Dengue Encephalitis

Case History: An 18-year-old patient came with complaints of fever and weakness in lower limbs for seven days. Lab investigation showed reduced platelets and Dengue positive serolology.

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Figure 1a:  T2W show hyperintensity in thalami and brainstem.

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Figure 1b

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Figure 2: FLAIR images showing hyperintensity in occipital whitematter ,b/l thalami , mid brain,pons and b/l cerebellar hemispheres.

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Figure 3: FLAIR images  showing hyperintensity  in occipital whitematter ,b/l thalami , mid

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Figure 4: FLAIR images  showing hyperintensity  in occipital whitematter ,b/l thalami , mid

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Figure 5: FLAIR images  showing hyperintensity  in occipital whitematter ,b/l thalami , mid

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Figure 6: FLAIR images  showing hyperintensity  in occipital whitematter ,b/l thalami , mid 

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Figure 7: DWI Show diffusion restriction in thalami ,brainstem.

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Figure 8: DWI Show diffusion restriction in thalami ,brainstem.

Patient underwent MRI at 1.5 T with DWI. MRI shows hyperintensity in b/l occipital whitematter, b/l thalami, brainstem and pons and b/l cerebellar hemispheres.

DWI images showed diffusion restriction in b/l thalami,brainstem and b/l cerebellar hemispheres.

Diagnosis: Dengue encephalitis.

The diagnosis of dengue was confirmed by the serum antibodies to dengue and the presence of a dengue antigen in the cerebrospinal fluid.

Discussion: The Dengue virus is a single-stranded RNA virus of the Flaviviridae family causing Dengue fever and dengue hemorrhagic fever. Encephalopathy is a very common neurological complication of dengue fever. Dengue encephalopathy is usually secondary to multisystem derangement like shock, hepatitis, coagulopathy, and concurrent bacterial infection[1]. Dengue encephalitis is a different entity that occurs due to direct neuronal infiltration by the dengue virus. Dengue virus infections are among the most common cause for hospital admissions in western Maharashtra. It is estimated that 50 to 100 million infections and 25,000 fatalities occur worldwide every year.

The World Health Organization (WHO) surveillance shows that global incidence is rising[4]. Numerous neurological manifestations like transverse myelitis[2], myositis[5], and Gullian-Barre syndrome[6] have been reported. Dengue encephalopathy is a well-recognized and common entity with incidence ranging from 0.5 to 6.2 %[5]. The possible mechanisms are liver failure (hepatic encephalopathy), cerebral hypoperfusion (shock), cerebral edema (vascular leak), deranged electrolytes, and intracranial bleeding due to thrombocytopenia or coagulopathy, which is secondary to hepatic failure[7]. There are subsets of patients in whom the cause for neurological injury remains unclear even after excluding the above-mentioned indirect mechanisms. These raise the possibility of direct neuronal injury due to the dengue virus. Dengue is thought to be a non-neurotropic virus[3]. However, there are reports of the demonstration of dengue virus and IgM antigen in the cerebrospinal fluid (CSF) of patients with encephalopathy. There are case reports by Misra et al., from India[5], and Solomon et al., from Vietnam[2]. In the study described by Misra et al.[5], 11 patients were seen with confirmed dengue infection, but no CSF study was reported. Solmon et al.[2], diagnosed dengue encephalitis in nine patients, but virus or antibody was found in the CSF of only two cases. Kankirawatana et al.[8] and Kularatne et al.[9], had a similar study in which they showed the association of dengue with encephalitis.

On admission, our patient had a history suggestive of encephalopathy with shock, coagulopathy, metabolic acidosis, and deranged liver functions. This encephalopathy is usually explained by the abnormalities mentioned earlier in the text. However, subsequent evaluation with positive MRI and CSF showed evidence of encephalitis. This showed the co-existence of encephalopathy and encephalitis. The MRI findings noted in our case are most characteristic of JE and not commonly seen with dengue fever[10]. The pattern of involvement (bilateral thalamic involvement with foci of hemorrhage, with involvement of temporal lobe and brain stem) is very uncommon with dengue. There is only one similar case report by Kamble et al., with similar MRI findings [10]. This case is presented to highlight the possible extensive involvement of the brain by dengue virus.

References
1. Koley TK, Jain S, Sharma H, Kumar S, Mishra S, Gupta MD, et al. Dengue encephalitis. J Assoc Physicians India. 2003;51:422–3.
2. Solomon T, Dung NM, Vaughn DW, Kneen R, Thao LT, Raengsakulrach B, et al. Neurological manifestations of dengue infection. Lancet. 2000;355:1053–9.
3. Nathanson N, Cole GA. Immunosuppression and experimental virus infection of the nervous system.Adv Virus Res. 1970;16:397–428.
4. Dengue haemorrhagic fever; diagnosis, treatment, prevention, and control. Geneva: WHO; 2005. World Health Organisation.
5. Misra UK, Kalita J, Syam UK, Dhole TN. Neurological manifestations of dengue virus infection. J Neurol Sci. 2006;244:117–22.
6. Sulekha C, Kumar S, Philip J. Guillain-Barre syndrome following dengue fever. Indian Pediatr.2004;41:948–50.
7. Varatharaj A. Encephalitis in the clinical spectrum of dengue infection. Neurol India. 2010;58:585–91.
8. Kankirawatana P, Chokephaibulkit K, Puthavathana P, Yoksan S, Somchai A. Dengue infection presenting with nervous system manifestation. J Child Neurol. 2000;15:544–47.
9. Kularatne SA, Pathirage MM, Gunasena S. A case series of dengue fever with altered consciousness and electroencephalogram changes in Sri Lanka. Trans R Soc Trop Med Hyg. 2008;102:1053–4.
10. Kamble R, Peruvamba JN, Kovoor J, Ravishankar S, Kolar BS. Bilateral thalamic involvement in dengue infection. Neurol India. 2007;55:418–19.

Harpreet Singh, MD, JP Scan Private Diagnostic Center, Khanna, Punjab, India