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British Journal of Radiology (2007) 80, e293-e295
© 2007 British Institute of Radiology
doi: 10.1259/bjr/54355671
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Case report

Central pontine myelinolysis in a case of cerebral malaria

C J Das, MD, DNB and R Sharma, MD

Radiology, AIIMS, New Delhi, 110 029, India

Correspondence: Dr Raju Sharma, Additional Professor, Department of Radio-Diagnosis, All India Institute of Medical Sciences, New Delhi -110029, India. E-mail: raju152{at}yahoo.com


   Abstract
Top
 Abstract
Introduction
 Case report
 Discussion
 References
 
Central pontine myelinolysis (CPM) is a clinical condition characterized by myelin destruction in the rostral part of the pons. It is commonly found in association with alcoholism, rapidly corrected hyponatraemia and electrolyte abnormalities. We describe here an unusual case of CPM occurring in a patient with cerebral malaria.


   Introduction
Top
 Abstract
 Introduction
Case report
 Discussion
 References
 
Central pontine myelinolysis (CPM) is characterized by myelin destruction in the rostral part of the pons involving all descending and ascending fibre pathways, with the exception of the ventrolateral tract [1]. Although the original descriptive term "central pontine myelinolysis" is commonly used, demyelination is often observed outside the pons [2]. It is commonly found in association with alcoholism, chronic nutritional deficiency, rapidly corrected hyponatraemia, systemic disorders associated with electrolyte abnormalities, chronic liver and lung diseases, diabetes mellitus and malignancy [3]. We describe here a case of CPM occurring in a patient with cerebral malaria.


   Case report
Top
 Abstract
 Introduction
 Case report
Discussion
 References
 
A 37-year-old man was admitted to a private hospital complaining of high-grade fever with chills and rigor of 7 day duration. He also reported a single episode of tonic clonic seizure followed by altered sensorium that had progressively worsened during the previous 24 h. His pertinent laboratory investigations at the time of admission were unremarkable. He was moved to our hospital in a coma. He had a history of malaria, which had been treated 2 years earlier. His medication included frusemide, vitamin B12 and folate. Physical examination revealed pallor and hepatosplenomegaly. His blood pressure was 160/120 mmHg, his heart rate was 110 beats per minute, his respiration rate was 20 per min, his temperature was 39°C, and his oxygen saturation was 83% in room air. On neurolgical examination, he scored 6 on the Glasgow Coma Scale (GCS). He had a Na+ level of 152 mmol dl–1 and K+ level of 4.5 mmol dl–1. Testing of arterial blood gases revealed a pH of 7.42 and a PaCO2 of 23 mmHg. Haematological parameters revealed a haemoglobin level of 6.8 g dl–1 and a leukocyte count of 14400 cells µl–1. Thick peripheral blood smears revealed the presence of Plasmodium falciparum with a parasitaemia level of 0.1%. Examination of the cerebrospinal fluid (CSF) revealed cells with a protein level of 22 g dl–1, glucose level of 83 mg dl–1 and chloride level of 113 mmol dl–1. No parasites were found in the CSF. A Gram stain, AFB stain and Indian ink stain were also negative. Non-contrast MRI was performed 48 h after the onset of coma, and revealed an altered area of signal intensity which was hypointense on a T1 weighted (T1W) (TR/TE 560/60) image (Figure 1Go) and hyperintense on a T2 weighted (T2W) (TR/TE 4500/120) image (Figure 2Go) localized to the central and dorsal parts of the pons involving the tegmentum with relative sparing of the ventral part. The involved area was also hyperintense on a fluid inversion recovery (FLAIR) (TI/TR/TE 2500/4500/120) image (Figure 3Go). During the course of the hospital stay, he developed azotaemia (serum creatinine 2.2 mg dl–1) and he required dialyses. Based on the clinical presentation and MR appearance, a diagnosis of cerebral malaria with central pontine myelinolysis (CPM) was suggested. He was treated with intravenous quinine hydrochloride and also underwent haemodialysis for his abnormal renal function. Blood pressure was controlled with amlodipine and clonidine. With treatment, the patient regained consciousness, but neurophysiological testing demonstrated defects in memorization tasks. A follow-up MRI scan performed 2 months after the onset of neurological symptoms showed no change in the pontine lesion (Figure 4Go). However, neuropsychological test scores returned to near normal.


Figure 1
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  		Figure 1. T1 weighted (TR/TE 560/60) axial image showing hypointensity localized to the central and dorsal parts of the pons involving the tegmentum with relative sparing of the ventral part.

 

Figure 2
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  		Figure 2. The involved areas appear hyperintense on theT2 weighted image (TR/TE 4500/120).

 

Figure 3
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  		Figure 3. FLAIR(TI/TR/TE 2500/4500/120) image.

 

Figure 4
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  		Figure 4. Repeat MRI(T2 weighted axial image) performed 2 months later showed no change in the pontine lesion.

 

   Discussion
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 Abstract
 Introduction
 Case report
 Discussion
References
 
CPM is a well-recognized clinical and radiological condition that was first described in 1959 by Adams and colleagues [1]. The symptoms of CPM include spastic hemiparesis, pseudobulbar palsy, changing levels of consciousness and coma [4]. A significant proportion of patients die, which may be preceded by a state of pseudocoma (locked-in syndrome). The principal abnormality is demyelination of the pons with relative neuronal sparing. Many of these patients have electrolyte abnormalities and symptoms that could be related to aggressive management of these electrolyte disturbances [5]. In more than 75% of cases, CPM is associated with chronic alcoholism or the rapid correction of hyponatraemia, but other conditions such as hypernatraemia, malnutrition, Addison's disease and renal failure, and diuretic usage have also been implicated [3]. The first case of CPM in a patient with cerebral malaria was reported by Kampfl et al [6].

Cerebral malaria is a life-threatening complication of Plasmodium falciparum infestation that occurs in approximately 2% of cases in endemic areas and it affects mainly children. Progressive neurological changes occur along with high fever and chills. The neurological manifestations are non-specific because of diffuse involvement of the brain. Extrapyramidal and neuropsychiatry manifestation as well as isolated cerebellar ataxia may occur. Coma may ensue, and approximately one-third of patients die [7].

There are few reports of neuroimaging findings in cerebral malaria. MRI is the investigation of choice. The most common MR finding being slightly increased brain volume, which is attributed to an increase in cerebral blood flow caused by vasodilatation and sequestration of infected erythrocytes [8]. Kampfl et al [6] in 1993 reported MR findings in a case of cerebral malaria showing pontine myelinolysis. Other reported brain lesions include myelinolysis in the upper medulla of cerebral malaria [9]. Our findings in this case are consistent with those described by Kampfl et al with the area of T2 hyperintensity located in the central and dorsal pons, sparing the ventral part. The hyperintensity had the characteristics of demyelination, which may be due to ischaemia or toxic injury. Similar cases of post-malarial demyelination presenting as acute disseminated encephalomyelitis (ADEM) and pseudobulbar palsy have also been reported [10, 11]. Pathological and experimental studies have focused on the effect of endothelial activation and non-specific immune inflammatory cytokines [12, 13, 14]. These factors could lead to vascular engorgement and vasodilatation leading to oedema. The differential diagnosis of isolated pontine hyperintensity includes pontine infarct caused by vascular insult, multiple sclerosis, hypertensive encephalopathy and low-grade glioma. The typical confluent T2 hyperintensity in the central pons with sparing of the periphery and corticospinal tracts excludes the possibility of perforating basilar artery infarct, which involves both central and peripheral pontine fibres. Diffusion-weighted imaging (DWI) is a relatively new MR technique, showing restriction of diffusion on DWI with a variable apparent diffusion coefficient (ADC) appearance varying from normal to mild hyperintensity [15, 16]. The possible mechanism for diffusion restriction in CPM is due to a shift of water in the hypernatraemic state from the extracellular interstitial compartment into either or both the intravascular compartment and within the glial cells. The decrease in free water in the interstitial space, combined with trapping of water within cells, would contribute to restricted diffusion [15, 16]. Pontine hypertensive encephalopathy typically does not spare the peripheral fibres. Moreover, the pontine lesion remains unchanged on repeat MRI. Multiple sclerosis was excluded on the basis that most of the demyelinating disease showed typical plaques elsewhere. Most of the pontine neoplasms are seen in paediatric patients. MR spectroscopy can aid in differentiating the neoplasm from CPM when the typical MR imaging appearance is absent.

In conclusion, we have described herein a patient with CPM occurring as a complication of cerebral malaria. MRI depicted the lesion characteristic and location elegantly. In the absence of profound electrolyte abnormality in a non-alcoholic patient with proper correction for hyponatraemia, the CPM may be attributed to the ischaemia or the toxic effect of the parasitized red blood cells in the cerebral microvasculature leading to capillary occlusion and damage.

Received for publication October 17, 2005. Revision received April 27, 2006. Accepted for publication September 15, 2006.


   References
Top
 Abstract
 Introduction
 Case report
 Discussion
 References
 

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This Article
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