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Flashcards in Neuroradiology Deck (22):

CT scan


● A conventional X-ray beam is rotated around the patient for image acquisition
● A computer reconstructs the data into axial or transverse images based on the Hounsfield attenuation of each pixel (based upon how much that tissue blocks the X-ray beam)
● Adjust Window and Level widths for soft tissue & bone windows
● Window level (wl)—”Brightness”
● Window width (ww)—”Contrast”




● Uses a magnetic field & applied radiofrequency pulses to obtain images
the patient is placed in a strong external magnetic field—up to ~ 3 tesla
An RF pulse is applied to manipulate how atoms align with the external field
As the atoms re-align with the external field, dissipated energy is measured and converted into an image
The vast majority of MRI is based upon the distribution of H nuclei (protons) in different tissues


IV contrast

Iodine based for CT
Gadolinium chelates for MRI
Blood-brain barrier breakdown allows contrast to pass from the intravascular to the extracellular space with subsequent enhancement (bright on CT and T1 MRI)
The pattern of enhancement helps to characterize a lesion and improves visualization of smaller lesions
Enhancement in and of itself is non-specific but denotes an “aggressive” underlying process
Risks: Nephropathy with iodinated agents, NSF with Gad chelates in the setting of renal failure


Imaging chars


The density of a tissue on CT is determined the degree that it attenuates the X-ray beam, expressed in Hounsfield units
Range is from +1000 to -1000
Pure water is set @ 0
In general, the higher the atomic number of the main component of the tissue, the higher the HU and brighter it looks on the image
Bright: bone (calcium) > blood (iron) > brain tissue
Dark: fluid > fat > Air (darkest)


Imaging chars


In general, the amount of water within a tissue determines its signal intensity on a particular MRI sequence, but tissues can vary greatly in signal (brightness) depending upon the sequence

Bright: Fat, types of blood (metHb), melanin
Dark: Water < cortical bone < air (darkest)
Bright: Water
Dark: cortical bone, blood (deoxyHb, hemosiderin), air


Imaging chars

Edema patterns

Vasogenic edema:
 Extracellular edema secondary to breakdown of the BBB
 Follows white matter tracts--”finger” like pattern Cytotoxic edema
Intracellular edema from disruption of Na-K pump
Involves both grey and white matter
Seen most often with an acute stroke


Imaging chars



Displacement of cingulate gyrus across midline beneath falx (aka “midline shift”)
Ipsilateral ventricle compressed, contralateral ventricle can enlarge from foramen of Monroe obstruction
Anterior cerebral artery displaced and compressed -> infarct


Imaging chars


Descending transtentorial (uncal)

Aka “uncal” herniation
Uncus and parahippocampal gyrus displaced medially, descend thru tentorial notch
Displaces and compresses brainstem, CN III
Can displace and compress posterior cerebral art -> infarct


Intracranial hemorrhage

Extra-axial hemorrhage

Subdural hemorrhage

● Cresent-shaped blood collection b/w arachnoid and inner layer of dura
● No dural attachments = can cross sutures
● 10-20% imaged head trauma patients
● > 30% autopsies with severe head trauma
● > 70% have other intracranial injuries
● From stretching and tearing of bridging veins as they enter the dural sinuses
● Poor prognosis
● 35-90% mortality, >2 cm thick=poor outcome


Intracranial hemorrhage

Extra-axial hemorrhage

Epidural hemorrhage

● Biconcave or lentiform blood collection in potential space b/w inner and outer layer of dura
● Does not cross suture lines
● Can cross falx and tentorium
● 1-4% imaged head trauma patients
● 5-15% patients with fatal head injuries
● 90% arterial, 10% venous
● 85-95% associated with skull fx, usually involving groove of the MMA


Intracranial hemorrhage

Extra-axial hemorrhage

Subarachnoid hemorrhage

● Blood collecting b/w pial and arachnoid membranes ● #1 cause of SAH is trauma (#2 = aneurysm)
● 33% with moderate brain injury (100% @ autopsy)
● Likely arises from tearing of veins in SAS
● Evolution and resolution much slower than for aneurysmal SAH


Intracranial hemorrhage

Extra-axial hemorrhage

Parenchymal hemorrhage

Differential dx

● Trauma (contusion, axonal injury)
● Hypertension (BG, thalami, dentate nuclei cerebellum)
● Hemorrhagic conversion of infarction ● Coagulopathy
● Underlying lesion
● Vascular – aneurysm, AVM
● Mass – primary or secondary
● Amyloid angiopathy



Acute infarct CT

● Interrupted blood flow resulting in cerebral ischemia/infarction with variable deficits

Dense artery sign
● Hyperdense M1 in 35-50% acute MCA infarcts
● “Dot” sign = occluded vessels in Sylvian fissure Loss of G/W distinction
● Seen in 50-70% infarcts in first 3 hours
● Insular ribbon sign, loss of deep gray nulcei
Gyral swelling and sulcal effacement
Occurs later, 12-24 hours


Acute infarct MRI

Hallmark of dx is restricted diffusion

● Reflects influx of water into cells as a result of failure of the Na/K pump secondary to energy depletion from ischemia, restricts water motion between cells and the interstitium (= CYTOTOXIC)
● + within minutes but can be reversible in some cases

T2 MRI images generally become + within 8 hrs
● Bright T2, dark T1 signal
● Loss of G/W interface, gyral expansion




● Elongated periventricular plaques-”Dawson fingers” perpendicular to the ventricles
● White matter, internal capsule, brainstem, corpus callosum, optic nerves, cord
● Atrophy of the brain and corpus callosum with long-standing disease
● CT-low density lesion
● MRI-much more sensitive than CT
● High signal plaques on T2
● T1-low but may not see plaques
● Active plaques may enhance, solid or ring-like; may demonstrate restricted diffusion


Intracranial infection

Cerebral abscess


● Early cerebritis (3-5d)
● Focal but not localized infection, mass of PMNs, edema, hemorrhage, and necrosis
● Late cerebritis (4-5d to 2 wks)
● Necrotic foci coalesce, vasc proliferation edema ● Early capsule (~2wks)
● Well-formed collagenous capsule, necrotic core
● Late capsule (wks-months)
● Central cavity shrinks, wall thickens


Intracranial infection

Cerebral abscess

Often demonstrates…

Often demonstrate restricted diffusion

Internal exudate limits water motion

Variable, most consistently seen with bacterial abscesses; less commonly seen with TB, parasites




Early imaging, especially CT, is negative
● Ventricular enlargement from arachnoid granulation obstruction

Inflammatory exudate can enhance
● T1 isointense to brain, T2 hyperintense

Imaging best for the imaging of complications
● Hydrocephalus
● Cerebritis, ventriculitis
● Vascular compl – arterial or venous thrombosis



Primary astrocytomas

Can make reasonable predictions about the tumor grade of astrocytomas based on the imaging appearance:
● The degree of heterogeneity of the tumor (i.e. necrosis, internal hemorrhage) increases with tumor grade
● The higher degree of internal enhancement usually correlates with higher grade (exception pilocytic astro Gr 1)

Focal white matter masses, can appear cortical if close to G/W interface
Enlargement and/or distortion of normal structures
+/- adjacent edema (vasogenic)


secondary metastatic disease

Focal, solid or ring-enhancing masses with surrounding vasogenic edema, mass effect

● 80% @ gray/white junction of cerebrum
● 15% cerebellum, 3% basal ganglia

● 50% cases have solitary met, 20% -2, 30% - >= 3

● Lung, breast, melanoma


Extra-axial meningioma

Accounts for 15-20% primary brain tumors
Most common intracranial extra-axial neoplasm in adults
Arise from arachnoid meningothelial (“cap”) cells
90% supratentorial
Symptoms depend upon location, size; up to 1/3 asymptomatic


Extra-axial vs intra-axial

Buckles/displaces adjacent brain
Expands ipsilateral subarachnoid space
CSF cleft between tumor and brain
Broad-based dural attachment

Expands involved brain
No subarachnoid space expansion, may be effaced
Spreads across well-defined boundries