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Table of Contents    
Year : 2019  |  Volume : 67  |  Issue : 1  |  Page : 273-275

Transient splenial hyperintensity in a rare case of chikungunya encephalitis

1 Department of Neuroradiology, Sri Bala Ji Action Medical Institute, New Delhi, India
2 Department of Gynaecology, Kasturba Hospital, New Delhi, India
3 Department of Neurology, Sri Bala Ji Action Medical Institute, New Delhi, India

Date of Web Publication7-Mar-2019

Correspondence Address:
Dr. Rupinder Singh
Department of Neuroradiology, Sri Bala Ji Action Medical Institute, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.253649

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How to cite this article:
Singh R, Kaur R, Pokhariyal P, Aggarwal R. Transient splenial hyperintensity in a rare case of chikungunya encephalitis. Neurol India 2019;67:273-5

How to cite this URL:
Singh R, Kaur R, Pokhariyal P, Aggarwal R. Transient splenial hyperintensity in a rare case of chikungunya encephalitis. Neurol India [serial online] 2019 [cited 2022 May 27];67:273-5. Available from: https://www.neurologyindia.com/text.asp?2019/67/1/273/253649


Chikungunya, a relatively rare and benign form of viral infection caused by a RNA-virus belonging to the genus Alphavirus of Togaviridae family transmitted by Aedes aegypti mosquito, was first recognized as an epidemic in India in Calcutta in 1963.[1] Recently chikungunya has reached an epidemic proportion in Delhi, India. Chikungunya infection typically induces a mild disease in humans, characterized by fever, myalgia, arthralgia, and rash. Neurological complications of chikungunya infection are infrequent and have been reported rarely, with encephalitis being the most common.[2] Transient signal abnormality solely involving the splenium of corpus callosum has been reported in encephalitis but not with chikungunya virus. We present the clinical and neuroimaging of chikungunya encephalitis showing transient splenial hyperintensity, a relatively unknown and rare manifestation.

A 19-year-old boy was admitted to the hospital with chief complaints of high-grade fever with chills and joint pains for 2 days. He had altered behavior, restlessness, irrelevant talking, and abnormal involuntary movements for the past 1 day. On the day of the admission, he developed altered sensorium along with a maculopapular rash all over the body. On physical examination, he was drowsy, disoriented, and not following commands. He was febrile (101.8°F) and his body mass index was 20 kg/m 2. His pulse rate was 86 per minute, blood pressure was 110/70 mmHg, and there was no superficial lymphadenopathy. His Glasgow Coma Scale (GCS) was 8/15 (E2M5V1), and pupils were equal and reacting. On examination decorticate posturing of the neck, generalized muscle rigidity, bilateral extensor plantars and brisk deep tendon reflexes were seen. Examination of the respiratory system, cardiovascular system, and abdomen were within normal limits. On the day of the admission investigations showed hemoglobin 12.9 g%, total leucocyte count 10,800/mm 3 (neutrophils 92.4%, eosinophils 0.0%, basophils 0%, lymphocytes 2.8%, monocytes 4.8%), platelet count 97,000 per mm 3, plasma glucose 90 mg/dl, sodium 124 mEq/dl, potassium 5.2 mEq/dl, blood urea 24 mg/dl, serum creatinine 0.7 mg/dl, serum bilirubin 1.96 mg/dl, total protein 7.2 g/dl (albumin 4.6 g/dl), aspartate aminotransferase 48 U/L, and alanine aminotransferase 15 U/L. He was managed with intravenous dexamethasone 12 mg/day and acyclovir and supportive care (ventilation). Subsequent investigations showed polymerase chain reaction (PCR) for chikungunya as positive. Tests for dengue antigen (nonstructural protein 1, NS1) and malaria antigen were negative.

Magnetic resonance imaging (MRI) of the brain done on the second day of the admission revealed hyperintensity of splenium of corpus callosum in T2/fluid attenuated inversion recovery (FLAIR) with restricted diffusion, subtle altered signal in bilateral frontal deep white matter seen on diffusion weighted imaging (DWI) [Figure 1], although T1 with contrast did not show any such abnormality [Table 1]. On lumbar puncture, cerebrospinal fluid (CSF) pressure was high (8–10 drops/s). CSF examination showed no cells, with glucose 60 mg/dl and protein 31 mg/dl. CSF PCR for herpes was negative. He started improving gradually with conservative management and was extubated after 2 days. A repeat MRI of the brain done after 7 days showed complete resolution of the splenial hyperintensity [Figure 2] and [Table 1]. He was discharged from the hospital after 8 days without any neurological deficit.
Figure 1: Initial Magnetic resonance imaging in case of chikungunya encephalitis, showing abnormal signals involving entire splenium of corpus callosum (“Boomerang sign”) on T2-weighted sagittal(A), diffusion-weighted sagittal image (C), and apparent diffusion coefficient sagittal image with ADC value of 0.34 ± 10_3 mm2/s (D) images with subtle increased signal intensity in deep white matter of bilateral frontal lobes on diffusion-weighted image axial (B)

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Table 1: Comparison of imaging features on initial and follow up MR (1 week)

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Figure 2: Repeat Magnetic resonance imaging done after 1week, showing complete resolution of splenial and white matter signal on T2-weighted sagittal (a) diffusion-weighted image axial (b) and FLAIR axial (c) images.

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Chikungunya virus belongs to the genome of alphaviruses and causes an acute viral infection characterized by fever, rash, and arthralgia. Neurological complications of chikungunya infection are infrequent and have been reported rarely in outbreaks in India and the Reunion Islands.[2] Various neurological complications have been described including meningoencephalitis, myeloradiculitis, myelitis, myeloneuropathy, Guillian–Barre syndrome, external ophthalmoplegia, facial palsy, sensorineural deafness, and optic neuritis. Our patient was infected during the recent epidemic in New Delhi, India. He presented with altered sensorium and irrelevant talking with a history of high-grade fever and rash and proved to be chikungunya positive by PCR. Such presentation has also been reported by Tournebize et al.,[3] who found altered mental status in 95% of the patients, headache in 30.4%, seizure in 26%, and motor dysfunction in 4.3% of their 23 cases. In 300 cases, Chandak et al.,[4] observed encephalitis in 55.1%, myelopathy in 14.3%, neuropathy in 14.3%, myeloneuropathy in 14.3%, and myopathy in 2% among various neurological syndromes.

Transient signal abnormality solely involving the splenium of corpus callosum on MRI is a rarely encountered finding in clinical practice. A well-defined focal hyperintensity of the splenium of corpus callosum is also known as Boomerang sign. Splenial lesions are visualized as hyperintense lesions on T2-weighted images, FLAIR, and/or DWI MRI. The occurrence of this abnormality was first described by Chason et al., as a transient postictal focal edema indicating transhemispheric propagation of seizure through the corpus callosum.[5] Since then, various etiological factors and pathophysiologic mechanisms have been proposed but none is well proven.[6] Various causes including epilepsy, overdose of antiepileptic drugs or sudden change of drug, infections such as Epstein Barr virus, malaria,  Salmonellosis More Details, measles, herpes simplex encephalitis, pre-eclampsia, vitamin B-12 deficiency, acute disseminated encephalomyelitis, multiple sclerosis, and trauma have been described in literature by different researchers.[6],[7],[8],[9]

The pathogenesis of the transient changes in the splenium of corpus callosum is still debatable. In encephalopathy/encephalitis, the presumed mechanism of acute intramyelinic edema is the separation of myelin layers leading to transient abnormalities on MRI.[10] Tada et al., proposed that splenial lesions may be secondary to intramyelinic edema and influx of inflammatory cells and macromolecules, combined with cytotoxic edema causes decreased apparent diffusion coefficient (ADC) levels. They suggested that ADC may return to normal if the cause is resolved quickly.[10] Breakdown of the blood–brain barrier producing transient focal edema has been implicated as another mechanism by some authors, especially in seizures.[9]

Chikungunya encephalitis has not yet been implicated in reversible splenial lesions on MRI. The frequently described association of seizures could not be seen in our patient as he never had convulsions in the past or during hospitalization. Although there is a report of splenial hyperintensity with recurrent herpes simplex encephalitis,[7] MRI finding of our case cannot be attributed to a herpetic etiology due to the lack of other suggestive MRI findings, CSF report, and most importantly, the negative PCR for herpes in CSF. The diagnosis of chikungunya encephalitis in this case was certain, and hence, this appears to be another cause of the typical disappearing splenium-of-corpus callosum lesion on MRI.

Transient hyperintensities of splenium of corpus callosum in MRI or Boomerang sign is an uncommon finding in clinical practice. Various causes have been documented in the literature with persistent seizures being the most common. To our knowledge, chikungunya encephalitis has never been described to cause such an abnormality. We report this case to document chikungunya encephalitis as a cause of transient MRI findings so that the treating physician must consider it along with other causes previously described, especially if the patient is not a known case of epilepsy or is not receiving any antiepileptic drug therapy.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initial will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Arankalle VA, Shrivastava S, Cherian S, Gunjikar RS, Walimbe AM, Jadhav SM, et al. Genetic divergence of Chikungunya viruses in India (1963-2006) with special reference to the 2005-2006 explosive epidemic. J Gen Virol 2007;88:1967-76.  Back to cited text no. 1
Chatterjee SN, Chakravarti SK, Mitra AC, Sarkar JK. Virological investigation of cases with neurological complications during the outbreak of hemorrhagic fever in Calcutta. J Indian Med Assoc 1965;45:314-6.  Back to cited text no. 2
Tournebize P, Charlin C, Lagrange M Neurological manifestations in Chikungunya: About 23 cases collected in Reunion Island Revue Neurologique 2009;165:48-51.  Back to cited text no. 3
Chandak NH, Kashyap RS, Kabra D, Karandikar P, Saha SS, Morey SH, et al. Neurological complications of Chikungunya virus infection. Neurol India 2009;57:177-80.  Back to cited text no. 4
[PUBMED]  [Full text]  
Chason DP, Fleckenstein JL, Ginsburg MI. Seattle, WA, USA Chicago: Old Smith Printers; 1996. Jun 21-27, Transient Splenial Edema in Epilepsy: MR Imaging Evaluation Proceedings of the 34th annual meeting of the American Society of Neuroradiology  Back to cited text no. 5
Conti M, Salis A, Urigo C, Canalis L, Frau S, Canalis GC. Transient focal lesion in the splenium of the corpus callosum: MR imaging with an attempt to clinical-physiopathological explanation and review of the literature. Radiol Med 2007;112:921-35.  Back to cited text no. 6
Tokumaru AM, Horiuchi K, Kaji T, Kohyama S, Sakata I, Kusano S. MRI findings of recurrent herpes simplex encephalitis in an infant. Pediatr Radiol 2003;33:725-8.  Back to cited text no. 7
Oster J, Doherty C, Grant PE, Simon M, Cole AJ. Diffusion-weighted imaging abnormalities in the splenium after seizures. Epilepsia 2003;44:852-4.  Back to cited text no. 8
Kim SS, Chang KH, Kim ST, Suh DC, Cheon JE, Jeong SW, et al. Focal lesion in the splenium of the corpus callosum in epileptic patients: Antiepileptic drug toxicity? AJNR Am J Neuroradiol 1999;20:125-9.  Back to cited text no. 9
Tada H, Takanashi J, Barkovich AJ, Oba H, Maeda M, Tsukahara H, et al. Clinically mild encephalitis/encephalopathy with a reversible splenial lesion. Neurology 2004;63:1854-8.  Back to cited text no. 10


  [Figure 1], [Figure 2]

  [Table 1]


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