radiology - pathology
TRANSCRIPT
Brain Pathology
Radiology - Pathology
Before You Begin
This module is intended primarily for pre-clinical studentslearning or reviewing pathophysiology.
Please note that this series will focus on how pathology presents in imaging studies. It assumes familiarity with fundamental anatomy. If you need to learn or review this core concept, please visit the “Anatomy” section of our website.
If material is repeated from another module, it will be outlined as this text is so that you are aware
Structure and function of the brain
• Layers of neurons and glial cells form the gray matter, which peripherally lines the gyri. Additional deep gray matter is present in the basal ganglia and thalami
• Deeper white matter tracts are composed of glial cells and myelinated nerve fibers, and is less densely cellular than gray matter
• Ventricles and subarachnoid space are filled with CSF. These spaces become more apparent with volume loss and some pathologic conditions
• The posterior fossa, including the brainstem and cerebellum, contain highly organized white matter tracts as well as gray matter
CT appearance of the normal brain
• Limited contrast resolution between gray and white matter; gray matter is hyperdense (whiter) compared to white matter due to cellularity
• Contrast resolution also limits evaluation of smaller white matter lesions
• X-rays must penetrate the calvarium, often leading to artifact, particularly at the skull base and in the posterior fossa
• Good for the evaluation of intracranial hemorrhage, volume loss, hydrocephalus
Normal CT appearance of the brain
*
*
Noncontrast CT demonstrates
normal gray-white differentiation
and cerebral volume
Note that the bone is white
(compare to MRI)
Streak artifact can
confound diagnosis of
pathology in the
brainstem and posterior
fossa
MR appearance of the normal brain
• Better contrast resolution allows differentiation between gray and white matter (T1 white matter = hyperintense/”whiter” than gray matter due to myelination, T2 white matter = hypointense/”grayer”)
• Fluid is T2 hyperintense
• Hemorrhage, protein, melanin is T1 hyperintense
• Not limited by photon starvation or beam hardening artifact in the posterior fossa
• Multiple pulse sequences can be used to differentiate between blood, CSF/simple fluid, etc.
• FLAIR
• Gradient/T2*/SWI
• DWI
Normal MR appearance of the brain: T1/T2
*
T2 T2 hyperinstense substances:
Water/Fluid/CSF
Fat
Gray matter is hyperintense to
white matter because of high
cellularity
CSF
Gray
White
Skull
Note that the skull bone is hypointense on
MRI whereas it was bright/radiodense on CT
The subcutaneous tissues (fat) are usually
hyperintense (bright) on MRISubcutaneous tissues
Normal MR appearance of the brain: T1/T2
*
T1 T1 hyperintense substances:
Hemorrhhage (subacute)
Fat
Protein
Melanin
Slow-flowing blood
T1 hypointense:
Highly-cellular tumors
White matter is hyperintense
to gray matter due to
myelinated nerve fibers
Normal MR appearance of the brain: FLAIR
*
*
FLAIR (fluid-attenuation
inversion recovery) images
suppress signal from normal
CSF or other simple fluid. The
image is otherwise T2-weighted
*If an area of CSF doesn’t suppress on FLAIR,
it is contaminated with something (elevated
protein, cells, blood)
FLAIR T2
Normal MR appearance of the brain: T2*
*
*
Gradient or susceptibility weighted
images (GRE/T2*/SWI) exploit local
magnetic field inhomogeneities,
making calcifications, such as in the
pineal gland, more conspicuous.
Because T2* images
increase artifacts, things
like aneurysm clips, VP
shunts, etc. can obscure
large portions of the image
due to “blooming”
Normal MR appearance of the brain: DWI
*
*
DWI (diffusion-weighted imaging)
evaluates the free flow of water. This is
disrupted when there is:
Intracellular water (cytotoxic edema)
Hypercellular tumor or abscess
Comparison is made with
the ADC (apparent diffusion
coefficient) image. True
restricted diffusion is bright
on DWI and dark on ADC
Abnormal: Restricted Diffusion
DWI—snow globe analogy
Note the Pittsburgh
reference and the large air
bubble in the snow globe.
Particles can freely
diffuse/move around when
shaken (normal brain)
In the NYC snow globe, there is a
tiny air bubble. It is more difficult for
particles to move around when
shaken (cytotoxic edema to brain
tissue after a stroke)
Basic Intracranial PathologyApproach to evaluation of
intracranial lesions:
1. Intra-axial vs extra-axial2. Enhancement3. Edema4. Mass effect5. Other findings:
hemorrhage, hydrocephalus, additional lesions, etc.
Intra- vs Extra-axial
EXTRA-axial masses demonstrate:
-CSF cleft
-Gray Matter “buckling”
-Intervening gray matter between
mass and white matter
T1 +C T1 -CT2
*This extra-axial mass is a meningioma.
Differential Diagnosis (extra-axial mass):
Metastasis
Lymphoma
Schwannoma
Plasmacytoma
Intra- vs Extra-axial
INTRA-axial masses:
NOT surrounded by CSF or gray matter
T1 +C T1 +C
*This intra-axial mass is a lung cancer
metastasis.
Differential Diagnosis (intra-axial mass):
Metastasis (if multiple, think mets!)
Primary brain neoplasms
Abscess
Enhancement
Metastases and high grade primary tumors
enhance due to disruption of the blood-
brain barrier (BBB) and neovascularity.
Low grade primary neoplasms typically do
not enhance, as the BBB is intact.
*Make sure to look at the
precontrast T1-weighted
images to ensure that
what you are calling
“enhancement” isn’t
intrinsic T1 shortening
T1 +C T1 -C
EnhancementT1 +C Ring Enhancing Mass Differential
“MAGICAL DR”:
M – metastasis
A – abscess
G – glioblastoma
I – infarction (subacute)
C – contusion
A – AIDS
L – lymphoma (immunosuppressed)
D – demyelination
R – radiation necrosis
Vasogenic vs Cytotoxic Edema
Vasogenic edema, (extracellular) due
to capillary permeability, predominantly
affects the white matter and can be
seen with tumors, infection, or
infarction
Cytotoxic edema, (intracellular) due to
failure of the Na/K ATPase pump,
affects dead/dying cells secondary to
infarction
T2 T2
Mass Effect
Types of mass effect:
Sulcal or ventricular effacement
Subfalcine herniation/”midline shift”
Uncal herniation
Tonsillar herniation
In this left MCA territory infarction:
1) Sulcal effacment (less CSF in sulci)
2) Partial effacement of the left lateral
ventricle (smaller than right)
3) Rightward midline shift
1
2
3
T2 T2
Masses Crossing the Corpus Callosum
Differential Diagnosis:
Glioblastoma (“butterfly glioma”)
Lymphoma
*Difficult to differentiate on imaging,
though GBM are more likely to be
necrotic or hemorrhagic
T1 +C FLAIR
Enhancing right parietal mass
with surrounding FLAIR signal
abnormality extending across
the splenium of the corpus
callosum
Other Findings
Hemorrhage
Most sensitive sequence = T2*
Can also see loss of FLAIR suppression in subarachnoid or
intraventricular hemorrhage
T1/T2-weighted signal characteristics are complex and depend on age of
blood
T2* FLAIR
Other Findings
Hydrocephalus
Can occur due to mass effect from a lesion (obstructive) or impaired
CSF reabsorption (communicating)
Bonus: Can you see a potential cause of this patient’s hydrocephalus
on this image?
CT -C
Other Findings
Can you see a potential cause of this patient’s hydrocephalus on this
image?
Intraventricular Hemorrhage layering in the occipital horns
CT -C
Other Findings
Multiple enhancing lesions
Raise suspicion for metastasis, particularly when lesions are
centered at the gray-white junction, though satellite lesions
remain a consideration.
CT +C CT +C
Differential Diagnosis Intra-axial Mass:ADULT
Supratentorial
Metastases
>> Primary Glial Neoplasm
Abscess
Infratentorial
Metastases
>> Hemangioblastoma
PEDIATRIC
Supratentorial
Primary Glial Neoplasm
Primitive Neuroectodermal tumor
Dysembryoplastic Neuroepithelial tumor
>>Metastases
Infratentorial
Juvenile Pilocytic Astrocytoma
Meduolloblastoma
Ependymoma
Hemangioblastoma
>> Metastases
*Age is important, with metastases most common in adults, though
narrowing the differential requires a thorough step-wise approach to
imaging and subsequent tissue sampling
Remember this approach:Approach to evaluation of
intracranial lesions:
1. Intra-axial vs extra-axial2. Enhancement3. Edema4. Mass effect5. Other findings:
hemorrhage, hydrocephalus, additional lesions, etc.
Cases
Use this approach to try to make the following diagnoses
Case 1
57M with dizziness, intermittent left sided paresthesia, and cognitive decline
Case 1T1 +C T2
Case 1
Avidly enhancing, dural-
based extra-axial mass
adjacent to the left temporal
lobe
Vasogenic edema and mass effect with
buckling of the left temporal gray matter
T1 +C T2
Meningioma
• Avidly enhancing extra-axial, dural-based mass
• Dural tail
• May see susceptibility artifact if calcified
• Benign WHO grade 1, but can have substantial mass effect and vasogenic edema in adjacent parenchyma, which is typically the reason for symptoms and resection.
Case 2
51M with vertigo and ataxia
Case 2T1 +C FLAIR
Case 2
Homogeneously enhancing mass in
the left periventricular white matter
with surrounding vasogenic edema
and mass effect
T1 +C FLAIR
Case 2
DWI ADC
Case 2
Restricted diffusion of the mass, with
surrounding edema
DWI ADC
CNS lymphoma
• Enhancing masses, typically in the periventricular white matter, thalamus, or basal ganglia
• Solid enhancement in immunocompetent patients, can be rim enhancing in immunocompromised patients
• Surrounding mass effect and vasogenic edema• Restricted diffusion due to hypercellularity• Can cross midline (ddx glioblastoma)
Case 3
65M with lung cancer and altered mental status
Case 3T2 T2
T1 +C
Case 3
Enlarged third and lateral ventricles
with normal size of the 4th ventricle
Obstructive hydrocephalus secondary
to enhancing metastatic mass at the
level of the cerebral aqueduct.
T2 T2
T1 +C
Metastases with hydrocephalus• Most metastases are parenchymal and frequently
centered at the gray-white junction due to highly-branching vasculature
• Multiple enhancing masses → high suspicion for metastatic disease
• Will enhance due to BBB disruption and neovascularity
• Mass effect with vasogenic edema → in this case, resulting in effacement of the cerebral aqueduct and hydrocephalus
Case 4
44yo F with altered mental status, left facial droop, and weakness
Case 4T1 +C T1 +C
Case 4
Diffuse pachymeningial (dural) enhancement
T1 +C T1 +C
Case 4T1 +C T2
Case 4
Multiple supra- & infra-tentorial ring enhancing masses with vasogenic edema
T1 +C T2
Case 4DWI ADC
Case 4
Masses demonstrate restricted diffusion
DWI ADC
Meningitis with abscess• CT: usually normal, may see hyperdensity in basilar
cisterns or sylvian fissures. If +C, may see meningeal enhancement
• MR: loss of FLAIR suppression in sulci, meningeal enhancement
• Complications: sinus thrombosis, abscess, empyema
Challenge Case
Don’t fall victim to satisfaction of search!
Challenge CaseFLAIR
Challenge CaseT1 +CT2* DWI ADC
Glioblastoma + Meningioma• Right frontal avidly enhancing dural based mass with
susceptibility on T2* images compatible with calcifcation. Mild local mass effect and edema. No restricted diffusion
• Right parietal enhancing mass with restricted diffusion and surrounding T2/FLAIR signal abnormality extending into the splenium of the corpus callosum. No hemorrhage or calcification
Glioblastoma + Meningioma• The glioblastoma was resected, but recurred, and the
right frontal meningioma remains stable (2 yrs later)
ConclusionImaging findings and localization can help narrow the differential diagnosis of intracranial pathologies, though tissue sampling is frequently necessary
END