Malaria is a vector-borne disease transmitted by the bite of an infected female anopheles mosquito presents with varied clinical manifestations. Neurological manifestations include headaches, confusion, convulsions, hemiplegia, ataxia, cerebral palsy, cortical blindness, and Guillain-Barre syndrome (GBS). We are presenting a case report of acute cerebellar ataxia in a 20-year-old male patient who presented with fever and positive for Plasmodium vivax and Plasmodium falciparum malaria antibodies.
Keywords: Cerebellar ataxia, cerebral malaria, cytoadherence, post malarial neurological syndrome
|How to cite this article:
Kumar PS, Manohar S, Siddeswari R, Mythili M. Acute cerebellar ataxia: A neurological manifestation in malaria. Ann Trop Med Public Health 2014;7:266-7
|How to cite this URL:
Kumar PS, Manohar S, Siddeswari R, Mythili M. Acute cerebellar ataxia: A neurological manifestation in malaria. Ann Trop Med Public Health [serial online] 2014 [cited 2021 Apr 11];7:266-7. Available from: https://www.atmph.org/text.asp?2014/7/6/266/155021
Malaria is a well-known cause of mortality and morbidity across the world, including India. Severe malaria is clinically characterized by confusion or drowsiness with extreme weakness (prostration). In addition, the following may develop: Cerebral malaria with generalized convulsions, pulmonary oedema, severe anemia, renal failure, hypoglycaemia, metabolic acidosis, circulatory collapse/shock, spontaneous bleeding and laboratory evidence of disseminated intravascular coagulation (DIC), andmacroscopic hemoglobinuria hyperthermia. Serious complications can arise in Plasmodium falciparum infection and also rarely in Plasmodium vivax. They may sometimes develop suddenly over a span of time as short as 12-24 h, and may lead to death if not treated promptly and adequately.  P. vivax is responsible for 21% of all severe malaria cases, P. falciparum for 71%, and mixed P. vivax and P. falciparum infections for 5%.  Rarely, adults (<3%) and children (>10%) suffer from a syndrome of neurological and psychiatric symptoms within two months after treatment of malaria, known as post-malarial neurological syndrome (PMNS). Psychosis (paranoia, mania, hallucinations, and delusions) are the most common sequelae. Hemiplegia, cerebral palsy, cortical blindness/deafness, impaired cognition and learning have been reported. Rare cases of Guillain-Barre syndrome (GBS) and cerebellar ataxia have also been observed. 
A 22-year-old male presented with chief complaints of tremulousness of limbs and swaying while walking. Twelve days prior to admission,he had high grade fever with chills that lasted for 5 days and one episode of generalized tonic clonic seizures that subsided with symptomatic treatment.He was not a known epileptic or alcoholic.He did not suffer from any psychiatric illness. Physical examination was unremarkable. Nervous system examination revealed staccato speech, hypotonia, dysmetria, finger-to-nose coordination, test positive, intentional tremor, overshooting (hypermetria), dysdiadochokinesia, grade 2 nystagmus, and rebound phenomenon. Fundus examination was normal.
Hemoglobin 13.5 gm%, red blood cells (RBC) count 5.15 million/cumm, white blood cells (WBC) count 10,000 cells/cumm, polymorphs 70%, lymphocytes 22%, eosinophils 2%, monocytes 6%, basophils 00%, haematocrit 42.7 vol%, platelet count 1.09 lakhs/cumm, mean corpuscular volume (MCV) 83.1 cumm, mean corpuscular hemoglobin (MCH) 26.2 pg, mean corpuscular hemoglobin concentration (MCHC) 31.6 g/dL, IgM Postive for P. vivax and P. falciparum. Random blood sugar 102 mg/dl, Blood urea: 38 mg/dl, the Widal test revealed S.typhi O-1:80 dilution, S.typhi H-1:160 dilution, chest radiography revealed a normal study, cerebrospinal fluid (CSF) analysis was normal. Computed tomography (CT) brain scan revealed a normal study. Magnetic resonsance imaging (MRI) brain revealed a normal study.
One of the dreaded manifestations of malaria is cerebral malaria. Cytoadherence, rosetting, and agglutination leading to sequestration of RBCs are central to the pathogenesis of falciparum malaria. Cerebral capillaries and venules are packed with parasitized erythrocytes and the brain is dotted with small foci of necrosis surrounded by glia (Durck nodes). These findings have been the basis of several hypotheses (one of which attributes to cerebral symptoms to mechanical obstructions of the vessels), but none is entirely satisfactory. Usually the neurologic symptoms appear in the second or third week of the infection, but they may be the initial manifestation.  Recent studies have demonstrated that P. vivax can cause both sequestrations-related and nonsequestration-related complications of severe malaria including cerebral malaria. Although P. vivax has been reported to cause cerebral symptoms in India and China.  In India about 50% of malaria cases which were reported are found to be caused by P. vivax. Vivax malaria generally has an uncomplicated course but sporadically, all complications usually associated with P. falciparum malaria have also been reported in vivax malaria.  The important neurological sequelae (PMS) in survivors were psychosis in 15 (5.06%), cerebellar ataxia in 14 (4.72%), hemiplegia in 5 (1.68%), extrapyramidal rigidity (EPR) in 4 (1.35%), peripheral neuropathy in 3 (1.01%), extrapyramidal rigidity (EPR) with trismus in 1 (0.33%) and isolated sixth nerve palsy in 1 (0.33%) patients and all showed complete recovery in further follow-up.  post malarial neurologic syndrome (PMNS) are known entities for decades. Delayed cerebellar ataxia is a new PMNS observed in the Indian Subcontinent during last two decades. The ataxic symptoms appeared after an afebrile period of 2-7 days and neurological examination revealed no other abnormality except a cerebellar syndrome interfering with normal gait and speech. Lower limbs were affected more than the upper limbs and the mean delay between the onset and fever and onset of cerebellar ataxia was 13 days. All the patients improved within one month without any residual deficit. Further follow-up for the next 4 weeks revealed no abnormality. 
In conclusion, mixed species infection is not uncommon in the locality where both species coexist. Here we are presenting a mixed species infection with cerebellar ataxia with positive antibodies to P. vivax and P. falciparum who has improved with antimalarial drugs. So we should not forget malaria in the differential diagnosis of acute neurological illness.
Diagnosis and Treatment of Malaria. (Directorate of National vector Borne Disease control Programme). Available from: http://nvbdcp.gov.in/Doc/Diagnosis-Treatment-Malaria-2013.pdf. [Last accessed on 2015 March 26].
Genton B, D’Acremont V, Rare L, Baea K, Reeder JC, Alpers MP, et al. Plasmodium vivax and mixed infections are associated with severe malaria in children: A prospective cohort study from Papua New Guinea. PLoS Med 2008;5:e127.
Agarwal AK, Chatterjee C. Malaria. In: Munjal YP, editor. API Textbook of Medicine. 9 th ed. Jaypee Brothers Medical Publishers Ltd; 2012. p. 1177-84.
Dr. Maguire J. Ch. 32. Infections of the Nervous system (Bacterial, Fungal, Spirochaetal, Parasitic) and Sarcoidosis. Adams and Victor’s Principles of Neurology, 10/e, Mc Graw Hill; 2014. p. 697-740.
Gandhi DJ, Nayak US, Shendurnikar N, Shah AR. Cerebral Malaria – a diagnostic and Therapeutic approach. Indian Pediatr 1990;27:651-7.
Islam N, Qamruddin K. Unusual complications in benign tertian malaria. Trop Geogr Med 1995;47:141-3.
Kochar DK, Shubhakaran, Kumawat BL, Kochar SK, Halwai M, Makkar RK, et al. Cerebral Malaria in Indian adults: A prospective study of 441 patients from Bikaner, north-west India. J Assoc Physicians India 2002;50:234-41.
Mohapatra MK, Panda BK, Das SP. Cerebellar ataxia in falciparum malaria – a report of two cases Indian J Malariol 2000;37:46-8.
Source of Support: None, Conflict of Interest: None