Pilocytic astrocytoma. Central neurocytoma.
Subependymoma.
Meningioma. Metastasis.
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.
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.
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.
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.
Occurs in anterosuperior portion of third ventricle near foramen of Monro.
Can cause acute hydrocephalus. Almost all are hyperdense. Variable T1 and
T2 signal.
Colloid cyst. Meningioma. Choroid plexus papilloma. Hamartoma. Glioma.
Vascular lesion. Granulomatous disease.
Germ cell tumors
Pineocytoma. In a male more likely to be a germinoma.

1 cm.
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.

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

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).

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.
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.
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.
Extension of enhancement along course of seventh and eighth nerves.
SATCHMO Sella (pituitary) tumor. Sarcoid. Aneurysm. Arachnoid cyst.
Teratoma. Craniopharyngioma. Hypothalamic glioma. Hamartoma of tuber
cinereum. Histiocytosis. Meningioma. Optic nerve glioma.

AMEN Acoustic (vestibular) schwannoma. Meningioma. Ependymoma.

Neuroepithelial cyst (arachnoid, epidermoid).
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.
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.
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.
Rare congenital hamartoma. More common in boys. Precocious puberty,
gelastic seizures, developmental delay, and hyperactivity. Wellcircumscribed, 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.
Granuloma with central caseous necrosis. Isodense or slightly hyperdense
nodules or small mass lesions.
Occurs in southwestern United States. Focal parenchymal granulomas are
rare. Hydrocephalus is common from complicating meningitis.
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.
Occurs in Midwest and southern United States. Meningitis is most common.
Multiple or solitary granulomas may occur.
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.

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.
Usually causes meningitis. Granulomas and small abscesses may occur.
Meningeal enhancement or multiple small enhancing granulomas or
microabscesses are usually seen.
Cryptococcosis.
50% occur in immunocompetent patients. Common infection in patients with
AIDS. Usually presents as meningitis. Granulomas can occur and are usually
multiple. Abscesses are less common. CT scans can be normal.
Cryptococcomas are small, usually multiple, solid-enhancing, peripheral
parenchymal nodules. Gelatinous pseudocysts can be seen.
Cystic lesion usually in basal ganglia. Perivascular spaces filled with
cryptococcal organisms. Usually found only in immunocompromised.
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.
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.
Atrophy, dilated ventricles, and calcifications. Periventricular white matter,
basal ganglia and cerebral hemisphere calcifications. In CMV, calcifications
are usually periventricular only.
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.
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.

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

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

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.
Demyelinating disease caused by a papova virus. Occurs only in
immunosuppressed patients, especially in AIDS.
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.
Tuberculous meningitis. Fungal meningitis. Racemose cysticercosis.
Sarcoidosis.

HIV encephalopathy. Toxoplasmosis. Cryptococcosis. Other fungal infections.

CMV and Herpes meningoencephalitis. Mycobacterial infection. PML.
Meningovascular syphilis.
Primary CNS lymphoma.
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.
Toxoplasmosis.
Multiple high T2 signal and enhancing mass lesions (1-4 cm) with
surrounding vasogenic edema. Larger lesions usually exhibit ring
enhancement. Unlike bacterial abscesses, toxoplasmosis lesions are not high
in signal on DWI. Preferred sites: Basal ganglia. White matter. Cortex. Main
differential consideration is primary CNS lymphoma.
Cryptococcosis.

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.
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.
Inherited disorder (leukodystrophy), affecting formation or maintenance of
myelin. Generally encountered within pediatric population.
Acquired disorder that affects normal myelin. Generally encountered within
adult population.

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).
MS.

Vasculopathy or hypercoagulable state.

Antiphospholipid syndrome (phospholipid antibody syndrome).

Hypercoagulable state with white matter and ischemic changes.
Normal anatomic finding. May mimic pathology. High T2 signal at tips of
frontal horns. Due to porous ependyma allowing transependymal flow of
CSF.
Age-related high T2 signal along entire length of lateral ventricles.
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.
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.
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.
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).
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

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

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 Nacetylaspartate).
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.
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.
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.
Normal to large head size. Less than 1 yo. Frontal white matter involvement.
No gray matter involvement.
Normal to large head size. less than 1 yo. Diffuse white matter involvement.
Vacuolization of cortical gray matter. deficiency of aspartoacylase, leads to
the buildup of NAA (MRS).
Occurs in acute hydrocephalus. May mimic periventricular white matter
disease. Important means of CSF reabsorption during ventricular obstruction.

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.
Communicating hydrocephalus. Dilated 4th ventricle can be seen in
communicating and non-communicating hydrocephalus.
Enlarged ventricles due to cerebral atrophy. Prominence of both sulci and
ventricles.
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.

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.
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).
Progressive hereditary disorder occuring in fourth and fifth decades.
Findings: Diffuse cortical atrophy. Caudate nucleus atrophy. Putamen atrophy.
Enlargement of frontal horns (heart-shaped).
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.
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).
High T1 signal: Dorsal brainstem. Ventrolateral thalamus. Lentiform nucleus.
Central corticospinal tracts. Low T2 signal: Posterior limb internal capsule
posterior portion.
High T1 signal: Anterior limb internal capsule. Cerebellar white matter.
High T1 signal: Genu of corpus callosum. Low T2 signal: Splenium of corpus
callosum.
Low T2 signal: Anterior limb internal capsule.
Adult appearance except for terminal myelination zones (periatrial and
adjacent to frontal horns)
Dark white matter on T2 (some minimal high-signal areas may persist
peripherally)
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.
Damage to brain from hypoxia/ischemia occurring in utero or around time of
delivery.
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.
Cortical irregularity and/or hydranencephaly.

Periatrial injury. No gliosis. Ex vacuo enlargement.

Periatrial gliosis: high T2 signal.
Watershed infarcts. Ulegyria. Variable deep, superficial white matter gliosis
and atrophy. Myelination delay. Injury to hippocampus and pons.
Occurs in term infants, premature infants greater than 26 weeks of
gestation. Periventricular gliosis. Ex vacuo ventriculomegaly. Apposition of
sulci to ventricular surface.

28 weeks .
26 weeks.
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.
Deep gray matter: Variable T1 and T2 signal. White matter: High T1 and low
T2 perirolandic cortex.
Deep gray matter: High T2 signal. White matter: High T2 perirolandic cortex.
Thinned gyri, atrophy.
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)
Congenital disorder with variable hypoplasia of optic nerves and complete or
partial absence of septum pellucidum. Squared-off appearance of frontal
horns.
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.
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.
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).
Congenital abnormalities. High T1 signal with fat supression. No mass effect.
Vessels course through these lesions. Occur because of persistence of
meninx primitiva.

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

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.
Islands of gray matter anywhere between ependymal surface and subcortical
white matter. May cause seizures.
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.
Porencephaly: encephalomalacia that communicates with ventricle.
Schizencephalic clefts are lined by gray matter. Porencephalic cysts are lined
by a thin layer of white matter.

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.
Cerebellar tonsillar ectopia (tonsils extend > 5 mm below foramen
magnum). Patients may be asymptomatic. May give rise to cervical spinal
cord syrinx.
Large posterior fossa with high tentorial insertion. Dilated cystic 4th ventricle
fills posterior fossa. Cerebellar vermis and hemispheres may be hypoplastic
or absent.
Altered signal in white matter and basal ganglia. Dural ectasia. Optic and
other gliomas. Sphenoid dysplasia. Thinning long bone cortex (ribbon ribs).
Plexiform neurofibromas. Caf au lait spots. Iris hamartomas (Lisch nodules).
Vascular stenoses.
Vestibular schwannomas. Meningiomas. Spinal glial tumors. Optic and other
gliomas.
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)

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.
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.