Imaging in Oncology
(Answer)
Evan W. Harris, MD
Assistant Professor of Radiology,
H. Lee Moffitt Cancer Center & Research Institute
Answer:
4. parenchymal (pial) arteriovenous malformation demonstrating areas of parenchymal
hemorrhage in addition to left subdural hematoma
Headache is such a common complaint and has so many etiologies that its correct
evaluation may be difficult to establish. While most patients with headaches do not have
underlying structural lesions, this possibility should be considered. Approximately one
third of patients with brain tumors present with an initial complaint of headache.
Evaluation of the intensity, quality, site, and duration of pain, as well as the presence
or absence of associated neurologic findings, helps to establish the underlying cause of
headache. The abrupt onset of a severe headache rather than a chronic headache in a
previously well patient is more likely due to an intracranial abnormality. Additionally,
headaches that are related to sleep disturbances, as well as headaches associated with
neurologic symptoms (eg, drowsiness, vision or limb problems, or seizures), are more
suggestive of an underlying structural lesion. Depending on the clinical impression,
follow-up investigations such as a CT scan or MRI of the head may provide helpful
information. When evaluating a CT scan and MRI of the head, the most important initial
factors in establishing an appropriate differential diagnosis for a visible intracranial
abnormality are the location of the abnormality and the age of the patients.
The origin of the abnormality or lesion should be first localized to either an
intracerebral/intra-axial or extracerebral/extra-axial location. This case involves an
adult with a primary intra-axial lesion (although a small extra-axial component also is
identified) within the anterior left temporal lobe. Following this initial categorization,
evaluation of attenuation on CT scans and signal intensity on MRI should help to focus the
differential diagnosis. The visualized left temporal lobe lesion demonstrates increased
attenuation on CT scans as well as areas of increased signal intensity on T1-weighted
images and decreased signal on T2-weighted images on MRI. The findings are consistent with
early sub-acute intracranial blood degradation products or hemorrhage.
Fresh intracerebral blood typically appears hyperdense on unenhanced CT of the head
when compared with normal brain. There is a linear relationship between CT attenuation and
hematocrit, hemoglobin concentration, and protein content. The attenuation of
uncomplicated intracerebral hematomas decreases with time, diminishing at an average of
1.5 Hounsfield units daily. Resolving intracerebral hemorrhage first liquefies and then
absorbs, with the process starting at the periphery and progressing centrally.
Intracerebral hematomas become virtually isodense with adjacent brain parenchyma after
approximately one to six weeks on CT scans.
On MRI, signal determinants of bland intracranial hematoma also progress in an orderly
stepwise fashion. Many factors influence the appearance of intracranial hemorrhage on MRI.
Intrinsic factors include macroscopic structure of clot, hemoglobin oxidation state, red
blood cell morphology, protein concentration/clot hydration, size/ location of hematoma,
and edema. Extrinsic factors that may influence the appearance of intracranial hemorrhage
on MRI include pulse sequences and field strength. Hyperacute intracranial hematoma (less
than two to six hours) contains intracellular oxyhemoglobin that will appear isointense to
hypointense on T1-weighted images and hyperintense on T2-weighted images. Acute
intracranial hematoma (hours to days) represents intracellular deoxyhemoglobin that
appears isointense to hypointense on T1-weighted images and hypointense on T2-weighted
images. Early subacute intracranial hematoma (days to weeks) contains intracellular
methemoglobin and appears hyperintense on T1-weighted images and hypointense on
T2-weighted images. Late 
sub-acute
intracranial hematoma (days to months) represents extracellular methemoglobin and appears
hyperintense on both T1- and T2-weighted images. Chronic intracranial hematoma (greater
than one month) contains hemosiderin and ferritin and appears isointense to hypointense on
T1-weighted images and hypointense on T2-weighted images.
The next step in evaluation requires creating a differential diagnosis for nontraumatic
intracranial hemorrhage in an adult. Very common causes for nontraumatic intracranial
hemorrhage include hypertension, aneurysm, and vascular malformation. Common causes
include embolic stroke with reperfusion, amyloid angiopathy, coagulopathy/blood dyscrasia,
drug abuse, and tumor. Uncommon causes include venous infarction, eclampsia, infective
endocarditis, septic emboli, vasculitis (fungal), and encephalitis.
In this case, T1-weighted sagittal MRI demonstrates tubular hypointense left
infratemporal structures (Fig 4). These are most consistent with the appearance of
arterialized draining veins. Additional hypointense foci within this lesion in the left
anterior temporal lobe likely represents fast-flowing blood/arterial supply. A
conventional cerebral arteriogram demonstrated blood supply from the anterior/temporal
branches of the left middle cerebral artery. Large, early-filling left infratemporal
draining veins are further visualized on subsequent images (Fig 5). Arteriovenous
malformations are congenital in nature and generally present during middle age. Most
common symptoms include hemorrhage (usually parenchymal), seizures, and headaches. More
than 80% are located supratentorially. The risk of bleeding is 2% to 3% per year, and
mortality is approximately 20% to 30% per bleeding episode.[1, 2] Multiple arteriovenous
malformations 
are seen in
Rendu-Osler-Weber disease and Wyburn-Mason syndrome. The major vascular supply is
generally from internal carotid artery (pial), but large arteriovenous malformations may
recruit external carotid artery (dural) vessels.
Answer 1 (dural arteriovenous malformation/fistula) is incorrect. The presence of a
small, associated subdural hematoma demonstrated as a peripheral, crescent-shaped area of
increased T1 signal should not cloud the diagnosis. Most dural arteriovenous
malformations/fistulae remain asymptomatic and occur in the posterior fossa. Occlusion of
a venous sinus is probably responsible for their formation. The common vessels that supply
the dural arteriovenous malformations are the occipital artery and meningeal branches of
the external carotid artery. Tentorial and small dural internal carotid artery or
vertebral artery branches also are frequent sources of supply.
The remaining choices (answers 2, 3, and 5) are incorrect as these entities also do not
explain the abnormal vascularity seen with a pial arteriovenous malformation. This would
be an atypical location for hypertensive hemorrhage or ruptured intracranial saccular
aneurysm. The common locations of hypertensive hemorrhage include the putamen/external
capsule (60% to 65%), the thalamus (15% to 25%), the pons (5% to 10%), the cerebellum (2%
to 5%), and the subcortical white matter (1% to 2%). More than 90% of intracranial
saccular aneurysms occur in the circle of Willis/middle cerebral artery bifurcation.
Aneurysms occur less commonly at distal sites in the intracranial circulation when they
are due to trauma or infection. Tumors that commonly bleed include pituitary adenoma,
anaplastic astrocytoma/glioblastoma multiforme, and metastases.
The patient's lesion was removed surgically without complications, and no neurological
deficit remained.
References
- Marks MP, Lane B, Steinberg GK, et al. Hemorrhage in intracerebral arteriovenous
malformations: angiographic determinants. Radiology. 1990;176:807-813.
- Chappell PM, Steinberg GK, Marks MP. Clinically documented hemorrhage in cerebral
arteriovenous malformations: MR characteristics. Radiology. 1992;183:719-724.
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