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Acute Inflammatory Demyelinating Polyneuropathy following Malaria is a rare clinical presentation. Few cases have been reported so far from India and abroad. Here we report such a case from this hospital and discuss the pathophysiology and management.

Acute inflammatory demyelinating polyneuropathy (AIDP),
Plasmodium falciparum,
IV immunoglobulin.

Acute inflammatory demyelinating polyneuropathy (AIDP) is acute, frequently severe and fulminant which is auto immune in nature characterized by rapidly developing areflexic ascending motor paralysis with or without sensory disturbances. 75% of cases are preceded 1-3 weeks by an acute infectious process usually respiratory or gastrointestinal. The reported microorganisms include Campylobacter jejuni, Mycoplasma, Human herpesvirus, CMV, E-B virus etc3. The AIDP following malaria is of rare occurrence. However recently several cases have been reported following both vivax and falciparum malaria1,5.

A 16 years boy from sonepur was admitted to this hospital on 18.06.2006 with complains of sudden weakness of both lower limbs and both upper limbs and inability to walk for 10 days. Twelve days back he had fever with chill and rigor for which he consulted local physicians and detected to be a case of Falciparum Malaria (slide +ve) and treated with chloroquine tablets. Next morning the patient noticed weakness and tingling sensation of both lower limbs. He was treated with IV fluids and multivitamin injection. The weakness rapidly progressed and after 2 days he developed weakness of both upper limbs and paralysis of both lower limbs leading to inability to walk. He was treated at the District Hospital with antimalarial drugs and referred to this Hospital.

On admission the patient was febrile (Temp. 99.80 F) conscious. There was mild pallor without icterus, clubbing, cyanosis, oedema or Thyroid enlargement. Pulse was 96/min, regular, B.P. was 120/80mm of Hg in both upper limbs. Respiration rate was 16/min. and abdominothoracic type. There was no sign of dehydration.

Neurological examination revealed normal higher intellectual functions with all cranial nerves intact without any pupillary abnormality. Motor examination showed normal bulk and tone of all muscles in upper and lower limbs. Power in both upper limbs were 3/5 grade in proximal groups and 4/5 grade in distal groups including hand grip weakness. Power in both lower limbs were 2/5 grade in proximal group (flexor, extensor around hip) and grade 3/5 around knee, ankle and feet. Power in trunk muscle and abdominal muscles were normal. Bladder and bowel were not involved. Coordination could not be tested and there was no involuntary movement. Deep Tendon reflexes in all four limbs were absent. Plantar was non responsive in both limbs. All the superficial reflexes were absent. Gait and Romberg’s test could not be done due to weakness. Sensory system examination showed all modalities intact. Autonomic nervous system was normal. Skull and spine was normal without any sign of meningitis.

Respiratory system, cardiovascular system, gastrointestinal system and other systems were normal.

There was no such past history. There was no history of SCD, TB, DM, HTN, exanthematous fever or dog bite. Family history was not suggestive.

Routine examination findings were-
HB – 9gm% ,TLC – 10,200/mm3, DC – N-64, L-30, E-6, M-0, B-0, ESR – 46mm 1st hour
ICT for Malaria – PFR ++
Serum – Na+ - 138m Eq/l, K+ - 4.2m Eq/l, Ca+ - 8mg%
Serum urea – 46mg%
Creatinine 1.5mg%

LFT – Serum Bilirubin – 1.3mg%(Total), 0.4mg% (Direct), SGOT- 42 IU/L, SGPT-97IU/L, Alkaline Phosphatase - 548IU/L. Chest X-ray PA view and X-ray of Lumbosacral spine were normal . Ultrasonogram of abdomen and pelvis was normal. CSF was clear with normal pressure, CSF cell count was 12/ml mostly lymphocytes, Glucose was 58mg%, protein 240mg% and gram stain and AFB were negative. Nerve conduction studies in both median, ulnar and common peroneal nerves revealed gross reduction in amplitude and motor nerve conduction velocity. The distal latency was grossly prolonged in all the nerves. F waves were absent in all the nerves. The sensory conduction in both median and common peroneal nerves was absent.

The patient was diagnosed to be a case of AIDP fllowing falciparum malaria. He was treated with full course of injection Artesunate and IV immunoglobulin 20g/day for 5 days. The patient improved after 3 days of completion of immunoglobulin . The power in all four limbs improved. On 10th day of admission the patient was discharged with follow up advise.

Acute inflammatory demyelinating polyneuropathy (AIDP) are seen following viral, bacterial infections or immunization and is uncommon following parasitic infection like malaria2. It is important to rule out other neurological syndromes that may be unmasked by febrile episode.

The pathogenesis of AIDP following malaria is not known. This is likely to be immunogenic that occurs after viral/bacterial infections.

Other possible mechanisms suggesting development of polyneuropathy following a parasitic infestation include:
• Parasitic emboli obstructing vasa nervosum.
• Release of neurotoxins.
• Associated metabolic and nutritional disturbances.
• Immune mediated capillary damage.
• Release of free radicals and tumors necrosis factor.

AIDP is a variant of GBS manifests as rapidly developing areflexic motor paralysis with or without sensory disturbances. The pattern is ascending type and first noticed as rubbery legs. Weakness typically evolves over hours to few days and frequently associated with tingling dysesthesia in extremities.

Legs are affected more than arms. All the reflexes are absent. Lower cranial nerves are frequently involved. Bladder involvement is rare. In severe cases autonomic dysfunction may occur, resulting in fluctuation of blood pressure, postural hypotension, cardiac dysrythmias.

Modified A.K. Asbury Criteria (for GBS):
Required Criteria:
• Progressive weakness of 2 or more limbs due to neuropathy
• Areflexia
• Disease course < 4 weeks
• Exclusion of other causes like vasculitis, botulism, diphtheria, porphyria, cauda equina syndrome.
Supportive Criteria:
• Relatively symmetric weakness
• Mild sensory involvement
• Facial or other cranial nerve involvement
• Absence of fever
• Typical CSF profile (Acellular , Increase protein level)
• Electrophysiological evidence of demyelination

Treatment is to be given as early as possible. In > 2 weeks of first motor symptoms, immunoglobulin is not effective. IVIg is administered as five daily injections for a total dose of 2g/kg body weight.

A course of plasmapheresis consisting of 40 to 50ml/kg, plasma exchange four times a week is usually employed. Combination has no advantage. Steroid has no role. In worsening phase critical care and ventilatory support is required.


In conclusion we report that falciparum malaria may present as AIDP and this possibility though uncommon must be taken into consideration while encountering patients in endemic areas.

1. Kanjalkar M, Karnad DR, Namayan RV, Shah PU: Guillain-Barre Syndrome following malaria, J. Infect 1999; 38: 48-50.
2. Sokrab RT, Eltahir A, Idris MN, Hamid M: GBS following acute falciaprum malaria, Neurology 2002, OCT, 22; 59(8), 1281-3.
3. Harrison’s Principle of Internal Medicine, 16th Edition, Vol – II, ; 365: P2513-14.
4. Corner DH, Herber JM, Parasitic infections of the pripheral nervous system in: Dyck PJ, Thomas PK, eds. Peripheral neuropathy, Philadelphia: WB Saunders; 1993 PP. 1338 – 90.
Chakravarty A, Ghosh B, Bhattacharyya R, Sengupta S, Mukherjee S: AIDS following

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