Download Spontaneously T1-Hyperintense Lesions of the Brain on MRI: A

Spontaneously T1-Hyperintense Lesions of the
Brain on MRI: A Pictorial Review
Sinan Cakirer, MD, Ercan Karaarslan, MD, and Arzu Arslan, MD
In this work, the brain lesions that cause spontaneously
hyperintense T1 signal on MRI were studied under seven
categories. The first category includes lesions with hemorrhagic components, such as infarct, encephalitis, intraparenchymal hematoma, cortical contusion, diffuse axonal
injury, subarachnoid hemorrhage, subdural and epidural
hematoma, intraventricular hemorrhage, vascular malformation and aneurysm, and hemorrhagic neoplasm. The
second category includes protein-containing lesions, such
as colloid cyst, craniopharyngioma, Rathke’s cleft cyst, and
atypical epidermoid. The third category includes lesions
with fatty components, such as lipoma, dermoid, and
lipomatous meningioma. Lesions with calcification or ossification, such as endocrine-metabolic disorder, calcified
neoplasm, infection, and dural osteoma, constitute the
fourth category, whereas the fifth category includes lesions
with other mineral accumulation, such as acquired hepatocerebral degeneration and Wilson disease. The sixth category includes melanin-containing lesions, such as metastasis from melanoma and leptomeningeal melanosis. The last
category is the miscellaneous group, which includes ectopic
neurohypophysis, chronic stages of multiple sclerosis, and
neurofibromatosis type I. The above-mentioned lesions are
presented with their typical T1-hyperintense images, and
the underlying reasons for those appearances in magnetic
resonance imaging are discussed.
The brain lesions that cause spontaneous T1 shortening on magnetic resonance imaging (MRI) were studied under seven categories in this article. These categories have included lesions with hemorrhagic
components, protein-containing lesions, fatty lesions,
This paper was presented at the RSNA 2002-88th Scientific Assembly and
Annual Meeting of the Radiological Society of North America, December
1-6, 2002, Chicago, USA.
From the Department of Radiology, Neuroradiology Section, Istanbul Sisli
Etfal Hospital, Istanbul, Turkey; the Department of Radiology, Istanbul
VKV American Hospital, Istanbul, Turkey; and the Department of Radiology, Kocaeli University Faculty of Medicine, Kocaeli, Turkey.
Reprint requests: Sinan Çakirer, 67 Ada, Kardelen 4/2, Daire 37, 81120
Atasehir, Istanbul, Turkey. E-mail: [email protected]
Curr Probl Diagn Radiol 2003;32:194-217.
© 2003 Mosby, Inc. All rights reserved.
0363-0188/2003/$30.00 ⫹ 0
doi:10.1016/S0363-0188(03)00026-4
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lesions with calcification or ossification, lesions with
other mineral accumulation, melanin-containing lesions, and a miscellaneous group (Table 1).
The purpose of our study is to review, illustrate, and
discuss the MRI findings of the brain lesions causing
T1 shortening with their typical T1-hyperintense appearances. The role of MRI in evaluating such lesions
has been emphasized.
Lesions with Hemorrhagic Components
Brain Infarcts
Infarction of brain tissue usually result from vascular occlusive diseases involving arteries or (very
rarely) veins. The arteries may be occluded for a
variety of reasons, most commonly because of atherosclerotic arterial disease, followed by cardiovasculogenic embolic occlusion, hypercoagulable states, arterial dissection, congenital anomalies, and neoplastic
infiltration or constriction of the arteries. Although the
arterial occlusion causes infarction of a specific vascular territory of the brain with the involvement of
cortical gray matter and subcortical white matter,
venous occlusions secondary to thrombophlebitis, hypercoagulable states, dehydration, oral contraceptive
usage, and tumoral encasement lead to areas of infarction that do not correspond to arterial distributions and
primarily affect the subcortical white matter rather
than cortical gray matter.1-4
The MRI appearance of cerebral infarcts depends
mainly on the age of infarct at the time of examination.
Areas of T1 shortening often develop within the zones
of subacute infarcts, starting on the second day. A
ribbon of high-signal intensity on T1-weighted scans
is seen following the contour of involved cerebral
cortex. This gyriform pattern may be caused by
petechial hemorrhage and biochemical changes caused
by laminar necrosis, ie, protein denaturation (Fig 1).
However, T1-hyperintense areas may be seen starting
Curr Probl Diagn Radiol, September/October 2003
TABLE 1. The lesions of brain with spontaneous T1 hyperintense signal characteristics on MRI
1. Hemorrhagic lesions
A. Infarcts: Subacture phase of arterial infarct associated with gyral hemorrhage and protein denaturation, embolic infarct associated
with reperfusion, and venous infarct
B. Infections, eg, herpes simplex encephalitis, cytomegalovirus encephalitis, and HIV encephalitis
C. Intraparenchymal hematoma: Traumatic, profuse hemorrhagic infarct, hypertensive hematoma, secondary to aneurysms and vascular
malformations, germinal matrix bleeding, amyloid angiopathy, coagulopathies, and blood dyscrasias
D. Cortical contusions
E. Diffuse axonal injuries
F. Subarachnoid hemorrhage: Traumatic, secondary to aneurysms and vascular malformations
G. Subdural and eipdural hematoma
H. Intraventricular hemorrhage: Traumatic, secondary to aneurysms and vascular malformations, periventricular hematomas dissectiing
into ventricles, germinal matrix bleeding, amyloid angiopathy, coagulopathies, and blood dyscrasias
I. Vascular malformations and aneurysms associated with intra- or perilesional hemorrhage and/or thrombosis: AVM, cavernous
malformation. aneurysm
J. Hemorrhagic neoplasms: Primary tumors such as pituitary adenomas, anaplastic astrocytoma, oligodendroglioma, glioblastoma
multiforme, and lymphoma (in immunocompromised patients); secondary tumors such as metastasis from melanoma, renal cell
carcinoma, choriocarcinoma, brochogenic carcinoma, and thyroid carcinoma
2. Protein-containing lesions
A. Colloid cyst of third ventricle
B. Craniopharynigoma
C. Rathke’s cleft cyst
D. Atypical epidermoid
3. Fatty lesions
A. Lipoma: pericallosal, cisternal, and intraventricular
B. Dermoid
C. Lipomatous meningioma
4. Calcified/ossified lesions
A. Endocrine-metabolic disorders: Hypo- or hyperparathyroidism, hypothryoidism, mitochondrial encephalopathies, Fahr disease (familial
cerebrovascular ferrocalcinosis), carbon monoxide poisoning, and idiopathic calcification
B. Calcified neoplasms: Craniopharyngioma, oligodendroglioma, choroid plexus papilloma, meningioma, pituitary adenoma, astrocytoma,
pericallosal lipoma, ependymoma, metastases from lung, breast, and gastrointestinal carcinomas
C. Infections: Toxoplasmosis, cytomegalovirus, rubella, herpes, tuberculosis, and cysticercosis infections
D. Dural osteomas
5. Lesions with other mineral accumulation
A. Acquired hepatocerebral degeneration
B. Wilson’s disease
6. Melanin-containing lesions
A. Melanoma metastases
B. Leptomeningeal melanosis
7. Miscellaneous
A. Ectopic neurohypophysis
B. Multiple sclerosis (chronic stage)
C. Neurofibromatosis type I
from the second day of infarct until the end of second
month if there is an associated area of hemorrhage
secondary to the dissolution of an embolus allowing a
reperfusion hemorrhage or to anticoagulant treatment
(Fig 2). Multifocal hemorrhagic infarcts suggest an
embolic source, such as subacute bacterial endocarditis. It is important to remember that hemorrhage within
cerebral infarcts may mimic other causes of atypical
hematomas, such as hemorrhagic neoplasms. Venous
pathologies, such as dural sinus thrombosis, should
also be considered as the underlying reason of hemorrhagic cerebral infarction. Additional T2-weighted
MRI sequences help to determine the exact stage of
Curr Probl Diagn Radiol, September/October 2003
infarct. Diffusion-weighted images show restricted
diffusion (high signal) in cerebral infarcts (Fig 1).1,3-9
Infections
Encephalitis is a diffuse inflammatory state of brain
tissue and most commonly develops secondary to viral
infections. Viral encephalitis is usually seen in immunocompromised patients. Herpes encephalitis is the
most common sporadic encephalitis in temperate climates and is caused by herpes simplex type I. Other
less-common viral agents are cytomegalovirus, human
immunodeficiency virus (HIV-1), and varicella-zoster
virus.10,11
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Fig. 2. Spin-echo T1-weighted axial image of a 32-year-old female
patient with a recent history of surgical resection of craniopharyngioma through a right pterional approach reveals an almost homogeneously hyperintense area of early subacute phase of hemorrhagic
infarction (arrow) in the distribution of right Heubner artery that
involves parts of head of caudate nucleus, internal capsule, and
putamen.
Fig. 1. Spin-echo T1-weighted axial (A) and fat-suppressed diffusionweighted axial (B) images of a 67-year-old female patient with a
left-sided hemiparesis that started 4 days previously reveal ribbons of
high-signal intensity following the contour of right opercular area
(arrowheads), representing an early phase of subacute infarct in the
distribution of middle cerebral artery on T1-weighted image. The
diffusion-weighted image clearly shows the infarct area with restricted
diffusion (high signal).
Herpes simplex encephalitis causes an acute fulminant hemorrhagic and necrotic type of meningoencephalitis that typically begins in the medial anterior
temporal and orbital surface of frontal lobes. As
herpes encephalitis progresses, patchy areas of hem-
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orrhage and abnormal contrast enhancement are common. Small hemorrhages within the edematous tissue
may be apparent on MRI as zones of T1 and/or T2
shortening (Fig 3). A rare alternative cause of rapidly
progressive edema and patchy hemorrhage in the
temporal lobe is thrombosis of the transverse sinus
with venous infarction in the patients with herpes
encephalitis. Involvement of the insular cortex, cingulate gyrus, and white matter lateral to the lenticular
nucleus is characteristic of herpes encephalitis. The
involvement of cingulate gyrus and contralateral limbic system is highly suggestive for herpes encephalitis.10-13
Intraparenchymal Hematoma
Intraparenchymal hematoma may result from
trauma, hemorrhagic transformation of cerebral infarct, hypertension, amyloid angiopathy, rupture of
aneurysms or vascular malformations, germinal matrix
bleeding, coagulopathy and blood dyscrasias, neoplastic lesions, and infectious lesions. Hypertension, amy-
Curr Probl Diagn Radiol, September/October 2003
Fig. 3. Spin-echo T1-weighted axial image of a 42-year-old male
patient with herpes simplex encephalitis reveals areas of gyriform
high-signal intensity along the anteromedial parts of left temporal lobe,
representing the subacute phase of patchy hemorrhagic areas.
loid angiopathy, and coagulopathy are the most common causes of nontraumatic intracranial hemorrhage
in the elderly, whereas patients younger than 50
usually have underlying vascular malformations and
aneurysms. Hypertensive bleeding is frequently observed in the region of the basal ganglia, thalami, and
internal capsules (Fig 4). Lobar or subcortical location
of hematomas is generally seen with amyloid angiopathy, vascular malformations, and aneurysms. Hemorrhagic transformation of cerebral infarcts is usually
seen 24 to 48 hours after the initial formation of
infarct. It has a common predilection for the basal
ganglia (Fig 5) and the cortex, and deep hemorrhagic
infarctions are often associated with proximal middle
cerebral artery occlusion.11,14-21
The signal-intensity characteristics of an intracranial hematoma depend on several factors, the most
important of which are listed as the age, size, location,
hemoglobin oxidation state of hematoma, degree of
clot retraction, extent of edema around hematoma, and
hematocrit level of the patient. The MRI appearance of
intracerebral hemorrhage on T1-weighted scans
changes during the first week of bleeding. Iron of
hemoglobin in the ⫹2 state becomes oxidized to the
⫹3 state in methemoglobin, which is strongly paraCurr Probl Diagn Radiol, September/October 2003
Fig. 4. Spin-echo T1-weighted (A) and gradient-echo T2-weighted (B)
axial images of a 67-year-old male patient with a history of longstanding hypertension and a right-sided hemiparesis that started 5 days
previously reveal a subacute stage of hematoma involving parts of
head of caudate nucleus, internal capsule, and putamen with highsignal intensity on T1-weighted images and very low-signal intensity on
T2*-weighted images (black arrows). There are areas of hemorrhages
at the same age within the left-sided corpus of the lateral ventricle
(white arrows) secondary to the dissection of parenchymal hematoma
into the ventricular system.
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Fig. 5. Spin-echo T1-weighted axial image of a 63-year-old male
patient with a history of longstanding hypertension reveals a hemorrhagic transformation of right putaminal infarct in the distribution of
lateral lenticulostriate branches of middle cerebral artery with the
high-signal intensity starting from the periphery and progressing
toward the center of infarct area (arrow).
magnetic during the early subacute phase of bleeding
that starts around the second day of bleeding. When
methemoglobin is initially intracellular, the hematoma
has a high signal on T1-weighted images that
progresses from periphery to center and a low signal
on T2-weighted images that is surrounded by a zone of
high T2 signal secondary to edema. When methemoglobin eventually becomes primarily extracellular during the late subacute phase of bleeding that starts
around the first to second week of bleeding, the
hematoma has a high signal on both T1- and T2weighted images. Cell lysis and watery dilution of
blood products accompany the oxidation of intracerebral hematomas, progressing inward from the periphery of the lesion. The combination of these events
converts the initially low-signal intensity of acute
hematomas on T2-weighted scans to high-signal intensity over a period of weeks. The concentric zones
of evolving signal intensity are typical of most spontaneous intracerebral hematomas.14-16
Cortical Contusion
Cortical contusions are the most common traumatic
injuries of brain parenchyma. They are often superficial lesions, reflecting bruising of the cortical surface
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Fig. 6. Spin-echo T1-weighted axial image of a 45-year-old male
patient with a history of recent head trauma reveals a hemorrhagic
area of cortical contusion involving right occipital pole with heterogeneous high-signal intensity (arrow).
against the adjacent osseous ridge and, less often, a
dural fold. Cortical contusions most frequently result
from acceleration/deceleration forces; however, a direct cortical contusion area may develop adjacent to a
skull fracture, as in the case of a depressed fracture.
Common locations include the anteroinferior portions
of temporal lobes, perisylvian cortex, anteroinferior
temporal lobes, and (less commonly) occipital pole.
Evidence of parenchymal damage usually should be
sought both immediately beneath and directly opposite
a skull fracture or scalp injury. Petechial cortical
contusions tend to coalesce into larger foci of hemorrhage, and they often become more evident within 24
to 48 hours after the initial trauma. The appearance of
contusion on MRI is an area of focal hemorrhage
involving the cerebral cortex and subcortical white
matter. The signal of cortical contusion depends on the
factors related to the hematoma. As the edema and
mass effect subside during the subacute phase, T1
shortening develops with a gyriform contour following
the cortical convolutions. The ribbon-like distribution
of subacute hemorrhage is commonly seen within
zones of contusion, resembling the pattern of T1
shortening in subacute infarction or anoxia (Fig 6).
Wide hemorrhagic areas may be associated with contusion in some severe cases.22-25
Curr Probl Diagn Radiol, September/October 2003
Diffuse Axonal (Shearing) Injuries
Diffuse axonal injuries, or shearing injuries, constitute the second most common traumatic injury of the
brain. Acceleration/deceleration injury, or shaking of
the brain, causes impaired axoplasmic transport, axonal swelling, and disconnection; thus, a state of
axonal transection. Diffuse axonal injury is frequently
observed near interfaces between tissues of different
consistency, so that shearing forces develop when
rotation or acceleration/deceleration forces impart different velocities and momentum to parenchyma on
each side of the tissue boundary. The most common
locations of shearing injuries are gray–white matter
junctions in the frontal and temporal lobes, corpus
callosum, fornix, brainstem, basal ganglia, and internal
capsule. The size of shearing injuries may range from
a few millimeters to centimeters. The lesions are
commonly microscopic and nonhemorrhagic; however, up to 50% of shearing injuries may be hemorrhagic (Fig 7).17,26-28
Subarachnoid Hemorrhage
Subarachnoid hemorrhage may result secondary to
a variety of underlying reasons, such as the trauma,
rupture of aneurysms (Fig 8), bleeding vascular malformations, hematomas dissecting into the cerebrospinal fluid, and coagulopathy. Subarachnoid hemorrhage
is not usually seen on MRI unless there is profuse
bleeding because the extravasated blood elements are
diluted within cerebrospinal fluid. Computed tomography is recommended for diagnosis of subarachnoid
hemorrhages. However, in the case of profuse bleeding into the subarachnoid space independent of the
underlying reason, hemoglobin may be deoxidized to
the deoxyhemoglobin state and further to the methemoglobin state, giving a hyperintense appearance on
T1-weighted images. Chronic stages of subarachnoid
bleeding may be characterized by the deposition of
hemosiderin on the pial surface of the brain, leading to
a thin hypointense rim appearance, especially prominent on T2-weighted images, called superficial siderosis.29,30
Fig. 7. Spin-echo T1-weighted axial image (A) and axial computed
tomographic image (B) of a 36-year-old male patient with a history of
recent head trauma reveal bilateral high-signal intensity foci of hemorrhagic shearing injuries in the thalami (black arrows) that were
detected as high-density foci (white arrows) on an emergent computed
tomographic study 4 days before MRI examination.
Epidural and Subdural Hematomas
Epidural hematomas usually result from traumatic
rupture of an epidural artery, often the middle meningeal artery, or of a dural venous sinus. The blood is
collected between the skull and outer layer of dura
mater with a typical biconvex shape. They do not cross
Curr Probl Diagn Radiol, September/October 2003
suture lines, except in cases of very large hematomas
associated with a diastatic fracture. Epidural hematomas cause compression of underlying brain parenchyma and subarachnoid spaces, and herniation is
commonly detected. Epidural hematomas are com-
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Fig. 8. Spin-echo T1-weighted axial images of a 41-year-old female patient who had a subarachnoid bleeding 3 days ago reveal (A) a saccular
aneurysm with a signal void at the bifurcation of right middle cerebral artery (white arrow) that is surrounded by hyperintense subacute bleeding
within the subarachnoid space (black arrow), and (B) bleeding filling the right sylvian fissure as well (black arrow).
monly associated with skull fractures but rarely can be
seen without fractures.14,22-24,31
Subdural hematomas usually result from the tearing of cortical arteries or veins where they enter the
subdural space. They have a typical crescentic shape
and are located between the inner layer of dura and
arachnoid layer. Subdural hematomas may cross
suture lines but not dural attachments. They usually
extend into the interhemispheric fissure. More than
two thirds of the subdural hematomas have significant associated lesions, such as subarachnoid hemorrhage, cortical contusion, and diffuse axonal
injuries.14,22-24,32,33
The signal intensity of epidural and subdural hematomas depends on several factors, but the most important factor is the age of the hematoma at the time of
examination. Acute hematomas are isointense or
slightly lower in signal intensity than cerebral parenchyma on T1-weighted images. The hematomas have
a high-signal intensity on T1-weighted images during
the whole subacute stage, whereas they have a lowsignal intensity secondary to the presence of intracellular methemoglobin during the early phase of the
subacute stage, and a high-signal intensity secondary
to the presence of extracellular methemoglobin during
the late phase on T2-weighted images (Fig 9). Mixed
signal intensities may be observed, especially for
200
Fig. 9. Spin-echo T1-weighted axial image of a 70-year-old female
patient with a history of recent head trauma reveals a right-sided
crescentic subdural hematoma along the temporo-occipital surface
(black arrows) with a hyperintense signal characteristic, representing
subacute phase of hematoma. Note that an additional focal area of
subdural hematoma is present along the right occipital pole (arrowhead).
subdural hematomas, as a result of rebleeding into the
hematomatous area.14,16,31-33
Curr Probl Diagn Radiol, September/October 2003
Vascular Malformations and Aneurysms
Fig. 10. Spin-echo T1-weighted axial image of a 2-day-old male
infant with a history of premature birth at 31 weeks of gestation shows
that bilateral lateral ventricles are enlarged with intraventricular posterior layering of hyperintense blood components secondary to germinal matrix bleeding. Note that both the amount and the myelination of
the white matter have seriously decreased. Septum pellucidum is also
absent.
Intraventricular Hemorrhage
Intraventricular hemorrhage may be seen as a result
of several conditions, such as trauma, bleeding secondary to vascular malformations and aneurysms,
periventricular hematomas dissecting into ventricles
(Fig 4), germinal matrix bleeding (Fig 10), amyloid
angiopathy, coagulopathies, and blood dyscrasias.
Hemorrhage commonly arises from fragile vessels in
the periventricular germinal matrix of premature newborns. Hematomas may remain confined to the subependymal region or rupture into the ventricular system, often causing secondary hydrocephalus. In adults,
hematomas in the posterior fossa or basal ganglia may
rupture into the fourth, third, or lateral ventricles. The
ventricles may be grossly expanded by thrombus.14,17,19,21,23,30,34-36
Curr Probl Diagn Radiol, September/October 2003
Arteriovenous malformations (AVMs) are the most
common symptomatic cerebral vascular malformations. AVMs may be sporadic, congenital, or associated with a history of trauma. They are angiogenically
immature lesions with continuing vascular remodeling. They are most commonly located in the supratentorial area (80-90%), whereas an infratentorial location is rare. AVMs contain multiple tightly packed
tortuous tubular flow void structures on T1- and
T2-weighted images secondary to patent arteries with
high blood flow. They may contain thrombosed vessels with variable signal, areas of hemorrhage in
various phases, calcification, and gliosis as well. The
signal-intensity characteristics of AVMs depend on
the presence of various components, as mentioned
previously. Areas of T1 shortening may be detected
secondary to thrombosis, hemorrhage, or calcification.
AVMs do not contain brain tissue within the nidus of
lesion. They are not usually associated with mass
effect, except in the case of a recent hemorrhage or
venous occlusion.14,16,19
Cavernous malformations, or cavernomas, are the
most common angiographically occult vascular malformations. They are angiogenically immature dynamic lesions with endothelial proliferation and
increased neoangiogenesis. Almost 75% of the cavernomas occur as solitary sporadic lesions, whereas
the rest of lesions are detected in the multiple
familial form. They are collections of sinusoidal
vascular spaces surrounded by a gliotic pseudocapsule without intervening neuroglial tissue. MRI
appearance of cavernous angiomas is highly characteristic. An aggregate, multinodular, or popcorn
morphology with prominent central zones of T1
shortening is surrounded by a characteristic rind of
T2 shortening that is attributable to the accumulation of hemosiderin from old hemorrhages (Fig 11).
Calcification may also contribute to low-signal intensity within and surrounding cavernous angiomas.
They may range in size from a few millimeters to
several centimeters in diameter. Any region of the
brain may be affected; however, supratentorial cavernomas occur more frequently than infratentorial
lesions. They have a propensity for repeated intralesional hemorrhage.14,16,20,37,38
Intracranial aneurysms constitute the most common
underlying reason for nontraumatic subarachnoid
hemorrhage, and they may cause areas of T1 shorten-
201
Fig. 11. Spin-echo T1-weighted axial image of a 40-year-old male
patient with a moderate degree of left-sided hemiparesis reveals a
lobulated, heterogeneously hyperintense lesion with a hypointense rim
(arrow), representing a cavernous malformation.
ing during the subacute phase of subarachnoid bleeding, as explained above. The aneurysms may be
saccular, fusiform, or blister-like structures. Saccular
aneurysms occur typically at arterial bifurcations, and
they are frequently located around the circle of Willis.
Saccular aneurysms greater than 25 mm in diameter
are referred to as giant aneurysms. The lumina of giant
saccular aneurysms may be at least partially occupied
by a thrombus that often has a lamellar or concentric
appearance. The layers of intermediate- and highsignal intensity caused by thrombi of different ages
and an additional zone of signal void layer representing the patent lumen are seen. This laminated internal
architecture is a hallmark of thrombosed aneurysm.
The circulation of blood within large-sized aneurysms
is often complex, with lower flow velocities and less
turbulence than is typically present within the lumen
of smaller aneurysms. As a result, large aneurysms
may demonstrate mixed intraluminal signal intensity
on MRI scans. It may be difficult to distinguish
between slowly flowing but patent components of the
aneurysm and intraluminal thrombus on standard spinecho scans. Flow-sensitive sequences are important in
evaluating such cases.14,29,30,39,40
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Fig. 12. Spin-echo T1-weighed coronal (A) and fast spin-echo T2weighted coronal (B) images of a 27-year-old female patient reveal a
hemorrhagic adenoma with homogeneous high-signal intensity on
T1-weighted (black arrow) image. T2-weighted image shows that the
adenoma has a laminar appearance with hypo-, hyper-, and hypointense signal intensity from periphery to central (white arrows), suggesting the transition from early to late phase of subacute hemorrhage.
Hemorrhagic Neoplasms
Intracranial neoplasms, whether primary or metastatic, may be associated with hemorrhagic components. The reported incidence of hemorrhage in intracranial neoplasms varies from 1% to 15% in various
series. Higher grades of malignancy, presence of
neovascularity, presence of arteriovenous shunts
within the lesions, rapidly growing neoplasms with
associated necrosis, and vascular invasion by neoplasms may be the underlying factors contributing to
the bleeding within the neoplasms. Primary tumors,
such as pituitary adenomas, anaplastic astrocytoma,
oligodendroglioma, glioblastoma multiforme, and
lymphoma (in the case of immunocompromised pa-
Curr Probl Diagn Radiol, September/October 2003
Fig. 13. Spin-echo T1-weighted axial (A) and FLAIR coronal (B) images of a 52-year-old male patient with a left frontal opercular mass involving
cortical gray matter and subcortical white matter that has a high-signal intensity after gyral convolutions on T1-weighted image (arrow) and an
almost homogeneous high-signal intensity (arrow) on FLAIR image with associated profuse edema. The mass was surgically proven to be an
oligodendroglioma with hemorrhagic components.
Fig. 14. Spin-echo T1-weighted axial image of a 48-year-old female
patient with a right occipitotemporal mass lesion that has a peripheral
high-signal intensity (arrowheads) toward the cortical surface of mass.
The diagnosis was confirmed as anaplastic astrocytoma with hemorrhagic components at surgery.
tients), and secondary tumors, such as metastasis from
bronchogenic carcinoma, renal cell carcinoma, melanoma, choriocarcinoma, and thyroid carcinoma, are
the most common intracranial neoplasms associated
with hemorrhage.21,41-44
Curr Probl Diagn Radiol, September/October 2003
The MRI appearance of a hemorrhagic neoplastic
lesions is usually characterized by a more complex
heterogeneous pattern of bleeding, nonhemorrhagic
components that enhance after intravenous gadolinium
administration, disordered evolution of hemorrhagic
elements within the lesion, persisting peripheral
edema during the evolution of lesion, and mass effect.
Primary tumors are solitary, and metastatic tumors are
typically multiple.21,43,44
Pituitary adenomas are common, benign, slowly
growing tumors representing approximately half of
the sellar and parasellar neoplasms in adults. Pituitary adenomas commonly have intermediate signalintensity characteristics on T1- and T2-weighted
sequences. However, the cysts, hemorrhage, and
necrosis, which are more common in the case of
macroadenomas with a size of more 10 mm, may be
associated with adenomas, leading to a heterogeneous signal-intensity pattern (Fig 12). The pattern
of hemorrhage within pituitary adenomas varies
from homogeneous to heterogeneous. The hemorrhages within an adenoma are much more commonly microscopic and subclinical. Acute bleeding
into an adenoma may cause sudden enlargement of
the tumor, with compression on the optic chiasm
and on the rest of hypophyseal gland. Rapidly
developing visual impairment and endocrine dysfunction, usually accompanied by headache, is
203
Fig. 15. Spin-echo T1-weighted axial (A) and postgadolinium spinecho T1-weighted axial (B) images of a 35-year-old female patient
reveal typical butterfly appearance of a bifrontal mass that extends
through the genu of corpus callosum. The mass has a high-signal
intensity peripherally representing surgically proven hemorrhagic components, and it shows a strong peripheral enhancement after gadolinium administration.
204
Fig. 16. Spin-echo T1-weighted axial (A) and gradient-echo T2weighted axial (B) images of a 61-year-old male patient with a history
of surgical excision of malignant melanoma in his arm reveal a nodular
lesion of the left periventricular area with peripherally hyperintense
and centrally hypointense components on T1-weighted image (arrow).
The lesion is strongly hypointense on T2*-weighted image, representing its hemorrhagic nature (arrow). The single focus was surgically
removed, and the histologic examination confirmed the diagnosis of
melanotic malignant melanoma.
called pituitary apoplexy. Some observers suggest
an increased incidence of pituitary hemorrhage in
patients receiving bromocriptine therapy.43,45-47
Anaplastic astrocytoma, oligodendroglioma, glioblastoma multiforme, and lymphoma (in immunocompro-
Curr Probl Diagn Radiol, September/October 2003
Fig. 18. Spin-echo T1-weighted sagittal image of a 46-year-old
female patient presenting with headache and hydrocephalus reveals a
homogeneously hyperintense cystic lesion (arrow) within the third
ventricle. Note that surgically proven colloid cyst causes enlargement
of the ventricular system.
Fig. 17. Spin-echo T1-weighted axial image of a 74-year-male patient
shows several hyperintense nodular lesions at the gray–white matter
junction, representing hemorrhagic metastases from a known primary
bronchogenic carcinoma. The right frontal nodule (black arrow) has an
accompanying edema, whereas the left parietal nodule (white arrow)
causes no edema.
mised patients) are the other primary neoplasms associated with hemorrhage. Macroscopic hemorrhage is
relatively uncommon in glial tumors. Microscopic hemorrhage is a common pathological feature within highgrade gliomas. Oligodendrogliomas are relatively rare,
slowly growing gliomas with usually mixed histologic
patterns. They make up a disproportionate share of
lesions presenting with gross hemorrhage (Fig 13). Areas
of signal void are also seen at sites of clump-like
calcification. High-grade gliomas, including anaplastic
astrocytoma (Fig 14) and glioblastoma multiforme (Fig
15), are highly malignant neoplasms with necrosis and
neovascular proliferation that represent a likely source of
bleeding. Hemorrhage and necrosis also may be associated with primary brain lymphoma in immunocompromised patients.21,43-45
Metastases represent approximately one third of
intracranial tumors. They are usually located at the
gray–white matter interface of cerebral hemispheres.
Hemorrhage, calcifications, and cysts may be associated with metastatic tumors. Neoplasms, such as
melanoma (Fig 16), choriocarcinoma, hypernephroma,
Curr Probl Diagn Radiol, September/October 2003
Fig. 19. Spin-echo T1-weighted sagittal image of a 34-year-old
female patient reveals a well-circumscribed intrasellar lesion (arrow)
with high signal intensity that was surgically removed with a resultant
diagnosis of Rathke’s cleft cyst.
bronchogenic carcinoma (Fig 17), and thyroid carcinoma, usually cause hemorrhagic cerebral metastases.
The high-signal intensity of T1-weighted images suggest the presence of subacute or early chronic hemorrhagic elements within the lesion. Hemorrhagic metastases may simulate the appearance of cavernous
angiomas or other occult vascular malformations when
they are solitary.21,43,44
205
Fig. 20. Spin-echo T1-weighted coronal image of a 59-year-old male
patient reveals a left-sided suprasellar cystic mass with homogeneously
high-signal intensity. The mass was found to be an epidermoid cyst that
surrounded the supraclinoid segment of left internal carotid artery and
prechiasmatic optic nerve at surgery.
Fig. 21. Spin-echo T1-weighted sagittal image of a 36-year-old
female patient with dizziness reveals a pericallosal curvilinear hyperintense lipomatous mass associated with hypoplasia of the splenium of
corpus callosum (arrow).
Protein-containing Lesions
Colloid Cysts
Colloid cysts exclusively arise from the inferior
aspect of the septum pellucidum and protrude into the
anterior portion of the third ventricle between columns
of the fornix; however, some authors have reported the
presence of colloid cysts in unusual locations, such as
206
the posterior fossa and lateral ventricles. Typical
clinical presentation is with episodes of positional
headaches caused by intermittent hydrocephalus. The
third ventricle is enlarged to accommodate the cyst;
lateral ventricles are enlarged as the result of obstruction in foramen of Monro. The cysts are well-circumscribed, with hyperintense signal-intensity on both T1and T2-weighted sequences in almost 60% of the
patients due to protein and mucin content of the lesion;
however, they show variable signal-intensity characteristics in the rest of the patients, depending on the
content of the cyst (Fig 18). Thin rim enhancement
may be observed around the cyst, representing a
fibrous capsule, after intravenous gadolinium administration. Differential diagnosis from the masses, such
as meningioma and ependymoma, is not difficult
because of their typical features on MRI.48-50
Craniopharyngioma
Craniopharyngiomas are usually histologically benign but locally aggressive lesions arising from squamous epithelial rests along Rathke’s cleft. They may
present with a variety of signal intensities, sizes, and
morphologies on MRI pictures. Craniopharyngiomas
most commonly involve the suprasellar region, alone
or in combination with intrasellar components. The
midline location is typical. They are usually wellcircumscribed lobulated lesions with variable low-,
intermediate-, or high-signal on T1- and T2-weighted
images. T1-hyperintense components within craniopharyngiomas most often represent high protein content within cystic regions of the tumor. Experimental
studies and analysis of fluid from tumor cysts have
suggested that appreciable T1 shortening is usually
correlated with protein concentrations in the range of
10% to 30%. Calcification and hemorrhage may be
associated with craniopharyngiomas, causing variable
signal-intensity patterns on T1- and T2-weighted images.47,51
Rathke’s Cleft Cyst
Rathke’s cleft cysts are uncommon, benign cystic
lesions that are derived from the remnants of the
epithelium embryologically lining Rathke’s cleft (craniopharyngeal duct). They may be intrasellar in 50%
of the cases, suprasellar in 25% of the cases, and both
in 25% of the cases. The cysts are usually simple, lined
by a single epithelial layer. They may contain variable
amounts of protein, mucopolysaccharide, cellular debris, and cholesterol. Their signal intensity may be
Curr Probl Diagn Radiol, September/October 2003
Fig. 22. Spin-echo T1-weighted sagittal image (A) and fat-suppressed spin-echo T1-weighted axial image (B) of a 34-year-old female patient show
a well-circumscribed hyperintense mass (arrow) of the quadrigeminal cistern on T1-weighted image with a signal-void region around the
lipomatous mass due to chemical shift artifact, and fat-suppressed image reveals that the hyperintense signal of the qudrigeminal cistern lipoma
ceases totally (arrow).
Fig. 23. Spin-echo T1-weighted sagittal image of a 46-year-old male
patient with headache reveals a hyperintense lipoma along the floor of
hypothalamus in the suprasellar cistern (arrow).
Fig. 24. Spin-echo T1-weighted sagittal image of a 28-year-old
female patient shows an incidentally detected subependymal mass
with high-signal intensity (arrow) that ceased on fat-suppressed images. The diagnosis is the atrial lipoma.
Atypical Epidermoid Cysts
correspondingly high, low, or intermediate on T1- and
T2-weighted sequences, depending on the contents of
cystic lesions (Fig 19). Gadolinium enhancement is
usually absent.47,52
Curr Probl Diagn Radiol, September/October 2003
Epidermoid cysts are nonneoplastic, congenital,
or acquired extra-axial off-midline lesions that are
filled with desquamated cells and keratinaceous
debris. The prepontine and cerebellopontine angle
207
Fig. 26. Spin-echo T1-weighted sagittal image of a 25-year-old
female patient presenting with a longstanding history of visual impairment and a recent onset of severe headaches shows a suprasellar
high-intensity mass that was surgically proven as dermoid cyst, and
association of scattered hyperintense foci along the neighboring sulci
secondary to the rupture of cyst.
vessels. They frequently have signal intensities
similar to that of cerebrospinal fluid on MRI. Very
rarely, epidermoid cysts demonstrate short T1 and
T2 values resembling dermoid cysts (Fig 20). Such
masses usually contain viscous liquid components
containing relatively high concentrations of protein
and causing high-signal intensity on T1-weighted
scans. The lack of contrast enhancement is characteristic of epidermoid cysts.53-57
Fatty Lesions
Lipomas
Fig. 25. Spin-echo T1-weighted axial image (A) and fat-suppressed
fast spin-echo T2-weighted coronal images (B) of a 52-year-old female
patient with severe headache reveal a mass of the sylvian cistern that
is heterogeneously hyperintense on T1-weighted image with the cease
of high signal on fat-suppressed image. The mass was surgically
removed with the resultant diagnosis of dermoid cyst.
cisterns and suprasellar and parasellar areas are
common sites for epidermoid cysts. They are wellcircumscribed, spheroid, or multilobulated cystic
lesions. They usually cause encasement rather than
displacement of the neighboring cranial nerves and
208
Intracranial lipomas are uncommon congenital
malformations that result from persistence and abnormal differentiation of the meninx primitiva.
Microscopically, they are composed of adipose
tissue with a variable mixture of vascular elements,
musculo-collagenous fibers, and glial and ganglion
cells. They are located at or near the midline in 80%
to 95% of the cases. The common locations for
lipomas are as pericallosal (25-50%) (Fig 21),
sylvian fissure, quadrigeminal cistern (Fig 22), interpeduncular cistern, cerebellopontine angle cistern, cerebellomedullary cistern, chiasmatic-suprasellar cistern (Fig 23), and choroid plexus of the
atrium (Fig 24). Lipomas can be nodular or curvilinear. They may contain calcifications. Intracranial
lipomas are often asymptomatic and discovered
Curr Probl Diagn Radiol, September/October 2003
Fig. 27. Spin-echo T1-weighted axial image (A) and fat-suppressed
spin-echo T1-weighted axial image (B) of a 58-year-old female patient
with severe headache reveal a dura-based left parafalcian mass
(arrow) that has heterogeneous hyperintense components on T1weighted image with the cease of high signal intensity on fatsuppressed image. The mass was surgically removed with the resultant
diagnosis of lipomatous meningioma.
incidentally. The clinical findings, if present, are
usually related to associated anomalies, such as
corpus callosum dysgenesis (Fig 21). Lipomas are
characteristically hyperintense masses on T1- and
Curr Probl Diagn Radiol, September/October 2003
Fig. 28. Spin-echo T1-weighted axial image (A) and gradient-echo
T2-weighted axial image (B) of a 28-year-old female patient with the
diagnosis of Fahr disease reveal high signal-intensity areas within the
globus pallidi and thalami (arrowheads) in T1-weighted image, and
very low signal-intensity areas within the globus pallidi (arrows) in
T2*-weighted image.
less hyperintense masses on T2-weighted sequences, with decreased signal intensity on fatsuppressed sequences on MRI. A more specific clue
to the diagnosis of lipoma and other lipid-containing
masses is the chemical shift artifact, which is simply
209
Fig. 29. Spin-echo T1-weighted sagittal image of a 49-year-old
female patient with seizures shows a temporo-occipital mass with
heterogeneous hyperintense and hypointense components. The histologic examination of surgically removed mass detected abundance of
dense calcifications within an oligodendroglioma with no evidence of
hemorrhage.
related to the difference in resonant frequencies
between fat and water protons. This artifact is
displayed as a region of signal void at fat–water
interfaces and hyperintensity at water–fat interfaces,
along the frequency encoding axis.57-61
Dermoid Cysts
Dermoid cysts are benign, slowly growing cystic
lesions arising from ectodermal cells enclosed intracranially during embryogenesis that are filled with
lipid material, cholesterol, desquamated cells, and
keratinaceous debris. Dermoid cysts may contain skin
appendages, such as hair follicles, sweat glands, and
sebaceous glands, in addition to squamous epithelium.
Calcification is rare. They are found most commonly
in the parasellar region. They are well-circumscribed
extra-axial lesions with high signal on T1-weighted
images and variable signal intensity on T2-weighted
images. The lipid content of dermoid cysts causes
high-signal intensity on T1-weighted scans (Fig 25).
The fluid–fluid or fluid– debris levels may be present
within the cystic lesions. They do not enhance after
gadolinium administration. Dermoid cysts may leak or
rupture, releasing their content into the subarachnoid
210
Fig. 30. Spin-echo T1-weighted coronal image (A) and axial computed tomography image (B) of a 63-year-old female patient with
left-sided decrease of hearing reveals a nodular mass attached to the
dura just at the postero-medial margin of internal acoustic canal with
peripheral hypointense and central hyperintense appearance (white
arrow) on T1-weighted image, and hyperdense lesion (black arrow) on
tomography. The mass was surgically removed with the resultant
diagnosis of dural osteoma.
space and ventricular system. The resultant appearance of scattered lipid droplets within sulci and cisterns is seen (Fig 26). Some patients may experience
chemical meningitis, particularly when the contents of
a ruptured cyst extend beyond the ventricles to involve
the subarachnoid spaces. The rupture of dermoid cysts
may even cause noncommunicating hydrocephalus.53,57,62,63
Lipomatous Meningioma
Meningiomas are the most common intracranial
extra-axial tumors. They are usually benign, slowly
Curr Probl Diagn Radiol, September/October 2003
Fig. 31. Spin-echo T1-weighted axial image of a 38-year-old male
patient who presented in a stuporous state with hepatic cirrhosis and
high serum level of ammonium reveals symmetrical high signal intensity
of bilateral globus pallidi (arrows). Additional high signal-intensity
areas in the cerebral peduncles, dentate nuclei of cerebellum with the
clinical findings of patient suggested the diagnosis of acquired hepatocerebral degeneration.
growing neoplasms; however, they may rarely reveal
malignant behavior. They are well-circumscribed, dural-based lesions. They may cause compression of
adjacent brain parenchyma, encasement of arteries,
and compression of dural venous sinuses. The most
common locations for meningiomas are the parasagittal area, convexity, sphenoid ridge, parasellar area,
posterior fossa, optic nerve sheath, and intraventricular
region. They are usually isointense with cortical gray
matter on all MRI sequences with a prominent gadolinium enhancement. Calcification is a frequently detected characteristic of the lesions. Necrosis, cysts, and
hemorrhage may be associated in around 25% of the
masses. Dural tail reaction that is characterized by
thickened dura tapering away from the tumor is
characteristic, but not pathognomonic, for meningiomas.55,64,65
Lipomatous meningiomas are relatively rare, benign tumors that are characterized either by an admixture of mature adipocytes and meningioma or the
production of lipids by neoplastic meningothelial cells
Curr Probl Diagn Radiol, September/October 2003
Fig. 32. Spin-echo T1-weighted axial image (A) and sagittal image
(B) of 13-year-old female patient with the diagnosis of Wilson’s
disease show symmetrical high-signal intensity characteristics of bilateral globus pallidi and nigrostriatal pathways (arrows).
assuming a lipoblast-like appearance. The lipomatous
changes are thought to appear as a result of metaplastic
changes of meningothelial cells. The signal intensity
of lipomatous meningiomas is heterogeneous, but
hyperintense components are detected on both T1- and
T2-weighted images secondary to the presence of lipid
(Fig 27).64-67
211
Fig. 34. Spin-echo T1-weighted sagittal image of a 15-year-old male
patient with growth hormone deficiency shows a bright spot along the
floor of third ventricle (arrow) associated with the absence of pituitary
stalk and hypoplasia of adenohypophysis within the sella turcica.
Lesions with Calcified or Ossified
Components
Endocrine–Metabolic Disorders
The signal intensity of calcification is usually characterized by hypointense appearance in both T1- and
T2-weighted sequences on MRI. However, the presence
of diamagnetic calcium salts and association with other
paramagnetic cations, such as iron and manganese, may
paradoxically cause T1 shortening in some cases. The
size and configuration of calcium deposits are also
important determinants of the signal intensity of calcification. Hypo- or hyperparathyroidism, hypothyroidism,
mitochondrial encephalopathies, Fahr disease (familial
cerebrovascular ferrocalcinosis or bilateral striopallidodentate calcinosis) (Fig 28), carbon monoxide poisoning, and idiopathic calcification are commonly presented with intracranial calcifications.68-72
Fig. 33. Spin-echo T1-weighted axial image (A) and FLAIR axial
image (B) of a 41-year-old male patient with a history of surgical
removal of melanotic malignant melanoma from the right supraorbital
region reveal nodular areas (arrows) of right temporal lobe and corpus
callosum with high signal intensity on T1-weighted sequence, and
iso-mild hyperintense signal to gray matter on FLAIR sequence. The
lesions were surgically removed with the resultant diagnosis of nonhemorrhagic metastases of melanoma.
Calcified Neoplasms
Primary neoplasms, such as craniopharyngioma,
oligodendroglioma (Fig 29), choroid plexus papilloma, meningioma, pituitary adenoma, astrocytoma,
pericallosal lipoma, ependymoma, and metastases
from lung, breast, and gastrointestinal carcinomas may
contain areas of calcification.47,72-78
Infections
Previous inflammatory diseases developing secondary to toxoplasmosis, cytomegalovirus, rubella, her-
212
Curr Probl Diagn Radiol, September/October 2003
Fig. 35. Spin-echo T1-weighted axial image of a 42-year-old male
patient with the diagnosis of multiple sclerosis reveals multiple periventricular chronic plaque lesions with peripheral high signal intensity.
Note the association of ventricular enlargement concordant with
longstanding course of the disease.
incompletely understood. Enlargement and hyperplasia of protoplasmic astrocytes in the cerebral and
cerebellar cortex, basal ganglia, and diencephalic nuclei are seen in acute forms of hepatocerebral degeneration. Gray and white matter necrosis with cavitation, gliosis, and myelin degeneration may occur in
chronic forms. A variety of different MRI findings
have been reported in these patients. Hyperintense
signal changes on T1-weighted sequences and hypointense or isointense signal changes on T2-weighted
sequences have been reported in the basal ganglia,
subthalamic area, quadrigeminal plate, cerebral peduncles, internal capsules, and anterior pituitary gland
(Fig 31). Bilateral symmetrical hyperintensity of the
globus pallidus particularly is reported in T1-weighted
images in 52% to 100% of patients with chronic liver
diseases. This hyperintense signal change on T1weighted images is reported to be caused by the
deposition of manganese, most probably reflecting the
presence of an adaptive process designed to improve
the efficacy of ammonia detoxification by astrocytes.
The signal hyperintensity may reverse after liver
transplantation.82-84
Wilson’s Disease
pes, tuberculosis, and cysticercosis infections may
cause foci of calcifications.10,68,70
Dural Osteomas
Osteomas are benign proliferations of bone located
in the skull or paranasal sinuses. The dural osteomas
are very rarely detected lesions. The signal intensity of
dural osteomas is characterized by a hyperintense
appearance on T1- and T1-weighted images, probably
secondary to fibro-fatty stromal components (Fig
30).79-81
Lesions with Other Mineral
Accumulation
Acquired Hepatocerebral Degeneration
Acquired hepatocerebral degeneration is a rare,
nonhereditary, irreversible neurologic syndrome that
occurs in patients with chronic liver disease associated
with multiple metabolic insults. Most of the disorders
of cerebral function develop rapidly and result mainly
in a disturbance of consciousness ranging from confusion to stupor to coma and death. The pathophysiology and the locations of the cerebral injuries are
Curr Probl Diagn Radiol, September/October 2003
Wilson’s disease is an autosomal-recessive disease
that is characterized by decreased functional serum
ceruloplasmin levels and altered copper metabolism
with increased urinary excretion of copper. The disease usually presents in childhood with abnormal toxic
copper deposition in tissues, resulting in cirrhosis, and
degenerative changes in the basal ganglia and brainstem. The signal-intensity changes on MRI are similar
to those of acquired hepatocerebral degeneration (Fig
32).85-87
Melanin-containing Lesions
Melanoma
Melanoma develops from melanocytes that are
derived from neural crest cells. Melanoma typically
causes hemorrhagic intracranial metastases (Fig 16);
however, cerebral metastases may demonstrate hyperintense appearances on T1-weighted images and almost isointense to gray-matter appearance on T2weighted images secondary to melanotic melanoma,
even in the absence of hemorrhage (Fig 33). The
presence of melanin molecules within the melanocytes
with its unpaired electrons is believed to account for
213
Fig. 36. Spin-echo T1-weighted axial image (A) and fast spin-echo T2-weighted axial image (B) of a 10-year-old male patient with the diagnosis
of neurofibromatosis type I reveal heterogeneously high signal-intensity areas of bilateral globus pallidi, internal capsules, and partially putamina
on T1-weighted image and corresponding iso- to mildly hyperintense signal areas on T2-weighted image.
the observed paramagnetic effects on signal intensity.
Amelanotic metastases from primary melanomas are
not associated with shortening of T1 or T2 values in
the absence of hemorrhage.43,72,88
Neurocutaneous Melanosis
Neurocutaneous melanosis is a rare neuroectodermal dysplasia that is characterized by the proliferation of melanocytes in leptomeninges associated
with multiple congenital pigmented or giant hairy
cutaneous nevi. It may change into primary central
nervous system melanoma. The patients reveal multiple meningeal-based lesions usually less than 3 cm
in diameter with intermediate- to high-signal intensity on T1-weighted images and variable signal
intensity on T2-weighted images. The lesions reveal
strong gadolinium enhancement. Vermian hypoplasia, arachnoid cysts, and Dandy–Walker malformation may be seen in association with neurocutaneous
melanosis.88-90
214
Miscellaneous Lesions
Ectopic Neurohypophysis
The normal neurohypophysis demonstrates highsignal intensity on T1-weighted images. T1 shortening
of the neurohypophysis seems to reflect enhanced
relaxation of water protons in the vicinity of neurosecretory vesicles that function in the storage and secretion of oxytocin and vasopressin. On sagittal MRI, the
neurohypophyseal focus of T1 shortening lies immediately anterior to the dorsum sella and has been
referred to as the posterior pituitary bright spot. The
bright spot can be seen as an ectopic zone of T1
shortening representing the functional neurohypophysis along the floor of the third ventricle (Fig 34). This
bright spot fails to develop in the normal intrasellar
location because of impaired formation of the pituitary
infundibulum, which normally transmits carrier-bound
neuropeptide hormones from the hypothalamus to the
neurohypophysis. The failure of development of the
pituitary infundibulum and hypoplasia of the adeno-
Curr Probl Diagn Radiol, September/October 2003
hypophysis may be isolated abnormalities or part of a
midline dysgenesis syndrome.47,91,92
Chronic Phase of Multiple Sclerosis
Multiple sclerosis is the most common demyelinating disease. The plaque lesions of multiple sclerosis have usually low- to intermediate-signal intensity on T1-weighted images and high-signal
intensity on T2-weighted images with or without
gadolinium enhancement depending on the activity
of disease. Chronic plaque lesions of multiple sclerosis may be characterized by peripheral T1 shortening (Fig 35). The basis for such peripheral T1
shortening is undetermined but may be related to the
accumulation of myelin degradation products. The
finding is normally noted in the context of longstanding disease. Long-standing multiple sclerosis
may also be associated with ventricular and sulcal
enlargement, associated with variable degrees of
cerebral atrophy.93-97
Neurofibromatosis Type I
Neurofibromatosis type I is the most common
neurocutaneous syndrome with an autosomal-dominant transmission. Focal areas of high-signal intensity
are present in the basal ganglia (most commonly
globus pallidi), thalami, hippocampal gyri, and brainstem. The lesions are benign, multiple, nonenhancing
signal areas with minimal or no mass effect. They are
thought to represent hamartomas, spongiotic, or vacuolar changes of myelin with usually high signal on
T2-weighted images and intermediate to slightly high
signal on T1-weighted images (Fig 36). Although the
precise reason for the signal-intensity changes is not
clear, it may be attributed to an admixture of areas of
myelin breakdown and remyelination of initially destroyed myelin and probable association of microcalcifications. They may show spontaneous regression
over time by serial MRI.98-101
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