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Table of Contents
CASE REPORT
Year : 2017  |  Volume : 5  |  Issue : 1  |  Page : 51-53

A rare case of young stroke in 16 years old female with Plasmodium vivax malaria infection


1 Junior Resident, Department of General Medicine, Dudhrej road, Surendranagar, Gujarat, India
2 Assistant Professor, Department of General Medicine, Dudhrej road, Surendranagar, Gujarat, India
3 Associate Professor, Department of General Medicine, Dudhrej road, Surendranagar, Gujarat, India

Date of Web Publication30-Aug-2018

Correspondence Address:
M K Marvaniya
Assistant Professor, Department of General Medicine, Dudhrej road, Surendranagar, Gujarat
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2347-6486.240227

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  Abstract 


Malaria is the most important parasitic disease in the world, in terms of both prevalence and mortality. Infection rate is high due to raise of strains resistant to the antimalarial medicines & social factors. Although cerebral malaria due to Plasmodium Vivax (P. Vivax) is rare, few cases with multiple cerebral infarct following P. Vivax infection have been reported. Plasmodium Falciparum (P. falciparum) malaria infections are thought to account for the vast majority of cerebral malaria cases and various neurological manifestations. Stroke is extremely unknown in cases of P.Vivax malaria. Here we report a rare case of young stroke with cerebral malaria in P. Vivax infection.

Keywords: Plasmodium Vivax Malaria, Stroke


How to cite this article:
Gediya N U, Marvaniya M K, Parmar D A, Gediya U S. A rare case of young stroke in 16 years old female with Plasmodium vivax malaria infection. J Integr Health Sci 2017;5:51-3

How to cite this URL:
Gediya N U, Marvaniya M K, Parmar D A, Gediya U S. A rare case of young stroke in 16 years old female with Plasmodium vivax malaria infection. J Integr Health Sci [serial online] 2017 [cited 2021 Nov 30];5:51-3. Available from: https://www.jihs.in/text.asp?2017/5/1/51/240227




  Introduction Top


In India, malaria is an endemic disease and an important treatable cause of mortality. The prevalence of malaria being reported to be 19%.[1] Commonly described with classical febrile illness with rigors and chills it can have atypical manifestations too. Neurological involvement as cerebral malaria has been described more commonly in falciparum malaria than vivax . Here we present a case of plasmodium vivax malaria with atypical manifestation as cerebro vascular accident with left hemiparesis.


  Case Report Top


16 years old female presented to emergency department with chief complaints of fever since ten days , intermittent in nature associated with chills and rigors with generalized headache and altered sensorium since one day with diminished movements in left upper and lower limb. On general examination patient was febrile and had tachycardia. Blood pressure was normal. Other general examination was normal. On systemic examination, altered consciousness was present with disorientation to time place and person and paucity of movements of left upper and lower limbs, patient had left upper motor neuron facial palsy too. There were no signs of meningeal irritation. On investigation peripheral blood smear showed P. Vivax ring forms and complete blood count – Haemoglobin-9.7gm/dl , Total Leucocyte count- 10100/cumm, RBC count -4.01 million/cumm, Platelet count - 165000/cumm. Serum Creatinine was 1.2mg/dl. Electrolytes were within normal limits [sodium-139.4 mEq/L , Potassium -3.92mEq/L, Chloride – 104.2mEq/L] . Serum SGPT was 70IU/L, SGOT was 55IU/L. Coagulation profile was within normal limits [BT- 1 MIN 30 SEC, CT- 2 min 45 SEC , APTT -28.1 SEC, PT- 16 SEC]. Plasmodium antigen test was done which was suggestive of only P.Vivax infection and negative for plasmodium falciaprum. In view of altered sensorium with left hemiparesis in a young patient magnetic resonance imaging was done which showed right frontal lobe infarct [Figure 1][Figure 2][Figure 3]. The rest of the brain parenchyma and both lateral ventricles appeared normal.
Figure 1: Iso-to-hypo intense areas on T1W image

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Figure 2: Multiple discrete hyper intense lesions on T2W image

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Figure 3: Multiple discrete hyper intense lesions on Diffusion W image

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Other possible causes of stroke were ruled out. Cardio embolic stroke due to infective endocarditis was ruled out with transthoracic Echocardiography being normal. SLE and Antiphospholipid antibody syndrome were ruled out by negative ANA profile and Anticardiolipin antibody test. Vertebral artery dissection was ruled out by normal MR Angiography. Cerebrospinal fluid examination was also normal [ Appearance –clear, Protein- 48mg/dl , Glucose - 75mg/dl, Total cells- 4/cumm, AFB stain and GRAM stain was negative, Adenosine Deaminase was 3 mg/dL] . Hence, as a diagnosis of exclusion final diagnosis of acute P.Vivax malaria with ischemic stroke was made. Patient was started on treatment with intravenous antimalarial artesunate and intravenous ceftriaxone along with fluid therapy and other supportive treatment. The patient showed recovery in the sensorium by third day and power in left upper and lower limb also improved to MRC grade of 4/5 at the time of discharge. Patient was advised physiotherapy. On follow up at the end of one month, the patient was fully recovered.


  Discussion Top


P. Vivax malaria infection rarely causes cerebral malaria and associated neurological complications. However, the neurological manifestations like behaviour changes, altered sensorium, seizure, ataxia, hemiparesis, psychosis, acute demyelinating polyneuropathy and late bilateral facial paralysis have been described in few studies.[2] Two mechanisms have been reported for the neurological complications in malaria. The mechanical theory indicates that cerebral malaria causes cerebral capillary and venules occlusion by parasitized erythrocytes. This results in thrombosis, anoxia, infarct and tissue necrosis. According to humoral theory non-specific vasoactive inflammatory substances producing changes in the capillary permeability results in compromisation of blood flow, impaired tissue perfusion and cellular hypoxia. Among these mediators tumour necrosis factor alpha and interlukin-2 are important mediators.[3] Our case is a young female who had the rare presentation of cerebrovascular accident by vivax malaria which was proven by exclusion of other causes and improvement with antimalarials. So this is a noteworthy case which suggests to consider possibility of malaria in a febrile patient presenting with neurological deficit in malaria endemic areas.



 
  References Top

1.
Haanshuus CG, Chandy S, Manoharan A, Vivek R, Mathai D, Xena D, Singh A, Langeland N, Blomberg B, Vasanthan G, Sitaram U. A high malaria prevalence identified by PCR among patients with acute undifferentiated fever in India. PLoS One. 2016 Jul 7;11(7):e0158816.  Back to cited text no. 1
    
2.
Garg RK, Karak B, Misra S. Neurological manifestations of malaria: an update. Neurology India. 1999 Apr 1;47(2):85.  Back to cited text no. 2
    
3.
Leopoldino JF, FUKUJIMA M, Gabbai AA. Malaria and stroke: case report. Arquivos de neuro-psiquiatria. 1999 Dec;57(4):1024-6.  Back to cited text no. 3
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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