| Article Access Statistics|
| Viewed||4917 |
| Printed||142 |
| Emailed||5 |
| PDF Downloaded||173 |
| Comments ||[Add] |
| Cited by others ||6 |
Click on image for details.
|Year : 2003 | Volume
| Issue : 3 | Page : 397-398
Hemiplegia: An initial manifestation of Japanese encephalitis
Nalini A, Arunodaya GR, Taly AB, Swamy HS, Vasudev MK
Departments of Neurology, National Institute of Mental Health and Neuro Sciences, Bangalore - 560 029
Department of Neurology, National Institute of Mental Health & Neuro Sciences, P.O. No. 2900, Bangalore - 560029
A 7-year-old boy from an area endemic to Japanese encephalitis (JE) manifested with acute febrile illness, left hemiplegia and preserved consciousness during the prodromal phase of illness. The child developed features of encephalitis 48 hours after the onset of hemiplegia. IgM MAC ELISA for JE virus revealed high titers in the serum and cerebrospinal fluid suggestive of JE. MRI of the brain showed asymmetrical bilateral thalamic hyperintense lesions on T2 weighted image, considered diagnostic of JE. Hemiplegia during the prodromal phase or as an initial symptom of JE is rather unusual.
|How to cite this article:|
Nalini A, Arunodaya G R, Taly A B, Swamy H S, Vasudev M K. Hemiplegia: An initial manifestation of Japanese encephalitis
. Neurol India 2003;51:397-8
Japanese encephalitis (JE) was first recognized as a clinical entity in 1871. The disease progresses through prodromal, encephalitic and convalescent stages. Children below 15 years bear the brunt of the disease. We describe a 7-year-old child who presented with fever and left hemiplegia with preserved consciousness during the prodromal stage of illness, and after 48 hours developed features of the encephalitic stage of JE.
A 7-year-old boy presented with acute onset of high-grade fever with chills and rigors associated with headache. A day later he developed left hemiplegia and left facial weakness with well-preserved consciousness. Evaluation on the third day of the illness revealed a conscious, alert and well-oriented child with normal speech. Fundi were normal. The child had a left hemiplegia with mild spasticity and left facial weakness. Twenty-four hours later, the child developed altered behavior with visual hallucinations and on the 5th day developed three episodes of primary generalized tonic clonic seizures and lapsed into altered sensorium. After 8 days there was progressive improvement in the neurological condition and by the 15th day of the illness he regained consciousness and obeyed simple commands. He had a left-sided hemiparesis with facial weakness. He also had mild right hemiparesis with spasticity. All stretch reflexes were brisk, and plantar response was extensor bilaterally. One month later the child was conscious, alert and speaking sentences, however the left hemiparesis was persistent.
ESR was 94 mm at first hour and became normal after two weeks. Lumbar CSF examination on the 3rd day of the illness revealed 340 cells / cumm, all lymphocytes, protein of 114 mg% and glucose of 66 mg%. IgM MAC ELISA for JE virus revealed titers of 226 units in serum and 223 units in CSF, strongly suggestive of JE. The ELISA test for antimycobacterial antibodies was negative. A repeat CSF examination done on the 8th day of the illness revealed 10 cells, all lymphocytes, protein of 27 mg% and glucose of 70 mg%. CT scan brain on the second day of admission revealed diffuse cerebral edema. MRI of the brain performed on the 28th day after the onset of illness revealed asymmetrical hypointensity on T1 [Figure - 1] and asymmetrical hyperintense signals involving both the thalami on T2 weighted sequences. Axial FLAIR images also showed hyperintense foci involving both the thalami [Figure - 2] and small areas of hyperintense foci in the right frontal and parietal cortices. Diffusion weighted sequences applied in three orthogonal directions showed asymmetrical hyperintense foci in both the thalami. These lesions were hyperintense on diffusion coefficient maps, suggesting the fluid content to be proteinaceous.
Hemiplegia as an initial manifestation of JE is a rare phenomenon. Our patient was from an area endemic to JE. He presented with a dense hemiplegia at the onset of illness and progressed to the encephalitic stage after 48 hours. The CSF IgM MAC ELISA titer was diagnostic of JE. A single CSF antibody titer of 100 units or more is strongly suggestive of JE even in patients hailing from endemic areas. MRI of the brain revealed bilateral asymmetrical thalamic lesions which are characteristic of JE, particularly in endemic areas. Bilateral symmetrical thalamic lesions are also seen in metabolic diseases such as Wilson's disease, anoxic encephalopathy and childhood hepatocerebral degeneration. However, the clinical and laboratory features of these diseases are distinctive compared to JE. Similar thalamic lesions are also seen in cerebral deep venous system thrombosis and basilar artery occlusion, but MRI brain did not reveal evidence of venous thrombosis and diffusion weighted images with apparent diffusion coefficient maps were also suggestive of thalamic necrosis and not infarction.
The pathological lesions in JE are polymorphic and diffuse involving various parts of the neuraxis. Multiple small necrolytic lesions are observed in the superficial cortical and deep gray matter. Gliomesenchymal nodules in gray matter are important pathological lesions and these are often found in children less than 15 years of age. JE typically involves the thalami. Rarely, basal ganglia and cerebellum are affected. It is also known to involve the brainstem, cerebral cortex, hippocampus, and white matter. It is possible that the thalamic lesions caused by the virus occurred prior to the encephalon involvement resulting in the hemiplegia. During the convalescent period the child was noticed to have mild right-sided weakness, which could be explained by the left thalamic involvement.
|1.||Desai A, Ravi V, Guru SC, et al. Detection of autoantibodies to neural antigens in the CSF of Japanese encephalitis patients and correlation of findings with the outcome. J Neurol Sci 1994;122:109-16. [PUBMED] |
|2.||Shankar SK, Rao VT, Mruthyunjayana BP, et al. Autopsy study of brains during an epidemic of Japanese encephalitis in Karnataka. Ind J Med Res 1983;78:431-40. |
|3.||Miyake M. The pathology of Japanese encephalitis - a review. Bull WHO 1964; 30:153. [PUBMED] |
|4.||Pradhan S, Pandey N, Shashank S, et al. Parkinsonism due to predominant involvement of substantia nigra in Japanese encephalitis. Neurology 1999;53:1781-6. [PUBMED] [FULLTEXT]|
|5.||Abe T, Kojima K, Shoji H, et al. Japanese encephalitis. J Magn Reson Imaging 1998;8:755-61. [PUBMED] |