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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
Hemangioblastoma features
Syrinx
Most common intradural tumor in thoracic region
Inverting Papilloma
Esthesioneuroblastoma
Three most common primary (mets by far more common) skull
base malignant tumors
Cholesteatoma
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
Thyroglossal duct
Lymphangiomas
Subgaleal hematoma
Intracranial air, pneumocephalus, may be seen with what
fractures
Subdural hematomas
Subarachnoid hemorrhage
Intraventricular hemorrhage
Cortical contusions
Subfalcial herniation
Uncal herniation
Transtentorial Herniation
Leptomeningeal cyst
Duret hemorrhage
Nonaccidental trauma head findings
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).
Fogging effect
Lacunes
Beginning at the genu and working back, the internal capsule
carries somatotopically organized fibers
Perivascular spaces
Arteriovenous malformations
Cavernous malformations
Venous malformations
Radiation necrosis
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
Leptomeningeal carcinomatosis
Most common primary cerebellar neoplasm in adult
population.
Capillary hemangioblastomas
Meningioma
Central neurocytoma
Subependymoma
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.
Pineoblastoma
Pineocytoma
Pineal cysts
Pituitary adenomas
Craniopharyngioma
Schwannoma
Most helpful imaging feature in distinguishing vestibular
schwannomas
Suprasellar Masses
Cerebellopontine Masses
Intracranial lipomas
Arachnoid cysts
Brain Coccidioidomycosis
Brain Blastomycosis
Brain Histoplasmosis
CNS Aspergillosis
CNS Mucormycosis
CNS Candidiasis
Most frequently reported CNS fungal infection.
CNS Cryptococcosis
Gelatinous pseudocyst
Cysticercosis
Echinococcosis
Amebic meningoencephalitis
Neurosyphilis
Creutzfeldt-Jakob disease
Meningitis forms causing thick meningeal enhancement
(pachymeningeal)
HIV Encephalopathy
Most common opportunistic CNS infection in AIDS
Toxoplasmosis
Most common AIDS CNS fungal infection
Dysmyelination
Demyelination
Ependymitis granularis
Senescent periventricular hyperintensity
Marchiafava-Bignami disease
Radiation Leukoencephalitis
Radiation Necrosis
Parkinson disease
Huntington disease
Wilson disease
Pelizaeus-Merzbacher Disease
HYPOXIC ISCHEMIC ENCEPHALOPATHY (HIE)
Hydranencephaly
Hypoxic ischemic encephalopathy occuring within 1st
trimester
Alobar holoprosencephaly
Semilobar holoprosencephaly
Lobar holoprosencephaly
Schizencephaly
Chiari II malformations
Chiari I malformations
Dandy-Walker Malformations
Tuberous sclerosis
Sturge-Weber Syndrome
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.
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.
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.
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.
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.
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.
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.
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.