Neuroradiology Flashcards

1
Q

CT scan

chars

A

● 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”

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2
Q

MRI

chars

A

● 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

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3
Q

IV contrast

A

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

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4
Q

Imaging chars

CT

A

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)

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5
Q

Imaging chars

MRI

A

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

T1
Bright: Fat, types of blood (metHb), melanin
Dark: Water < cortical bone < air (darkest)
T2
Bright: Water
Dark: cortical bone, blood (deoxyHb, hemosiderin), air

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6
Q

Imaging chars

Edema patterns

A

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

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7
Q

Imaging chars

Herniation

subfalcine

A

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

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8
Q

Imaging chars

Herniation

Descending transtentorial (uncal)

A

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

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9
Q

Intracranial hemorrhage

Extra-axial hemorrhage

Subdural hemorrhage

A

● 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

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10
Q

Intracranial hemorrhage

Extra-axial hemorrhage

Epidural hemorrhage

A

● 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

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11
Q

Intracranial hemorrhage

Extra-axial hemorrhage

Subarachnoid hemorrhage

A

● 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

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12
Q

Intracranial hemorrhage

Extra-axial hemorrhage

Parenchymal hemorrhage

Differential dx

A

● 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

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13
Q

Infarction

Acute infarct CT

A

● 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

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14
Q

Acute infarct MRI

Hallmark of dx is restricted diffusion

A

● 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

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15
Q

Demyelination

MS

A

● 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

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16
Q

Intracranial infection

Cerebral abscess

Stages

A

● 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

17
Q

Intracranial infection

Cerebral abscess

Often demonstrates…

A

Often demonstrate restricted diffusion

Internal exudate limits water motion

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

18
Q

Leptomeningitis

imaging

A

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

19
Q

Neoplasms

Primary astrocytomas

A

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)

20
Q

secondary metastatic disease

A

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

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

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

Types
● Lung, breast, melanoma

21
Q

Extra-axial meningioma

A

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

22
Q

Extra-axial vs intra-axial

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

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