DOI:10.2214/AJR.07.2249
AJR 2007; 189:720-725
© American Roentgen Ray Society
MRI of Cerebral Microhemorrhages
Marisa Kastoff Blitstein1 and
Glenn A. Tung1
1 Both authors: Department of Diagnostic Imaging, Brown Medical School, Rhode
Island Hospital, 593 Eddy St., Providence, RI 02903.
Received November 4, 2006;
accepted after revision April 19, 2007.
Address correspondence to M. K. Blitstein
(marisa_kastoff{at}alumni.brown.edu).
Abstract
OBJECTIVE. The purpose of this pictorial essay is to discuss the
differential diagnosis of cerebral microhemorrhages on T2*-weighted
gradient-echo MRI.
CONCLUSION. Cerebral amyloid angiopathy and chronic systemic
hypertension are the two most common causes of cerebral microhemorrhages. Less
common causes include diffuse axonal injury, cerebral embolism, cerebral
autosomal dominant arteriopathy with subcortical infarcts and
leukoencephalopathy, multiple cavernous malformations, vasculitis, hemorrhagic
micrometastasis, radiation vasculopathy, and Parry-Romberg syndrome.
Keywords: cerebral microhemorrhages • MRI
Introduction
Cerebral microhemorrhages have been defined as multiple ovoid foci of
marked loss of signal intensity on T2*-weighted, gradient-recalled
echo MRI. Compared with FLAIR and turbo spin-echo T2-weighted sequences, the
T2*-weighted gradient-echo sequence has greater sensitivity for the
local magnetic field inhomogeneity produced by microscopic deposits of
hemosiderin that can remain in macrophages for years after microhemorrhage.
Cerebral microhemorrhages, also known as microbleeds or lacunar hemorrhages,
must be differentiated from vascular flow voids and cerebral calcifications.
Size criteria have been inconsistent. Whereas most studies define
microhemorrhages as being smaller than 5 mm in diameter, an upper limit of 10
mm is sometimes used [1]. Once
thought to be an incidental finding, cerebral microhemorrhages are now
recognized as a marker of microangiopathy and have diagnostic and prognostic
implications. We discuss common, uncommon, and rare causes of cerebral
microhemorrhages.
Common Causes
Congophilic Amyloid Angiopathy
Congophilic amyloid angiopathy is progressive deposition of amyloid within
small- to medium-sized blood vessels leading to fibrinoid necrosis and
vascular fragility. Congophilic amyloid angiopathy is a major cause of primary
lobar intracranial hemorrhage in the elderly and is a common cause of cerebral
microhemorrhages. In patients older than 60 years, the diagnosis of
congophilic amyloid angiopathy should be suspected if there are two or more
lobar hemorrhages of any duration, areas of high signal intensity in the white
matter, and multiple cerebral microhemorrhages at the corticomedullary
junction (Figs. 1A and
1B). As the number of
microhemorrhages increases, so does the risk for intracerebral lobar
hemorrhage and associated neurologic impairment
[2].
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Fig. 1A —76-year-old woman with congophilic amyloid angiopathy.
Transaxial T2*-weighted gradient-echo MR images show innumerable
microhemorrhages predominantly at cerebral gray–white matter junction.
Microhemorrhages are not present in basal ganglia, pons, or cerebellum. Large
focal hemorrhages are present in left superior parietal lobe (arrows,
A) and right inferior parietal lobe (arrow, B).
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Fig. 1B —76-year-old woman with congophilic amyloid angiopathy.
Transaxial T2*-weighted gradient-echo MR images show innumerable
microhemorrhages predominantly at cerebral gray–white matter junction.
Microhemorrhages are not present in basal ganglia, pons, or cerebellum. Large
focal hemorrhages are present in left superior parietal lobe (arrows,
A) and right inferior parietal lobe (arrow, B).
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Hypertensive Cerebral Angiopathy
Hypertensive cerebral angiopathy is the development of intimal hyperplasia
and hyalinosis in deep penetrating brain arterioles as the result of chronic
systemic hypertension. These microangiopathic changes can lead to subclinical
cerebral microbleeding. Unlike congophilic amyloid angiopathy, cerebral
microhemorrhages associated with chronic hypertension are more commonly found
in the thalamus, basal ganglia, cerebellum, and pons, sites of hypertensive
intracerebral hematoma (Figs.
2A and
2B). It is postulated that
hypertensive cerebral microhemorrhage is a risk factor for subsequent
intracerebral hematoma [3].
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Fig. 2A —71-year-old man with history of chronic hypertension,
dementia, and multiple strokes who presented with new right-sided weakness.
Transaxial T2*-weighted gradient-echo MR image shows hemorrhage in
left basal ganglia (solid arrow) and multiple microhemorrhages in
left putamen (solid arrowhead), right caudate nucleus head (open
arrow), and thalamus (open arrowhead).
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Fig. 2B —71-year-old man with history of chronic hypertension,
dementia, and multiple strokes who presented with new right-sided weakness.
Transaxial T2*-weighted gradient-echo MR image shows
microhemorrhage (arrowhead) in basis pontis and left peridentate
cerebellum.
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Uncommon Causes
Diffuse Axonal Injury
Diffuse axonal injury is a type of traumatic brain injury in which
torsional forces generated by rapid acceleration or deceleration of the head
cause the shearing of axons. Areas most vulnerable to shear injury include the
cerebral gray–white matter junction, splenium of the corpus callosum,
and dorsolateral brainstem. Diffuse axonal injury is recognized as multiple
small foci of hyperintensity on FLAIR, T2-weighted, and occasionally
diffusion-weighted MR images owing to the presence of white matter edema from
the axonal shear injury. Diffuse axonal injury can be accompanied by petechial
tissue-tear microhemorrhages that are more apparent on T2*-weighted
MR images than on images obtained with other sequences
[4] (Figs.
3A,
3B, and
3C).
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Fig. 3A —14-year-old boy with postconcussive syndrome and
microhemorrhages from diffuse axonal head injury. Unenhanced CT scan at
presentation shows single punctuate hemorrhage in right frontal lobe and
extensive scalp hematoma.
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Fig. 3B —14-year-old boy with postconcussive syndrome and
microhemorrhages from diffuse axonal head injury. FLAIR (B) and
T2*-weighted gradient-echo (C) MR images obtained 6 months
after A show bilateral corticomedullary microhemorrhages evident only
on gradientecho MR images.
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Fig. 3C —14-year-old boy with postconcussive syndrome and
microhemorrhages from diffuse axonal head injury. FLAIR (B) and
T2*-weighted gradient-echo (C) MR images obtained 6 months
after A show bilateral corticomedullary microhemorrhages evident only
on gradientecho MR images.
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Neurovasculitis
Vasculitis is inflammation of the blood vessel wall usually associated with
ischemia from compromise of the vessel lumen. Neurovasculitis is considered
primary when the vasculitis is confined to the CNS and secondary when a
systemic disorder or meningitis causes inflammatory vasculopathy. In primary
angiitis of the CNS, vasculitis is isolated to the vessels of the CNS, most
commonly the arterioles, and is characterized by brain ischemia and
microhemorrhages at the corticomedullary junction. CNS vasculitis that
complicates bacterial meningitis is an example of secondary neurovasculitis
and is the result of either direct angioinvasion by the microbe or collateral
vascular injury from the host inflammatory response to meningeal infection.
Ischemic infarction, occasionally with hemorrhage, typifies the imaging
presentation and may be associated with cerebral microhemorrhages
[5,
6]
(Fig. 4).
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Fig. 4 —23-year-old man with sickle cell trait and cerebral
vasculitis secondary to meningococcal meningitis. Transaxial
T2*-weighted gradient-echo MR image shows numerous microhemorrhages
and larger hemorrhages at corticomedullary junction.
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Cerebral Cavernous Malformations
Cavernous malformations are a type of low-flow cerebral vascular
malformation characterized by tightly packed, variably thickened vascular
channels that lack both elastic fibers and smooth muscle. Unlike pial
arteriovenous malformation, low-flow cavernous malformation is not associated
with a nidus or enlarged supplying arteries. Multiple cavernous malformations
are found in as many as 33% of sporadic cases and in as many as 75% of cases
of familial disease. One unusual presentation of cavernous malformation than
can be indistinguishable from cerebral microhemorrhages on
T2*-weighted gradient-echo MRI is type 4 cavernous malformation.
According to the classification scheme of Zabramski et al.
[7], type 4 cavernous
malformation may represent a minute form of cavernous malformation or a
histologically distinct precursor (Figs.
5A and
5B).
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Fig. 5A —9-month-old girl with family history of cerebral cavernous
malformation who presented with 1-month history of simple focal seizure.
Transaxial T1-weighted (A) and T2*-weighted (B)
gradient-echo MR images show subacute hematoma (arrow, B) and
vasogenic edema associated with right parietal cavernoma. In this child,
multiple microhemorrhages on gradient-echo MRI are consistent with other
smaller cavernous malformations (type 4 cerebral cavernous malformation).
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Fig. 5B —9-month-old girl with family history of cerebral cavernous
malformation who presented with 1-month history of simple focal seizure.
Transaxial T1-weighted (A) and T2*-weighted (B)
gradient-echo MR images show subacute hematoma (arrow, B) and
vasogenic edema associated with right parietal cavernoma. In this child,
multiple microhemorrhages on gradient-echo MRI are consistent with other
smaller cavernous malformations (type 4 cerebral cavernous malformation).
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Rare Causes
Hemorrhagic micrometastasis from melanoma or renal cell carcinoma can
manifest as cerebral microhemorrhages, and microhemorrhages have been reported
after external beam radiation with or without methotrexate in therapy for
lymphoblastic leukemia [8]
(Figs. 6A,
6B,
6C, and
6D).
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Fig. 6A —48-year-old man with hemorrhagic micrometastasis from renal
cell carcinoma. Transaxial T2*-weighted gradient-echo MR images
show microhemorrhages in right frontal (arrowhead, A), left
occipital (arrow, A), and left temporal (arrow,
B) lobes.
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Fig. 6B —48-year-old man with hemorrhagic micrometastasis from renal
cell carcinoma. Transaxial T2*-weighted gradient-echo MR images
show microhemorrhages in right frontal (arrowhead, A), left
occipital (arrow, A), and left temporal (arrow,
B) lobes.
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Fig. 6C —48-year-old man with hemorrhagic micrometastasis from renal
cell carcinoma. Contrast-enhanced T1-weighted images show small enhancing foci
consistent with hemorrhagic micrometastasis in right frontal
(arrowhead, C), left occipital (arrow, C), and
left temporal (arrow, D) lobes.
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Fig. 6D —48-year-old man with hemorrhagic micrometastasis from renal
cell carcinoma. Contrast-enhanced T1-weighted images show small enhancing foci
consistent with hemorrhagic micrometastasis in right frontal
(arrowhead, C), left occipital (arrow, C), and
left temporal (arrow, D) lobes.
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Cerebral autosomal dominant arteriopathy with subcortical infarcts and
leukoencephalopathy (CADASIL) is an inherited form of cerebral arteriopathy
that leads to precocious demyelination and ischemic white matter infarction.
The underlying defect in CADASIL affects smooth-muscle cells in small blood
vessels that are affected by a unique type of nonarteriosclerotic
amyloid-negative angiopathy characterized by the presence of granular
osmiophilic deposits at electron microscopy. The clinical features of CADASIL
include recurrent ischemic events, cognitive deficits, migraine with aura, and
psychiatric disorders. MRI may show symmetric confluent areas of high signal
intensity in the frontal and anterior temporal lobe white matter and within
the external capsules. Cerebral microhemorrhages have been reported to occur
in 25–70% of cases of CADASIL but have no characteristic distribution
[2] (Figs.
7 and
8).
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Fig. 7 —56-year-old man with biopsy-proven cerebral autosomal
dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
Transaxial T2*-weighted gradient-echo MR image shows extensive
confluent areas of high signal intensity in cerebral white matter, right
frontal lobar hemorrhage (arrow), and single microhemorrhage
(arrowhead) in right superior parietal lobe.
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Fig. 8 —62-year-old man with biopsy-proven cerebral autosomal
dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
Transaxial FLAIR MR image shows extensive and confluent areas of high signal
intensity in cerebral white matter and three microhemorrhages.
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Parry-Romberg syndrome, also known as progressive facial hemiatrophy, is
rare disorder of possible neurovascular origin characterized by unilateral
wasting of the facial skin and subcutaneous tissue with variable involvement
of underlying musculoskeletal and neural tissue. This disorder may be a form
of linear scleroderma called coup de sabre, which is characterized by linear
atrophy of the forehead likened to a saber strike. Fifteen percent of patients
with Parry-Romberg syndrome have neurologic manifestations, including
epilepsy, migraine, hemiplegia, ptosis, and enophthalmos. Findings on brain
MRI are usually ipsilateral to the facial hemiatrophy and include
leptomeningeal enhancement, diffuse areas of high signal intensity in the
white matter, unilateral focal infarctions in the corpus callosum, and
multiple intracranial aneurysms
[9]. We encountered one case of
Parry-Romberg syndrome in which unilateral cerebral microhemorrhages were
found ipsilateral to facial hemiatrophy (Figs.
9A and
9B).
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Fig. 9A —33-year-old man with Parry-Romberg syndrome (facial
hemiatrophy). Transaxial FLAIR MR image shows skin and soft-tissue atrophy of
left frontal scalp and multifocal areas of high signal intensity in white
matter, confluent in left parietooccipital lobe, and ipsilateral to forehead
hemiatrophy.
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Fig. 9B —33-year-old man with Parry-Romberg syndrome (facial
hemiatrophy). Transaxial T2*-weighted gradient-echo MR image shows
scattered microhemorrhages in left frontal lobe, thalamus, and
parietooccipital white matter.
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Acknowledgments
The authors acknowledge Stephen Salloway and Michael Vecchione for their
contribution of case material for this article.
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Abstract
Introduction
