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Year : 2018  |  Volume : 21  |  Issue : 3  |  Page : 233-234

Transient hemorrhagic demyelination following insect bite

1 Department of Radiodiagnosis, PGIMER, Chandigarh, India
2 Department of Neurology, PGIMER, Chandigarh, India

Date of Web Publication4-Sep-2018

Correspondence Address:
Dr. Sameer Vyas
Department of Radiodiagnosis and Imaging, PGIMER, Chandigarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/aian.AIAN_428_17

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How to cite this article:
Vyas S, Paruthi C, Goyal MK, Khandelwal N. Transient hemorrhagic demyelination following insect bite. Ann Indian Acad Neurol 2018;21:233-4

How to cite this URL:
Vyas S, Paruthi C, Goyal MK, Khandelwal N. Transient hemorrhagic demyelination following insect bite. Ann Indian Acad Neurol [serial online] 2018 [cited 2023 Feb 8];21:233-4. Available from:


An 18-year-old boy presented with a history of insect bite while sleeping. He noticed pain in his hand, which woke him up, and mild local redness. However, no bite marks were seen. Thirty minutes later, he developed progressive difficulty in breathing and after 6 h became unconscious. There was no history of seizures, fever, headache, or systemic complaints. There was no history suggestive of stridor. At presentation, Glasgow Coma Scale was M2E2V2. He was intubated immediately on arrival. External ocular movements were normal by Doll's maneuver, and pupils were reacting to the light. Deep tendon reflexes were all brisk, and plantar responses were bilaterally extensor. Magnetic resonance imaging (MRI) revealed multiple T2- and fluid-attenuated inversion recovery (FLAIR) hyperintense foci in the corpus callosum and bilateral cerebral white matter, with associated microhemorrhages [Figure 1]. Electroencephalography revealed background slowing in theta to delta range suggestive of diffuse encephalopathy. He was put on ventilator support and was managed symptomatically. He received intravenous methylprednisolone in a dosage of 1 g daily for 5 days. He progressively improved, and 15 days later, he had complete resolution clinically and radiologically [Figure 2].
Figure 1: Magnetic resonance imaging brain (at the time of symptoms), fluid-attenuated inversion recovery (a), and T2-weighted (b) images showing hyperintensities in bilateral white matter (arrowhead) and corpus callosum (arrow). Corpus callosum showing microhemorrhages on magnitude (c) and phase (d) susceptibility-weighted images and diffusion restriction on diffusion (e) and apparent diffusion coefficient (f) images

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Figure 2: Magnetic resonance imaging brain after 3 weeks showing complete resolution on T2- (a) and diffusion-weighted (b) images

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Insect bite is a common occurrence and usually presents with inflammatory changes at the local site. Depending on the type of insect and the patient's immune response, the inflammatory reaction may vary from local redness and tenderness to severe swelling, necrosis, and even systemic anaphylactic response. Neurological symptoms and encephalopathy following insect bite occur when the insect is a vector or carrier for viral or rickettsial infection. While mosquitoes cause various viral encephalitides such as West Nile and Japanese encephalitis, ticks cause Lyme disease and rickettsial infections. These have an incubation period, about 4–10 days for most infections.

Encephalitis or encephalopathy caused by the insect itself rather than it acting as a vector may also occur.[1] This occurs due to the effect of the toxins released in the bite,[2] such as high alpha-latrotoxin in black widow spider bite, which causes massive presynaptic release of acetylcholine, or neuromuscular excitotoxins in certain spider bites.[3] Apart from these, encephalopathies due to insect bite might also be due to inflammatory reaction in the central nervous system (CNS). Inflammation in CNS leads to demyelination and thus could be picked up on MRI as T2 and FLAIR hyperintensities.

Toxic leukoencephalopathy occurs due to white matter damage, and various toxic agents have been implicated. These include chemotherapeutic drugs, antimicrobials, cranial irradiation, drugs of abusive, and various other environmental toxins. It presents with altered mental status and variable neurobehavioral deficits.[4] Acute phase of leukodystrophy is characterized by MR abnormalities in the form of T2 and FLAIR hyperintensities with diffusion restriction in the white matter, mainly in periventricular region.[5] Removal of exposure to the offending agent leads to improvement, and clinical reversal is accompanied by radiological reversal.[6] These transient white matter imaging abnormalities are likely due to cytotoxic or intramyelinic edema, which has been thought to occur due to various causes. Chemotherapeutic agents lead to demyelination and myelin vacuolation due to macrophage infiltration. Some may cause microvascular injury, injury to the capillary endothelium, or even excitotoxic damage to the neurons. Free radical-mediated injury is also speculated.[5]

However, insect bite as a cause of leukoencephalopathy has not been described earlier. The exact cause is not known. We think that white matter damage due to some unknown toxins in the insect bite would have been a cause. As it was accompanied by hemorrhages, microvascular injury is the most probable explanation. Microvascular injury leads to disruption of the blood–brain barrier which would have caused the accompanying transient white matter changes. Furthermore, direct toxic effect due to some unknown toxin would explain the relatively rapid onset of clinical symptoms, without any significant incubation period as in vector-borne infective encephalitis.

To conclude, we describe insect bite as a cause of toxic hemorrhagic leukoencephalopathy which has not been described earlier. A variety of toxins have been known to cause leukoencephalopathy, but through this case, we wish to highlight that a number of other still unknown toxins may cause this. In view of clinical symptoms and history of suspected exposure to any toxin, this entity should be considered after exclusion of the other diagnosis. MRI in the acute phase is able to detect white matter abnormalities. Removal of exposure to the offending agent is of utmost importance.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

   References Top

Salimi H, Cain MD, Klein RS. Encephalitic arboviruses: Emergence, clinical presentation, and neuropathogenesis. Neurotherapeutics 2016;13:514-34.  Back to cited text no. 1
Graudins A. Venomous arthropods. In: Shannon MW, Borron SW, Burns MJ, editors. Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose. 4th ed. Philadelphia: Saunders Elsevier; 2007. p. 433-54.  Back to cited text no. 2
Tankersley MS, Ledford DK. Stinging insect allergy: State of the art 2015. J Allergy Clin Immunol Pract 2015;3:315-22.  Back to cited text no. 3
Filley CM, Kleinschmidt-DeMasters BK. Toxic leukoencephalopathy. N Engl J Med 2001;345:425-32.  Back to cited text no. 4
McKinney AM, Kieffer SA, Paylor RT, SantaCruz KS, Kendi A, Lucato L, et al. Acute toxic leukoencephalopathy: Potential for reversibility clinically and on MRI with diffusion-weighted and FLAIR imaging. AJR Am J Roentgenol 2009;193:192-206.  Back to cited text no. 5
Wartenberg KE, Patsalides AD, Yepes M. Transient diffusion-weighted imaging changes in a patient with reversible leukoencephalopathy syndrome. Acta Radiol 2004;45:674-8.  Back to cited text no. 6


  [Figure 1], [Figure 2]


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