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CT and MR Imaging of Nontraumatic Neurologic Emergencies

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

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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].

View larger version (131K): [in this window] [in a new window] [as a PowerPoint slide]   Arthur W. Goodspeed, 4th President, 1903-1904

View larger version (131K): [in this window] [in a new window] [as a PowerPoint slide]   James B. Bulitt, 5th President, 1904-1905

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View larger version (108K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (123K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (122K): [in this window] [in a new window] [as a PowerPoint slide]   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.

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].

View larger version (131K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2A. —Dural sinus thrombosis in 38-year-old woman with headache. Unenhanced axial CT scan shows hyperdense appearance of superior sagittal sinus (arrows), consistent with thrombosis.

View larger version (78K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (125K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (123K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (163K): [in this window] [in a new window] [as a PowerPoint slide]   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).

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

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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.

View larger version (132K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (148K): [in this window] [in a new window] [as a PowerPoint slide]   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.

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

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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].

View larger version (79K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (166K): [in this window] [in a new window] [as a PowerPoint slide]   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).

View larger version (87K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (128K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (82K): [in this window] [in a new window] [as a PowerPoint slide]   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).

View larger version (55K): [in this window] [in a new window] [as a PowerPoint slide]   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.

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].

View larger version (136K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (147K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (152K): [in this window] [in a new window] [as a PowerPoint slide]   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.

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

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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].

View larger version (127K): [in this window] [in a new window] [as a PowerPoint slide]   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).

View larger version (136K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (130K): [in this window] [in a new window] [as a PowerPoint slide]   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).

View larger version (132K): [in this window] [in a new window] [as a PowerPoint slide]   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.

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).

View larger version (148K): [in this window] [in a new window] [as a PowerPoint slide]   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.

View larger version (145K): [in this window] [in a new window] [as a PowerPoint slide]   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

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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.

References

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1. Beauchamp NJ Jr, Bryan RN. Acute cerebral ischemic infarction: a pathophysiologic review and radiologic perspective. AJR 1998;171:73-84[Free Full Text]
2. Meyer JT, Gorey MT. Differential diagnosis of nontraumatic intracranial hemorrhage. Neuroimaging Clin N Am 1998;8:263-293[Medline]
3. Ameri A, Bousser MG. Cerebral venous thrombosis. Neurol Clin 1992;10:87-111[Medline]
4. Zimmerman RD, Ernst RJ. Neuroimaging of cerebral venous thrombosis. Neuroimaging Clin N Am 1992;2:463-485
5. Deschiens MA, Conard J, Horellou MH, et al. Coagulation studies, factor V Leiden, and anticardiolipin antibodies in 40 cases of cerebral venous thrombosis. Stroke 1996;27:1724-1730[Abstract/Free Full Text]
6. Zuber M, Toulon P, Marnet L, Mas JL. Factor V Leiden mutation in cerebral venous thrombosis. Stroke 1996;27:1721-1723[Abstract/Free Full Text]
7. de Bruijn SF, Stam J, Koopman MM, Vandebroucke JP. Case-control study of risk of cerebral sinus thrombosis in oral contraceptive users and in carriers of hereditary prothrombotic conditions: the Cerebral Venous Thrombosis Study Group. BMJ 1998;316:589-592[Abstract/Free Full Text]
8. Provenzale JM, Barboriak DP, Ortel TL. Dural sinus thrombosis associated with activated protein C resistance: MR imaging findings. AJR 1998;170:499-502[Abstract/Free Full Text]
9. Virapongse C, Cazenave C, Quisling R, Sarwar M, Hunter S. The empty delta sign: frequency and significance in 76 cases of dural sinus thrombosis. Radiology 1987;162:779-785[Abstract/Free Full Text]
10. Casey SO, Alberico RA, Patel M, et al. Cerebral CT venography. Radiology 1996;198:163-170[Abstract/Free Full Text]
11. Ozsvath RR, Casey SO, Lustrin ES, Alberico RA, Hassankhani A, Patel M. Cerebral venography: comparison of CT and MR projection venography. AJR 1997;169:1699-1707[Abstract/Free Full Text]
12. Vogl TJ, Bergman C, Villringer A, Einhaupl K, Lissner J, Felix R. Dural sinus thrombosis: value of venous MR angiography for diagnosis and follow-up. AJNR 1994;162:1191-1198
13. Keiper MD, Ng SE, Atlas SW, Grossman RI. Subcortical hemorrhage: marker for radiographically occult cerebral vein thrombosis on CT. J Comput Assist Tomogr 1995;19:527-531[Medline]
14. Keller E, Flacke S, Urbach H, Schild HH. Diffusion- and perfusion-weighted magnetic resonance imaging in deep cerebral vein thrombosis. Stroke 1999;30:1144-1146[Abstract/Free Full Text]
15. Einhaupl KM, Villringer A, Meister W, et al. Heparin treatment in sinus venous thrombosis. Lancet 1991;338:597-600[Medline]
16. Horowitz M, Purdy P, Unwin H, et al. Treatment of dural sinus thrombosis using selective catheterization and urokinase. Ann Neurol 1995;38:58-67[Medline]
17. Spearman MP, Jungreis CA, Wehner JJ, Gerszten PC, Welch WC. Endovascular thrombolysis in deep cerebral venous thrombosis. AJNR 1997;18:502-506[Abstract]
18. Hinchey J, Chaves C, Appignani B, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996;334:494-500[Abstract/Free Full Text]
19. Ay H, Buonanno FS, Schaefer PW, et al. Posterior leukoencephalopathy without severe hypertension: utility of diffusion-weighted MRI. Neurology 1998;51:1369-1376[Abstract/Free Full Text]
20. Schwartz RB, Mulkern RV, Gudbjartsson H, Jolesz F. Diffusion-weighted MR imaging in hypertensive encephalopathy: clues to pathogenesis. AJNR 1998;19:859-862[Abstract]
21. Schwartz RB, Jones KM, Kalina P, et al. Hypertensive encephalopathy: findings on CT, MR imaging, and SPECT imaging in 14 cases. AJR 1992;159:379-383[Abstract/Free Full Text]
22. Schwartz RB, Bravo SM, Klufas RA, et al. Cyclosporine neurotoxicity and its relationship to hypertensive encephalopathy: CT and MR findings in 16 cases. AJR 1995;165:627-631[Abstract/Free Full Text]
23. Hauser RA, Lacey DM, Knight MR. Hypertensive encephalopathy: magnetic resonance imaging demonstration of reversible cortical and white matter lesions. Arch Neurol 1988;45:1078-1083[Abstract]
24. Truwit CL, Denaro CP, Lake JR, DeMarco T. MR imaging of reversible cyclosporine A-induced neurotoxicity. AJNR 1991;12:651-659[Abstract]
25. Schaefer PW, Buonanno FS, Gonzalez RG, Schwamm LH. Diffusion-weighted imaging discriminates between cytotoxic and vasogenic edema in a patient with eclampsia. Stroke 1997;28:1082-1085[Abstract/Free Full Text]
26. Edvinsson L, Owman C, Sjoberg N-O. Autonomic nerves, mast cells, and amine receptors in human brain vessels: histochemical and pharmacologic study. Brain Res 1976;115:377-393[Medline]
27. Gardner DJ, Gosink BB, Kallman CE. Internal carotid artery dissections. J Ultrasound Med 1991;10:607-614[Abstract]
28. Steinke W, Rautenberg W, Schwartz A, Hennerici M. Noninvasive monitoring of internal carotid artery dissection. Stroke 1994;25:998-1005[Abstract]
29. Hoffman M, Sacco RL, Chan S, Mohr JP. Noninvasive detection of vertebral artery dissection. Stroke 1993;24:815-819[Abstract/Free Full Text]
30. Sturznegger M, Mattle HP, Rivoir A, Rihs F, Schmid C. Ultrasound findings in spontaneous extracranial vertebral artery dissection. Stroke 1993;24:1910-1921[Abstract/Free Full Text]
31. Biousse V, D'Anglejan-Chatillon J, Massiou H, Bousser MG. Head pain in non-traumatic carotid artery dissection: a series of 65 patients. Cephalalgia 1994;14:33-36[Medline]
32. Anxionnat R, Roy D, Bracard S, et al. Dissection of intracranial vertebral arteries revealed by subarachnoid hemorrhage: report of seven cases. J Neuroradiol 1994;21:1-16[Medline]
33. Bogousslavsky J, Regli F. Ischemic strokes in adults younger than 30 years of age: cause and prognosis. Arch Neurol 1987;44:479-482[Abstract]
34. Provenzale JM. Dissection of the internal carotid and vertebral arteries: imaging findings. AJR 1995;165:1099-1104[Abstract/Free Full Text]
35. Brandt T, Hausser I, Orberk E, et al. Ultrastructural connective tissue abnormalities in patients with spontaneous cervico-cerebral artery dissections. Ann Neurol 1998;44:281-285[Medline]
36. Houser OW, Baker HL Jr. Fibromuscular dysplasia and other uncommon diseases of the cervical carotid artery: angiographic aspects. AJR 1968;104:201-212[Abstract/Free Full Text]
37. Caplan LR, Zarins CK, Hemmati M. Spontaneous dissection of the extracranial vertebral arteries. Stroke 1985;16:1030-1038[Abstract/Free Full Text]
38. Schievink WI, Mokri B, O'Fallon WM. Recurrent spontaneous cervical-artery dissection. N Engl J Med 1994;330:393-397[Abstract/Free Full Text]
39. Schievink WI, Mokri B, Piepgras DG. Spontaneous dissections of cervicocephalic arteries in childhood and adolescence. Neurology 1994;44:1607-1612[Abstract/Free Full Text]
40. Lisovoski F, Rousseaux P. Cerebral infarction in young people: a study of 148 patients with early cerebral angiography. J Neurol Neurosurg Psychiatry 1991;54:576-579[Abstract]
41. Sherman DG, Hart RG, Easton JD. Abrupt change in head position and cerebral infarction. Stroke 1981;12:2-6[Abstract/Free Full Text]
42. Levy C, Laissy JP, Raveau V, et al. Carotid and vertebral artery dissections: three-dimensional time-of-flight MR angiography and MR imaging versus conventional angiography. Radiology 1994;190:97-103[Abstract/Free Full Text]
43. Kitanaka C, Tanaka J, Kuwahara M, Teraoka A. Magnetic resonance imaging study of intracranial vertebrobasilar artery dissections. Stroke 1994;25:571-575[Abstract]
44. Ozdoba C, Sturnegger M, Schroth G. Internal carotid artery dissection: MR imaging features and clinical-radiologic correlation. Radiology 1996;199:191-198[Abstract/Free Full Text]
45. Hosoya T, Watanabe N, Yamaguchi K, Kubota H, Onondera Y. Intracranial vertebral artery dissection in Wallenberg syndrome. AJNR 1994;15:1161-1165[Abstract]
46. Hosoya T, Adachi M, Yamaguchi K, Haku T, Kayama T, Kato T. Clinical and neuroradiological features of intracranial vertebrobasilar artery dissection. Stroke 1999;30:1083-1090[Abstract/Free Full Text]
47. Kirsch E, Kaim A, Engelter S, et al. MR angiography in internal carotid artery dissection: improvement of diagnosis by selective demonstration of the intramural hematoma. Neuroradiology 1998;40:704-709[Medline]
48. Leclerc X, Godefroy O, Salhi A, Lucas C, Leys D, Pruvo JP. Helical CT for the diagnosis of extracranial carotid artery dissection. Stroke 1996;27:461-466[Abstract/Free Full Text]
49. Leclerc X, Lucas C, Godefroy O, et al. Helical CT for the follow-up of cervical internal carotid artery dissections. AJNR 1998;19:831-837[Abstract]
50. Ho DD, Hirsch M. Acute viral encephalitis. Med Clin North Am 1985;69:415-429[Medline]
51. Morawetz RB, Whitley RJ, Murphey DM. Experience with brain biopsy for suspected herpes encephalitis: review of forty consecutive cases. Neurosurgery 1983;12:654-657[Medline]
52. Mertens G, Ieven M, Ursi D, Pattyn SR, Martin JJ, Parizel PM. Detection of herpes simplex virus in the cerebral spinal fluid of patients with encephalitis using the polymerase chain reaction. J Neurol Sci 1993;118:213-216[Medline]
53. Koelfen W, Freund M, Guckel F, Rohr H, Schultze C. MRI of encephalitis in children: comparison of CT and MRI in the acute stage with long-term follow-up. Neuroradiology 1996;38:73-79[Medline]
54. Davis JM, Davis KR, Kleinman GM, Krichner HS, Taveras JM. Computed tomography of herpes simplex encephalitis with clinicopathological correlation. Radiology 1978;129:409-417[Abstract]
55. Hindmarsh T, Lindqvist M, Olding-Stenkvist E, Skoldenberg B, Forsgren M. Accuracy of computed tomography in the diagnosis of herpes simplex encephalitis. Acta Radiol 1986;369:192-196
56. Schroth G, Gawehn J, Thron A, Valibracht A, Voigt K. Early diagnosis of herpes simplex encephalitis by MRI. Neurology 1987;37:179-183[Abstract/Free Full Text]
57. Damaerel P, Wilms G, Robberecht W, et al. MRI of herpes simplex encephalitis. Neuroradiology 1992;34:490-493[Medline]
58. Tien RD, Felsberg GJ, Osumi AK. Herpes virus infections of the CNS: MR findings. AJR 1993;161:167-176[Abstract/Free Full Text]
59. Soo MS, Tien RD, Gray L, Andrews PI, Friedman H. Mesenrhombencephalitis: MR findings in nine patients. AJR 1993;160:1089-1093[Abstract/Free Full Text]
60. Deresiewicz RL, Thaler SJ, Hsu L, Zamani AA. Clinical and neuroradiographic manifestations of eastern equine encephalitis. N Engl J Med 1997;336:1867-1874[Abstract/Free Full Text]
61. White ML, Edwards-Brown MK. Fluid attenuated inversion recovery (FLAIR) MRI of herpes encephalitis. J Comput Assist Tomogr 1995;19:501-505[Medline]
62. Kato T, Ishii C, Furusho J, Endo T, Tazaki I. Early diagnosis of herpes encephalopathy using fluid-attenuated inversion recovery pulse sequence. Pediatr Neurol 1998;19:58-61[Medline]
63. Tsuchiya K, Katase S, Yoshino A, Hachiya J. Diffusion-weighted MR imaging of encephalitis. AJR 1999;173:1097-1099[Abstract/Free Full Text]
64. Burke JW, Mathews VP, Elster AD, Ulmer JL, Mclean FM, Davis SB. Contrast-enhanced magnetization transfer saturation imaging improves MR detection of herpes simplex encephalitis. AJNR 1996;17:773-776[Abstract]

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