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Year : 2014  |  Volume : 62  |  Issue : 1  |  Page : 67--68

A case of frontal lobe infarct in Plasmodium vivax infection

OP Jatav, Ashish Singhal, Ajay Pal Singh 
 Department of General Medicine, Gajra Raja Medical College, Gwalior, Madhya Pradesh, India

Correspondence Address:
Ashish Singhal
Department of General Medicine, Gajra Raja Medical College, Gwalior, Madhya Pradesh

How to cite this article:
Jatav O P, Singhal A, Singh AP. A case of frontal lobe infarct in Plasmodium vivax infection.Neurol India 2014;62:67-68

How to cite this URL:
Jatav O P, Singhal A, Singh AP. A case of frontal lobe infarct in Plasmodium vivax infection. Neurol India [serial online] 2014 [cited 2020 Jul 10 ];62:67-68
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Malaria is a mosquito-borne infectious disease caused by protists of the genus Plasmodium. According World Health Organization (WHO) estimates, there were about 219 million cases of malaria in 2010 and an estimated 660,000 deaths. [1] In South-East Asia, the second most affected region in the world, India has the highest malaria burden (with an estimated 24 million cases/year). [1] Cerebral malaria due to Plasmodium vivax, although rare, has been reported from Indonesia, India and Papua New Guinea. Recently cases with multiple cerebral infarcts following P. vivax infection has been reported from Korea. [2] Here, we report a case of frontal lobe cerebral infarct in P. vivax infection.

A 30-year-old female patient presented with the complaints of fever since 15 days and headache and altered sensorium since 1 day. Fever was intermittent and was associated with chills and rigor. At the other facility peripheral blood smear showed P. vivax rings and hemoglobin was 6.6 g/dL, total leukocyte count was 11000/mm 3 and platelet count was 1.66 lakhs/mm 3 . Neurological examination revealed neck rigidity and Kernig's sign. The patient was put on intravenous artesunate and ceftriaxone; fluids, antipyretics and other supportive treatment were also given. On the next day repeat investigations revealed: Hemoglobin of 6.9 g/dL, mild deranged liver function test (serum glutamic oxaloacetic transaminase: 51 IU/L, serum glutamic-pyruvic transaminase: 46 IU/L) and slightly low serum protein (total protein - 6.19 g/dL and albumin - 2.5 g/dL). Ultra sound abdomen showed hepatomegaly and splenomegaly. A packed cell has been transfused for severe anemia management. Magnetic resonance imaging brain done the next day showed infarct involving right frontal lobe [Figure 1]a-c. Cerebrospinal fluid examination was normal. Patient improved on antimalarial therapy and was discharged on day-5.{Figure 1}

P. vivax accounts for nearly half of all malaria infections and is now recognized as a cause of complications and death. WHO defines cerebral malaria as unarousable coma in a patient with P. falciparum asexual parasitemia after other causes of encephalopathy have been excluded. Almost all patients with cerebral malaria present with fever, rigors and/or chills. Altered sensorium might be present from the outset or might develop slowly over a period of several days. Signs of irritability, restlessness or psychotic behavior can be the initial manifestations of cerebral involvement. Neck stiffness is occasionally encountered, but other signs of meningism are uncommon in our experience. In patients with P. vivax infections behavior changes, altered sensorium, seizures, cerebellar manifestations and ataxia, hemiparesis, aphasia, psychosis, acute inflammatory demylienating polyneuropathy and late bilateral facial paralysis have been described [3] and some of the cases may develop multi-organ involvement.

Two mechanisms have been proposed for the neurological complications in malaria. The mechanical theory [4] suggests that cerebral capillary and venules occlusion by parasitized erythrocytes is caused by direct action of the parasite on the erythrocyte, distorting its morphology, altering the elasticity and plasticity and changing its surface properties. By the impaired capillaries flow and adhesion to the endothelium and other blood cells (forming aggregates, "rosettes") obstruction supervenes. This results in thrombosis, anoxia and infarct and tissue necrosis. In more serious cases, further endothelial damage produces an increase in capillary permeability and even hemorrhages. According to the humoral [4] theory the action of non-specific vasoactive inflammatory substances producing changes in the capillary permeability results in compromisation of blood flow, impaired tissue perfusion and cellular hypoxia. Among the mediators tumor necrosis factor alpha and interleukin-2 are the important mediators in the inflammatory process. This theory holds that the more severe cases of malaria, especially cerebral malaria, are the result of an exacerbated inflammatory response of the host.

Only single case of cerebral infarct has been reported as a manifestation of P. vivax infection until date. [2] Our patient was young with no known risk factors for ischemic stroke developed a frontal lobe cerebral infarct during the acute phase of P. vivax malarial infection. We feel the cerebral infarction is related to P. vivax infection however the exact mechanisms are not clear. P. vivax malaria is considered to be benign infection, However, it can be complicated by thrombocytopenia, cerebral malaria and acute renal, hepatic and pulmonary dysfunctions and death. [5]


1WHO World Malaria Report 2012 FACT SHEET. Available from: [Last accessed on 2013 Mar 19, 7 pm IST].
2Young-Kyoung J, Minn YK, Soo-Jin C, Kwon KH. Multiple cerebral infarcts following acute Plasmodium vivax infection. Korean J Stroke 2012;14:149-51.
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4Leopoldino JF, Fukujima MM, Gabbai AA. Malaria and stroke. Case report. Arq Neuropsiquiatr 1999;57:1024-6.
5Limaye CS, Londhey VA, Nabar ST. The study of complications of vivax malaria in comparison with falciparum malaria in Mumbai. J Assoc Physicians India 2012;60:15-8.