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CASE REPORT  
Year : 2017  |  Volume : 10  |  Issue : 3  |  Page : 734-736
Dengue encephalitis with cerebellar involvement: A rare case report


1 Department of Medicine, King George's Medical University, Lucknow, Uttar Pradesh, India
2 Department of Anesthesiology, King George's Medical University, Lucknow, Uttar Pradesh, India
3 Department of Obstetrics and Gynaecology, King George's Medical University, Lucknow, Uttar Pradesh, India

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Date of Web Publication21-Aug-2017
 

   Abstract 


Dengue is the most important arthropod-borne viral infection of humans. Clinical presentation of dengue fever ranged from mild clinical febrile illness to severe life-threatening conditions. Many unusual neurological manifestations have been reported with dengue fever. These include aseptic meningitis, encephalitis, myelitis, intracranial hemorrhage, and mono/polyneuropathies. Here, we report a case who presented with cerebellar syndrome with sinus bradycardia as the initial manifestation of dengue fever.

Keywords: Acute cerebellar syndrome, dengue fever, neurological complication

How to cite this article:
Patel ML, Shyam R, Pushkar DK, Sachan R. Dengue encephalitis with cerebellar involvement: A rare case report. Ann Trop Med Public Health 2017;10:734-6

How to cite this URL:
Patel ML, Shyam R, Pushkar DK, Sachan R. Dengue encephalitis with cerebellar involvement: A rare case report. Ann Trop Med Public Health [serial online] 2017 [cited 2019 Nov 15];10:734-6. Available from: http://www.atmph.org/text.asp?2017/10/3/734/213181



   Introduction Top


Dengue fever is a common arboviral infection in the tropical countries resulting in significant morbidity and mortality. Its incidence is toward rising trend in many tropical countries with periodic peaks in epidemic proportions reported following monsoon rains. Global incidence of dengue has drastically increased in the last few years. It is estimated that 390 million people gets dengue infections per year, of which 96 million manifest apparently.[1]

The clinical presentation of dengue infection has a wide spectrum, ranging from mild clinical febrile illness to severe illness. Few patients develop life-threatening complication such as dengue hemorrhagic fever, which is associated with plasma leakage and shock. In recent years, the virological characteristics of dengue viruses have been changing, resulting in widespread neurological complications.

Acute liver failure, acute kidney injury, and multiorgan failure are known complications.[2] However, many unusual manifestations have been reported with dengue, and there are many reports of neurological manifestations. These include aseptic meningitis, encephalitis, myelitis, intracranial hemorrhage, and mono/polyneuropathies.[3] The pathophysiological basis of these neurological manifestations is not fully understood. Cerebellar involvement in dengue infection is not clearly defined. We report a patient of dengue fever who presented with cerebellar syndrome with sinus bradycardia as the initial manifestation.


   Case Report Top


A 16-year-old previously healthy young boy from the rural area of Lucknow city admitted in medical emergency with a history of fever from the past 3 days, speech abnormality and difficulty in walking since last 1 day. On the day of admission, he looked ill and was febrile. On examination, the blood pressure was 110/70 mmHg with no postural hypotension, bradycardia (pulse rate - 48/min), and respiratory rate was 18/min. At the time of admission, he was fully conscious and oriented. He did not have any other apparent source of infection or any focal neurological deficit. There was no neck stiffness, skin rash, hemorrhage, lymphadenopathy, or arthritis. On neurological examination, he was conscious and oriented with a Glasgow coma scale score of 15/15. He had dysarthria and horizontal nystagmus with bilateral dysmetria, dysdiadochokinesia, and incoordination. His gait was wide-based and ataxic with a tendency to fall to the right side more than to the left. The rest of the neurological examination including tone, power, and sensation was normal, but knee reflex was pendular in nature.

His investigation results on admission were hemoglobin 13.0 g%, leukocyte count 4600/mm 3, platelets 32,000/mm 3, hematocrit 40.5%, and erythrocyte sedimentation rate 16 mm/h. Blood film showed leukopenia, lymphocytosis, and thrombocytopenia suggestive of an acute viral infection. Liver transaminases showed a 9–10 fold rise above the upper limit of normal (alanine aminotransferase 408 U/l, aspartate aminotransferase 513 U/l). Renal function, electrolytes, and blood glucose were normal. CPK-MB was 0.949 ng/ml. Other investigations such as high-sensitive troponin-T, pro-BNP, and two-dimensional echocardiography of the heart were normal. Nonstructural protein 1 test for dengue antigen was positive.

His fever subsided by the 4th day of the illness, but the cerebellar symptoms and signs persisted. The platelet count continued to drop reaching up to 25,000/mm 3 by the 5th day of illness. However, no evidence of plasma leakage or shock occurred. He was managed with intravenous and oral fluid replacement. Dengue IgM antibodies by enzyme-linked immunosorbent assay were positive on the 7th day of the illness. Serology for antinuclear cytoplasmic antibody, mycoplasma, herpes simplex virus, Epstein–Barr virus, human immunodeficiency virus, and cytomegalovirus antibodies were not detected. The venereal disease research laboratory test was negative. Magnetic resonance imaging (MRI) of the brain with gadolinium contrast was performed on 12th day of illness showing signal intensity alteration patchy enhancement in the pons, medulla, superior, and middle cerebellar peduncles [Figure 1] and [Figure 2]. The patient refused consent for lumbar puncture.
Figure 1: T2 saggital section showing signal intensity alteration and enhancement in mid brain, pons and cerebellar peduncles

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Figure 2: T2 Flair axial section showing signal intensity alteration and enhancement in mid brain and cerebellar peduncles

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The patient was discharged from hospital on day 14 when platelet count returned to normal. His cerebellar signs progressively improved and the patient was discharged with partial recovery with advice to follow-up in medical outdoor.


   Discussion Top


Neurological complications occur in 0.5%–7.4% of patients with dengue infection.[4] Neurological complications have been classified into dengue virus encephalopathy, dengue virus encephalitis, immune-mediated syndromes (acute disseminated encephalomyelitis, myelitis, Guillain–Barré syndrome, and brachial neuritis), neuromuscular complications (hypokalemic paralysis, transient benign muscle dysfunction, and myositis), and dengue-associated stroke. Immune-mediated mechanisms as well as direct tropic effects of the virus have been postulated to cause these neurological manifestations, and dengue antigen has been demonstrated in the brain in some patients with dengue encephalitis.[5]

Postinfectious cerebellar syndrome has been described in several viral infections, but the association with dengue has been reported in very few instances.[6],[7] In these reports, the onset of cerebellar symptoms varied from 2 days to 2 weeks after the onset of fever.[6],[8] We report a unique case of dengue fever who presented with acute onset cerebellar signs with sinus bradycardia at the time of admission. The gradual recovery of the symptoms in our case suggests a possible self-limiting nature of the disease. The MRI scan of the brain revealed signal intensity alteration and patchy enhancement in the pons, medulla, superior, and middle cerebellar peduncles.

In a study done by Hegde et al., in eight patients suffering from dengue encephalitis, in which all cases exhibited abnormal cerebellar findings in MRI.[9] In addition, MRI signal changes were also noted in the brainstem, thalamus, basal ganglia, internal capsule, insula, medial temporal lobe, cortical, and cerebral white matter. In another study done in four patients with dengue-associated cerebellar features, the MRI showed hyperintensity of cerebellum in T2 sections in two patients while it was normal in the other two.[6],[7]

Acute cerebellitis in relation to virus infection can be primary infective or postinfective.[10] Acute primary infective cerebellitis mostly occurs secondary to infections such as varicella zoster virus, Epstein–Barr virus, measles, mumps, rubella, herpes simplex virus, and Coxsackie virus. Postinfective cerebellitis have been reported as a consequence of varicella zoster virus, Coxsackie virus, Epstein–Barr virus, and human immunodeficiency virus infection. Considering the time of onset of the symptoms, our patient seems to represent a primary infective cerebellitis associated with dengue infection.

Cardiac rhythm abnormalities, including ventricular arrhythmia, atrial fibrillation, and atrioventricular block, have been observed during the acute stage of dengue hemorrhagic fever. Rhythm disturbances, such as bradycardia and ventricular ectopic, have also been reported during the convalescence period of dengue fever. In our patient, sinus bradycardia was present on the day of admission. Being asymptomatic, no specific treatment was given for it. Sharda et al. also reported bradycardia in 8 out of 48 dengue patients.[11]


   Conclusion Top


With this case report, we signify the occurrence of acute cerebellitis as a presenting manifestation of dengue infection thus adding to the neurological complications of the expanded dengue syndrome.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Bhatt S, Gething PW, Brady OJ, Messina JP, Farlow AW, Moyes CL, et al. The global distribution and burden of dengue. Nature 2013;496:504-7.  Back to cited text no. 1
    
2.
Rajapakse S, Rodrigo C, Rajapakse A. Treatment of dengue fever. Infect Drug Resist 2012;5:103-12.  Back to cited text no. 2
    
3.
Gulati S, Maheshwari A. Atypical manifestations of dengue. Trop Med Int Health 2007;12:1087-95.  Back to cited text no. 3
    
4.
Carod-Artal FJ, Wichmann O, Farrar J, Gascón J. Neurological complications of dengue virus infection. Lancet Neurol 2013;12:906-19.  Back to cited text no. 4
    
5.
Lum LC, Lam SK, Choy YS, George R, Harun F. Dengue encephalitis: A true entity? Am J Trop Med Hyg 1996;54:256-9.  Back to cited text no. 5
    
6.
Weeratunga PN, Caldera HP, Gooneratne IK, Gamage R, Perera WS, Ranasinghe GV, et al. Spontaneously resolving cerebellar syndrome as a sequelae of dengue viral infection: A case series from Sri Lanka. Pract Neurol 2014;14:176-8.  Back to cited text no. 6
    
7.
Karunarathne S, Udayakumara Y, Fernando H. Epstein-Barr virus co-infection in a patient with dengue fever presenting with post-infectious cerebellitis: A case report. J Med Case Rep 2012 30;6:43.  Back to cited text no. 7
    
8.
Verma R, Sharma P, Garg RK, Atam V, Singh MK, Mehrotra HS. Neurological complications of dengue fever: Experience from a tertiary center of north India. Ann Indian Acad Neurol 2011;14:272-8.  Back to cited text no. 8
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9.
Hegde V, Aziz Z, Kumar S, Bhat M, Prasad C, Gupta AK, et al. Dengue encephalitis with predominant cerebellar involvement: Report of eight cases with MR and CT imaging features. Eur Radiol 2015;25:719-25.  Back to cited text no. 9
    
10.
Sawaishi Y, Takada G. Acute cerebellitis. Cerebellum 2002;1:223-8.  Back to cited text no. 10
    
11.
Sharda M, Gupt A, Nagar D, Soni AK. Dengue fever: An additional cause for bradycardia. J Assoc Physicians India 2014;62:362-3.  Back to cited text no. 11
    

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Correspondence Address:
Munna Lal Patel
Department of Medicine, King George Medical University, C-28, Sec-J Aliganj, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ATMPH.ATMPH_93_17

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