DOI:10.2214/AJR.07.7095
AJR 2008; 191:S25-S27
© American Roentgen Ray Society
AJR Teaching File: Acute Onset Headache
Ashok Jayashankar1,
Stephen M. Sabourin and
Mark E. Mullins
1 All authors: Department of Radiology, B-115, Emory University School of
Medicine, 1364 Clifton Rd. NE, Atlanta, GA. 30322.
Received April 29, 2008;
accepted after revision April 29, 2008.
Address correspondence to A. Jayashankar
(ajayash{at}emory.edu).
Keywords: headache • intraparenchymal lobar hematoma
Clinical History
A 60-year-old hypertensive man presents with acute onset of headache. He
denies any history of trauma.
Radiologic Description
An unenhanced axial CT scan of the head
(Fig. 1A) shows an acute
intraparenchymal hematoma centered in the paramedian left parietal lobe
parenchyma. A hyperdense nodule is noted along the periphery of the hematoma
ventromedially. MR images (Figs.
1B,
1C,
1D) show signal characteristics
(T1 isointensity, T2 hypointensity) in the hematoma that are most consistent
with acute blood products. Gadolinium-enhanced imaging shows enhancement of
the peripheral nodule.
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Fig. 1A —60-year-old hypertensive man with acute onset of headache and
no history of trauma. Unenhanced axial CT scan of head illustrates hematocrit
level (curved arrow) and hyperdense nodular focus along periphery
(straight arrow).
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Fig. 1B —60-year-old hypertensive man with acute onset of headache and
no history of trauma. Axial unenhanced T1-weighted MR image of brain
illustrates signal heterogeneity (inside circle) without apparent
intrinsic T1 hyperintensity in left parietal lobe in region of abnormalities
identified on A.
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Fig. 1C —60-year-old hypertensive man with acute onset of headache and
no history of trauma. Axial unenhanced gradient-recalled echo T2*-weighted
susceptibility MR image of brain illustrates decreased signal (in
oval) most consistent with blood products. No other remote lesions were
identified on this examination.
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Fig. 1D —60-year-old hypertensive man with acute onset of headache and
no history of trauma. Axial contrast-enhanced T1-weighted MR image of brain
illustrates nodular exophytic enhancement along (arrowhead), smooth
rim enhancement around (straight arrow), and hematocrit level
(curved arrow) within a left parietal lobar hematoma. No other remote
lesions were identified on this examination.
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Differential Diagnosis
The differential diagnosis for an intraparenchymal lobar hematoma includes
primarily hypertensive hemorrhage, vascular anomalies (such as arteriovenous
malformation or cavernous malformation), hemorrhagic neoplasm, hemorrhagic
infarction (including both ischemic arterial and venous), amyloid angiopathy,
and trauma. In most cases, this differential diagnosis may be modified
significantly by the imaging and the clinical scenario. Many other rare causes
may be considered; including multiple sclerosis, mycotic aneurysm rupture, and
vasculitis. An extended differential diagnosis may be obtained from many
modern textbooks and refined as indicated on the basis of the individual
patient.
Diagnosis
The diagnosis in this patient is hemorrhagic metastatic melanoma.
Commentary
Differentiation of a benignintraparenchymal hematoma from a hemorrhagic
neoplasm is a commonly encountered clinical scenario. Although CT may offer
some clues to the presence of an underlying neoplasm (atypical location,
multiple hemorrhagic sites, disproportionate edema, or, as in this patient, a
nodule along the periphery of the hematoma), MRI, with its superior
sensitivity for the detection of blood products and spatial resolution, is
considered the technique of choice
[1]. On MRI, several features,
when present, are suggestive of hemorrhagic neoplasms. First, a
mixed-intensity appearance of the hematoma suggests underlying malignancy.
This is thought to be due to multiple episodes of bleeding into the tumor,
resulting in blood products at different stages of evolution
[1,
2]; an appearance such as this
is nonspecific and may be due to nontumoral causes as well. Second, the
identification of abnormal soft-tissue signal characteristics in or adjacent
to the hematoma suggests neoplasm; in these situations, the abnormal soft
tissue presumably corresponds to nonhemorrhagic tumor. Enhancement of the
soft-tissue signal, as in this patient, is most characteristic of malignancy.
Third, the predictable sequence of T1 and T2 signal intensity characteristics
seen in nonneoplastic hematomas is often not observed with malignancies.
Specifically, several studies have shown persistence of the deoxyhemoglobin
phase (T2 hypointensity) for several days and even weeks in cases of
hemorrhagic neoplasms [1,
2]. In contrast, nonneoplastic
hematomas characteristically show deoxyhemoglobin signal characteristics only
in the acute phase, typically only a few days. Fourth, the appearance of T1
hyperintensity (subacute methemoglobin) centrally or eccentrically in the
hematoma rather than at the periphery suggests underlying neoplasm. Fifth, the
presence of a discontinuous or irregular hemosiderin rim in the late stage of
evolution is more consistent with a neoplastic hematoma. Finally, although
nonneoplastic hematomas generally show decreasing edema over time, neoplastic
hematomas are often associated with persistent or increasing edema. It must be
emphasized that although these features may serve as useful guidelines, they
must be interpreted in the context of the overall clinical picture because
they are relatively nonspecific. Even so, in most cases, reliable
differentiation of a benign intraparenchymal hematoma from a hemorrhagic
neoplasm requires repeated imaging over time and, even then, biopsy may be
needed.
In most situations, the patient's clinical scenario and initial imaging
appearance—both unenhanced head CT and contrast-enhanced brain
MRI—are used to determine whether any additional imaging workup such as
arteriovenous imaging (with CT, MRI, or catheter angiography) is indicated. If
the cause is not trauma, something underlying the lobar hematoma presumably
bled. The hematoma may have obliterated the lesion that bled, or it may be
evident with the CT, MRI, and vascular imaging that can be combined at the
time of presentation. If no direct lesion is identified at the site of
hematoma, other lesions may be seen, thus suggesting a relationship—for
example, amyloid angiopathy, familial cavernous malformations, and signs of
old classic hypertensive hemorrhages are useful in this regard. After an
unrevealing battery of initial imaging, follow-up imaging (usually brain MRI
with contrast material) is performed, typically within approximately 2 weeks'
time, in the hope that the acute blood products, brain swelling, and mass
effect will have abated and perhaps an underlying lesion may be identified.
The primary clinical goal is to identify any underlying process before it can
progress or bleed again, perhaps with more serious morbidity or mortality than
at presentation.
In this patient, the CT finding of a hyperdense nodule along the periphery
of the hematoma initially suggests a satellite hematoma rather than a
hyperdense mass. Hyperdensity is thought to result primarily from increased
cellularity, blood products, or mineralization. The homogeneous appearance of
this nodule suggests a mass is most likely, and mineralization is least
likely, of these possibilities. Contrast-enhanced CT would not likely have
been of help to characterize this lesion (it was not performed in this case);
this case further illustrates the usefulness of MRI to further characterize CT
results. Enhancement on gadolinium-enhanced MR images further supports a
neoplastic cause. Open brain biopsy (i.e., resection) showed metastatic
melanoma. This was the only lesion that the patient had intracranially, thus
underscoring the fact that many (
50%) solitary brain tumors are
metastases. Pathologic assessment of this lesion revealed that most of the
nodule was not hemorrhagic, and that the nodular hyperdensity on unenhanced CT
was caused by dense cellularity. This is supported by the signal
characteristics on MRI, wherein there is a lack of intrinsic T1
hyperintensity—no evidence for methemoglobin or melanin
contents—or decreased signal on susceptibility or gradient-recalled echo
imaging.
Malignant melanoma is the third most common neoplasm to metastasize to the
CNS, behind only lung and breast cancer
[3]. Melanomas are also among
the most common intracranial metastases to hemorrhage
[4]. Although the brain is the
most common site of metastasis in the head from melanoma
[3], several other intracranial
and extracranial structures, including the meninges, choroid plexus, orbit,
internal auditory canal, and parotid gland, can be involved
[5]. Two distinct patterns of
metastatic melanoma have been described on MRI: a melanotic (T1
hyperintensity, T2 hypointensity) and an amelanotic pattern (T1 hypointensity,
T2 hyperintensity). Although Isiklar et al.
[6] showed that the melanotic
imaging pattern is highly specific for melanin-containing metastases, other
studies have shown a much weaker association
[7]. For example, Woodruff et
al. [7] found no melanin in a
resected metastasis with the melanotic imaging pattern. They postulate that
the T1 hyperintensity seen in the melanotic pattern is more likely due to
intralesional hemorrhage than to the paramagnetic effects of melanin.
Therefore, the association of the melanotic imaging pattern with
melanin-containing metastases is, at best, controversial. The amelanotic
pattern is nonspecific and has not been shown to correlate with either the
presence or the absence of melanin in the metastasis.
Objective
The educational objective of this teaching article is to describe the
features that help differentiate a hemorrhagic neoplasm from a benign
intraparenchymal hematoma and to describe the typical patterns of intracranial
metastatic mela noma.
Conclusion
Several features are helpful in differentiating hemorrhagic neoplasms from
nonneoplastic hematomas on MRI. Metastatic melanoma to the brain has a variety
of appearances, including a melanotic pattern that shows T1 hyperintensity and
T2 hypointensity.
References
- Destian S, Sze G, Krol G, Zimmerman RD, Deck MD. MR imaging of
hemorrhagic intracranial neoplasms. AJR1989; 152:137
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- Atlas SW, Grossman RI, Gomori JM, et al. Hemorrhagic intracranial
malignant neoplasms: spin-echo MR imaging. Radiology1987; 164:71
–77[Abstract/Free Full Text]
- Escott EJ. A variety of appearances of malignant melanoma in the
head: a review. RadioGraphics 2001;21
: 625–639[Abstract/Free Full Text]
- Mandybur TI. Intracranial hemorrhage caused by metastatic tumors.
Neurology 1977;27
: 650–655[Abstract/Free Full Text]
- Atlas SW, Grossman RI, Gomori JM, et al. MR imaging of intracranial
metastatic melanoma. J Comput Assist Tomogr1987; 11:577
–583[Medline]
- Isiklar I, Leeds NE, Fuller GN, Kumar AJ. Intracranial metastatic
melanoma: correlation between MR imaging characteristics and melanin content.
AJR 1995; 165:1503
–1512[Abstract/Free Full Text]
- Woodruff WW Jr, Djang WT, McLendon RE, Heinz ER, Voorhees DR.
Intracerebral malignant melanoma: high field-strength MR imaging.
Radiology 1987;165
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Clinical History
Radiologic Description
