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Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) following plasmodium vivax malaria--a case report.


Neurological manifestations following malaria is uncommon with a prevalence of 0.12%. It is 299 times more common in complicated falciparum malaria than uncomplicated type. [1] Most of the post malarial neurological symptoms (PMNS) are seen with P. falciparum infection. PMNS following P. vivax infection is much rarer but there is no epidemiological data regarding the actual incidence. AIDP following P. vivax infection is very rarely reported. Our patient presented with AIDP and facial diplegia following recent recovery from P. vivax infection and after a thorough search no other causative factor could be elicitated. In this case the neurological manifestations could be considered to be the consequence of P. vivax infection.

Case Report

A 22 year old male, presented with weakness of all four limbs for two weeks. He had a history of high fever with chill and rigor for five days, about two week prior to the development of quadriparesis. There was no history of cough, diarrhea or rash. His fever was diagnosed to be due to vivax malaria by demonstration of trophozoites of P. vivax in peripheral blood smear (Figure 1) and positive P. vivax antigen test. He received three doses of oral chloroquine (600 mg stat, 600 mg after 24 hours and 300 mg after 48 hours of first dose) and advised for oral primaquine (15 mg x 14 days). After an afebrile period of ten days, he developed progressive weakness of lower limbs involving both the proximal and distal muscles. Weakness gradually ascended rostrally to involve his upper limbs within a time span of one week. He also had subjective sensory symptoms and aching pain in lower limbs. During second week of his illness he developed difficulty in deglutition, dribbling of saliva from both angle of mouth and inability to close both eyelids and eventually facial diplegia. At the end of second week the patient was completely bed ridden. There was no history of any root pain, girdle like sensation, anaesthesia, and hyperesthesia or bladder/bowel involvement. Examination revealed, bilateral lower motor neuron type of Facial nerve palsy and hypoactive gag reflex. Limbs were hypotonic. Power was diminished in all four limbs (lower limb-1/5 and upper limb-2/5) associated with generalised areflexia. Plantar reflex was non responsive bilaterally. Exteroceptive and proprioceptive sensory modalities were unaffected. Complete hemogram, liver, renal, thyroid Function tests, blood glucose and electrolytes were within normal limit. HIV serology was negative. Peripheral blood smear did not show any malaria parasite. P. falciperum antigen was negative. CSF study showed albuminocytological dissociation (cell count: 5/cmm all mononuclear cells and protein: 282 mg/dl). CSF glucose-60 mg/dl. CSF gram stain, AFB stain, fungal and mycobacterial culture were negative as well as negative HSV PCR study. Chest X-ray and MRI brain and spinal cord were normal. Nerve conduction study showed decreased CMAP amplitude in both upper and lower limbs with conduction block in left median, left ulnar and right peroneal nerve with significantly decreased conduction velocity (<70%) and markedly increase distal latency (>130%) with absent SNAP in upper limb with preserved sural SNAP with absent 'H' and 'F reflex in both upper and lower limbs consistent with a diagnosis of AIDP. The patient was treated with plasmapheresis. Signs of improvement noted at the end of first week. Tone and power of limbs improved over next two weeks and he was able to take food orally during this period. He was discharged in stable condition after three weeks from his admission.


In this patient the diagnosis of AIDP was evident from clinical features and later on confirmed by the typical CSF changes and nerve conduction studies. AIDP usually occurs following upper respiratory tract infections and gastrointestinal infections. The most frequently identified organisms are Campylobacter jejuni and cytomegalo virus. [2] Other infections known to trigger AIDP are HIV, Epstein-Barr virus, Hemophilus, Influenza, Coxsackie and herpes simplex. Surprisingly in our patient the development of AIDP was heralded by infection with P. vivax. The patient developed AIDP after an interval of ten days afebrile period. After extensive search for common etiological agents of AIDP, we failed to find any; neither the patient had any prior history of respiratory, gastrointestinal infection or vaccination. P. vivax malaria was considered as benign in the past but the scenario has changed. There is increasing incidence of serious complications being reported in association with P. vivax malaria. Neurological complications after P. falciparum is not uncommon and it encompasses cerebral malaria, myelitis and post malarial neurological syndrome characterized by an acute confusional state, acute psychosis, inappropriate speech, visual hallucination, convulsion, tremor, and hypotonia. [1] PMNS occurs after the clearance of parasitemia and is not a manifestation of cerebral malaria. On the contrary, neurological involvement is very rare in P. vivax malaria and it ranges from ADEM, cerebral malaria and myelitis during parasitemia and PMNS. [3,4] P. vivax malaria as a cause of AIDP is extremely uncommon and only few cases have been reported before. [5-7] Though unclear, the possible pathogenic mechanisms responsible for neuronal insult in malaria is immune mediated myelin and axonal damage. Immune mediated peripheral nerve damage may also see in a previously infected person due to memory immune response. [8] Parasitic emboli obstructing vasa nervosum, release of neurotoxins, metabolic, immune-mediated capillary damage, release of free radicals and cytokines are also hypothesized for the developpment of polyneuropathy. [9] Temporary demyelination of peripheral nerves can occur following vascular occlusion by parasites.

As par few literatures, long term use of chloroquine in arthritis patients may cause areflexic weakness. [10,11] But there are no evidence of similar incident with short term use of chloroquine in malaria. Again normal electrolytes level and thyroid profile virtually exclude any possibility if channelopathy in this patient. Acute transverse myelopathy could also be reasonably excluded by a normal MRI of spine. Facial diplegia has previously been reported following P. vivax infection. [11] In our patient facial diplegia can be considered as a spectrum of AIDP.


This case report is concerned with the development of AIDP and facial diplegia following P. vivax infection. To the best of our knowledge this combination of PMNS following P. vivax malaria has not as been reported before.


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[3.] Kochar DK, Saxena V, Singh N, Kochar SK, Kumar SV, Das A Plasmodium vivax malaria. Emerg Infect Dis. 2005; 11(1):132-34.

[4.] Moulick A, Maitra S, Sarkar BS, Jana A, Sarkar S. Vivax malaria presenting with myelitis: a rare complication. J Clin Diagn Res. 2013;7(5):914.

[5.] Padmini R, Maheshwari MC. P. vivax malaria complicated by peripheral neuropathy with electrophysiological studies. J Assoc Physicians India. 1980;28:152-6

[6.] Chakravarty A, Ghosh B, Bhattacharyya R, Sengupta S, Mukherjee S. Acute inflammatory demyelinating polyneuropathy following plasmodium vivax malaria. Neurol India. 2004;52(1):130-1.

[7.] Kanjalkar M, Karnad DR, Narayana RV, Shah PU. Guillain-Barrel syndrome following malaria. J Infect. 1999;38:48-50.

[8.] Wijesundere A, Guillain Barre Syndrome in plasmodium falciparum malaria. Postgrad Med J 1992;68 (799):367-377.

[9.] Conner DH, Herber JM. Parasitic infections of the peripheral nervous system. In: Dyck PJ, Thomas PK, eds. Peripheral Neuropathy. Philadelphia: WB Saunders; 1993. 1338-90

[10.] Becerra-Cunat JL, Coll-Canti J, Gelpi-Mantius E, Ferrer-Avellf X, Lozano-Sanchez M, Millan-Torne M, et al. Chloroquine-induced myopathy and neuropathy: progressive tetraparesis with areflexia that simulates a polyradiculoneuropathy. Two case reports. Rev Neurol. 2003; 36(6):523-6. [Article in Spanish]

[11.] Sim JE, Choi YC, Kim WJ. Facial Diplegia in Plasmodium vivax Malaria. J Clin Neurol. 2010;6:102-3.

Source of Support: Nil

Conflict of interest: None declared

Tony Ete, Sumantro Mondal, Debanjali Sinha, Kaushik Bhar, Soumik Sarkar, Jyotirmoy Pal, Alakendu Ghosh

Institute of Post Graduate Medical Education and Research, Kolkata, West Bengal, India

Correspondence to: Tony Ete (

DOI: 10.5455/ijmsph.2014.020220141

Received Date: 23.01.2014

Accepted Date: 02.03.2014
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Title Annotation:CASE REPORT
Author:Ete, Tony; Mondal, Sumantro; Sinha, Debanjali; Bhar, Kaushik; Sarkar, Soumik; Pal, Jyotirmoy; Ghosh,
Publication:International Journal of Medical Science and Public Health
Date:Apr 1, 2014
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