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TOPIC OF THE ISSUE: LETTER TO EDITOR
Year : 2010  |  Volume : 58  |  Issue : 4  |  Page : 595-596

Acute disseminating encephalomyelitis with hemorrhage following dengue


1 Department of Medicine, Christian Medical College and Hospital, Ludhiana - 141 008, Punjab, India
2 Department of Radiodiagnosis, Christian Medical College and Hospital, Ludhiana - 141 008, Punjab, India

Date of Acceptance17-Jul-2010
Date of Web Publication24-Aug-2010

Correspondence Address:
Uttam George
Department of Radiodiagnosis, Christian Medical College and Hospital, Ludhiana - 141 008, Punjab
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.68661

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How to cite this article:
Gera C, George U. Acute disseminating encephalomyelitis with hemorrhage following dengue. Neurol India 2010;58:595-6

How to cite this URL:
Gera C, George U. Acute disseminating encephalomyelitis with hemorrhage following dengue. Neurol India [serial online] 2010 [cited 2019 Aug 23];58:595-6. Available from: http://www.neurologyindia.com/text.asp?2010/58/4/595/68661


Sir,

During an outbreak of dengue in north-west India, a 27-year-old male presented with history of fever, myalgias and vomiting for 5 days. He later presented with two episodes of generalized tonic-clonic seizures. On admission, he was comatose and unresponsive to painful stimulus, and his pupils were reactive to light with equal and reacting pupils. Investigations revealed hemoglobin of 10.7 g/dl, hematocrit of 32%, white cell count of 11 x 10 9 /L, platelet count of 19 x 10 9 /L, blood urea of 102 mg/dl, serum creatinine of 1.9 mg/dl, alanine aminotransferase (ALT) of 1,457 U/L, aspartate aminotransferase (AST) of 832 U/L, total protein of 4.8 g/dl, albumin of 2.3 g/dl, total bilirubin of 1.7 mg/dl and direct bilirubin of 0.16 mg/dl. Dengue-specific antibody was negative at admission with rising titer to 59.7 units (normal ≤10 units) 3 days later. Electroencephalography revealed background activity of 5-6 Hz intermixed with delta waves. Cerebrospinal fluid examination showed absent cells and mild rise in protein (58 mg/dl) and glucose (162 mg/dl; blood glucose was 190 mg/dl). cerebrospinal fluid (CSF) polymerase chain reaction for herpes simplex virus was negative while serology for Japanese encephalitis could not be performed due to nonavailability. Magnetic resonance imaging (MRI) of the brain showed confluent hyperintensities on T2-weighted and T2 FLAIR images in the periventricular and subcortical white matter bilaterally in the frontal and parietal lobes and also left temporal lobe with involvement of U-fibers at some locations [Figure 1]a, b. Symmetrical involvement of the thalami [Figure 2]a, mid-brain, pons, middle cerebellar peduncle as well as the cerebellar hemispheres was also seen [Figure 2]d. T2* images showed small areas of hemorrhage involving both thalami as well as the cerebellum [Figure 2]b and e. The thalami, pons and cerebellar hemispheres showed restricted diffusion on DWI [Figure 2]c and f. These MR features following a viral-like prodrome, with rising dengue-specific antibody titers suggesting a diagnosis of postdengue acute disseminated encephalomyelitis (ADEM). In view of the extensive demyelination, a course of high-dose corticosteroids was administered. The patient showed good response and slowly regained consciousness with gradual recovery of power in the limbs. At 8 months follow-up, he was asymptomatic with no neurological deficits. Repeat MRI showed near-complete resolution of all the lesions with minimal hemorrhagic residues in both thalami and cerebellum.
Figure 1 : Axial T2 FLAIR (a) and sagittal T2-weighted (b) images showing extensive involvement of the frontal and parietal lobes, including the subcortical U fibers

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Figure 2 : T2 FLAIR and T2-weighted images showing involvement of the thalamus (a), pons and cerebellum (d), with the presence of hemorrhage on T2* (b and e) and restricted diffusion on DWI (c and f)

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Neurological complications of dengue include encephalitis, transverse myelitis, Guillain Barre syndrome, neuromyelitis optica and ADEM. [1],[2],[3] Imaging studies in ADEM following dengue are few. In the patient described by Brito et al., [4] the MRI showed white matter lesions in the centrum semiovale, corona radiata, callosal-septal interface and thalamus and in the patient examined by Yamamoto et al., [5] thoracic spinal cord showing demyelinating lesion was described. [5] Our patient had extensive involvement of the frontal, parietal and temporal white matter as well as the corpus callosum. White matter lesions also involved the brainstem, bilateral thamalmi and cerebellum. DWI showed restricted diffusion in the lesions in the thalamus, brainstem and cerebellum. An additional finding in our patient was the presence of hemorrhage involving the thalami and cerebellar hemispheres. The hemorrhagic foci were within corresponding areas of restricted diffusion. This coincident location may be explained by acute inflammation or vasculitis with subsequent vessel occlusion and wall necrosis leading to the hemorrhage. [6] In the absence of histopathological evidence, the pathogenesis with these MRI lesions can only be hypothesized. These MRI features are similar to the findings seen in patients with ADEM, suggesting an immune-mediated pathogenetic mechanism. The hemorrhagic manifestation in addition could be explained by the existing coagulopathy. The follow-up scan at 8 months showed near-complete resolution with minimal hemorrhagic residues in the thalamus and cerebellar hemispheres [Figure 3]. Such hemorrhagic foci in dengue with demyelination have not been reported. Identifying such a pattern should prompt a work-up for dengue, especially in the endemic regions as well as in travelers frequenting such locations.
Figure 3 : Follow-up magnetic resonance imaging at 8 months shows minimal residual changes in the thalamus (a) with near-complete resolution of the frontal and parietal white matter involvement (a and b)

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 » References Top

1.Solomon T, Dung NM, Vaughn DW, Kneen R, Thao LT, Raengsakulrach B, et al. Neurological manifestations of dengue infection. Lancet 2000;355:1053-9.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.Cam BV, Fonsmark L, Hue NB, Phoung NT, Poulsen A, Heegaard ED. Prospective case controlled study of encephalopathy in children with dengue hemorrhagic fever. Am J Trop Med Hyg 2001;65:848-51.  Back to cited text no. 2      
3.Misra UK, Kalita J, Syam UK, Dhole TN. Neurological manifestations of dengue virus infection. J Neurol Sci 2006;244:117-22.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Brito CA, Sobreira S, Cordeiro MT, Lucena-Silva N. Acute disseminated encephalomyelitis in classic dengue. Rev Soc Bras Med Trop 2007;40:236-8.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]  
5.Yamamoto Y, Takasaki T, Yamada K, Kimura M, Washizaki K, Yoshikawa K. Acute disseminated encephalomyelitis following dengue fever. J Infect Chemother 2002;8:175-7.  Back to cited text no. 5      
6.Lee HY, Chang KH, Kim JH, Na DG, Kwon BJ, Lee KW, et al. Serial MR Imaging Findings of acute hemorrhagic leukoencephalitis: a case report. AJNR Am J Neuroradiol 2005;26:1996-9.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]  


    Figures

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