Article Figures & Data
Figures
- Fig 1.
Patterns of diffusion restriction on admission MR imaging in children with retinopathy-positive cerebral malaria. Numbers in each category are reported as No. (%). Examples of each observed pattern are illustrated with accompanying description.
- Fig 2.
IWMDR on initial brain MR imaging in children with cerebral malaria. A–C, Axial diffusion-weighted images in 3 different comatose children with acute cerebral malaria. There are confluent regions of diffusion restriction in the subcortical white matter without involvement of the cortex or deep gray matter. D–F, Axial DWI in a different patient demonstrates a similar pattern of white matter hyperintensity on diffusion-weighted images, with corresponding hypointensity on ADC maps, consistent with true diffusion restriction. Axial T2-weighted image demonstrates subtle regions of corresponding T2 hyperintensity.
Tables
- Table 1:
Clinical characteristics and outcomes associated with IWMDR in children with cerebral malariaa
IWMDR+ IWMDR− OR 95% CI P Value Clinical characteristics Admission temperature (°C) 38.9 ± 1.1 38.8 ± 1.2 1.11 0.87–1.42 .40 Plasma lactic acid levels (mmol/L) 5.4 ± 3.6 6.9 ± 4.5 0.91 0.85–0.98 .02 Systolic blood pressure (mm Hg) 41.2 ± 214.7 74.9 ± 137.6 1.00 0.99–1.00 .14 HIV status 5 (9.6%) 32 (16.3%) 0.55 0.20–1.48 .23 Reported preadmission seizure 53 (89.8%) 171 (83.0%) 1.80 0.72–4.52 .21 Plasma glucose level (mmol/L) 6.4 ± 2.1 6.7 ± 3.6 0.97 0.89–1.06 .49 Plasma HRP-II levels 10.2 ± 10.2 10.8 ± 10.1 0.99 0.96–1.02 .67 Received anticonvulsant at admission 35 (57.4%) 148 (71.2%) 0.55 0.30–0.98 .04 Admission Blantyre coma scale score 1.4 ± 0.6 1.3 ± 0.6 1.44 0.90–2.31 .13 Admission white blood cell count × 10−9/L 10.5 ± 7.9 11.3 ± 7.9 0.98 0.95–1.03 .51 Platelet count × 10−9/L 56 ± 60 59 ± 64 1.00 1.00–1.00 .81 EEG characteristics Average voltage (μV) 128.9 ± 50.7 104.5 ± 53.5 1.01 1.00–1.02 .02 Maximum voltage (μV) 251.1 ± 75.8 219.4 ± 88.5 1.00 0.99–1.01 .06 Sleep architecture 20 (55.6%) 66 (55.5%) 1.00 0.47–2.13 .99 Dominant rhythm frequency (Hz) 2.3 ± 0.9 2.4 ± 1.7 NA NA .56 Variability 24 (66.7%) 69 (58.0%) 1.45 0.66–3.17 .35 Reactivity 20 (58.8%) 45 (40.5%) 2.10 0.96–4.58 .06 General slowing 35 (97.2%) 105 (90.5%) 3.67 0.46–29.4 .22 Paradoxic reactivity 10 (50%) 17 (37.0%) 1.70 0.59–4.93 .32 Asymmetry 7 (19.4%) 34 (28.8%) 0.60 0.24–1.49 .27 Outcomes Overall coma duration (hrs) 47.5 ± 25.3 74.8 ± 43.9 0.98 0.97–0.99 <.001 Full recovery 55 (90.2%) 148 (71.2%) 3.70 1.50–9.10 .004 Survival with sequelae 5 (8.2%) 27 (13.0%) 0.60 0.22–1.63 .32 Death 1 (1.6%) 33 (15.9%) 0.09 0.01–0.67 .02 Note:—HRP-II indicates histidine-rich protein, a marker of parasite burden; IWMDR+, subjects with purely subcortical white matter abnormalities, excluding those with cortical DWI abnormalities and those with basal ganglia DWI abnormalities; IWMDR−, those who did not meet criteria for IWMDR+; NA, not applicable.
↵a Values are No. (%) or means.
- Table 2:
Conditions with reversible/transient white matter diffusion restriction and their pathophysiology
Condition Proposed Pathophysiology Relevance to Cerebral Malaria Acute toxic leukoencephalopathy Intramyelinic edema, myelin vacuolization Endothelial injury is a pathophysiologic mechanism in CM38 Capillary endothelial injury Direct toxic demyelination16 Hypoglycemia Energy failure leading to excitatory edema21 Hypoglycemia is a frequent complication in children with severe falciform malaria39; local/focal hypoglycemia may occur due to sludging even in the absence of systemic hypoglycemia Peri-/postictal state Increased metabolic demand leading to energy failure and resultant cytotoxic and vasogenic edema40 Seizures, often recurrent, are a frequent manifestation of CM and associated with worse outcome29 Penumbra of ischemic infarct Early white matter ischemic injury with axonal swelling and intramyelinic edema13 Sequestration in postcapillary venules of the brain and venous congestion are central to CM pathogenesis25 Demyelination Immune-mediated perivenular inflammation and demyelination41 Vascular inflammatory markers are associated with CM, and perivenular inflammation is thought to contribute to CM pathogenesis38
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