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LETTERS TO EDITOR
Year : 2018  |  Volume : 66  |  Issue : 5  |  Page : 1483-1484

Facial palsy: An unusual complication of vivax malaria


Department of Medicine, Employee's State Insurance- Post Graduate Institute of Medical Science and Research and ESIC Medical College Hospital, Joka, Kolkata, West Bengal, India

Date of Web Publication17-Sep-2018

Correspondence Address:
Dr. Anirban Ghosh
Department of Medicine, ESI.-PGIMSR and ESIC Medical College and Hospital, Joka, Kolkata .- 700 104, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.241337

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How to cite this article:
Sengupta RS, Datta J, Ghosh A, Chakraborty S, Sarkar A. Facial palsy: An unusual complication of vivax malaria. Neurol India 2018;66:1483-4

How to cite this URL:
Sengupta RS, Datta J, Ghosh A, Chakraborty S, Sarkar A. Facial palsy: An unusual complication of vivax malaria. Neurol India [serial online] 2018 [cited 2018 Oct 23];66:1483-4. Available from: http://www.neurologyindia.com/text.asp?2018/66/5/1483/241337




Sir,

Post-malaria neurological syndrome (PMNS) is a very unusual complication of severe malaria. This complication usually occurs after recovery of malaria and is a self-limiting complication with no long-term sequelae, the pathogenesis of which is little understood. The time from eradication of systemic parasitemia to the development of this syndrome can be up to 2 months.[1]

A 33-year old male patient was admitted with high-grade fever associated with chills and rigors. Peripheral blood smears and rapid diagnostic test revealed Plasmodium vivax. He was given chloroquine and primaquine as his glucose 6-phosphate dehydrogenase (G6PD) enzyme was normal and he was subsequently discharged. After 2 weeks, he presented to us with history of left-sided facial weakness. Examinations revealed lower motor type of facial palsy of the left side without involvement of any long tracts [Figure 1]. Otoscopic examination was performed to rule out local pathology such as otitis media or vesicles within the ear cavity (herpes zoster oticus).
Figure 1: Left sided facial palsy with normal MRI brain imaging

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Magnetic resonance imaging (MRI) of the brain [Figure 1] and cerebrospinal fluid (CSF) study did not reveal any abnormality. In the index case of facial palsy, blood smears were initially positive and thereafter, negative for malarial parasite; however, other causes of facial palsy such as chronic suppurative otitis media, meningitis, and herpes zoster were reasonably ruled out. The temporal association of facial weakness and a preceding history of vivax malaria infection with gradual recovery of facial palsy, makes vivax malaria as the most probable etiology of facial nerve palsy. He was discharged with a short course of prednisolone and gradual improvement was noted on follow-up visits.

PMNS is a self-limiting complication, manifested in the form of acute-onset confusional state, convulsions, psychiatric problems, acute disseminated encephalomyelitis, and focal neurological deficits such as cranial nerve palsy occurring after successful treatment of malaria, with a latency of a few weeks to months.[2] One Indian article described malarial polyneuritis including Guillain–Barre like presentation and mononeuritis syndromes involving facial, trigeminal, optic, ulnar, or lateral popliteal nerves.[3] The other manifestations of PMNS described were cerebellar syndromes, postural hypotension, subarachnoid hemorrhage, and extrapyramidal syndromes.[3] Although it usually occurs after infection with P.falciparum, a few case reports of occurrence of neurological disorders have been described in association with vivax malaria also.

The pathogenesis of facial palsy in malaria has been little understood. It has been postulated that occlusion of the vasa nervosum by malarial parasites causes hypoxic damage or temporary demyelination of the neurological structures.[4] Another hypothesis states that release of inflammatory cytokines such as interleukin (IL)-2, IL-6, and tumor necrosis factor cause direct neurological injury.[3] Both mechanisms are true for falciparum malaria. However, whether or not the same process is applicable in the case of vivax malaria is a matter of debate.

PMNS is a self-limiting condition and usually does not require any active intervention. The role of corticosteroids in the severe form of PMNS is doubtful. A clinical entity called corticosteroid responsive encephalopathy may benefit from corticosteroids.[5]

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 » References Top

1.
Nguyen TH, Day NP, Ly VC, Waller D, Nguyen HP, Bethell DB, et al. Post-malaria neurological syndrome. Lancet 1996;348:917-21.  Back to cited text no. 1
    
2.
Singh AK, Chakraborti S, Subhranag S. Post malaria -neurological syndrome-A case of Bell's Palsy after plasmodium vivax malaria. J Nepal Paediatr Soc 2013;33; 66-67.  Back to cited text no. 2
    
3.
Garg RK, Karak B, Misra S. Neurological manifestations of malaria: An update. Neurol India 1999;47:85-91.  Back to cited text no. 3
[PUBMED]  [Full text]  
4.
Markley JD, Edmond MB. Post-malaria neurological syndrome: A case report and review of the literature. J Travel Med 2009;16:424-30.  Back to cited text no. 4
    
5.
Schnorf H, Diserens K, Schnyder H, Chofflon M, Loutan L, Chaves V, et al. Corticosteroid responsive postmalaria encephalopathy characterized by motor aphasia, myoclonus, and postural tremor. Arch Neurol 1998;55:417-20.  Back to cited text no. 5
    


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