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|LETTERS TO EDITOR
|Year : 2018 | Volume
| Issue : 5 | Page : 1483-1484
Facial palsy: An unusual complication of vivax malaria
Rimi Som Sengupta, Joydip Datta, Anirban Ghosh, Samir Chakraborty, Anirban Sarkar
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 Publication||17-Sep-2018|
Dr. Anirban Ghosh
Department of Medicine, ESI.-PGIMSR and ESIC Medical College and Hospital, Joka, Kolkata .- 700 104, West Bengal
Source of Support: None, Conflict of Interest: None
|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
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.
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).
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. One Indian article described malarial polyneuritis including Guillain–Barre like presentation and mononeuritis syndromes involving facial, trigeminal, optic, ulnar, or lateral popliteal nerves. The other manifestations of PMNS described were cerebellar syndromes, postural hypotension, subarachnoid hemorrhage, and extrapyramidal syndromes. 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. Another hypothesis states that release of inflammatory cytokines such as interleukin (IL)-2, IL-6, and tumor necrosis factor cause direct neurological injury. 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.
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Conflicts of interest
There are no conflicts of interest.
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