herpes simplex 2ncephaIitis [HSE) has been well described by computed tomography (CT) 113 and by Eon-enhanced magnetic resonance imaging (MRI) iZj. We present a case of Gd-DTPA enhanced MRI of HSE and its evolution under antiviral therapy.
T.“_
A &I-year-old man presented with a convulsive episode preceded by four days of fever. His workup was generally negative except for slight pleocytosis and protein elevation in the cerebrospinal fluid (,CSF) and electroencephalographic (EKG) Ghanges over the right hemisphere. Three days after admission the computed tomography [CT) (Figure 1) demonstrated two non-enhancing, well demarcated regions of hypodensity in the right temporal lobe. On magnetic resonance imaging (MRI, three days later (Figure 2), the corresponding regions showed isointenity on TI-weighted images and hyperintensity on T&weighted images. Minima! mass effect was present. The Gd-DTPA-enhanced images [Figure 2) &owed meningeal enhancement about the right temporal lobe. These finding confirmed t clinical suspicion of herpes simplex encephali [HSE) and antiviral therapy with acyclovir was
A
epeat CT (Figure 3) ‘10 days after the initial CT demonstrated hemorrhage in the anterior right temporal lesion as well as meningeal enhancement
From the Departments of Radiology (P.S.. J.M.G.) and Neurology [SE.), Hadassah University Hospital, Jerusalem, Israel. Address all reprint requests to: John M. Gomori. M.D., Department of Radiology, Hadassah University Hospital, FE.0 Box 12000, Jerusalem 91120 Israel. Received JuIJ 1990; revised February 1991. 0 2391 by EIsevier Science Publishmg CO., hc. 655 Avenue of the Americas, New York, NY 10010 0899/7071/971$3.50
B
wvo hypodense ?a1 lobe.
1 Enhanced non-enhancing
ax:a! ZT scans demonstrate regions in the right tempo-
122
CLINICAL IMAGING VOL. 15, NB3. 2
SWITZER ET AL.
type appears
the initial
exposure.
Frequently
i
dxmcteris:lcal;y acutely years after the causative virus
) e&anced axlai ZT . [A) lanenhanced and ( scans demonstrate hemorrhage at right temporal lobe tip (A.), meningeal enhancement ( ), and enhancement 3f the lesion near the atrium of the right lateral ventricle [C).
PI
E 2. (A) unenhanced and (S] Gd-DTPA Tl-weighted image (5001'10 = TRITE) and T&weighted image (22OQi80) (C) axial MRI scans through the temporal lobes demonstrate the two lesions and the meningeal enhancement.
not appreciated on the initial CT. F’oilow up M a (Figure 4) 17 days after the initial CT showed subacute anterior temporal lobe hemorrhage, decrease of the TZ-weighted images, hyperintensity of the temporal lobe lesions, decreased mass effect, and almost complete resolution of the meningeal enhancement. However, now there was significant new parenchymal enhancement in the two right temporal regions.
A
exiensim to the frontal and pariecal khe is common bilateral [Z). e lesions are frequently diagnosis of HSE is important so that effective antiviral drugs can be istered (6). CT has oeen previously reported to pful in the diagnosis of HSE, while it is usually negative in other cases of acute viral encepha!itis (1). There is initially a decrease in the parenchymal density in the affected
4. [A) unenhanced and ] Gd-DTPA enhanced Tl-weighted image (450110) and T2-weighted image (22001 30)(6)axial MN scans demonstrate the hemorrhagic region :n the tip of the right temporai lobe and enhancement of :he two lesions. The meningeal enhancement has resolved.
.mxJ
is not isolared md anti y titres have significant false negative results (3) wever, characteristic inclusion bodies are seen biopsy specimens. Neuronal destruction results in cytotoxic edema augmented by secondary vasogenic edema and the frequent formation of glial nodules. Vascular necrosis may lead to petechia1 hemorrhages (4). HSE has a eferential involvement of the limbic system (5). ue to the universal latency of this virus in the Gasserian gangtion, ther is marked predilection for the temporal lobe. The asal ganglia are spared while
B
124
SWITZER
ET AL.
CLINICAL
IMAGING VOL. 15, NO. 2
extension to the parietal or frontal lobe. Foci of subacute hemorrhage may be demonstrated on T?1weighted or 3%weighted images depending on their age. In our case the meningeal enhancement vias Seen better on the MRI because of the lack of obscuration by the adjacent bony structures. The follow-up MRI showed parenchymal enhancement and resolution of the meningeal enhancement. The delayed appearance of parenchymal enhancement is similar to the time course of enhancement of infarctions. The presence of hemorrhage is also suggestive of HSE. In the acute phase, both CT and Ml31 will demonstrate the hemorrhage. However, in the subacute phase, unenhanced M be more sensitive to the presence of subac rhage. In conclusion, Gd-DTPA-enhanced nart of the routine protocol for the investigation of suspected HSE.
lobe. As noted, the lesions may be bilateral and the basal ganglia are spared (1). Contrast enhancement characteristically shows a diffuse parenchymal or gyral pattern with enhancement of the Sylvian fissure. Mass effect may be present due to swelling of the affected parenchyma. Wemorrhage into the affected parenchyma has been reported. All of these CT changes depend on the timing of the scan during the illness. The earliest reported enhancement occurred on the third day of the illness while the longest lasting enhancement occurred at 39 days (7). In most cases of non-herpetic acute viral enchephalitis CT shows no abnormalities in the ac-ute phase. In two of 17 cases, delayed CT showed evidence of basal ganglia calcifications and hypodense lesions in the basal ganglia, thalamus, and periventricular white matter (1). The typical MRI changes of HSE are caused by an increase in water content and breakdown of the blood-brain barrier in affected areas (8, 9). These are manifested by a decreased signal on T1-weighted images and increased signal on TZ-weighted images. These changes are in the characteristic distribution involving the temporal lobe or lobes with possible
Weisberg L, Greenberg r, Stazio A. Zompaseu ~omographrc findings in acute viral encephalitis in adults with emphasis on herpes simplex encephalitis. Computerized Medical Imaging and Graphics 1988;12:385-392. Schroth 6, Gawehn J, Thron A, Valibracht A, Voigt K. Early diagnosis of herpes simplex encephalitis by MRI. Neurology 1987;37:179-183. Nahmias AJ, Whiley RJ, Visintine AN. et al. Herpes simplex virus encephalitis: Laboratory evaluations and their diagnostic significance. J Infect Dis 1982;145:829-836. Sze G. MR of infections and inflammatory disease. in Bradley W, Stark D (eds): Magnetic Resonance tmaging. St. Louis: Mosby, 1987 pp 316-343. Damasio AR, Hoesen GW. The limbic system and the !ocalisation of herpes simplex encephalitis. J Neuroi Neurosurg Psychiatry 1985;48:297-301, Skdldenberg B, Alestig K, Burman L, et al. Acyclovir versus vidarabine herpes simplex encephalitis. Randomized multicenpatients. Lancet +re study in consecutive Swedish 1984;2:707-711. 3avis TM, Kenneth RD, Kleinmann MG, Kirchner H§, Taveras JM. Computed tomography of herpes simplex encephalitis with clinicopathological correlation. Radiology 1978; 129:409-417. Zse G, Zimmerman RD. The magnetic resonance imaging of infections and inflammatory diseases. Radio1 Clin North Am 1988;26:839-859. Davidson HD, Steiner RR. Magnetic resonance imaging in infections of the central nervous system. AJNR 1985;6:499504.
T.“_
A &I-year-old man presented with a convulsive episode preceded by four days of fever. His workup was generally negative except for slight pleocytosis and protein elevation in the cerebrospinal fluid (,CSF) and electroencephalographic (EKG) Ghanges over the right hemisphere. Three days after admission the computed tomography [CT) (Figure 1) demonstrated two non-enhancing, well demarcated regions of hypodensity in the right temporal lobe. On magnetic resonance imaging (MRI, three days later (Figure 2), the corresponding regions showed isointenity on TI-weighted images and hyperintensity on T&weighted images. Minima! mass effect was present. The Gd-DTPA-enhanced images [Figure 2) &owed meningeal enhancement about the right temporal lobe. These finding confirmed t clinical suspicion of herpes simplex encephali [HSE) and antiviral therapy with acyclovir was
A
epeat CT (Figure 3) ‘10 days after the initial CT demonstrated hemorrhage in the anterior right temporal lesion as well as meningeal enhancement
From the Departments of Radiology (P.S.. J.M.G.) and Neurology [SE.), Hadassah University Hospital, Jerusalem, Israel. Address all reprint requests to: John M. Gomori. M.D., Department of Radiology, Hadassah University Hospital, FE.0 Box 12000, Jerusalem 91120 Israel. Received JuIJ 1990; revised February 1991. 0 2391 by EIsevier Science Publishmg CO., hc. 655 Avenue of the Americas, New York, NY 10010 0899/7071/971$3.50
B
wvo hypodense ?a1 lobe.
1 Enhanced non-enhancing
ax:a! ZT scans demonstrate regions in the right tempo-
122
CLINICAL IMAGING VOL. 15, NB3. 2
SWITZER ET AL.
type appears
the initial
exposure.
Frequently
i
dxmcteris:lcal;y acutely years after the causative virus
) e&anced axlai ZT . [A) lanenhanced and ( scans demonstrate hemorrhage at right temporal lobe tip (A.), meningeal enhancement ( ), and enhancement 3f the lesion near the atrium of the right lateral ventricle [C).
PI
E 2. (A) unenhanced and (S] Gd-DTPA Tl-weighted image (5001'10 = TRITE) and T&weighted image (22OQi80) (C) axial MRI scans through the temporal lobes demonstrate the two lesions and the meningeal enhancement.
not appreciated on the initial CT. F’oilow up M a (Figure 4) 17 days after the initial CT showed subacute anterior temporal lobe hemorrhage, decrease of the TZ-weighted images, hyperintensity of the temporal lobe lesions, decreased mass effect, and almost complete resolution of the meningeal enhancement. However, now there was significant new parenchymal enhancement in the two right temporal regions.
A
exiensim to the frontal and pariecal khe is common bilateral [Z). e lesions are frequently diagnosis of HSE is important so that effective antiviral drugs can be istered (6). CT has oeen previously reported to pful in the diagnosis of HSE, while it is usually negative in other cases of acute viral encepha!itis (1). There is initially a decrease in the parenchymal density in the affected
4. [A) unenhanced and ] Gd-DTPA enhanced Tl-weighted image (450110) and T2-weighted image (22001 30)(6)axial MN scans demonstrate the hemorrhagic region :n the tip of the right temporai lobe and enhancement of :he two lesions. The meningeal enhancement has resolved.
.mxJ
is not isolared md anti y titres have significant false negative results (3) wever, characteristic inclusion bodies are seen biopsy specimens. Neuronal destruction results in cytotoxic edema augmented by secondary vasogenic edema and the frequent formation of glial nodules. Vascular necrosis may lead to petechia1 hemorrhages (4). HSE has a eferential involvement of the limbic system (5). ue to the universal latency of this virus in the Gasserian gangtion, ther is marked predilection for the temporal lobe. The asal ganglia are spared while
B
124
SWITZER
ET AL.
CLINICAL
IMAGING VOL. 15, NO. 2
extension to the parietal or frontal lobe. Foci of subacute hemorrhage may be demonstrated on T?1weighted or 3%weighted images depending on their age. In our case the meningeal enhancement vias Seen better on the MRI because of the lack of obscuration by the adjacent bony structures. The follow-up MRI showed parenchymal enhancement and resolution of the meningeal enhancement. The delayed appearance of parenchymal enhancement is similar to the time course of enhancement of infarctions. The presence of hemorrhage is also suggestive of HSE. In the acute phase, both CT and Ml31 will demonstrate the hemorrhage. However, in the subacute phase, unenhanced M be more sensitive to the presence of subac rhage. In conclusion, Gd-DTPA-enhanced nart of the routine protocol for the investigation of suspected HSE.
lobe. As noted, the lesions may be bilateral and the basal ganglia are spared (1). Contrast enhancement characteristically shows a diffuse parenchymal or gyral pattern with enhancement of the Sylvian fissure. Mass effect may be present due to swelling of the affected parenchyma. Wemorrhage into the affected parenchyma has been reported. All of these CT changes depend on the timing of the scan during the illness. The earliest reported enhancement occurred on the third day of the illness while the longest lasting enhancement occurred at 39 days (7). In most cases of non-herpetic acute viral enchephalitis CT shows no abnormalities in the ac-ute phase. In two of 17 cases, delayed CT showed evidence of basal ganglia calcifications and hypodense lesions in the basal ganglia, thalamus, and periventricular white matter (1). The typical MRI changes of HSE are caused by an increase in water content and breakdown of the blood-brain barrier in affected areas (8, 9). These are manifested by a decreased signal on T1-weighted images and increased signal on TZ-weighted images. These changes are in the characteristic distribution involving the temporal lobe or lobes with possible
Weisberg L, Greenberg r, Stazio A. Zompaseu ~omographrc findings in acute viral encephalitis in adults with emphasis on herpes simplex encephalitis. Computerized Medical Imaging and Graphics 1988;12:385-392. Schroth 6, Gawehn J, Thron A, Valibracht A, Voigt K. Early diagnosis of herpes simplex encephalitis by MRI. Neurology 1987;37:179-183. Nahmias AJ, Whiley RJ, Visintine AN. et al. Herpes simplex virus encephalitis: Laboratory evaluations and their diagnostic significance. J Infect Dis 1982;145:829-836. Sze G. MR of infections and inflammatory disease. in Bradley W, Stark D (eds): Magnetic Resonance tmaging. St. Louis: Mosby, 1987 pp 316-343. Damasio AR, Hoesen GW. The limbic system and the !ocalisation of herpes simplex encephalitis. J Neuroi Neurosurg Psychiatry 1985;48:297-301, Skdldenberg B, Alestig K, Burman L, et al. Acyclovir versus vidarabine herpes simplex encephalitis. Randomized multicenpatients. Lancet +re study in consecutive Swedish 1984;2:707-711. 3avis TM, Kenneth RD, Kleinmann MG, Kirchner H§, Taveras JM. Computed tomography of herpes simplex encephalitis with clinicopathological correlation. Radiology 1978; 129:409-417. Zse G, Zimmerman RD. The magnetic resonance imaging of infections and inflammatory diseases. Radio1 Clin North Am 1988;26:839-859. Davidson HD, Steiner RR. Magnetic resonance imaging in infections of the central nervous system. AJNR 1985;6:499504.
