|Year : 2011 | Volume
| Issue : 2 | Page : 204-205
A rare cause of Guillain-Barre syndrome
K.A.S. Praveen, D.K.S. Subrahmanyam
Department of medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry, India
|Date of Submission||11-Mar-2011|
|Date of Acceptance||21-Mar-2011|
|Date of Web Publication||23-Aug-2011|
Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry
Source of Support: None, Conflict of Interest: None
| Abstract|| |
The Guillain-Barre syndrome (GBS) is an acute, acquired, autoimmune disorder of the peripheral nervous system, triggered by infections and other immunogenic stimuli; however, the exact cause of this disease is not fully understood. The malarial parasite as a cause of GBS is very rare and there are only few reports in the literature. Here, we report a case of acute flaccid quadriparesis with generalized areflexia following malaria caused by Plasmodium vivax, which improved with plasmapheresis.
Keywords: Demyelination, Guillain-Barre syndrome, nerve conduction study, place, Plasmodium vivax malaria
|How to cite this article:|
Praveen K, Subrahmanyam D. A rare cause of Guillain-Barre syndrome. Int J Nutr Pharmacol Neurol Dis 2011;1:204-5
| Introduction|| |
Guillain-Barre syndrome (GBS) is an acute demyelinating polyradiculoneuropathy of the peripheral nervous system, triggered by infections and other immunogenic stimuli. The neurological complications of malaria are usually seen with Plasmodium falciparum, due to sequestration of infected erythrocytes in the venules of the brain; these are less frequent with malaria caused by Plasmodium vivax. The neurological complications are cerebral malaria, intracranial hemorrhage, cerebral arterial occlusion, transient extrapyramidal, and neuropsychiatric manifestations,  and, rarely, GBS. These complications occur frequently in children compared to adults.
| Case Report|| |
A 60-year-old female presented to (Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry, India with a history of high-grade intermittent fever, accopmanied with chills and rigors of one-week duration. On day seven of the fever, she developed a sudden onset of weakness in both lower limbs, which ascended to involve the upper limbs also. There was no history of unconsciousness, abnormal movements, bowel or bladder disturbance, facial weakness, difficulty in vision/speech, recent vaccination, or root pain. There was also no history of recent respiratory or gastrointestinal infections or drug intake, except for chloroquine. On examination, her pulse rate was 88 per minute, blood pressure 130/80 mm Hg, and respiratory rate 18 per minute. The central nervous system (CNS) examination revealed normal higher mental functions; the cranial nerves were intact, and there was a lower motor neuron-type of quadriparesis. Power was diminished in all muscle groups of the lower limbs to grade 1/5 of the Medical Research Council (MRC) scale, while power in the upper limbs had diminished to 3/5 of the MRC scale in the proximal (Shoulder girdle) muscle group, and 4/5 at the elbow, wrist, and other distal muscles, with a handgrip of 60%. The patient's sensory system was normal. All deep tendon reflexes were absent and the plantar response was flexor.
Laboratory investigations revealed hemoglobin of 9.6 g/dl and TLC - 12.7 × 10 9 /L. The peripheral smear showed the malarial parasite P vivax. The cerebrospinal fluid (CSF) study showed albuminocytological dissociation (CSF cell count was 5 cells/mm 3 , protein 326 mg%, and sugar 43 mg%, with a corresponding blood sugar of 120 mg/dl). The nerve conduction studies (NCS) showed prolongation of distal latencies in the motor nerves, and a decrease in the compound motor action potential (CMAP) in the median, ulnar, peroneal, and tibial nerves. The nerve conduction velocities in the median, ulnar, peroneal, and tibial nerves were reduced, with absent tibial H-reflex.
The patient received treatment with chloroquine for Plasmodium vivax malaria, and her fever had subsided when she presented with acute flaccid quadriparesis. The diagnosis of GBS was established on the basis of the clinical findings, NCS and CSF findings The patient received plasmapheresis, four times every other day, along with physiotherapy. The muscle power gradually improved and two weeks later, the patient was discharged from the hospital with a muscle power of 3/5 in both lower limbs and 4/5 in the upper limbs.
| Discussion|| |
The GBS usually occurs following viral upper respiratory tract infections and gastrointestinal infections, among most frequently indentified is Campylobacter jejuni.  Other infections known to trigger GBS are HIV, cytomegalovirus, Epstein-Barr virus, Hemophilus influenzae, mycoplasma, toxoplasmosis, influenza virus, Coxsackie, herpes simplex, and Escherichia More Details coli. Plasmodium vivax malaria as a cause of GBS is very rare and there are only few case reports in the literature. ,,,
The pathogenic mechanism implicated in postinfectious GBS is molecular mimicry and cross-reactivity. The exact mechanism behind the demyelination of the peripheral nervous system in malaria remains unknown, but immune-mediated damage is believed to be the cause. The release of certain cytokines and other immunological mediators during the asexual stage of malarial infection can mediate an immune response. As there is a short delay between infection and the onset of neurological symptoms, it may be attributed to the immunologically mediated damage, following a memory immune response in a patient who has been previously infected with malaria.  Jae Eun Sim et al. reported the presence of elevated titers of anti-MAG and anti-GD1b in the CSF, suggesting the autoimmune-mediated mechanism of GBS.  The pathogenesis has also been attributed to immune-mediated capillary damage, toxic oxygen radicals, tumor necrosis factor, parasitic emboli obstructing the vasa nervorum, neurotoxin release, and nutritional and metabolic disturbances.  The malarial parasite damaging the peripheral nerves by vascular occlusion, can lead to temporary demyelination, and recovery after the disappearance of the parasitemia and establishment of normal blood flow in the vasa nervosum. 
In this patient, the history and neurological signs suggested GBS, which was confirmed by NCS and CSF analyses. In a study conducted by Kanjalkar et al., the average interval between the fever and the onset of weakness was 15 days (range, 1-6 weeks).  This case report showed that GBS following Plasmodium vivax malaria had a milder course, as compared to Plasmodium falciparum malaria. In this case, there was a delay of six days between the fever and onset of weakness, and there was no respiratory muscle weakness or autonomic disturbance. The standard treatment of GBS was either with intravenous immunoglobulin or plasma exchange, as both had equal efficacy. This patient received chloroquine for Plasmodium vivax malaria and four single plasma volume exchanges for GBS, on alternate days. The patient's muscle power gradually recovered partially over a period of two weeks and she was discharged from hospital for regular follow-up.
In conclusion, a milder form of GBS can occur following Plasmodium vivax malaria. As autoimmune etiology plays a role in its pathogenesis, early diagnosis and treatment with plasma exchange or intravenous immunoglobulins has a better outcome.
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