INTRODUCTION:
AIDP following Malaria is a rare clinical presentation. Few cases have been reported so far from India and abroad. It is usually acute onset with rapidly developing areflexic ascending motor paralysis with or without sensory disturbances. Though various mechanisms are postulated it is more likely immunogenic. It responds to I/V immunoglobulin along with anti malarial therapy. Early therapeutic measures lead to good prognosis.

CASE REPORT:
A 16years boy admitted on 18.06.2006 with sudden weakness of all four limbs following 2 days of fever with chill and rigor. Detected to be Falciparum malaria (slide test) and treated locally with chloroquin referred to this hospital.

On admission the patient was febrile, conscious with mild pallor. Other vital signs were normal. Respiratory, CVS and Gastrointestinal system were normal. Neurological examination revealed normal higher intellectual functions without any cranial nerve involvement or pupillary abnormality. Motor examination showed normal bulk and tone of all muscles. Power in both U/L were 3/5 in proximal and 4/5 in distal groups including handgrip weakness. Power in both lower limbs were 2/5 around hip and 3/5 around knee, ankle and feet. There was no abnormal movement. Deep tendon reflexes were absent in all four limbs. Plantar was nonresponsive. All superficial reflexes were absent. Sensory system, autonomic nervous systems were normal without bladder and bowel involvement.

Routine blood examination findings showed Hb- 9gm%, ICT for malaria- PFR ++ and DC, TLC, ESR were normal. Serum electrolytes, urea, creatinine, FBS, and LFT were normal. Chest X-Ray, X-Ray of L.S. Spine and USG of abdomen and pelvis were normal. CSF picture was normal. Nerve conduction study of both median, ulnar and common peroneal nerves revealed gross reduction in amplitude and motor nerve conduction velocity, with prolonged distal latency, and absence of F waves. Sensory was absent in all the nerves.

The patient was treated with full course of injection Artesunate and IV immunoglobulin 24g/day for 5 days. The patient improved after 3 days of completion of immunoglobulin. The patient was discharged in 10th day of admission after fully recovery.

DISCUSSION:
AIDP is seen following viral (herpes virus, CMV, E-B virus etc) bacterial (Campilobacter jejuni, Mycoplasma) or immunization. But it is uncommon following parasitic infection like malaria. It is important to rule out other neurological syndromes that may be unmasked by febrile illness. The pathogenesis of AIDP following malaria is not known. This is possibly to be immunogenic like that occur after viral or bacterial infection. Other possible mechanisms of polyneuropathy may be due to parasitic emboli obstructing vasa nervosum, release of neurotoxins, associated metabolic and nutritional disturbances, immune mediated capillary damage, and release of free radicals and tumor necrosis factors.

AIDP is a variant of GBS encountered rarely following malaria (few case reports after Vivax, Falciparum). Early institution of I/V immunoglobulin results full recovery. Steroid has no role.