AJR 2000; 174:289-299
© American Roentgen Ray Society
Centennial Dissertation Honoring
Arthur W. Goodspeed, MD and James B. Bullitt, MD |
CT and MR Imaging of Nontraumatic Neurologic Emergencies
James M. Provenzale1
1
Department of Radiology, Duke University Medical Center, Box 3808, Durham, NC
27710.
Received September 23, 1999;
accepted after revision October 25, 1999.
Address correspondence to J. M. Provenzale.
Introduction
The emergency department physician who is ordering a neuroimaging study
must balance multiple conflicting concerns. First, establishing a diagnosis
quickly and accurately is necessary in an era when patients view emergency
department services as a substitute for routine health care. The expectation
of many patients that a definitive diagnosis for nonacute medical problems
will be reached during an emergency department visit causes an increased
strain on emergency department resources. One result is that diagnostic tests,
including imaging studies, are overused. Second, concerns about legal
liability lead some emergency department physicians to order unnecessary tests
as a means of avoiding allegations of misdiagnosis or delay in diagnosis.
Third, emergency department physicians must limit unnecessary expenditures
while still providing appropriate medical care, a task made more difficult by
the financial constraints of managed health care. This complex decision-making
process is made even more difficult by the lack of scientifically validated
algorithms for ordering CT and MR imaging.
Four nontraumatic neurologic emergencies encountered by the emergency
department radiologist will be presented, with an emphasis on clinical
features and imaging findings that aid in the diagnosis. Some nontraumatic
neurologic emergencies (e.g., stroke and nontraumatic subarachnoid hemorrhage)
are more common than the entities discussed here but are well described in
numerous sources [1,
2].
Dural Sinus Thrombosis
Dural sinus thrombosis is a neurologic condition that occurs in young and
middle-aged adults. This condition can present with a number of clinical
features caused by either increased intracranial pressure (manifested by
headache, papilledema, and confusion) or ischemia and infarction
[3,
4]. The major entities with
which dural sinus thrombosis can be confused on clinical grounds are migraine
headache and pseudotumor cerebri. CT and MR imaging play a fundamental role in
distinguishing dural sinus thrombosis from these entities. The superior
sagittal sinus and transverse sinus are the dural sinuses most commonly
affected. Venous infraction caused by retrograde extension of thrombus into
the cerebral veins is one of the feared complications of dural sinus
thrombosis (Fig. 1A,
1B,
1C). In addition, marked
increases in intracranial pressure as a result of venous outflow obstruction
can lead to coma and death [3,
4]. For these reasons, early
identification of dural sinus thrombosis is important and may be
lifesaving.
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Fig. 1A. —Hemorrhagic venous infarction in 41-year-old woman with dural sinus
thrombosis. Unenhanced axial CT scan shows hyperdense appearance of superior
sagittal sinus (arrowheads) and straight sinus (solid
arrow), consistent with thrombosis. Note hemorrhagic lesion in right
frontal lobe (open arrow). Subcortical location and hemorrhagic
nature of lesion are typical of venous infarction.
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Fig. 1B. —Hemorrhagic venous infarction in 41-year-old woman with dural sinus
thrombosis. Contrast-enhanced coronal T1-weighted MR image obtained same day
as A shows replacement of flow voids of superior sagittal sinus
(straight arrow) and straight sinus (curved arrow) by
thrombus that is isointense with gray matter. Note mild rim enhancement of
thrombus.
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Fig. 1C. —Hemorrhagic venous infarction in 41-year-old woman with dural sinus
thrombosis. Axial T2-weighted MR image shows more extensive region of
hemorrhage (arrows) than that seen in A. Note hypointense
signal intensity of thrombus in superior sagittal sinus (arrowheads),
which simulates flow void.
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A wide variety of factors predisposing to dural sinus thrombosis has been
reported; pregnancy and puerperium, oral contraceptive use, dehydration,
infection at sites adjacent to dural sinuses (e.g., mastoiditis), and
compression by tumor are the most common
[3,
4]. The role of hypercoagulable
states has attained increasing importance over the past few years, especially
in patients not having these risk factors
[5,
6]. Furthermore, the presence
of two factors may predispose patients to a much higher risk than only one.
For instance, one study found that women using oral contraceptives have a
13-fold risk of dural sinus thrombosis compared with age-matched control
subjects not using such medication; however, oral contraceptive users who have
a hereditary hypercoagulable state have a 30-fold risk
[7]. Activated protein C
resistance is one major form of hypercoagulable state that appears to increase
the risk of dural sinus thrombosis. This hypercoagulable state is found in
2-3% of control subjects, but in some studies, it has been reported in 10-21%
of patients with dural sinus thrombosis
[5,
6]. In a previous study at the
author's institution, four of the first five patients with dural sinus
thrombosis tested positive for activated protein C resistance
[8].
CT features of dural sinus thrombosis include a hyperdense dural sinus on
unenhanced CT (Figs. 2A,
2B,
3A,
3B and
3C) and an unenhanced central
portion of the affected sinus after administration of contrast material (the
"empty delta" sign)
[9]. However, the diagnosis of
dural sinus thrombosis is often difficult to establish on CT for a number of
reasons. The affected sinus may not be perpendicular to the imaging plane;
this position would render the empty delta sign useless. Also, a normal dural
sinus may appear hyperdense (especially in children). CT venography is a
recently developed imaging study that offers greater sensitivity and
specificity than routine contrast-enhanced CT in the diagnosis of dural sinus
thrombosis [10,
11]. On CT venography, dural
sinus thrombosis is seen as the absence of opacification of the affected dural
sinus on projectional images (Fig.
2A,
2B) and as a filling defect in
the dural sinus on source images
[10,
11].
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Fig. 2B. —Dural sinus thrombosis in 38-year-old woman with headache. CT
venogram, lateral view, shows opacification of anterior portion of superior
sagittal sinus (curved arrow), inferior sagittal sinus
(arrowheads), and internal cerebral veins (open arrow).
Posterior portion of superior sagittal sinus (solid arrows) is not
opacified because of thrombosis.
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Fig. 3A. —Transverse sinus thrombosis in 8-month-old female infant who had
recently undergone resection of suprasellar mass. Unenhanced axial CT scan
shows hyperdense appearance of left transverse sinus (arrowhead),
consistent with thrombosis. Note pneumocephalus (arrows) resulting
from recent surgery.
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Fig. 3B. —Transverse sinus thrombosis in 8-month-old female infant who had
recently undergone resection of suprasellar mass. Unenhanced axial T1-weighted
MR image shows abnormal signal (arrows) replacing expected flow void
in left transverse sinus.
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Fig. 3C. —Transverse sinus thrombosis in 8-month-old female infant who had
recently undergone resection of suprasellar mass. Collapsed image from
three-dimensional time-of-flight MR venogram (in which all data are viewed
looking caudad) shows normal flow in superior sagittal sinus (solid
straight arrow) and right transverse sinus (curved arrow) but
absence of flow in expected location of left transverse sinus (open
arrows).
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MR imaging also offers substantial benefits over conventional CT in the
diagnosis of dural sinus thrombosis. On MR imaging, dural sinus thrombosis is
manifested by replacement of the flow void of the dural sinuses or major veins
by abnormal signal intensity (Figs.
1A,
1B,
1C and
3A,
3B,
3C). On unenhanced T1-weighted
images, the thrombosed dural sinus generally appears isodense or hyperdense
relative to gray matter (Fig.
3A,
3B,
3C); after administration of
contrast material, the central portion of the sinus typically fails to enhance
[4] (Fig.
1A,
1B,
1C). On T2-weighted images, the
thrombosed dural sinus is typically hyperintense or isointense with gray
matter but may be hypointense and simulate a normal flow void
[4] (Fig.
1A,
1B,
1C). Typical MR venography
findings consist of the absence of signal consistent with thrombosis in the
affected dural sinus [12]
(Fig. 3A,
3B,
3C).
Venous infarction, a major complication of dural sinus thrombosis, is
typically subcortical and often hemorrhagic
[13] (Fig.
1A,
1B,
1C). The infarcts are in
relatively close proximity to the thrombosed dural sinus; on occasion,
infarcts reflecting thrombosis of veins coursing into the affected sinus may
be seen on each side of a thrombosed dural sinus. Information from
diffusion-weighted MR studies indicates that frank infarction may be preceded
by reversible vasogenic edema (seen as regions of decreased signal intensity
on diffusion-weighted images)
[14]. On MR perfusion imaging
studies, increased relative cerebral blood volume and prolonged mean transit
time, reflecting venous congestion, have been reported in areas of vasogenic
edema [14].
Typical treatment of dural sinus thrombosis consists of anticoagulation by
IV heparin followed by oral warfarin
[15]. This therapy is
generally successful, but in patients with advanced disease more aggressive
therapy is warranted. In such patients, infusion of thrombolytic agents with a
microcatheter positioned in the affected dural sinus has proven effective
[16]. Thrombosis of the deep
cerebral venous system (i.e., internal cerebral veins, vein of Galen, and
straight sinus) is a life-threatening condition because severe cerebral edema
and infarction of the basal ganglia and thalamus can result. Because risk of
permanent severe neurologic dysfunction and death is high and systemic
anticoagulation is often unsuccessful, aggressive measures such as direct
infusion of thrombolytic agents into the thrombus via a microcatheter placed
in the vein of Galen may be necessary
[17].
Reversible Posterior Leukoencephalopathy Syndrome
The reversible posterior leukoencephalopathy syndrome is clinically
manifested by headache, visual disturbance, decreased level of consciousness,
and seizures. The syndrome is known by other names such as hypertensive
encephalopathy and posterior reversible encephalopathy syndrome
[18,
19,
20,
21,
22,
23]. The syndrome typically
occurs in acute elevation of systemic blood pressure, in preeclampsia or
eclampsia, or after treatment with a variety of immunosuppressive agents
(e.g., cyclosporin A, cisplatin, FK-501, and tacrolimus)
[18,
22,
24]. Occasionally, reversible
posterior leukoencephalopathy syndrome may occur after only moderate elevation
of systemic blood pressure
[18,
19]. The exact mechanism by
which this syndrome occurs is not known with certainty, but recent evidence
points to vasogenic edema from loss of autoregulation in cerebral blood
vessels [19,
25]. Reversible posterior
leukoencephalopathy syndrome is an emergency condition because patients may
proceed to cerebral infarction and death if not appropriately treated
[19]. Treatment consists of
reversal of hypertension (if present) or removal of other causative
agents.
Typical imaging features of reversible posterior leukoencephalopathy
syndrome include hypodense regions within posterior white matter regions on
unenhanced CT scans and areas of hyperintense signal on T2-weighted MR images
[18,
20,
21,
22,
23,
24] (Fig.
4A,
4B). After administration of
contrast material, lesions do not enhance. Occasionally, cortical regions are
also involved. The predilection for involvement of white matter of the
occipital and parietal lobes is reported to result from decreased innervation
of arteries of these regions by autonomic fibers relative to the remainder of
the cerebral circulation [26].
After appropriate treatment, almost complete resolution of white matter
abnormalities is seen.
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Fig. 4A. —Posterior white matter abnormalities caused by reversible posterior
leukoencephalopathy syndrome in 38-year-old man with severe hypertension,
headache, vomiting, and seizures. Unenhanced axial CT scan shows bilateral
hypodense white matter lesions (arrowheads) that are more marked in
posterior brain regions.
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Fig. 4B. —Posterior white matter abnormalities caused by reversible posterior
leukoencephalopathy syndrome in 38-year-old man with severe hypertension,
headache, vomiting, and seizures. Axial T2-weighted MR image obtained 1 day
after A shows regions of hyperintense signal intensity
(arrows) in abnormal regions seen in A. Lesions terminate at
gray—white matter junction, consistent with vasogenic edema. After
control of hypertension, central nervous system symptoms resolved.
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Diffusion-weighted MR imaging has provided insights into the pathogenesis
of reversible posterior leukoencephalopathy syndrome by showing that signal
abnormalities on T2-weighted MR images are associated with vasogenic rather
than cytotoxic edema [19,
20,
25]. However, on
diffusion-weighted images, lesions of reversible posterior leukoencephalopathy
syndrome often appear isointense rather than hypointense as expected in
vasogenic edema [20]. This
finding is probably caused by the net effect of a combination of decreased
signal intensity on diffusion-weighted images (from vasogenic edema) and
increased signal intensity caused by T2 prolongation effects (T2
"shine-through" effect). Although lesions are often isointense
with normal brain tissue on diffusion-weighted images, on apparent diffusion
co-efficient maps increased signal intensity from heightened water
diffusibility (i.e., vasogenic edema) is seen
[20,
25].
Dissection of the Cervicocephalic Arteries
Dissection of the carotid and vertebral arteries was once considered
uncommon. However, improvements in carotid sonography and development of
cross-sectional imaging techniques such as MR imaging and CT angiography have
allowed more patients to be examined in a noninvasive manner. Thus, dissection
is diagnosed with increased frequency. This discussion centers on the use of
MR imaging and CT angiography to diagnosis dissection. Detailed discussion of
sonography of this entity can be found in a number of sources
[27,
28,
29,
30].
Patients typically present with headache or neck ache (approximately 75% of
patients with carotid dissection)
[31] (Fig.
5A,
5B,
5C,
5D). In rare instances,
patients may present with subarachnoid hemorrhage from rupture of the
intramural hematoma through the adventitia
[32]. Because headache and
neck ache are nonspecific and common in the general population, the diagnosis
of arterial dissection is often delayed, requiring multiple visits to
physicians. Nevertheless, the diagnosis should be strongly considered in
certain circumstances. Headache or neck ache with oculosympathetic paresis
(Horner's syndrome) should suggest the diagnosis of carotid dissection (Fig.
6A,
6B), especially if the
headache is retroorbital
[33].
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Fig. 5A. —Bilateral internal carotid artery dissections in 44-year-old man who
developed right-sided neck pain and right Horner's syndrome a few days after
downhill skiing. He had no history of direct trauma. Catheter angiogram of
right common carotid artery, lateral view, shows long segment of luminal
narrowing in high cervical segment (arrows), consistent with
dissection, and extending up to level of skull base.
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Fig. 5B. —Bilateral internal carotid artery dissections in 44-year-old man who
developed right-sided neck pain and right Horner's syndrome a few days after
downhill skiing. He had no history of direct trauma. Unenhanced axial
T1-weighted MR image shows narrowing of flow void of right internal artery
with eccentric hyperintense intramural hematoma that expands outer diameter of
artery (straight arrow). Note normal caliber of left internal carotid
artery (curved arrow).
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Fig. 5C. —Bilateral internal carotid artery dissections in 44-year-old man who
developed right-sided neck pain and right Horner's syndrome a few days after
downhill skiing. He had no history of direct trauma. Catheter angiogram of
left common carotid artery, lateral view, shows pseudoaneurysm
(arrow) resulting from dissection in cervical segment. Because
dissection did not extend to skull base, it is not seen in B.
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Fig. 5D. —Bilateral internal carotid artery dissections in 44-year-old man who
developed right-sided neck pain and right Horner's syndrome a few days after
downhill skiing. He had no history of direct trauma. Two-dimensional
time-of-flight MR angiogram shows, adjacent to left internal carotid artery,
small focal region (straight arrow) of abnormal flow, corresponding
to pseudoaneurysm seen in C. Note narrowing of right internal carotid
artery (curved arrow) corresponding to dissection in A.
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Fig. 6A. —Right internal carotid artery dissection in 42-year-old woman with
right-sided neck pain and oculosympathetic paresis (Horner's syndrome). Source
image from CT angiogram shows marked narrowing of right internal carotid
artery (curved arrow) compared with left internal carotid artery
(straight arrow) because of dissection. Note that soft tissue
immediately surrounding artery does not differ from normal muscle (unlike
appearance seen on MR image in Figure
5A,
5B,
5C,
5D).
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Fig. 6B. —Right internal carotid artery dissection in 42-year-old woman with
right-sided neck pain and oculosympathetic paresis (Horner's syndrome).
Three-dimensional reconstruction from CT angiogram of right internal carotid
artery shows long segment of arterial narrowing (arrows) beginning
distal to carotid bifurcation. Note more focal segment of narrowing
(arrowhead) in mid portion of stenosis.
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Although dissection can occur after trauma, it is largely unrecognized that
most dissections occur in the absence of trauma or after only trivial trauma
[34]. For this reason, the
diagnosis of dissection is often unsuspected when a history of trauma is not
evident. Because a number of risk factors predispose patients to arterial
dissection (e.g., underlying abnormalities of collagen fibers, fibromuscular
dysplasia, Marfan's syndrome, cystic medial necrosis, type IV Ehlers-Danlos
syndrome), one might consider these features useful to direct imaging studies
for patients at high risk of dissection
[35,
36,
37,
38,
39]. However, most patients
with arterial dissection do not have these diseases at presentation. This lack
of predisposing factors limits the importance of these features in
establishing the diagnosis.
Dissection of the cervicocephalic arteries is a neurologic emergency
because of the increased risk of cerebral infarction. Although infarction
occurs in only a minority of patients with dissection, in some studies it is
one of the most common causes of stroke in young and middle-aged adults
[33,
40]. The cause of cerebral
infarction in most patients is the propagation of emboli from
fibrin—platelet aggregates that form at sites of intimal injury, rather
than a low-flow state caused by arterial occlusion. Infarction can occur while
the artery is merely stenosed.
The most common site of extracranial carotid dissection is a few
centimeters above the carotid bifurcation (Figs.
5A,
5B,
5C,
5D and
6A,
6B), distal to the typical
site of atheromatous disease
[36,
39]. The most common site of
intracranial carotid dissection (much less frequent than the extracranial
form) is the supraclinoid segment of the internal carotid artery. Vertebral
artery dissection is less common than carotid artery dissection but may lead
to more profound neurologic deficits than carotid dissection because brainstem
infarction may result. The most common site of vertebral artery dissection is
at the level of the C1—C2 complex where the artery courses over the
lateral masses of these vertebral bodies
[41].
Before development of MR imaging, catheter angiography was considered the
study of choice for depiction of carotid and vertebral dissection (Figs.
5A,
5B,
5C,
5D and
7A,
7B,
7C). On catheter angiography,
typical findings included arterial stenosis (Fig.
5A,
5B,
5C,
5D) or occlusion alone or in
association with pseudoaneurysm formation (Figs.
5A,
5B,
5C,
5D and
7A,
7B,
7C). Because of its
noninvasive nature allowing thin-section images through vessels, MR imaging
has replaced catheter angiography for the diagnosis of arterial dissection at
many institutions (Figs. 5A,
5B,
5C,
5D and
7A,
7B,
7C). The principal findings on
MR imaging are narrowing of the flow void of the arterial lumen (or in the
case of occlusion, replacement of the flow void by abnormal signal) and within
the arterial wall a periarterial collar of abnormal signal (Fig.
5A,
5B,
5C,
5D) representing intramural
hemorrhage [34,
42,
43,
44,
45]. The periarterial collar
frequently widens the external diameter of the artery (Fig.
5A,
5B,
5C,
5D) and in one study was
particularly helpful in establishing the diagnosis
[42]. The periarterial collar
is frequently eccentric, with a wider diameter on one side of the lumen than
on the other side [42] (Fig.
5A,
5B,
5C,
5D). During the first few days
after dissection, the periarterial collar can be relatively isointense
compared with muscle on both T1- and T2-weighted images
[43,
46]. At this point, the
diagnosis can be made by the presence of narrowed arterial flow void and
widening of the outer diameter of the artery
[44]. Fat-suppressed
T1-weighted images can increase the conspicuity of the hematoma
[44]. Pseudoaneurysms are seen
as either focal regions of abnormal signal intensity (representing partial
thrombosis or slow flow) (Fig.
7A,
7B,
7C) or a circular or oval
region of flow void larger than the parent artery. After the first few days,
the periarterial collar becomes hyperintense on T1-weighted images (Fig.
5A,
5B,
5C,
5D) and subsequently
hyperintense on T2-weighted images
[47]. This finding is present
for months [32,
43].
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Fig. 7A. —Pseudoaneurysm formation caused by vertebral artery dissection in
50-year-old woman with headache. Unenhanced axial T1-weighted MR image shows
mass (arrow) adjacent to medulla in expected location of right
vertebral artery.
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Fig. 7B. —Pseudoaneurysm formation caused by vertebral artery dissection in
50-year-old woman with headache. Source image from three-dimensional
time-of-flight MR angiogram shows flow (arrow) consistent with right
vertebral artery pseudoaneurysm within mass shown in A. Absence of flow
void in lesion is probably caused by slow flow in pseudoaneurysm.
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Fig. 7C. —Pseudoaneurysm formation caused by vertebral artery dissection in
50-year-old woman with headache. Catheter angiogram of right vertebral artery,
lateral view, shows abnormal dilatation of artery (arrow) consistent
with pseudoaneurysm.
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On MR angiography, the findings of arterial dissection include narrowing of
the arterial lumen (Fig. 5A,
5B,
5C,
5D) and pseudoaneurysm
formation (seen as a region of bright signal projecting outside the expected
confines of the arterial lumen) (Fig.
7A,
7B,
7C). On source images (Fig.
7A,
7B,
7C), the periarterial rim
typically has signal intensity that is between the bright signal of flowing
blood and the dark signal of background tissue. The time-of-flight MR
angiography technique is generally favored for diagnosis of arterial
dissection because the periarterial signal abnormality will typically be seen
as a result of T1 shortening
[34,
47]. On the other hand,
intramural hematoma will not generally be seen on phase-contrast MR imaging
because only moving blood causing phase shifts will generate signal intensity
[47]. Specific techniques can
be used to better depict the intramural hematoma. One method for isolating the
intramural hematoma from the bright signal of flowing blood uses a saturation
pulse placed caudad to the site of suspected dissection. This pulse will
saturate arterial flow signal within the slab (black blood technique)
[47]. Intramural hematoma will
then appear as a region of hyperintense signal intensity adjacent to the
affected artery. Some investigators have claimed that a three-dimensional
spoiled gradient-echo technique is superior to MR angiography in evaluation of
vertebrobasilar artery dissections because it is more sensitive for depiction
of a false lumen [45,
46]. However, until controlled
trials comparing the two methods are performed, spin-echo MR imaging and MR
angiography will continue to remain the preferred MR methods for diagnosis of
arterial dissection.
The development of CT angiography using helical techniques has allowed
rapid thin-section depiction of vessels and excellent anatomic detail on
three-dimensional reconstructed images. The finding of arterial dissection on
source images is revealed by narrowing or occlusion of the contrast-filled
lumen (Fig. 6A,
6B), alone or combined with a
contrast-filled pseudoaneurysm
[48]. Unlike MR imaging, in
which the intramural hematoma typically has abnormal signal characteristics
that are conspicuous, on CT angiography the hematoma appears bland and
isodense relative to soft tissue (Fig.
6A,
6B). However, on both studies
the residual lumen is generally eccentric in location relative to the hematoma
[49].
Herpes Simplex Virus Type I Encephalitis
Encephalitis caused by herpes simplex virus type 1 is the most common cause
of sporadic (nonepidemic) encephalitis in immunocompetent individuals in the
United States [50].
Encephalitis resulting from this agent is a neurologic emergency because it is
associated with high morbidity and mortality and because the infection is
eminently treatable in early stages by acyclovir therapy. Patients present
with low-grade fever, headache, and mental status alterations. Until
relatively recently, the definitive method of diagnosis was brain biopsy
[51]. However, identification
of the virus in cerebrospinal fluid via an amplification method using a
polymerase chain reaction technique has become possible. This technique
substantially reduces the need for biopsy
[52].
In the early stages of the infection, CT changes indicating herpes simplex
virus type 1 are subtle or absent. In one recent study of children with a
variety of types of encephalitis, only two of 10 patients who underwent CT
during the first 6 days after the onset of symptoms had abnormal findings
[53]. When present on
unenhanced CT, early abnormal findings may include a mild decrease in
attenuation of one or both temporal lobes and insula, subtle effacement of
temporal lobe sulci, and narrowing of the sylvian fissure
[54]. In later stages,
affected regions further decrease in attenuation, and parenchymal swelling
increases (Fig. 8A,
8B,
8C,
8D). At this point, lesions
also become more extensive and occasionally extend to include inferior
surfaces of the frontal lobes. CT contrast enhancement is usually mild or
absent [55].
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Fig. 8A. —61-year-old woman with 6-day history of encephalopathy caused by
herpes simplex type 1 encephalitis. Unenhanced axial CT scan shows right
temporal lobe hypodensity and swelling (solid arrow), narrowing of
right sylvian fissure, and hypodensity in right insula (open
arrows).
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Fig. 8B. —61-year-old woman with 6-day history of encephalopathy caused by
herpes simplex type 1 encephalitis. Contrast-enhanced axial T1-weighted MR
image obtained 2 days after A shows mild gyriform contrast enhancement
of right temporal lobe (arrowheads). Note absence of right temporal
lobe sulci (arrows) caused by swelling, compared with left temporal
lobe.
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Fig. 8C. —61-year-old woman with 6-day history of encephalopathy caused by
herpes simplex type 1 encephalitis. Axial T2-weighted MR image shows increased
signal intensity in right temporal lobe (open arrows) and inferior
frontal region (solid arrow).
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Fig. 8D. —61-year-old woman with 6-day history of encephalopathy caused by
herpes simplex type 1 encephalitis. Axial T2-weighted MR image shows increased
signal intensity in right insula (open arrows) and temporal lobe,
anterior aspect of cingulate gyrus and subcallosal region (curved
arrow), and left insula (solid straight arrow). Note sparing of
basal ganglia.
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|
MR imaging is more sensitive than CT in detecting brain involvement by
herpes simplex 1 encephalitis because of the high signal contrast in affected
regions relative to uninvolved brain tissue on T2-weighted MR images
[56] (Fig.
8A,
8B,
8C,
8D). Lesions that appear
hyperintense on T2-weighted MR images are more extensive than on CT images
obtained at the same stage (Fig.
8A,
8B,
8C,
8D). On unenhanced T1-weighted
images, lesions appear mildly or moderately hypointense; contrast enhancement
is usually mild, with a gyriform or patchy pattern of enhancement (Fig.
8A,
8B,
8C,
8D). Small foci of hemorrhage
are seen commonly on MR imaging and were reported in 50% of patients in one
small series [57]. Variations
from the typical pattern of cerebral involvement include contrast enhancement
of the trigeminal nerve or other cranial nerves and extension of abnormal
signal into the cingulate gyrus (Fig.
8A,
8B,
8C,
8D) or brainstem
[58,
59]. (Contrast enhancement of
the trigeminal nerve may reflect reactivation of virus from a previous latent
infection of the trigeminal ganglion, and extension of the abnormal signal
into the cingulate gyrus may reflect transmission of the infection from the
hippocampus along its efferent pathways.) Lack of basal ganglia involvement
despite involvement of the adjacent internal capsule is common (Fig.
8A,
8B,
8C,
8D) and may be one means of
distinguishing herpes simplex 1 encephalitis from other entities (e.g.,
infarction) and other forms of encephalitis
[57]. For example, basal
ganglia involvement is common in eastern equine encephalitis
[60]. Herpes simplex 1
encephalitis can further be distinguished from infarction because encephalitis
frequently involves both the medial and lateral aspects of the temporal lobe
and involves territory supplied by both the middle cerebral artery and the
posterior cerebral artery (Figs.
8A,
8B,
8C,
8D and
9A,
9B). This pattern would be
atypical for infarction. Herpes simplex 1 encephalitis can be distinguished
from a neoplasm involving the temporal lobe because the inferior frontal lobe
and contralateral temporal lobe and insula are frequent sites for herpes
simplex 1 encephalitis, but not for tumors (Figs.
8A,
8B,
8C,
8D and
9A,
9B).
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Fig. 9A. —50-year-old man with 4-day history of confusion and somnolence
caused by herpes simplex type 1 encephalitis. Axial T2-weighted MR image shows
markedly increased signal in left temporal lobe and mildly increased signal
intensity in right medial temporal lobe (arrow). Findings of diffuse
bilateral temporal lobe involvement would not be expected in tumor or
infarction.
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Fig. 9B. —50-year-old man with 4-day history of confusion and somnolence
caused by herpes simplex type 1 encephalitis. Coronal contrast-enhanced
T1-weighted MR image shows thick contrast enhancement in medial left temporal
lobe (straight arrows) and smaller region of contrast enhancement in
right hippocampus (curved arrow). Compare thickness of contrast
enhancement in left temporal lobe with thin gyriform enhancement seen in
Figure 8A,
8B,
8C,
8D.
|
|
Recent developments in MR imaging allow even more sensitive detection of
herpes simplex 1 encephalitis than is possible with routine spinecho MR
imaging. Fluid attenuated inversion recovery (FLAIR) technique is reported to
define the extent of herpes simplex 1 encephalitis involvement better than
routine spin-echo images [61,
62]. Diffusion-weighted MR
imaging is another relatively recent advancement that is sensitive to brain
alterations in encephalitis
[63]. During the acute stage
of the infection, affected brain regions are seen as areas of increased signal
on diffusion-weighted images, probably from cytotoxic edema. Although
published reports of diffusion-weighted MR evaluation of encephalitis are
still limited, occasionally FLAIR imaging is more sensitive than
diffusion-weighted MR imaging for depiction of brain lesions, possibly because
of relatively minor degrees of cytotoxic edema in some patients
[63]. MR magnetization
transfer technique has been used as a means of better depicting the extent of
involvement compared with routine contrast-enhanced T1-weighted imaging. Using
this technique, areas of abnormal enhancement are occasionally more extensive
than regions of involvement as shown on spin-echo T2-weighted images
[64].
Summary
This review has highlighted some of the disease processes that produce
diagnostic difficulty in the emergency neuroradiology setting. Because
radiologists are often the first individuals to consider these entities, they
must be familiar with the clinical features that suggest the diagnosis.
Furthermore, acquaintance with the various imaging findings of these diseases
will allow early diagnosis and will help limit the severe complications that
follow these neurologic emergency conditions if left untreated.
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Introduction
Dural Sinus Thrombosis
