1

Computed Tomography
Hyperdense Lesions
HENRY SU, MD, PHD

A B C
2I CT CTA Conventional
angiogram
CASE A: A 66-year-old man presenting with sudden-onset left-sided weakness. CT, computed tomography;
CTA, CT angiogram.

A B C D
I CT I CT I CT I CT
CASE B: A 77-year-old man with a history of lung cancer. CT, computed tomography.

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4 Brain and Coverings

A B C D
2I CT CTA MIPS T1 Post gad

E F G
FLAIR Susc PET
CASE C: A 73-year-old man with depression, falls, and difficulty completing sentences. CT, computed tomog-
raphy; CTA, CT angiogram; FLAIR, fluid attenuated inversion recovery; gad, gadolinium; MIPS, maximum
intensity projections; PET, positron emission tomography; Susc, susceptibility.

A B C
2I CT T1 Post gad

D E
ADC Post gad
after treatment
CASE D: A 56-year-old man with generalized tonic-clonic seizures. ADC, apparent diffusion coefficient; CT,
computed tomography; gad, gadolinium.

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DESCRIPTION OF FINDINGS
Case A: A small focus of hyperdensity
is present in the left middle cerebellar
peduncle. The CT angiogram demon-
strates a tangle of vessels just lateral to
this focus of hemorrhage. A conventional
catheter angiogram confirms the pres-
ence of an arteriovenous malformation
with arterial supply from the left ante-
rior inferior cerebellar artery and pon-
tine perforators and early filling of the
straight, transverse, and sigmoid sinuses.
The lesion was subsequently treated with
liquid embolic material (not shown).
Case B: A left occipital lesion demon-
strates peripheral hyperdensity. There is
surrounding edema with local mass effect
and effacement of the left occipital horn.
After administration of contrast, super-
imposed enhancement is seen along the
peripheral portions of the mass. On the
coronal reformats, an additional smaller
hyperdense right cerebellar lesion with
ring enhancement is noted. Given the
patients history of lung cancer, these find-
ings are consistent with lung metastases.
Case C: Small, discrete hyperdensities
measuring 150 to 200 HU are consistent
with calcifications in the left occipital lobe.
Surrounding parietal occipital hypoden-
sity and effacement of the left ventricular
atrium are noted. CT angiogram maxi-
mum intensity projection image does not
demonstrate abnormal associated ves-
sels. Gadolinium-enhanced, T1-weighted
MRI shows no associated enhancement.
Marked T2/FLAIR hyperintense signal is
noted correlating with the CT hypoden-
sity. Gradient echo imaging shows cal-
cific foci appearing as punctate foci of
susceptibility. PET imaging demonstrates
a predominantly hypometabolic lesion.
Pathologic evaluation after surgical resec-
tion revealed an oligodendroglioma.
Case D: A CT scan of the brain demon-
strates a mass lesion centered in the left
anterior basal ganglia. There is an irregu-
lar hyperdense rim with a hypodense
center. On MRI, the rim enhances and
has restricted diffusion characterized by
hypointensity on the ADC images. The
findings are suggestive of a hypercellu-
lar lesion with internal necrotic or cystic
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Computed Tomography Hyperdense Lesions 5
c omponents. The patient was given a diag-
nosis of lymphoma, and marked improve-
ment of the enhancing lesion occurred
after IV methotrexate was administered.
DIAGNOSIS
Case A: Intraparenchymal cerebellar hem-
orrhage resulting from an arteriovenous mal-
formation
Case B: Metastatic lung cancer
Case C: Oligodendroglioma grade 2 (proven
by pathology)
Case D: Lymphoma
SUMMARY
The differential diagnosis of CT hyperdense
lesions usually revolves around hemorrhagic
products, calcifications, or hypercellular
lesions. CT attenuation value of hyperdense
lesions in the brain can be helpful in determin-
ing the etiology. Attenuation of hyperdense
hemorrhage in the brain ranges from 60 to 100
HU. Calcifications typically have Hounsfield
units in the hundreds. Care must be taken
when measuring small hyperdensities because
volume averaging can underestimate the
Hounsfield units. MRI susceptibility-weighted
images can also be helpful for differentiating
these entities. Intraparenchymal hemorrhage
demonstrates susceptibility (low signal) with
marked enlargement or blooming of the
hemorrhage compared with its actual size.
Calcification typically shows low signal with
little to no blooming. Dense cellular packing
does not show susceptibility.
Determining the etiology of an intraparen-
chymal hemorrhage is important because it
will affect prognosis, treatment, and manage-
ment. CT angiography is highly sensitive and
specific for identifying an underlying vascular
lesion. Approximately 15% of intraparenchy-
mal hemorrhages result from vascular lesions
such as arteriovenous malformations and fis-
tulae, aneurysms, dural venous sinus throm-
bosis, moyamoya disease, and vasculitis. If an
underlying vascular lesion is not identified,
common causes of intraparenchymal hemor-
rhage in elderly patients should be considered.
Hemorrhages due to anticoagulation are usu-
ally large, lobar hemorrhages, and hyperten-
sive hemorrhages typically are located in the
deep gray nuclei, brainstem, and cerebellum.
6 Brain and Coverings
If anticoagulation and hypertension are not
considerations, a gadolinium-enhanced MRI
with gradient echo sequences is obtained to
evaluate for other causes, such as amyloid
angiopathy, underlying neoplasms, and cav-
ernous malformations. Amyloid angiopathy
is characterized by a lobar hemorrhage with
associated gray/white matter junction micro-
hemorrhages and/or leptomeningeal hemosid-
erosis on susceptibility-weighted sequences.
Neoplasms that produce intraparenchymal
hemorrhage include high-grade gliomas and
metastatic tumors, such as melanoma and
renal cell carcinoma. Frequently, an underly-
ing enhancing mass is identified after admin-
istration of IV gadolinium. However, an
underlying mass can be obscured by the hem-
orrhage, and follow-up MRI is recommended
if no clear cause for the parenchymal hemor-
rhage is identified and neoplasm remains in
the differential diagnosis. Cavernous malfor-
mations may be the cause of acute intrapa-
renchymal hemorrhage in young children and
young adults. They typically have a hetero
genous popcorn appearance with a complete
hemosiderin rim on T2-weighted images and
no surrounding edema. After acute hemor-
rhage, there is edema and the hemosiderin
rim may be obscured. Clues to the etiology
are age and associated classic cavernous mal-
formations in other brain locations (particu-
larly in the familial form).
Calcifications can be either benign or asso-
ciated with pathology. Intraparenchymal cal-
cifications are nonspecific and can be seen
in a variety of etiologies, including normal
deposition in the basal ganglia, prior cerebral
insult (e.g., infection, inflammation, or isch-
emia), vascular abnormalities (e.g., cavernous
malformations, arteriovenous malformations,
and fistulae), or neoplasms. Primary intraaxial
central nervous system neoplasms that show
calcifications include astrocytomas, oligoden-
drogliomas, or, rarely, glioblastomas. Case C is
a grade 2 oligodendroglioma. Low-grade oligo-
dendrogliomas are slowly growing neoplasms
typically located in a cortical/subcortical loca-
tion, most commonly in the frontal lobe. They
may cause scalloping of the adjacent calvar-
ium. The majority demonstrate calcification
and about 50% show variable enhancement.
Differentiation from other neoplasms is not
definitively possible with imaging alone.
On CT, increased attenuation due to dense
cellular packing usually is seen with lym-
phoma and other small, round, blue-cell
tumors, such as peripheral neuroectodermal
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tumors and medulloblastomas, but increased
density also can be seen in glioblastomas. Lym-
phoma is characteristically located in the deep
white matter and deep gray nuclei. On MRI,
the high cellularity is reflected by isointensity
to brain parenchyma on T2-weighted images,
restricted diffusion with hyperintensity on
diffusion-weighted images, and hypointensity
on ADC maps. Lymphoma typically demon-
strates avid homogenous enhancement in
immunocompetent patients. In immunocom-
promised patients, lymphomas may demon-
strate rim enhancement with nonenhancing
regions of central necrosis. In contrast with
acute hemorrhage, lymphomas do not have
susceptibility. Lymphomas usually rapidly
respond to treatment with IV methotrexate,
radiation therapy, or steroids.
DIFFERENTIAL DIAGNOSIS
Acute hemorrhage
Calcification
Highly cellular neoplasms
Previous contrast
PEARLS
Underlying etiologies for acute intrapa-
renchymal hemorrhage should be further
assessed by CT angiogram.
When patients with intraparenchymal
hemorrhage have negative CT angiogram
findings and no history of hypertension or
anticoagulation, a gadolinium-enhanced
MRI with gradient echo sequences should
be performed to assess for underlying
malignancy and amyloid angiopathy,
respectively.
Increased attenuation on CT examina-
tion due to dense cellular packing usually
is seen with lymphoma and other small,
round, blue-cell tumors. These lesions usu-
ally show dense, homogeneous enhance-
ment and restricted diffusion and do not
have susceptibility.
Attenuation of hyperdense hemorrhage in
the brain typically ranges from 60 to 100
HU, whereas calcifications typically have
Hounsfield units in the hundreds. Calcifica-
tions have little to no blooming on suscep-
tibility-weighted images, in contrast with
hemorrhage, which has marked blooming.
 Computed Tomography Hyperdense Lesions 7

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