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he emergency department physi-

cian who is ordering a neuroimag-

ing study must balance multipleconflicting concerns. First, establishing a di-

agnosis quickly and accurately is necessary in

an era when patients view emergency depart-

ment 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 emer-

gency department visit causes an increased

strain on emergency department resources.

One result is that diagnostic tests, including

imaging studies, are overused. Second, con-

cerns about legal liability lead some emer-

gency department physicians to order

unnecessary tests as a means of avoiding alle-gations of misdiagnosis or delay in diagnosis.

Third, emergency department physicians must

limit unnecessary expenditures while still pro-

viding 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 emergen-

cies encountered by the emergency depart-

ment radiologist will be presented, with an

emphasis on clinical features and imaging

findings that aid in the diagnosis. Some non-traumatic neurologic emergencies (e.g.,

stroke and nontraumatic subarachnoid hem-

orrhage) are more common than the entities

discussed here but are well described in nu-

merous sources [1, 2].

Dural Sinus Thrombosis

Dural sinus thrombosis is a neurologic con-

dition that occurs in young and middle-agedadults. This condition can present with a num-

ber of clinical features caused by either in-

creased intracranial pressure (manifested by

headache, papilledema, and confusion) or is-

chemia and infarction [3, 4]. The major entities

with which dural sinus thrombosis can be con-

fused on clinical grounds are migraine head-

ache and pseudotumor cerebri. CT and MR

imaging play a fundamental role in distinguish-

ing dural sinus thrombosis from these entities.

The superior sagittal sinus and transverse sinus

are the dural sinuses most commonly affected.

Venous infarction caused by retrograde exten-

sion of thrombus into the cerebral veins is oneof the feared complications of dural sinus

thrombosis (Fig. 1). In addition, marked in-

creases in intracranial pressure as a result of

venous outflow obstruction can lead to coma

and death [3, 4]. For these reasons, early identi-

fication of dural sinus thrombosis is important

and may be lifesaving.

A wide variety of factors predisposing to

dural sinus thrombosis has been reported;

pregnancy and puerperium, oral contracep-

tive use, dehydration, infection at sites adja-

cent to dural sinuses (e.g., mastoiditis), and

compression by tumor are the most common

[3, 4]. The role of hypercoagulable states hasattained 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 pa-

tients to a much higher risk than only one.

T

CT and MR Imaging of NontraumaticNeurologic Emergencies

James M. Provenzale

1

Centennial Dissertation

Honoring Arthur W. Goodspeed, MDand James B. Bullitt, MD

Arthur W. Goodspeed4th President

19031904

James B. Bullitt5th President

19041905

Received September 23, 1999; accepted after revision October 25, 1999.

1

Department of Radiology, Duke University Medical Center, Box 3808, Durham, NC 27710. Address correspondence to J. M. Provenzale.

AJR2000;174:289299 0361803X/00/1742289 American Roentgen Ray Society

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BA

C

Fig. 1.Hemorrhagic venous infarction in 41-year-old woman with dural sinus thrombosis.A, Unenhanced axial CT scan shows hyperdense appearance of superior sagittal sinus(arrowheads) and straight sinus (solidarrow), consistent with thrombosis. Note hemor-rhagic lesion in right frontal lobe (open arrow). Subcortical location and hemorrhagic na-ture of lesion are typical of venous infarction.B, Contrast-enhanced coronal T1-weighted MR image obtained same day as A shows re-placement 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 enhance-ment of thrombus.C, 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 si-nus (arrowheads), which simulates flow void.

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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 contracep-

tive users who have a hereditary hypercoag-

ulable state have a 30-fold risk [7].

Activated protein C resistance is one major

form of hypercoagulable state that appearsto increase the risk of dural sinus thrombo-

sis. This hypercoagulable state is found in

23% of control subjects, but in some stud-

ies, it has been reported in 1021% of pa-

tients with dural sinus thrombosis [5, 6]. In

a previous study at the authors institution,

four of the first five patients with dural si-

nus thrombosis tested positive for activated

protein C resistance [8].

CT features of dural sinus thrombosis in-

clude a hyperdense dural sinus on unen-

hanced CT (Figs. 2 and 3) and an unenhanced

central portion of the affected sinus after ad-

ministration of contrast material (the emptydelta sign) [9]. However, the diagnosis of

dural sinus thrombosis is often difficult to es-

tablish 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 (espe-

cially in children). CT venography is a re-

cently developed imaging study that offers

greater sensitivity and specificity than routine

contrast-enhanced CT in the diagnosis of du-

ral sinus thrombosis [10, 11]. On CT venog-

raphy, dural sinus thrombosis is seen as the

absence of opacification of the affected dural

sinus on projectional images (Fig. 2) and as a

filling defect in the dural sinus on source im-

ages [10, 11].

MR imaging also offers substantial bene-fits over conventional CT in the diagnosis of

dural sinus thrombosis. On MR imaging, du-

ral sinus thrombosis is manifested by replace-

ment of the flow void of the dural sinuses or

major veins by abnormal signal intensity

(Figs. 1 and 3).

On unenhanced T1-weighted

images, the thrombosed dural sinus generally

appears isodense or hyperdense relative to

gray matter (Fig. 3); after administration of

contrast material, the central portion of the si-

nus typically fails to enhance [4] (Fig. 1). On

T2-weighted images, the thrombosed dural

sinus is typically hyperintense or isointense

with gray matter but may be hypointense andsimulate a normal flow void [4] (Fig. 1). Typ-

ical MR venography findings consist of the

absence of signal consistent with thrombosis

in the affected dural sinus [12] (Fig. 3).

Venous infarction, a major complication of

dural sinus thrombosis, is typically subcortical

and often hemorrhagic [13] (Fig. 1). The in-

farcts 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 re-

versible vasogenic edema (seen as regions of

decreased signal intensity on diffusion-

weighted images) [14]. On MR perfusion im-

aging studies, increased relative cerebral bloodvolume and prolonged mean transit time, re-

flecting venous congestion, have been reported

in areas of vasogenic edema [14].

Typical treatment of dural sinus thrombosis

consists of anticoagulation by IV heparin fol-

lowed by oral warfarin [15]. This therapy is

generally successful, but in patients with ad-

vanced disease more aggressive therapy is

warranted. In such patients, infusion of throm-

bolytic 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 Ga-

len, and straight sinus) is a life-threatening con-dition because severe cerebral edema and

infarction of the basal ganglia and thalamus can

result. Because risk of permanent severe neuro-

logic dysfunction and death is high and sys-

temic anticoagulation is often unsuccessful,

aggressive measures such as direct infusion of

thrombolytic agents into the thrombus via a mi-

crocatheter placed in the vein of Galen may be

necessary [17].

Fig. 2.Dural sinus thrombosis in 38-year-old woman with headache.A, Unenhanced axial CT scan shows hyperdense appearance of superior sagittal sinus (arrows), consistent with thrombosis.B, CT venogram, lateral view, shows opacification of anterior portion of superior sagittal sinus (curved arrow), inferior sagittal sinus (arrowheads), and internal cerebralveins (open arrow). Posterior portion of superior sagittal sinus (solidarrows) is not opacified because of thrombosis.

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Reversible Posterior

Leukoencephalopathy Syndrome

The reversible posterior leukoencephalopa-

thy syndrome is clinically manifested by head-

ache, visual disturbance, decreased level of

consciousness, and seizures. The syndrome is

known by other names such as hypertensive en-

cephalopathy and posterior reversible encepha-

lopathy syndrome [1823]. The syndrome

typically occurs in acute elevation of systemic

blood pressure, in preeclampsia or eclampsia, or

after treatment with a variety of immunosup-

pressive agents (e.g., cyclosporin A, cisplatin,

FK-501,

and tacrolimus) [18, 22, 24]. Occa-

sionally, reversible posterior leukoencephalopa-

thy syndrome may occur after only moderate

elevation of systemic blood pressure [18, 19].

The exact mechanism by which this syndrome

BA

Fig. 3.Transverse sinus thrombosis in 8-month-old female infant whohad recently undergone resection of suprasellar mass.A, Unenhanced axial CT scan shows hyperdense appearance of lefttransverse sinus (arrowhead), consistent with thrombosis. Note pneu-mocephalus (arrows) resulting from recent surgery.B, Unenhanced axial T1-weighted MR image shows abnormal signal(arrows) replacing expected flow void in left transverse sinus.C, Collapsed image from three-dimensional time-of-flight MR venogram (inwhich all data are viewed looking caudad) shows normal flow in superiorsagittal sinus (solid straight arrow) and right transverse sinus (curvedarrow) but absence of flow in expected location of left transverse sinus(open arrows).

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occurs is not known with certainty, but recent

evidence points to vasogenic edema from lossof 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]. Treat-

ment consists of reversal of hypertension (if

present) or removal of other causative agents.

Typical imaging features of reversible pos-

terior leukoencephalopathy syndrome in-

clude hypodense regions within posterior

white matter regions on unenhanced CT

scans and areas of hyperintense signal on T2-

weighted MR images [18, 2024] (Fig. 4).

After administration of contrast material, le-sions 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 de-

creased innervation of arteries of these regions

by autonomic fibers relative to the remainder

of the cerebral circulation [26].

After appropri-

ate treatment, almost complete resolution of

white matter abnormalities is seen.

Diffusion-weighted MR imaging has provided

insights into the pathogenesis of reversible poste-rior leukoencephalopathy syndrome by showing

that signal abnormalities on T2-weighted MR im-

ages are associated with vasogenic rather than

cytotoxic edema [19, 20, 25]. However, on diffu-

sion-weighted images, lesions of reversible poste-

rior 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 de-

creased 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 diffu-sion-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, im-

provements in carotid sonography and develop-

ment of cross-sectional imaging techniques such

as MR imaging and CT angiography have al-lowed more patients to be examined in a nonin-

vasive manner. Thus, dissection is diagnosed

with increased frequency. This discussion cen-

ters on the use of MR imaging and CT angiogra-

phy to diagnosis dissection. Detailed discussion

of sonography of this entity can be found in a

number of sources [2730].

Patients typically present with headache or

neck ache (approximately 75% of patients

with carotid dissection) [31] (Fig. 5). In rare

instances, patients may present with subarach-

noid hemorrhage from rupture of the intramu-

ral hematoma through the adventitia [32].

Because headache and neck ache are nonspe-cific and common in the general population,

the diagnosis of arterial dissection is often de-

layed, requiring multiple visits to physicians.

Nevertheless, the diagnosis should be strongly

considered in certain circumstances. Headache

or neck ache with oculosympathetic paresis

(Horners syndrome) should suggest the diag-

nosis of carotid dissection (Fig. 6), especially

if the headache is retroorbital [33].

Fig. 4.Posterior white matter abnormalities caused by reversible posterior leukoencephalopathy syndrome in 38-year-old man with severe hypertension, headache, vom-iting, and seizures.A, Unenhanced axial CT scan shows bilateral hypodense white matter lesions (arrowheads) that are more marked in posterior brain regions.B, 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 graywhite matter junction, consistent with vasogenic edema.After control of hypertension, central nervous systemsymptoms resolved.

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Although dissection can occur after trauma, it

is largely unrecognized that most dissections oc-cur in the absence of trauma or after only trivial

trauma [34]. For this reason, the diagnosis of dis-

section 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 fi-

bers, fibromuscular dysplasia, Marfans syn-

drome, cystic medial necrosis, type IV Ehlers-

Danlos syndrome), one might consider these

features useful to direct imaging studies for pa-

tients at high risk of dissection [3539]. How-ever, 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 dis-

section, 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 in-farction in most patients is the propagation of

emboli from fibrinplatelet 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 ca-

rotid dissection is a few centimeters above the

carotid bifurcation (Figs. 5 and 6), distal to the

typical site of atheromatous disease [36, 39].

BA

Fig. 5.Bilateral internal carotid artery dissections in 44-year-old man who developedright-sided neck pain and right Horners syndrome a few days after downhill skiing. Hehad no history of direct trauma.A, Catheter angiogram of right common carotid artery, lateral view, shows long segmentof luminal narrowing in high cervical segment (arrows), consistent with dissection, andextending up to level of skull base.B, Unenhanced axial T1-weighted MR image shows narrowing of flow void of right in-

ternal artery with eccentric hyperintense intramural hematoma that expands outer di-ameter of artery (straight arrow). Note normal caliber of left internal carotid artery(curved arrow).C, Catheter angiogram of left common carotid artery, lateral view, shows pseudoaneu-rysm (arrow) resulting from dissection in cervical segment. Because dissection did notextend to skull base, it is not seen in B.D, Two-dimensional time-of-flight MR angiogram shows, adjacent to left internal carotidartery, small focal region (straightarrow) of abnormal flow, corresponding to pseudo-aneurysm seen in C. Note narrowing of right internal carotid artery (curved arrow) cor-responding to dissection in A.

D

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The most common site of intracranial carotid

dissection (much less frequent than the extracra-

nial form) is the supraclinoid segment of the in-

ternal carotid artery. Vertebral artery dissection

is less common than carotid artery dissection

but may lead to more profound neurologic defi-

cits than carotid dissection because brainstem

infarction may result. The most common site of

vertebral artery dissection is at the level of the

C1C2 complex where the artery courses over

the lateral masses of these vertebral bodies [41].Before development of MR imaging, cathe-

ter angiography was considered the study of

choice for depiction of carotid and vertebral

dissection (Figs. 5 and 7). On catheter angiog-

raphy, typical findings included arterial steno-

sis (Fig. 5) or occlusion alone or in association

with pseudoaneurysm formation (Figs. 5 and

7). Because of its noninvasive nature allowing

thin-section images through vessels, MR im-

aging has replaced catheter angiography for

the diagnosis of arterial dissection at many in-

stitutions (Figs. 5 and 7). The principal find-

ings on MR imaging are narrowing of the flow

void of the arterial lumen (or in the case of oc-clusion, replacement of the flow void by ab-

normal signal) and within the arterial wall a

periarterial collar of abnormal signal (Fig. 5)

representing intramural hemorrhage [34, 42

45]. The periarterial collar frequently widens

the external diameter of the artery (Fig. 5) and

in one study was particularly helpful in estab-

lishing the diagnosis [42]. The periarterial col-

lar is frequently eccentric, with a wider

diameter on one side of the lumen than on the

other side [42] (Fig. 5). 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 re-gions of abnormal signal intensity (represent-

ing partial thrombosis or slow flow) (Fig. 7) 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. 5) and subsequently

hyperintense on T2-weighted images [47].

This finding is present for months [32, 43].

On MR angiography, the findings of arterial

dissection include narrowing of the arterial lu-

men (Fig. 5) and pseudoaneurysm formation

(seen as a region of bright signal projecting out-

side the expected confines of the arterial lumen)

(Fig. 7). On source images (Fig. 7), the periarte-rial rim typically has signal intensity that is be-

tween 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 be-

cause the periarterial signal abnormality will

typically be seen as a result of T1 shortening

[34, 47]. On the other hand, intramural he-

matoma 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 sus-

pected dissection. This pulse will saturate arte-

rial flow signal within the slab (black blood

technique) [47]. Intramural hematoma will then

appear as a region of hyperintense signal inten-sity adjacent to the affected artery. Some investi-

gators have claimed that a three-dimensional

spoiled gradient-echo technique is superior to

MR angiography in evaluation of vertebrobasi-

lar artery dissections because it is more sensitive

for depiction of a false lumen [45, 46]. How-

ever, 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 arte-

rial dissection.

The development of CT angiography using he-

lical techniques has allowed rapid thin-section de-

piction of vessels and excellent anatomic detail onthree-dimensional reconstructed images. The

finding of arterial dissection on source images is

revealed by

narrowing or occlusion of the con-

trast-filled lumen (Fig. 6), 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 he-

matoma appears bland and isodense relative to

Fig. 6.Right internal carotid artery dissection in 42-year-old woman with right-sided neck pain and oculosympathetic paresis (Horners syndrome).A, Source image from CT angiogram shows marked narrowing of right internal carotid artery (curved arrow) compared with left internal carotid artery (straightarrow)

because of dissection. Note that soft tissue immediately surrounding artery does not differ from normal muscle (unlike appearance seen on MR image in Figure 5).B, Three-dimensional reconstructionfrom CT angiogram of right internal carotid artery shows long segment of arterial narrowing (arrows) beginning distal to carotid bi-furcation. Note more focal segment of narrowing (arrowhead) in mid portion of stenosis.

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soft tissue (Fig. 6). 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 emer-

gency because it is associated with high morbid-ity 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 rel-

atively recently, the definitive method of diagno-

sis was brain biopsy [51]. However, identification

of the virus in cerebrospinal fluid via an amplifi-

cation 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 chil-

dren 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 unen-

hanced CT, early abnormal findings may in-

clude a mild decrease in attenuation of one or

both temporal lobes and insula, subtle efface-

ment of temporal lobe sulci, and narrowing ofthe sylvian fissure [54].

In later stages, affected

regions further decrease in attenuation, and pa-

renchymal swelling increases (Fig. 8). 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].

MR imaging is more sensitive than CT in

detecting brain involvement by herpes simplex

1 encephalitis because of the high signal con-

trast in affected regions relative to uninvolved

brain tissue on T2-weighted MR images [56]

(Fig. 8). Lesions that appear hyperintense on

T2-weighted MR images are more extensive

than on CT images obtained at the same stage

(Fig. 8). On unenhanced T1-weighted images,

lesions appear mildly or moderately hypo-

intense; contrast enhancement is usually mild,

with a gyriform or patchy pattern of enhance-

ment (Fig. 8). Small foci of hemorrhage are

seen commonly on MR imaging and were re-ported in 50% of patients in one small series

[57]. Variations from the typical pattern of ce-

rebral involvement include contrast enhance-

ment of the trigeminal nerve or other cranial

nerves and extension of abnormal signal into

the cingulate gyrus (Fig. 8) or brainstem [58,

59]. (Contrast enhancement of the trigeminal

nerve may reflect reactivation of virus from a

previous latent infection of the trigeminal gan-

glion, and extension of the abnormal signal into

BA

Fig. 7.Pseudoaneurysm formation caused by vertebral artery dissection in 50-year-old woman with headache.A, Unenhanced axial T1-weighted MR image shows mass (arrow) adjacent to medulla in expected location ofright vertebral artery.B, Source image from three-dimensional time-of-flight MR angiogram shows flow (arrow) consistent with rightvertebral artery pseudoaneurysm within mass shown in A. Absence of flow void in lesion is probably caused byslow flow in pseudoaneurysm.C, Catheter angiogram of right vertebral artery, lateral view, shows abnormal dilatation of artery (arrow ) con-sistent with pseudoaneurysm.

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Fig. 8.61-year-old woman with 6-day history of encephalopathy caused by herpes simplex type 1 encephalitis.A, Unenhanced axial CT scan shows right temporal lobe hypodensity and swelling (solidarrow), narrowing of right sylvian fissure, and hypodensity in right insula (openarrows).B, Contrast-enhanced axial T1-weighted MR image obtained 2 days after A shows mild gyriform contrast enhancement of right temporal lobe (arrowheads). Note absenceof right temporal lobe sulci (arrows) caused by swelling, compared with left temporal lobe.C, Axial T2-weighted MR image shows increased signal intensity in right temporal lobe (open arrows) and inferior frontal region (solidarrow).D, 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 straightarrow). Note sparing of basal ganglia.

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the cingulate gyrus may reflect transmission of

the infection from the hippocampus along its ef-

ferent pathways.) Lack of basal ganglia involve-

ment despite involvement of the adjacent internal

capsule is common (Fig. 8) and may be one

means of distinguishing herpes simplex 1 en-cephalitis 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 en-

cephalitis can further be distinguished from in-

farction because encephalitis frequently involves

both the medial and lateral aspects of the tempo-

ral lobe and involves territory supplied by both

the middle cerebral artery and the posterior cere-

bral artery (Figs. 8 and 9). This pattern would be

atypical for infarction. Herpes simplex 1 enceph-

alitis can be distinguished from a neoplasm in-

volving the temporal lobe because the inferior

frontal lobe and contralateral temporal lobe andinsula are frequent sites for herpes simplex 1 en-

cephalitis, but not for tumors (Figs. 8 and 9).

Recent developments in MR imaging allow

even more sensitive detection of herpes simplex

1 encephalitis than is possible with routine spin-

echo MR imaging. Fluid attenuated inversion re-

covery (FLAIR) technique is reported to define

the extent of herpes simplex 1 encephalitis in-

volvement better than routine spin-echo images

[61, 62]. Diffusion-weighted MR imaging is an-

other relatively recent advancement that is sensi-

tive 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 fromcytotoxic edema. Although published reports of

diffusion-weighted MR evaluation of encephali-

tis 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 com-

pared 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 dis-

ease processes that produce diagnostic diffi-

culty in the emergency neuroradiology setting.

Because radiologists are often the first individ-

uals to consider these entities, they must be fa-

miliar 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 neu-

rologic emergency conditions if left untreated.

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Fig. 9.50-year-old man with 4-day history of confusion and somnolence caused by herpes simplex type 1 encephalitis.A, Axial T2-weighted MR image shows markedly increased signal in left temporal lobe and mildly increased signal intensity in right medial temporal lobe (arrow). Findingsof diffuse bilateral temporal lobe involvement would not be expected in tumor or infarction.B, Coronal contrast-enhanced T1-weighted MR image shows thick contrast enhancement in medial left temporal lobe (straight arrows) and smaller region of contrastenhancement in right hippocampus (curved arrow). Compare thickness of contrast enhancement in left temporal lobe with thin gyriform enhancement seen in Figure 8.

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