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Review
. 2014 Jul 18:13:276.
doi: 10.1186/1475-2875-13-276.

Magnetic resonance imaging during life: the key to unlock cerebral malaria pathogenesis?

Sanjib Mohanty, Terrie E Taylor, Sam Kampondeni, Mike J Potchen, Premanand Panda, Megharay Majhi, Saroj K Mishra, Samuel C Wassmer  1
Affiliations
Review

Magnetic resonance imaging during life: the key to unlock cerebral malaria pathogenesis?

Sanjib Mohanty et al. Malar J. .

Abstract

Understanding the mechanisms underlying the pathophysiology of cerebral malaria in patients with Plasmodium falciparum infection is necessary to implement new curative interventions. While autopsy-based studies shed some light on several pathological events that are believed to be crucial in the development of this neurologic syndrome, their investigative potential is limited and has not allowed the identification of causes of death in patients who succumb to it. This can only be achieved by comparing features between patients who die from cerebral malaria and those who survive. In this review, several alternative approaches recently developed to facilitate the comparison of specific parameters between fatal, non-fatal cerebral malaria and uncomplicated malaria patients are described, as well as their limitations. The emergence of neuroimaging as a revolutionary tool in identifying critical structural and functional modifications of the brain during cerebral malaria is discussed and highly promising areas of clinical research using magnetic resonance imaging are highlighted.

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Figures

Figure 1
Figure 1
CT scans of adult CM patients from India showing mild to severe brain swelling. Non-enhanced 8 mm transverse sections of a control patient (A) and two acute CM patients showing mild and severe cerebral oedema (B and C, respectively). Images were obtained within 6 hours of admission at Ispat General Hospital in Rourkela, Orissa, India, as part of another study [52] and using a Philips W1000 third generation CT scan. Brain swelling observed in (B) and (C) was defined as loss of cerebrospinal fluid space, small ventricles, absence of sulci, and/or compression of the cisterns. Mild brain swelling was defined as local or diffuse effacement of sulci and Sylvian fissure without compression of the supratentorial ventricular system (B). Severe swelling was defined as diffuse obliteration of sulci, Sylvian fissure and basal cisterns, together with an important mass effect causing near total obliteration of the supratentorial ventricular system and generalized hypodensity of brain parenchyma (C).
Figure 2
Figure 2
MRI of paediatric patient with fatal CM from Malaŵi presenting severe brain swelling. Admission axial T2 scan (TR 3140, TE 123) of a 4 years old male child with fatal retinopathy-positive CM performed at Queen Elizabeth Central Hospital in Blantyre, Malaŵi (A). Severe brain swelling is observed, with complete loss of sulcal markings. (B) shows a lower slice depicting severe brainstem compression resulting from the swelling. A mid-sagittal T1 Flair image (TR 2311, TE 26, ET 2) of the same patient reveals the complete effacement of all basilar cisterns and the 4th ventricle, as well as severe brainstem compression (C). Finally, (D) shows potential diffuse restricted diffusion in the cerebral cortex and white matter. The child succumbed from respiratory failure 3 hours after these images were obtained.
Figure 3
Figure 3
MRI of paediatric CM survivor from Malaŵi during the acute phase and at follow-up. Admission axial T2 scan (TR2960, TE122) of a 2 years old male Malaŵian child with retinopathy-positive CM performed at Queen Elizabeth Central Hospital in Blantyre, Malaŵi. There is severe brain swelling with total loss of sulcal markings and grey-white differentiation (A). The same child presents mild diffuse atrophy one month later during the post-discharge follow-up visit (B).
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