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Neurology India, Vol. 52, No. 1, January-March, 2004, pp. 130-131 Letter To Editor Acute inflammatory demyelinating polyneuropathy following plasmodium vivax malaria Chakravarty A, Ghosh B, Bhattacharyya R, Sengupta S, Mukherjee S Division of Neurology, Vivekananda Institute of Medical Sciences and B. R. Singh Hospital and Research Centre, Calcutta Code Number: ni04044 Sir, Acute Inflammatory Demyelinating Polyneuropathy (AIDP), seen following viral, bacterial infections or immunization, is uncommon following parasitic infection. We could locate 11 cases of Guillain Barre Syndrome (GBS) following malarial illness from the literature. Eight of these cases were following P. Falciparum infection and three were following P. Vivax infection.[1] We report a case of AIDP / GBS following P. Vivax malaria that needed ventilatory support. A 39-year-old male developed fever with chill and rigor. His hematological examination showed ring forms of P. vivax. He was treated with chloroquine (total 1500mg base) and primaquine (total 210 mg). He became asymptomatic in about five days. On the eleventh day following onset of fever, the patient developed tingling sensations in both the lower limbs from the feet up to the knees and both hands. The next day he noticed weakness of both the lower limbs, he could not get up from the squatting position and could not climb stairs. In the night he developed retention of urine. On the following day he was bed-bound and could not move his fingers adequately and could not raise his arm above the bed. He was admitted to the hospital where he developed difficulty in speaking, swallowing and had nasal regurgitation. He was not dyspnoeic at that stage. There was no history of any other illness preceding or following malaria and there was no history of recent immunization. On examination, his speech volume was low. There were bilateral VII, IX and X nerve palsies. Secretion accumulated in the throat. There was hypotonia in all the muscles of all four limbs. Muscle power was 2/5 in the upper limbs and 0/5 in the lower limbs. The sensory system was normal. Superficial reflexes were normal and all deep tendon jerks were absent. Chest expansion was 5 cm on deep inspiration and single breath count was 26. Chest examination was normal. Peripheral smear examination showed no malarial parasite. Falciparum antigen test was negative and urinary porphobilinogen was absent. CSF study revealed: cells -3/cmm (all lymphocytes), sugar 78mg%, protein 208 mg%. Conduction studies in both median, ulnar, peroneal and posterior tribal nerves revealed gross reduction in motor nerve conduction velocity (MNCV) and CMAP amplitude in all the nerves; distal latency grossly prolonged in all the nerves; F waves absent in all the nerves; temporal dispersion seen in all four limbs; H-reflexes absent in both sides; and SNAP absent in both median, ulnar and sural nerves. The weakness progressed and the patient developed respiratory difficulty. He was ventilated. He was given IV immunoglobulin 24g/day for five days. The patient started improving 2 days after IVIG was completed and could be weaned off the ventilator after one week. He went home after about one month and could walk unaided. AIDP / GBS following malaria is rare. It is important to rule out other neurological syndromes that may be unmasked by a febrile episode. A review of 12 cases of GBS (11 previously reported and the present one) revealed that eight patients had preceding falciparum malaria and four had vivax infections. All but three patients (including the present one) had distal symmetric sensory deficits. Paralysis was mild in seven cases (three due to P. Vivax and four due to P. Falciparum) and recovered completely in 2-6 weeks without any specific treatment. Four patients with falciparum malaria developed severe paralysis with respiratory failure, and three patients died. This appears to be the first case report of severe GBS following P. Vivax malaria requiring ventilatory support and IVIG therapy. The pathogenesis of GBS following malaria infection is not known. This is likely to be immunogenic like that occurring after viral or bacterial infections. Other mechanisms suggested for the development of polyneuropathy following a parasitic infection include parasitic emboli obstructing vasa nervosum, release of neurotoxins, associated metabolic and nutritional disturbance, immune-mediated capillary damage, release of free radicals and tumor necrosis factor.[2] References
Copyright 2004 - Neurology India |
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