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Magnetic resonance imaging patterns of paediatric brain infections: a pictorial review based on the Western Australian experience
Insights into Imaging volume 13, Article number: 160 (2022)
Paediatric brain infections are relatively uncommon, but it is important for radiologists to recognise the disease and provide accurate differential diagnoses. Magnetic resonance imaging (MRI) plays an important role in determining the most likely causative pathogen—either in the setting of an unwell child with acute infectious encephalitis, or in the evaluation of a child for sequela of prior infection. Image analysis can, however, be difficult since a particular pathogen can cause variable MRI findings across different geographic environments, and conversely, a particular appearance on MRI may be caused by a variety of pathogens. This educational review aims to identify some of the key MRI patterns seen in paediatric brain infections and present example cases encountered in Western Australia. Based on (i) the predominant type of signal abnormality (restricted diffusion versus T2 hyperintensity) and (ii) the distribution of signal abnormality throughout the brain, this review presents a framework of six key MRI patterns seen in paediatric brain infections, with an emphasis on acute infectious encephalitis. There is general utility to these MRI patterns—each suggestive of a group of likely diagnostic possibilities which can be calibrated according to institution and local environment. The pattern-based framework of this review can be easily transitioned into daily radiological practice, and we hope it facilitates the formation of accurate differential diagnoses in paediatric brain infections.
There are several key MRI patterns in the setting of paediatric brain infections, which are common across geographic boundaries.
Mechanism of dissemination (such as haematogenous or neural spread) and patient age (maturity of immune system) contribute to imaging appearances.
Patterns based on abnormal restricted diffusion can manifest primarily in supratentorial white matter, supratentorial grey matter, or in the corpus callosum.
Patterns based on abnormal high T2 signal can manifest primarily in supratentorial white matter, the basal ganglia/thalami, or the posterior fossa.
Each pattern suggests a group of differential diagnoses, which can be calibrated according to institution and geographic environment.
Paediatric brain infections are an uncommon but important disease group. Through the use of magnetic resonance imaging (MRI), radiologists are central to the process of establishing differential diagnoses—either in the setting of an unwell child with acute infectious encephalitis (acute inflammation of brain parenchyma) or in the evaluation of a child for sequela of prior infection. However, establishing an accurate differential diagnosis can be challenging, as there are heterogeneous MRI findings described in the literature. A particular pathogen can cause variable brain MRI findings across different geographic environments, and a particular appearance on MRI may be caused by a variety of pathogens. For example:
Burkholderia pseudomallei, a gram negative aerobic bacterium found in tropical and subtropical areas, manifests primarily as supratentorial brain abscesses in Southeast Asia due to bacteraemic spread following ingestion of contaminated food/water . In comparison, Burkholderia manifests as rhomboencephalitis in Northern Australia, relating to nasopharyngeal mucosal colonisation during the wet season, followed by retrograde spread of bacteria to the brainstem .
The pattern of restricted diffusion in deep and periventricular white matter (with a radiating pattern which appears to follow the deep medullary veins) is a well-documented finding in neonatal viral encephalitis, albeit across different geographic environments—such as by rotavirus in Korea and by Chikungunya virus in the Reunion Islands [2, 3].
Although these examples highlight the importance of reviewing regional datasets so that differential diagnoses can be tailored to the local environment, they also reveal the existence of imaging patterns which are common across geographic boundaries. The purpose of this educational review is to illustrate some of the key patterns of brain infections as seen on MRI, describe possible pathophysiologic mechanisms for these patterns, and present example cases encountered in Western Australia. The emphasis is on patterns of acute infectious encephalitis, although patterns relating to post-infectious sequela will also be discussed. Non-infectious aetiologies, such as autoimmune and metabolic conditions, have not been the focus of this review. Whilst other educational reviews on brain infections may present information categorised by microbial types, the structure of this review is to document a pattern-based framework that can be useful for narrowing the differential diagnosis and can be easily implemented into daily radiological practice.
Key patterns of paediatric brain infections on MRI
The MRI patterns and example cases presented in this review are derived from a set of 95 microbiology-proven cases of brain infection in Western Australia, corroborated with the findings of published literature. Patient cases were identified through retrospective analysis of MRI and microbiology data for children treated at Perth Children’s Hospital and Prince Margaret Hospital for Children in Western Australia (WA) between the start of 2010 and March 2021. Ethics approval was obtained through the Western Australian Governance, Evidence, Knowledge and Outcomes (GEKO) system. The mean age of patients included in the data set was 2 years and 6 months (range 0 months through to 15 years and 9 months), with a similar gender distribution (51 males versus 44 females). Upon analysis of MRI cases, the following two factors were found to be of the highest diagnostic value in determining the causative pathogen in paediatric brain infection:
The predominant type of signal abnormality (restricted diffusion versus T2 hyperintensity)
The distribution pattern of signal abnormalities throughout the brain
Based on the above factors, six key MRI patterns relating to paediatric brain infection were identified, as listed below:
Restricted diffusion in supratentorial white matter
Restricted diffusion in supratentorial grey matter
Restricted diffusion in corpus callosum
T2 hyperintensity in supratentorial white matter
T2 hyperintensity in the basal ganglia and/or thalami
T2 hyperintensity in the posterior fossa
Using generic axial and coronal templates of the brain, stylised images representing each pattern were hand drawn using graphics software (following a format inspired by de Oliveira et al.’s incisive article on toxic and metabolic brain disorders) . These stylised images, along with descriptions of sub-patterns, are detailed in Fig. 1. The pathogens encountered in Western Australia, pertaining to each pattern and sub-pattern, are summarised in Table 1—discrepancy between the number of patterned cases and number of microbiology-proven cases of brain infection relates to the large proportion of microbiology-proven cases (particularly of viral aetiology) with normal or near-normal MRI studies.
In the following sections, each pattern is discussed in further detail, with exploration of possible pathophysiologic mechanisms, the types of causative pathogens (with example cases), and corroboration with the published literature.
Pattern 1: Restricted diffusion in supratentorial white matter
The presence of restricted diffusion typically indicates cytotoxic oedema, with less common causes including high viscosity and high cellularity (as seen with pyogenic abscesses) . The mechanism for restricted diffusion which bilaterally and relatively symmetrically involves deep and periventricular white matter, with a radiating pattern which appears to follow the deep medullary veins, that is not fully understood. Potential mechanisms include neuroaxonal tropism (activation of toll-like receptors and subsequent inflammatory response), perivenular invasion or venous ischaemia . Nevertheless, in neonates, two important pathogens implicated in this pattern are parechovirus and enterovirus infection [6,7,8]. The cytotoxic oedema seen on diffusion-weighted imaging (DWI) is the predominant imaging feature, with corresponding signal abnormalities on T1 (hyperintensity)- and T2 (hypointensity)-weighted imaging being relatively subtle . The extent of restricted diffusion can range from florid (pattern 1A—Fig. 2) to mild (pattern 1B—Fig. 3), and cystic encephalomalacia can be seen as a sequelae of severe white matter injury . Rotavirus, adenovirus, Chikungunya and herpes simplex virus (HSV) have also been described in the literature as producing similar appearances on DWI in neonates [2, 3, 9, 10]. As a memory aid, the differential list of parechovirus, adenovirus, rotavirus, enterovirus, Chikungunya and HSV conveniently spells the mnemonic P-A-R-E-C-H.
Pattern 2: Restricted diffusion in supratentorial grey matter
Cytotoxic oedema involving grey matter, as seen on DWI, represents a heterogeneous group which can be divided into three sub-patterns for the purposes of this review.
In the first sub-pattern, mainly observed in infants and young children, scattered and asymmetric foci of restricted diffusion (pattern 2A) suggest haematogenous spread of disease. This could relate to occlusion/inflammation of small distal vessels as seen with septic emboli, particularly in immunocompromised children (Fig. 4) [11, 12], or alternatively with spread of viral particles across the immature blood brain barrier as seen with herpes simplex virus (HSV) infection (Fig. 5) [10, 13]. Early detection of HSV encephalitis and assessment of disease extent is best assessed on DWI [13, 14], although differentiation between early HSV encephalitis and septic emboli can be difficult. Progression of lesions (within days) to form confluent areas of cortical/subcortical signal abnormality is suggestive of HSV encephalitis [13,14,15], whereas abscess formation is consistent with septic emboli [11, 12].
A second sub-pattern of supratentorial grey matter diffusion restriction in infants and young children corresponds to neural spread of disease, as opposed to the previously described haematogenous spread. As can be observed with HSV in older children, cytotoxic oedema can affect the mesial temporal and insular cortices (pattern 2B—Fig. 6), relating to spread of viral particles along meningeal branches of the trigeminal ganglion [10, 14].
In a third sub-pattern of supratentorial grey matter diffusion restriction, infection can lead to ischaemic stroke, resulting in cytotoxic oedema (restriction on DWI) in distinct vascular territories (pattern 2C). Although not an infectious encephalitis per se, the child will nevertheless present unwell with acute neurological signs, and it is important to recognise the role of recent infection in the child’s presentation. The chicken pox virus is a notable cause, leading to post-varicella arteriopathy (Fig. 7) [16, 17]. Microbes such as HSV, EBV, enterovirus and TB (Fig. 8) have also been implicated in the literature [16, 17].
Pattern 3: Restricted diffusion in corpus callosum
Cytotoxic lesions of the corpus callosum (CLOCCs) are encountered in a number of settings, including infection, inflammation and trauma; in children, the most common cause is infection [18, 19]. The vulnerability of the corpus callosum, in particular the splenium, is thought to relate to an increased number of cytokine (and ultimately glutamate) receptors, which in conjunction with its rich blood supply (from both anterior and posterior circulations) makes the corpus callosum vulnerable to cytokinopathy in settings such as infection [19, 20]. Whilst various patterns of callosal involvement have been described, the most common pattern in children is an ovoid lesion centred midline within the splenium (Fig. 9) [18, 19]. Typical infectious agents implicated in CLOCCS include influenza (most common), herpesviridae and gastrointestinal pathogens (e.g. rotavirus, Escherichia coli and Salmonella enteritis) [18,19,20]. In the paediatric cohort, the reversibility of CLOCCS (within 1–2 weeks) typically confers a favourable prognosis; conversely, persistence of restricted diffusion within the corpus callosum should prompt consideration of non-infectious aetiologies (e.g. metabolic or traumatic) .
Pattern 4: T2 hyperintensity in supratentorial white matter
Diffuse or confluent supratentorial white matter T2 hyperintensities, in the absence of DWI changes related to cytotoxic oedema, suggest abnormalities such as gliosis and/or encephalomalacia (as the end-product of prior or longstanding infection) [21, 22]. In the neonatal setting, congenital TORCH infections (toxoplasma, other, rubella, cytomegalovirus and herpes simplex virus) come to mind as important differentials with manifestations in supratentorial white matter [21,22,23]. The presence of calcification is likewise an indicator of brain parenchymal injury during the early stages of life, arising from parenchymal necrosis in conjunction with an immature immune system and the impaired phagocytic ability of macrophages .
The timing of TORCH infection is central to its imaging manifestations . Early in-utero infection, such as during the early stages of the second trimester of pregnancy, is more likely to result in malformations of cortical development (lissencephaly-pachygyria or polymicrogyria), brain volume loss and diffuse white matter abnormality (pattern 4A—Figs. 10, 11 and 12) [23,24,25,26]. Conversely, TORCH infection during late third trimester of pregnancy is seen without neuronal migration abnormality, and any long-term neurodevelopmental sequelae are typically less severe (pattern 4B—Fig. 13) [23,24,25]. Although post-natal imaging depicts the sequela of infection rather than ongoing infectious encephalitis, being able to differentiate between early and late in utero TORCH infection has important prognostic implications, and establishes the utility of MRI in the work-up of infants and young children with abnormal neurology/development.
Whilst there is overlap in the imaging features of different TORCH infections, certain findings can help distinguish between cases of congenital neurotoxoplasmosis and cytomegalovirus (CMV) infection. Congenital neurotoxoplasmosis (Figs. 10 and 11) is characterised by hydrocephalus, parenchymal volume loss, necrosis with abscess formation, and calcifications (typically coarse and random in distribution); chorioretinitis with vision impairment is a supportive clinical feature [23, 26]. In comparison, congenital CMV (Figs. 12 and 13) is characterised by anterior temporal pole cysts, parietal/peritrigonal white matter T2 hyperintensity, microcephaly and calcifications (typically periventricular); sensorineural hearing loss is a supportive clinical feature, and may be the initial trigger for investigation [24,25,26].
When there is supratentorial white matter hyperintensity and the typical peritrigonal distribution of CMV is not observed (in an otherwise developmentally normal brain), non-TORCH infections should be considered. For example, Streptococcus pneumoniae can cause diffuse white matter injury involving the centrum semiovale bilaterally . Non-infectious differentials for the anterior temporal pole cysts seen in congenital CMV include megalencephalic leukoencephalopathy with subcortical cysts (MLC) and Aicardi-Goutières syndrome (AGS) .
Pattern 5: T2 hyperintensity in the basal ganglia and/or thalami
A number of pathogens exhibit tropism for the basal ganglia and/or thalami, including Epstein-Barr virus (EBV), varicella zoster virus (VZV), Flaviviridae (such as Dengue virus, West Nile virus, Murray Valley encephalitis virus and Japanese encephalitis virus), cryptococcus and tuberculosis [13, 23, 24, 28,29,30,31,32]. The mechanisms by which these pathogens affect deep brain structures is not fully understood, and may relate to a number of factors including the high inherent metabolic activity of the basal ganglia and thalami, in conjunction with their vascular supply . In particular settings, such as with cryptococcal infection, infiltration of deep brain structures via perivascular spaces has been described [32, 34]. Post-inflammatory, genetic and metabolic causes should also be considered in pathology of the basal ganglia and thalami, and clinical history is fundamental [13, 28, 30, 31].
EBV infections present with bilateral T2 hyperintense lesions of the basal ganglia and thalami, with variable symmetry, variable restricted diffusion and typically no gadolinium enhancement (Fig. 14) [13, 14, 23, 29]. Extension into the infratentorial brain may occasionally occur, and variable cortical grey matter involvement has been reported [23, 29]. Imaging features of cryptococcal infection reflect spread of disease along perivascular spaces, with formation of gelatinous pseudocysts predominantly in the basal ganglia—this gives rise to ‘bubble-like' lesions which are T2 hyperintense and may have a small component of restricted diffusion (Fig. 15) [24, 32]. Cases of flavivirus encephalitis were not available in our data set, but literature describes the presence of bilateral T2 hyperintensities in the thalami, with or without basal ganglia involvement [23, 30]. Although not known to be neurotropic for deep brain structures, respiratory pathogens (such as influenza virus, parainfluenza virus, respiratory syncytial virus, adenovirus and Streptococcus pneumoniae) have also been associated with lesions in the thalami (often symmetric), with a minority of cases leading to acute necrotising encephalitis (ANEC) [30, 35].
Pattern 6: T2 hyperintensity in the posterior fossa
Rhombencephalitis, with high T2 signal in the brainstem and/or cerebellum, can be associated with different infectious aetiologies—each with their own mechanism for affecting the posterior fossa. Enterovirus, which can initially present as a gastrointestinal illness or as a rash involving the hands and feet of infants and young children, spreads along peripheral nerves to gain access to the central nervous system where it has a predilection for ventral horn cells of the spinal cord and the brainstem . When enterovirus causes rhombencephalitis, MRI typically demonstrates T2 hyperintensity of the dorsal pons and medulla oblongata (pattern 6A—Fig. 16), and there may be involvement of the midbrain, dentate nuclei and upper cervical cord (serotypes E-71 and E-68 are often cited as the causative agent) [36,37,38,39]. More specific to the Northern Australian setting, neuromelioidosis results from nasopharyngeal mucosal colonisation by Burkholderia, followed by retrograde spread to the brainstem to cause rhombencephalitis (cranial nerve deficits may be clinically apparent) and spread of micro-abscesses along longitudinal white matter and commissural tracts (pattern 6B—Fig. 17) [1, 40, 41]. Rim-enhancing brain abscesses may eventually develop in the posterior fossa and/or contralateral supratentorial compartment (Fig. 18) [1, 40, 41]. Although not encountered in our dataset, other pathogens implicated in rhombencephalitis include rotavirus, Listeria monocytogenes (e.g. from pre-cooked meats and unpasteurised milk), VZV and HSV [1, 42,43,44,45]. Viruses which affect the basal ganglia and thalami, such as EBV and flaviviridae, may also occasionally manifest in the posterior fossa [23, 28, 29].
This educational review offers a practical framework for approaching paediatric brain infections. The key MRI patterns described in this review are each suggestive of a group of diagnostic possibilities—grounded in pathophysiology and corroborated by published literature, with flexibility for calibration according to institution and local environment (an example summary for Western Australia is shown as Fig. 19). The pattern-based framework of this review can be easily transitioned into daily radiological practice, and we hope it can facilitate the formation of accurate differential diagnoses in paediatric brain infections.
Availability of data and materials
The dataset used and/or analysed during the current study are available from the corresponding author on reasonable request.
Apparent diffusion coefficient
Acute necrotising encephalitis
Cytotoxic lesion of the corpus callosum
Herpes simplex virus
Mild encephalitis with reversible splenial lesion
Megalencephalic leukoencephalopathy with subcortical cysts
Magnetic resonance imaging
Varicella zoster virus
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Consent for review of retrospective imaging and microbiological data was obtained through the Western Australian Governance, Evidence, Knowledge and Outcomes (GEKO) system—reference number 42052.
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Yang, CW.R., Mason, M., Parizel, P.M. et al. Magnetic resonance imaging patterns of paediatric brain infections: a pictorial review based on the Western Australian experience. Insights Imaging 13, 160 (2022). https://doi.org/10.1186/s13244-022-01298-1
- Infectious encephalitis
- Viral encephalitis
- Differential diagnosis
- Diagnostic imaging
- Magnetic resonance imaging