Posted by Dr. Bijoykumar Barik on Thursday, 22nd July 2010ABSTRACT:
Delayed cerebellar ataxia is a rare acute self limiting complication of falciparum malaria . This complication is predominantly found in Sri Lanka though few cases have been reported from India and Africa [2,4]. We have recently encountered such a patient in our hospital. The case is described below with pertinent literatures reviewed.
Delayed cerebellar ataxia, Plasmodium falciparum
Delayed cerebellar ataxia found in falciparum malaria is usually an acute self limiting and isolated ataxia without cerebral involvement . The patient usually shows features of midline cerebellar involvement and is characterized by cerebellar gait and truncal ataxia [1,4]. Most of the patients are afebrile before the onset of symptoms [1,4].
A 45 year old engineer was admitted to the hospital in September '07 with complaints of difficulty in maintaining balance with a tendency to fall in all directions for the past four days. He developed high grade fever, intermittent in nature associated with chills and rigor and subsided with profuse sweating. He was admitted in the local hospital and was detected having falciparum malaria by MP slide and was treated with anti-malarials and antibiotics. The patient became afebrile after five days and was discharged. Four days later He developed instability of gait such that he lurched and fell in all directions – this left him unable to walk. He was then referred to our hospital for further investigations and management.
There was no history of diabetes mellitus, hypertension, tuberculosis or sickle cell disease.
Family history is also not suggestive of diabetes mellitus, hypertension, tuberculosis or sickle cell disease.
On admission the patient was found to be conscious afebrile. There was mild pallor, no cyanosis, icterus, clubbing, edema, Lymph node or thyroid enlargement, JVP was not raised, Pulse was 80/ min regular, B.P. 150/ 84 mm of Hg, Respiratory rate of 18/ min and temperature was 36.4 ° C.
Neurological examination revealed normal higher mental function. All cranial nerves were found normal. Motor system examination revealed normal bulk, tone and power. The gait was broad based with irregular stepping and a tendency to fall in all direction. No sensory impairment or autonomic involvement was found. On finger nose testing revealed past pointing; the knee heel shin test was found to be clumsy bilaterally. Disdiadochokinesia was present bilaterally. The deep tendon reflexes were normal, plantar was bilaterally flexor. The cranium and spine was normal and there were no signs of meningeal irritation.
The respiratory, cardiovascular, and gastrointestinal system was found to be normal.
On investigation Hb% was 11.2 gm/dl, DC N72 E3 L25; Total leukocyte count was 7100/cmm and ESR was 6 mm in 1st hr. Routine blood biochemistry Fasting blood glucose 110 mg/dl, urea 28 mg/dl, creatinine 1.4 mg/dl, serum Na+ 147mEq/l and K+ 4.0 mEq/l. Malaria parasite by ICT was found to be positive. CT scan of brain was found to be normal and no abnormality was detected by pure tone audiometry bilaterally. CSF study was found to be normal.
The patient was diagnosed as having delayed cerebellar ataxia following falciparum malaria. He was treated with a full course of inj. Artesunate for 5 days. The patient rapidly improved and by the 5th day he was able to walk on his own. The cerebellar signs disappeared on the 6th day and he was discharged with advice after 7 days of admission.
Neurologic features found in malaria are usually not consistent; the commonest being altered sensorium followed by seizures . But cerebellar involvement is the most consistent neurological manifestation of complicated as well as uncomplicated malaria as Purkinje cells are susceptible to damage due to hyperpyrexia .
RBCs with parasitized P. falciparum adhere to the endothelial wall of capillaries in a certain phase of its cycle. Parasites derive some nutrition from endothelium. This phenomenon occurs maximally in the capillaries of brain . Focal hemorrhage or non hemorrhagic infarcts in cortex, basal ganglia, thalamus, pons and cerebellum have all been described in cerebral malaria . Immunologic mechanism, as a cause for delayed cerebellar ataxia has been postulated; cerebellar demyelination following falciparum malaria has been reported in several patients from Sri Lanka and India occurring several days after recovery [1,4]. The CT scan of brain is normal [1,2]. The disease has an excellent prognosis with complete recovery in 3 months [2,4]. The patients are treated symptomatically though some physicians prefer to use steroids.
Cerebellar involvement in falciparum malaria may be due to selective clogging of cerebellar micro vasculatures with parasitized RBCs, perivascular hemorrhage, microscopic infarcts, shrinkage of purkinje cells and perivascular clusters of microglia, carrying a high mortality rate [1,3] or, may be due to immunologic mechanism as in the case of delayed cerebellar ataxia [1,4].
Delayed cerebellar ataxia is a rare complication of cerebellar involvement following falciparum malaria and may be considered in the differential diagnosis in patients showing cerebellar signs especially if the patient gives a past history of fever. This is the first reported case of delayed cerebellar ataxia from our institution.
1. Adult cerebral malaria: prognostic importance of Imaging findings and correlation with postmortem findings; Tufail F. Patankar, MD, Dilip R. Karnad, MD, Prashant G. Shetty, MD, Anand P. Desai, MD, Srinivasa R. Prasad, MD;Radiology 2002;224:811-816
2. Delayed cerebellar ataxia following Falciparum malaria: Hussam Alsoub, MD : Annals of Saudi Medicine,1999;Vol 19, no. 2: 128-129
3. MR of cerebral malaria; Yves Sébastien Cordoliani, Jean-Luc Sarrazin, Dominique Felten, Eric Caumes, Cristophe Lévêque, Alain Fisch; AJNR Am Neuroradiol 19:871-874, May 1998