Neuroradiology Flashcards
CT scan
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● 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”
MRI
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● 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
CT
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
MRI
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
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
Herniation
subfalcine
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
Herniation
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
Infarction
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
Demyelination
MS
● 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