Chapter 28 Imaging of the Neurologic System Flashcards
What are the three layers of meninges from out to in
Dura
Arachnoid
Pia
Where is contrast (iodinated) injected dyring myelography?
Subarachnoid space
CT can be appropriate modality for dx of IVDE if two ‘criteria’ met - what scenario
- Chondrodystrophic breeds with myelopathy due to suspected IVDE
- Assume extruded material contains mineralised contens of haemorrhage
What imaging modality (be specific) and findings?
T2W fast spin echo (A) and postcontrast T1W (B) magnetic resonance images of the brain of a dog with a cerebral mass.
Note the exceptional intracranial contrast resolution. The fat within the cancellous bone of the calvaria is very T1 hyperintense and moderately T2 hyperintense. The dense cortical bone has no signal (black) because it lacks hydrogen protons.
Normal brain tissue is light gray, and cerebrospinal fluid in the right lateral ventricle is T1 hypointense and very T2 hyperintense. In the T2W images the normal myelinated white matter of the right cerebrum (arrow) is hypointense to the gray matter.
Perilesional vasogenic edema is present in the left cerebral white matter. This has prolonged T1 and T2 relaxation times, making the white matter T1 hypointense and T2 hyperintense. As expected for vasogenic edema, the T2 hyperintensity tracks along the white matter that makes up the internal capsule, centrum semiovale and into the corona radiata, extending into individual gyri of the cerebrum, and into the diencephalon.
In A, the borders of the mass are difficult to distinguish from the vasogenic edema in the left cerebrum. However, in B, marked gadolinium enhancement of the mass occurs, consistent with vascularization and lack of a functional blood-brain barrier.
What imaging modality is this?
CT myelogram
What is apperance of boone in MRI and why?
Hypointense, because tissues devoid of hydrogen –> signal void
When can mri be superior to CT re bone imaging?
When St pathologic tissues infiltrate
Sagittal T2W image of the humerus of a dog with osteosarcoma. A fat saturation technique has been applied, so if normal, the entire humerus should appear dark (because of suppression of marrow fat), similar to the humeral condyle and scapula (white arrows). Instead, marked T2 prolongation of nearly the entire humerus and adjacent soft tissues is evident. A portion of the cranial cortex (underlying periosteal new bone; arrowheads) appears irregular with faintly increased signal, indicating neoplastic infiltration.
What contrast is usually used in CT?
And MRI?
Iodinated
Gadolinium-based
What is HFU of air?
water?
Acute blood?
Air -1000
Water 0
Blood 60 - 100
What are CT densities
Air
Lung
Fat
Water
Soft tissues
Mineral
Dense bone
Metal
List 3 reasons soft tissues may appear more hypoattenuating than normal
And if more hyperattenuating than usual?
Cystic/fluid filled, necrotic, oedematous
Haemorrhage, mineral, metal, densely cellular, densely fibrotic
From what molecule are MRI signals produced
hydrogen atoms i.e. abudant in water and lipid
Generally speaking, what are T1W and prtoton density images good for?
And T2W?
T1W and prtoton density images good for anatomic detail
T2W good for pathology.
Except T1W good for pathologic tissue with short T1 values e.g. lesions containing fat, methemoglobin, gadolinium contrast
What is an advantage of T2 FLAIR
Advantages of T2 FLAIR images include the ability to distinguish “pure” fluid structures (nulled signal) from solid but high-water-content lesions such as edema within tissue (high signal) and the improved conspicuity of hyperintense lesions compared with spin echo T2W images.
This sequence is particularly advantageous for periventricular or perisulcal lesions that are hyperintense on T2W images that blend into the hyperintense cerebrospinal fluid (Figure 28.16). It is important to recognize, however, that quite often high-protein mucinous fluid (e.g., within the tympanic, nasal, or paranasal cavities/sinuses) will not completely attenuate.
T2W fast spin echo (top) and T2 fluid-attenuated inversion recovery (FLAIR) (bottom) images of a dog with cerebrocortical pathology following seizures. Note how the hyperintense lesions (arrows) could be overlooked on the T2W spin echo image because they blend into the adjacent hyperintense sulci. Because cerebrospinal fluid in the sulci is attenuated on the T2 FLAIR image, hyperintense lesions are much more conspicuous. The cause of the lesions is presumed to be excitatory toxicity related to excessive neurotransmitters, given the history of seizures and the propensity to affect the cingulate gyri (as seen here); however, other causes of T2W hyperintensity must be considered.
What is STIR good for
Vertebral and paravertebral ST pathology because high signal fo fat within marrow is supressed., enabling detection of remaining pathology.
Sagittal short tau inversion recovery (STIR) image of a dog with myeloma of the body of the L3 vertebra. With suppression of the normal high signal of marrow fat in the vertebral bodies, the hyperintense neoplasm is highly conspicuous.
What does diffusion weighted imaging show
Molecular motion or diffusion of water, which is significantly altered in many diseases.
Discriminated between cytotoxic and vasogenic oedema
List 3 MRI fat supression techniques
STIR
Dixon Technique
Spectral Fat Saturation
A: Sagittal T2W
B: T1W precontrast
C: T1W postcontrast
D: T1W postcontrast with fat suppression
On the T2W image (A), there is a mass extending from the body of L4 into the epidural space and compressing the spinal cord. Cranial to the vertebral lesion, the spinal cord is hyperintense, spanning the length of several vertebrae (arrowheads). Note within the field of view and within anatomic structures such as the vertebrae, there exists a wide range of signal intensities that make it difficult to differentiate normal anatomy from pathologic changes. Specifically, there is a hyperintense area within the body of L2 (white arrow). In other vertebrae, there is heterogenous signal intensity that may or may not be pathologic (open arrows in T13 and L7). On the T1W precontrast image (B), the hyperintense area in the body of L2 remains hyperintense (white arrow). Although this likely represents benign fatty infiltration of the cancellous bone (fat is hyperintense on fast/turbo spin T1W and T2W images), pathologic change cannot be excluded from consideration. Following intravenous contrast medium administration (C), it is difficult to tell if the T1 hyperintense area in the L2 vertebra enhances (white arrow), whereas in L7, contrast enhancement (open arrow) is evident when the image is compared to the precontrast T1W image. In T13, it is also difficult to determine if the area enhances (open arrow). On T1W images with fat suppression (D), removal of the signal from fat imparts a more uniform low signal (dark) background appearance to the vertebrae. This better enables the identification of lesions that do enhance (e.g., in T13, L4, and L7) because they become more conspicuous. In the body of L2, the previously T1 hyperintense region is now hypointense, which supports the presence of fat within the cancellous bone (white arrow).
Which two MR angiography techniques dont require use of ocntrast?
Time of flight and phase-contrast MRA
What is spectroscopy?
Graphical display of chemical enviroment allowing quantification of normal and abnormal metabolites
List 6 substances with high intensity on T1W images
And 5 on T2W images
On a T1W image, substances with short T1 relaxation (e.g., fat) have high signal intensity and appear “hyperintense” or bright, whereas those with long relaxation (e.g., cerebrospinal fluid) appear “hypointense” or dark
On a T2W image, substances with long T2 relaxation (e.g., cerebrospinal fluid) will be bright, and substances with short T2 relaxation (e.g., muscle) will be dark.
Fat, which has intermediate T2 relaxation, has an intermediate bright intensity. Normal cellular tissues (e.g., brain gray matter) will appear gray on both T1W and T2W images. Normal white matter is T2 hypointense (see Figure 28.3) and T1 hyperintense relative to gray matter
Why doe the following pathologic processes (oedema, necrosis, demyelination, inflammation, gliosis, many neoplasms) result in T1 and T2 prolongation?
Associated with an increase in unbound water.
Although the tissues are still solid, they now contain more freely mobile water molecules, resulting in T2 and T1 prolongation while increasing signal intensity on a T2W image and decreasing signal on a T1W image relative to normal. On the other hand, when fluid becomes protein bound, as is seen with mucin or marked cerebrospinal fluid inflammation, water molecules become less mobile, and T2 and T1 shortening occur, resulting in decreased signal on a T2W image and increased signal on a T1W image
How does gadolinium work to enhance image?
Gadolinium is paramagnetic
(Meaning that in the presence of a magnetic field it will strengthen field)
In what sequence os gadolinium viewed
T1W
Which 3 CNS structures normally enhance with gadolinium and why?
Pituitary, choroid plexus and meninges
because capillaries are fenestrated and allow passive diffusion.
HOw does vasogenic oedema typically behave in white matter?
How does it appear on CT?
And T1W MR
and T2W MR
Migrates along white matter fibre tracts more readily than tightly integrated cortical grey matter
On CT = hypoattenuating
On T1W hypointense
On T2W hyperintense
How woudl a brain lesion eg neoplasia + perilesional oedema appear on post-contrast T1W images
Leson hyprintense
Oedema hypointense
List author recommended 5 brain sweuences
T1W (pre- and post-contrast)
T2W
T2W FLAIR
T2*W (good for haemorrhage)
Name 3 types of brain oedema
Vasgenic
Cytotoxic (usually result of ischaemia)
Interstitial (from transependymal migrartion of CSFinto periventricular white matter. Often with hydrocephalus)
List 3 types of hydrocephalus
Non-communicating (due to obstruction)
Communication (due to increased production of decreased reduced resorption
Compensatory (due to loss of brain parenchyma)
What 3 brainchanges shoudl you look for with mass effect lesions
- Midline shift
- Ventricular compression
- Effacement of sulci
List 5 imaging findings that point towards extra-parenchymal lesion
- Broad base
- Dural tail (=contiguous dural enhancement)
- Cleft of CSF between mass and brain
- Buckling of white/grey matter junction
- Adjacent hyperostosis of skull
Once structural bran lesion is identified how shoudl it be further classified?
- Location
- Solitary, multifocal or diffuse
- Symmetric or random distribution
Shape, size, margination, attenuation/intensity, contrast enhancement, presence of associated findings (eg mass effect, oedema, haemorrage, necrosis, cavitation, cysts, atrophy, ventriculomegaly
What is the mnemonic for neurologic disorder ddx, and what does it stand for?
MIIND
M - Malformations
I - Inflammations
I - Injuries
N - Neoplasias
D - Degenerations
For myelography, what is contrast vol limit, injection location and why?
<8 ml
via lumbar puncture
to reduce risk of post-myelographic seizures
How are lesions involving SC categorised
Extradural
Intradural-extramedullary
Intramedullary
What is golf tee sign?
created where the hyperintense cerebrospinal fluid in the dorsal subarachnoid space abuts the mass (arrows), is evident, indicating extramedullary localization.
