Mikihiko TAKESHITA, Takeshi ISHII, Jun SAKAGUCHI, Masahiro IZAWA,
Kintomo TAKAKURA and Shigeru SENTO"
Department of Neurosurgery, Neurological Institute, Tokyo Women's Medical College *Department of Neurosurgery, Oyama Neurological Center
(Received July 15, 1993)
We studied CT and MRI imaging of patient with Japanese B encephalitis.
cally, the patient had masked face, dysarthria and delirium progressing to coma as
sequelae. T2-weighted MRI images clearly demonstrated high intensity localized in the
substantia nigra and basal ganglia, and showed the time sequence of the pathologic
changes.
Introduction
The number of patients with Japanese B ence-phalitis, which is widespread throughout Asia from the maritime provinces of Russia to South
India and Sri Lanka, has decreased to less than
100 per year in Japan since 1967 because of
intensive vaccination of children and public
hygienei). Early di'agnosis and treatment of Jap-anese B encephalitis is essential because of the
high mortality and morbidity rate and because blood antibody titers against Japanese B
ence-phalitis virus do not increase until the second or third week of illness. MRI images, particularly T2-weighted image, may be useful for early diagnosis because of their close correlation with MRI
find-ings and pathophysiology. We reported a case
with Japanese B encephalitis manifesting remark-ably changes in MRI.
Case Report
A 46-year-old male suffering from fever and
headache for two days was admitted to the hos-pital. When hospitalized, he was markedlycon-fused and generalized seizures were encountered. Temperature was 390C, and severe nuchal rigidity was presented. Masked face, dysarthria, cogwheel
rigidity of four extremities and tremor of bilateral
arms were noted. A spinal tap showed high
opening pressure and spinal fluid contained 108 mg/dl of protein, 68 mg/dl of glucose and 1,388
cells per cubic millimeter, 53% of which were lymphocytes. CT scan on admission demonstrated decreased attenuation value in the right crus cerebri and bilateral thalamus (Fig. 1). Serum complement fixation titer to japanese B
ence-phalitis virus was less than 1:4. 0n the 6th after onset, he lapsed into semicoma and quadriplegia
occurred. A tracheostomy was performed and
priodic use of a respirator was necessary. T2-weighted MRI images showed high intensity areain the right crus cerebri, right putamen and
bilateral thalamus (Fig. 2). Spinal fluid contained 102 mg/dl of protein, 74 mg/dl of glucose and 433
cells per cubic millimeter (N:L=85:348). With
diagnosis of viral encephalitis, we used intra-venous acyclovir (300 mg three times per day for7 days). Eleven days after onset, he seemed to be
mutic and barely responded to his name but
quadriplegia was still found and periodic use of a
respirator was necessary. Serum complement
fixation titer to Japanese B encephalitis virus had risen to 1:64. 0n the 25th day, T2-weighted MRI
77
Fig. 1 Axial plain CT on the 3rd day after onset demonstrates spotty low densities in
thalamus and decreased attenuation in the right crus cerebri (arrow).
the bilateral
Fig. 2 T2-weighted irnages (TR= 200, TE==110, excitation==2) on the 6th day show high intensity area in the right crus cerbri, right putamen and bitlateral thalamus (arrow).
area in the right crus cerebri, bilateral thalamus
and right putamen (Fig. 3). Serum complement
fixation titer to Japanese B encephalitis virus had decreased to 1:32. Spinal fluid contained 94 mg/dl of protein, 52 mg/dl glucose and 23 cells per cubic millimeter (N:L=3:20). Fifty-five days after onset, he first seemed aware of his surroundings, but still suffered from quadriaparesis, dysarthria,
in-tension tremor and incontinence. Three months
after infection, although quadriparesis with
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ticity, dysarthria and Babinski signs persisted, he was able to walk with the help of parallel bars.
T2-weighted MRI images showed high intensity
localized in the right substantia nigra, bilateral thalamus and right putamen (Fig. 4).
Discussion
The incidence of Japanese B encephalitis, which is a major concern in Asia, has dropped dramati-cally because of intensive vaccination and vector
Fig. 3 T2-wejghted image$ on the 25th day revea] expanding high intensity area in the right crus cerebri (arrow), bilateral thalamus and right putamen.
Fig. 4 T2-weighted images from the three months after onset show high intensity in the right substantia nigra (arrow), right putamen and bilateral thalamus.
control. However, mortality rates in the range of 20 to 50% are reported, and rates of permanent neurological sequelae are high when this ence-phalitis does occur2). Consequently, early diagno-sis of Japanese B encephalitis is essential, while no specific therapy for this encephalitis had been available.
The pathologic changes of inflammatory brain
disease demonstrated by MRI are the increase in water content and breakdown of the blood-brain barrier3). Particularly, the T2-weighted spin-echo technique to increased brain water content clearly
demonstrates inflammatory lesions. While the
pathophysiological pictures in viral infection depend on the infective agent and the host re-sponse and usually have a multifocal or diffuse
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inflammatory process, each encephalitis virus
may have distinctive involved areas. Pathologi-cally, Japanese B encephalitis virus is involved in the cerebral cortex, basal ganglia, brain stem and anterior horn of the spinal cord, particularly in
the thalamus and substantia nigra4)N6}. MRI
images in Japanese B encephalitis was reported by Shoji et ai.7)8) demonstrated abnormalities in the
thalamus and basal ganglia including putamen.
However, their Japanese B encephalitis patients were not studied serially from the early infectious
stage to the chronic stage. In our case,
T2-weighted MRI images demonstrated high
inten-sity localized in the substantia nigra and basal
ganglia, and showed the time sequence of' the
pathologic changes. The pathologic changes
caused by Japanese B encephalitis were better detected by MRI than CT.The sqperiority of MRI becomes more obvious
in the diagnosis of viral encephalitis, in that MRI allows an earlier-and therefore therapeutically more important-specific diagnosis because blood antibody titers against Japanese B encephalitis virus do not increase until the second or third week of illness.
Finally, MRI offers diagnostic advantages in
CNS inflammation of the meninges and extracere-bral complications, as it can show the individual
components and variable extent of the inflamma-tory process as a result of the alteration of the water content, water binding capacity, and blood
flow3}g).
Reference
1) Okuno T: An epidemiological review ofJapanese phalitis. WHO Stat Rep 31: 120-133, 1978
2) Kono K, Kim KH: Comparative epidemiological
tures of Japanese encephalitis in the Republic of Korea, China (Taiwan) and Japan: Bull WHO 30: 263-277,
1968
3) ing in infections of the central nervous system. AJNR 6:
499-504, 1985
4) HaymakerW,SabinAB:Topographicdistributionof lesions in central nervous system in Japanese B phalitis. Arch Neurol Psychiatry 57: 673-692, 1949
5) Takeya S: Histopathology of Japanese encephalitis. Adv Neurol'Sci 6: 75-94 1962
'6) Zimmerman HM: The pathology of Japanese B
phalitis. Am J Pathol 22: 965-991, 1946
7) Shoji H, Murakami T, Murai I et al: A follow-up study by CT and MRI in 3 cases of Japanese
itis. Neuroradiology 32: 215-219, 1990
8) Shoji H, Hirai Y, Kuwasaki N et al: Japanese encephalitis in the Kurume region of Japan: CT and MRI findings.J Neurol 236: 255-259, 1989
9) Schroth G, Kretzschmar K, Gawehn J et al:
Advantage of magnetic resonance imaging in the nosis of cerebral infections. Neuroradielogy 29: 120-126, 1987
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