facial diplegia has diverse etiologies , including viral and bacterial infections such as diphtheria , syphilis and lyme disease , and also protozoal infection in very rarely cases . a 20-year - old male patient was admitted to our hospital due to bilateral weakness of the upper and lower facial muscles . a peripheral blood smear demonstrated the presence of the asexual trophozoite stage of plasmodium vivax with ring - form trophozoites , which led to a diagnosis of malaria . a serum work - up revealed increased igg titers of antibodies to myelin - associated glycoprotein and ganglioside gd1b . the patient was administered antimalarial treatment , 1 week after which he showed signs of recovery . to our knowledge , this is the first case of facial diplegia after malaria infection , providing evidence that the mechanism underlying the condition is related to immune - mediated disease . facial diplegia can be induced by inflammatory , infective , traumatic , and infiltrative causes . keane found that benign and self - limited syndromes were responsible for one - half of cases.1 one of the most common underlying causes is guillain - barr syndrome ( gbs ) , which itself is attributable to nondescript respiratory or gastrointestinal infections , especially from viruses . serologic reports have found other types of bacterial infections , including mycoplasma pneumonia , lyme disease , and campylobacter jejuni.2 protozoal infection has also been suggested as a cause of gbs , but the incidence is reportedly very rare . a 20-year - old male patient was admitted to our hospital in july 2008 , due to bilateral weakness of the upper and lower facial muscles associated with facial palsy . four days before admission , he had experienced difficulty closing his eyelids and the next day felt facial weakness . on admission , his temperature was 38.3. neurological examination revealed his pupils to be isocoric with prompt reflexes to both direct and indirect light ; his extraocular movements were full and there was no nystagmus . bilateral facial weakness of the peripheral type was noted : the patient was unable to close his eyes tightly , smile , blow , or whistle . the patient 's deep tendon reflexes were normal and his sensory functions were not impaired . a peripheral blood smear demonstrated the presence of the asexual trophozoite stage of the protozoal parasite plasmodium vivax , with ring - form trophozoites . the patient 's hemoglobin was 13.8 g / dl and his white cell count was 3.9210/l , comprising 59.7% neutrophils . serum levels of glucose , sodium , and potassium were 116 mg / dl , 137 mm , and 4.7 mm / l , respectively . the patient 's cerebrospinal fluid ( csf ) was clear in appearance , cells were absent , and levels of protein and glucose were 34.7 mg / dl and 66 mg / dl , respectively . serologic tests for leptospiral infection , lyme disease , herpes simplex , varicella zoster , and epstein - barr virus were negative in the serum and csf . his igg index was 0.03 and his erythrocyte sedimentation rate was 38 mm / h . high titers of antibodies to myelin - associated glycoprotein ( mag ) were found to be 1,200 btu ( normal value , < 1,000 btu ) . titers of ganglioside gm1 igg and igm were not increased , but anti - gd1b igg titers were increased to 1,180 btu and anti - gd1b igm titers were within the normal range . contrast revealed enhancement of the right facial nerve . ultrasound evaluation of the abdomen revealed splenomegaly . sensory evoked potentials and visual evoked potentials were normal , and there were no observable r1 or r2 responses in the blink reflex test . on facial emg , denervation potentials founded in the bilateral orbicularis oculi , orbicularis oris , and frontalis muscles . antimalarial therapy with hydroxychloroquine sulfate was commenced , and the patient showed signs of recovery after 1 week . bilateral facial weakness is present in less than 1% of facial palsy patients , with facial paralysis resulting from a wide range of congenital abnormalities , cranial trauma , and infections . in the present case , all laboratory data , including serologic tests , were normal except for the anti - mag and anti - gd1b titers in csf . these results suggest that the cause of the facial diplegia is related to an immune - mediated condition , such as gbs . gbs is a form of peripheral neuropathy that is commonly triggered by infections and is related to immune - mediated mechanisms . a large number of infectious agents that mediate gbs have been identified , but protozoal parasitic infection has been reported in only a limited number of patients with leishmania donovani , p. falciparum , and p. vivax malaria.3 - 6 to our knowledge , only 22 cases of gbs after malarial infection have been reported , and this is the first case of facial diplegia after a malarial infection . the malaria parasite may damage the peripheral nerves by vascular occlusion , thus causing anoxic stagnation in the vasa nervosum , which leads to temporary demyelination and recovery after disappearance of the parasitemia and establishment of normal blood flow in the vasa nervosum . immune - mediated damage is believed to be the cause of gbs . in malaria , asexual - stage infections are accompanied by the release of cytokines and other immunological mediators.7 in our case , immunologic studies revealed that anti - mag and anti - gd1b titers were elevated , possibly indicating that the development of gbs after malaria infection is an immune - mediated disease rather than the result of direct damage by parasites.8 drug - induced polyneuropathy is unlikely , since paralysis occurred in our case before commencing treatment . p. falciparum malaria is associated with a poorer outcome compared with other types of malarial infection.5,6,9 in other reports , almost half of patients developed respiratory and bulbar paralysis , which ultimately leads to death . these findings are worse than those usually encountered in gbs.1 however , several p. vivax malaria patients , including our case , have survived and did not develop bulbar involvement.10 the relevant patient population is too small to allow us to draw a reliable conclusion , but we can assume that p. vivax malaria can be complicated by gbs , which has a low incidence of bulbar affection and a better clinical outcome than p. falciparum malaria .
backgroundfacial diplegia has diverse etiologies , including viral and bacterial infections such as diphtheria , syphilis and lyme disease , and also protozoal infection in very rarely cases.case reporta 20-year - old male patient was admitted to our hospital due to bilateral weakness of the upper and lower facial muscles . 
 examination revealed that the patient had a facial diplegia of the peripheral type . 
 a peripheral blood smear demonstrated the presence of the asexual trophozoite stage of plasmodium vivax with ring - form trophozoites , which led to a diagnosis of malaria . 
 a serum work - up revealed increased igg titers of antibodies to myelin - associated glycoprotein and ganglioside gd1b . 
 the patient was administered antimalarial treatment , 1 week after which he showed signs of recovery . to our knowledge , this is the first case of facial diplegia after malaria infection , providing evidence that the mechanism underlying the condition is related to immune - mediated disease.conclusionsfacial diplegia can manifest after p. vivax infection .