Magnetic resonance imaging findings in acute febrile encephalopathy in children

INTRODUCTION

Acute febrile encephalopathy is term commonly used to identify the condition in which altered mental status either accompanies or follows short febrile illness. The incidence is high in children and is associated with mortality and morbidity. It is a medical emergency and clinicians need to diagnose it accurately and timely.¹ The clinical features are nonspecific and with non-availability of many pathogen-specific microbiological investigations, etiological agent may remain elusive in a considerable proportion of cases.² Magnetic resonance imaging (MRI) brain with or without contrast is the recommended imaging. It plays an important role in understanding the pathophysiology, management and sometimes aetiology.

There is paucity of studies on MRI findings in acute febrile encephalopathy in children. This prospective observational study aims to study MRI findings in the setting of acute febrile encephalopathy in children between 1 month to 18 year of age group.

METHODS

Following institutional ethical committee clearance, this observational prospective study was conducted in patients of acute febrile encephalopathy admitted in PICU at tertiary care center. Informed written consent was taken from the patient/guardian.

Study design

It was an observational descriptive type of study.

Study duration

The duration of study was from January 2019 to December 2019.

Study sample

All children of age 1 month to 18 year of age group who had acute febrile encephalopathy admitted in PICU at tertiary care center during January 2019 to December 2019 and who satisfied the inclusion and exclusion criteria were selected in the study finally. 28 patients constituted the study sample.

Inclusion criteria

Patients between 1 month to 18 year of age group, admitted in PICU at tertiary care center, patients with altered state of consciousness lasting for >15 minutes and with fever ≤2 weeks duration with acute onset, patients with or without seizure, complex febrile seizure with altered sensorium, and MRI brain after cardiorespiratory, hemodynamic, and neurological stabilization were included.

Exclusion criteria

Patients with simple febrile seizure, space occupying lesion, metabolic encephalopathy, and endocrinal encephalopathy were excluded

In this study demographic data and detailed history of patient was taken and it includes age, gender, duration of illness, and time of presentation.

Operational definitions

Acute febrile encephalopathy

Acute febrile encephalopathy is term commonly used to identify the condition in which altered mental status either accompanies or follows short febrile illness.

Seizure

Transient occurrence of signs and symptoms resulting from abnormal excessive synchronous neuronal activity in the brain.

Febrile seizure

Seizure that occurs between the ages of 6 and 60 months with temperature of 38 °C (100.4 F) or higher, that are not the result of CNS infection or any metabolic imbalance, and that occur in the absence of history of prior afebrile seizure.

Complex febrile seizure is more prolonged (>15 min), and/or is focal, and/or recurs within 24 hours.

Method of collection of data

Method of collection of data included demographic data, presenting complaints, history and clinical features. All data was collected from patient in prescribed proforma.

MRI brain was done after cardiorespiratory, hemodynamic, and neurological stabilization

Data analysis

The MRI findings were analysed by all three paediatricians along with one neurologist.

The MRI sequences included T1, T2, fluid attenuated inversion recovery (FLAIR) T1 and T2, diffusion weighted images, apparent diffusion coefficient (ADC) and susceptibility weighted images.

RESULTS

This prospective observational study aims to study MRI findings in the setting of acute febrile encephalopathy in children between 1 month to 18 year of age group.

In the present study, MRI brain findings were normal in 17 out of 28 (59.5%) children. MRI brain findings were abnormal in 11 children (38.5%).

Diffuse cerebral oedema was found in 3 patients (10.5%). Focal bilateral symmetrical areas of T2 and FLAIR hyperintensity in basal ganglia and thalamus with restricted diffusion in 2 (7%) patients. T2 and FLAIR hyperintensity was seen in hippocampus in 2 patients 2 (7%). Features of haemorrhagic encephalitis was seen in 1 patient (3.5%). Restricted diffusion in DWI and dark on ADC in the region of right corona radiata was seen in 3 patients (10.5%).

DISCUSSION

Acute febrile encephalopathy is term commonly used to identify the condition in which altered mental status either accompanies or follows short febrile illness. It is associated with high mortality and morbidity. It is a medical emergency, requires support of a good intensive care unit. MRI brain is an essential modality in understanding the pathophysiology and in the management and sometimes aetiology.

There is paucity of studies on MRI findings in acute febrile encephalopathy in children. This prospective observational study aims to study MRI findings in the setting of acute febrile encephalopathy in children between 1 month to 18 year of age group.

In this study we analysed the MRI brain findings in 11 (29%) of the 28 children between one month and 18 years of age group who were admitted in PICU at tertiary care center with AFE during the period January 2019 to December 2019.

Diffuse cerebral oedema was found in 3 patients (10.5%). Focal bilateral symmetrical areas of T2 and FLAIR hyperintensity in basal ganglia and thalamus with restricted diffusion in 2 (7%) patients. T2 and FLAIR hyperintensity was seen in hippocampus in 2 patients 2 (7%). Features of haemorrhagic encephalitis was seen in 1 patient (3.5%). Restricted diffusion in DWI and dark on ADC in the region of right corona radiata was seen in 3 patients (10.5%).

Neuroimaging findings in childhood encephalitis differ from adults and range from normal MRI to severe haemorrhagic/necrotizing lesions and brain oedema. MRI may play an important role in determining the most likely causative pathogen. Image analysis can, however, be difficult at times since a particular pathogen can cause variable MRI findings, and a particular appearance on MRI may be caused by a variety of causes.^2,3

The association between abnormal brain MRI findings with severe clinical presentation and short-term outcome of encephalitis has been reported. The severity of brain MRI findings have been shown to correlate with length of hospitalization. Poor long-term outcome is associated with abnormal brain MRI findings.⁴

Clinical applications of MRI sequences used was as follows: T1 useful to define anatomy especially of midline structures; T2 useful to define the pathology especially of white matter; FLAIR useful to define white matter abnormalities especially near ventricles and sulci; diffusion weighted images (DWI) useful to identify early ischaemia, abscess, empyema and tumors; apparent diffusion coefficient (ADC) used along with DWI sequence to evaluate ischaemia; and susceptibility weighted images (SWI) useful to detect small haemorrhages.

Yang et al have proposed a pattern-based framework based on MRI findings that can be useful for narrowing the differential diagnosis in acute infectious encephalitis. Six key MRI patterns were proposed: 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; and T2 hyperintensity in the posterior fossa.³

MRI findings have been well described in certain conditions.

In dengue fever MRI shows T2W hyperintensity in bilateral thalami and globus pallidus. Hippocampus, temporal lobe and the pons may also be involved.² Priyal et al described MRI findings in eight cases of dengue encephalitis. The MRI showed mild-to-moderate hyperintensities on T2-weighted and FLAIR sequences and diffusion restriction on diffusion-weighted images. Micro-haemorrhages appear as blooming on susceptibility-weighted MRI. The areas involved were deep periventricular white matter, subcortical white matter, basal ganglia, thalami, infra-tentorium cerebellar white matter and brainstem, and occasionally in cortical grey matter. Among the four dengue viruses DENV2 and DENV3 are neurotropic.⁵

In separate studies Wei et al and Jayaraman et al discussed MRI findings in suspected cases of Japanese encephalitis (JE). The lesions appeared hyperintense in FLAIR and T2-weighted images and isointense to hypointense in T1-weighted images. The lesions involved thalamus, the basal ganglia, brainstem and hippocampus and the neocortex.^2,6 The authors also concluded that MRI is preferable to CT to detect early changes.⁶

Pichl et al have compared MRI findings in JE and dengue fever.⁷ The number of normal MRI scans was markedly higher in dengue with neurological manifestations than in JE. This suggests that patients with dengue suffered more from encephalopathy rather than encephalitis. In dengue fever lesions were most commonly reported in thalamus (29.4%), white matter (28.4%), and brain stem (19.6%). Intracranial haemorrhages were more common in dengue (MRI: 5.9%, CT 33.3%) than in JE. White matter lesions, cerebellar lesions, and minor intracranial haemorrhages were reported frequently in dengue encephalitis but never in JE. In JE lesions were most commonly reported in thalami (74%), basal ganglia (42.5%), and brain stem (32.6%). Basal ganglia and hippocampus lesions were reported much more frequently in JE than in dengue. Thalamic lesions were the most common focal finding in both JE and dengue fever.⁷

All HSV encephalitis cases have been reported to have frontal lobe changes on MRI (TW2 and FLAIR) and more than 90% had temporal lobe changes. Approximately one-third had basal ganglia or thalamic lesions.^2,8

Diogo et al reported the longitudinal evolution of the MRI brain findings of three cases of mother-to-child Chikungunya virus transmission.⁹ The initial scans showed brain cavitations with or without corpus callosum diffusion restriction. The follow up scans showed reduction in the volume of cavitations, with resolution of the restricted diffusion and increase in size of ventricles. Focal haemorrhages were seen in one case.

Lee reported neurologic manifestations of enterovirus 71 infections in Korea. Twenty-five patients underwent an MRI scan. Of these, 14 (56.0%) revealed the characteristic increased T2 and FLAIR images signal intensity in the posterior region of the brainstem and bilateral cerebellar dentate nuclei.¹⁰

In Varicella zoster the reported MRI findings include hyperintensities on T2W/FLAIR sequences and restriction in DWI in cerebellum and spinal cord. Cerebral cortex, basal ganglia, and deep white matter were also involved. Associated haemorrhages and necrosis were also reported.² Rodrigues et al reported that the most common findings in VZ were oedematous changes with hyperintense areas on the T2 sequence in the temporal and inferior frontal lobes.¹¹

Vyas et al analysed 16 patients with acute febrile encephalopathy in whom CSF latex agglutination, CSF culture, or CSF multiplex PCR were positive for H. influenzae. The MRI brain findings were meningitis, predominantly around frontoparietal lobes (43%), cerebritis (28%), ventriculitis (14%), and subdural collections (21.5%). One patient had features consistent with acute disseminated encephalomyelitis (ADEM). Four patients had normal MRI scan.¹²

Fujita et al reported a novel subtype of acute encephalopathy syndrome in childhood in a patient with influenza type A infection. Serial MRI studies were done on days 2, 4, 7, and 16. These findings were: acute necrotizing encephalopathy (ANE), mild encephalitis/encephalopathy with a reversible splenial lesion (MERS type II), acute cerebellitis, and acute encephalopathy with biphasic seizures and late reduced diffusion (AESD).¹³

Ramya et al reported MRI brain findings in influenza B. The scans showed bilateral, symmetric diffusion restriction of the amygdala, hippocampus, putamen, thalami, pons and regions of the peripheral cortex. Faint enhancement of the posterior optic nerves was observed bilaterally in postcontrast images. Diffuse cerebral oedema was also noted. Neuroimaging in ANE further shows symmetric necrosis of thalami, cortex, internal capsule and brain stem structures. Cytokine-mediated vascular inflammation and parenchymal cell apoptosis are the most proposed pathophysiological mechanisms for influenza-associated encephalopathy/encephalitis.¹⁴

A case of Mycobacterium bovis Bacillus Calmette-Guérin (BCG) strain meningitis and ventriculitis following BCG vaccination was reported by Furuichi et al brain MRI revealed hydrocephalus with widespread and disseminated enhancement lesions with thickening of the third ventricle floor, and brain tissue. Positive polymerase chain reaction (PCR) result for the Mycobacterium tuberculosis complex was obtained in the cerebrospinal fluid.¹⁵

In patients of HIV infection, the reported MRI brain findings were volume loss with widening of the ventricle and sulci. Reduced grey-white matter volume was seen in the medial frontal gyri.²

In study by Jayaraman, CMV imaging findings included microcephaly with ventriculomegaly, white matter volume loss, delayed myelination, and periventricular cysts. The abnormality in the cortex were a spectrum from dysgenesis to lissencephalic pattern. Periventricular calcifications/cysts with enlarged ventricles were also reported.²

In EBV encephalitis/encephalopathy the affected regions reported include the cerebral hemisphere, thalamus, basal ganglia, brain stem, cerebellum, the limbic system, and corpus callosum. The MRI was normal in about 40% of patients.¹⁶

Jayaraman et al have studied imaging in HHV6 and HHV7.¹⁷ Although HHV-6 has been established as a cause of encephalitis, the CNS sequelae of the closely related HHV-7 are largely unknown, particularly in immunocompetent patients. The authors demonstrated mildly increased abnormal T2 FLAIR signal involving bilateral medial temporal lobes and bilateral hippocampi in a patient of encephalitis in whom a human metagenomics CSF panel was positive only for HHV-7. Suspected microhaemorrhages (more extensive on right versus left) were reported on susceptibility weighted imaging (SWI). Akça et al have also reported severe encephalitis with human herpes virus-7 (HHV-7) and associated transient splenial lesion on MRI in an immunocompetent child.¹⁸

Chaitra et al reported MRI brain findings in Rabies encephalitis in a preschool child following post-exposure prophylaxis. T2/FLAIR sequences revealed hyperintensities in posterior 1/3 of pons, pontomedullary junction, medulla oblongata, and posterior part of left temporal gyri. Post-contrast MRI showed patchy heterogeneous enhancement in bilateral basal ganglia and external capsule. Bilaterally symmetrical hyperintensities in T2 and FLAIR images in basal ganglia, thalamus, and central grey matter of the cervical spinal cord extending to the dorsal segments have been reported.¹⁹

Encephalitis/encephalopathy is an extremely rare complication of Kawasaki disease. Keino et al reported a case of a previously healthy 8-month-old Japanese boy who had a prolonged seizure after febrile illness. Brain MRI showed restricted diffusion in the left subcortical white matter, that subsequently disappeared and still later mild left cerebral atrophy.²⁰

Maeda et al have reported T2 high signal intensities in bilaterally symmetrical and subcortical white matter and thalamus, and linear radial hyperintensities parallel to the cerebral vessels of the periventricular white matter. Diffuse white matter hyperintensity on the ADC map suggested vasogenic oedema.²¹ Mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) has also been reported in Kawasaki disease.²⁰

Moreno-Brauer et al studied the spectrum, evolution, and clinical relationship of MRI in 31 children with febrile infection-related epilepsy syndrome.²² The most frequent abnormalities were brain atrophy (74.2%) and T2/FLAIR changes (64.5%) that were mostly hippocampal (45.2%). Generalized brain atrophy was the most frequent type of atrophy (58%).

Mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) is a clinico-radiological syndrome mainly triggered by viral infection. Bacteria are relatively rare pathogens. Cranial MRI shows prolonged signal on T2, reduced diffusion on DWI, restricted water diffusion, and decreased ADC values in the splenium of corpus callosum.^23.24 The restricted diffusion in MERS may occur due to cytotoxic oedema, which is more pronounced in the splenium of corpus callosum, considering the high density of neurons, astrocytes, oligodendrocytes and cytokine and glutamate receptors in this area of brain.²⁴

The condition is subdivided into two types based on the extent of involvement. In MERS type 1, which is the more common type, lesions are limited to the splenium of corpus callosum. In MERS type 2 the lesions involve the whole corpus callosum or symmetric spread to the white matter.²⁵ Non-infectious causes of MERS include discontinuation of antiepileptic drugs, abrupt cessation of steroid therapy and hypoglycaemia.²⁶ MERS with extensive lesions (MERS type-2) is rarely associated with adenovirus. There are only three published cases of MERS type-2 associated with adenovirus infection.²¹

Sharma et al studied the role of diagnostic imaging in Rasmussen’s encephalitis and published a case report from Nepal.²⁷ Rasmussen’s encephalitis (RE) is a relatively rare chronic inflammatory neurological disease. The earliest abnormal MRI finding (stage 1) is cortical swelling with high signal intensity in the affected hemisphere in T2/FLAIR sequences. This stage lasts for up to 12 months. In the second stage, findings include focal or multifocal T2 and FLAIR high signal intensity areas involving the cortex or white matter of the affected hemisphere. This stage lasts for up to 22 months. In stage three there is atrophy of affected hemisphere characterized by widening of sulci and dilatation of lateral ventricle on the affected side. The final stage four is characterized by the disappearance of the abnormal signal, leaving a substantially atrophied cerebral hemisphere.

Bickerstaff’s brainstem encephalitis is characterized by ophthalmoplegia, ataxia, and disturbance of consciousness.²⁸ Usually, the findings are hyperintensity on T2-weighted images of the pons, medulla, thalamus, or cerebellum. MRI brain is normal in majority cases of Bickerstaff’s brainstem encephalitis and PET could be more insightful.

Safavi reported encephalitis caused by Balamuthia mandrillaris in a 3-year-old Iranian girl.²⁹ Balamuthia mandrillaris is a recently introduced causative agent of granulomatous amoebic encephalitis. Computed tomography (CT) scan and magnetic resonance imaging analyses revealed multiple mass lesions.

Limitations

Some shortcomings were identified in this study. The sample size was small, limiting the analysis's power. This study was done in a tertiary care center hence referral bias cannot be ruled out. Specific investigations for viral etiologies of AFE and autoimmune encephalitis were not done. Patients were not followed up long enough to study evolving changes in brain.

Despite these drawbacks, the study's strength was its rigorous methodology, prospective design and involvement of a neurologist in the study. MRI imaging is reported by radiologists. Reports are assumed to have final say in diagnosis. On part of paediatric physicians there is a considerable lack of understanding of MRI findings, its interpretations and implications on treatment and outcome of patients. Taking care of this lacunae is important in resource-limited setting. We anticipate that this research will help to bridge gaps in our existing understanding of etiopathology of AFE and improve patient outcome.

CONCLUSION

Acute febrile encephalopathy is a life-threatening condition. It poses challenges to the attending physician in the emergency room and in PICU. Aside from starting standard treatment directed at reducing intracranial pressure and seizures, it is important to identify the possible aetiology and pathophysiology for directing specific treatment. One modality that can address this issue is MRI brain. Paediatric intensive care physicians are not always updated regarding utility of MRI and its findings in acute febrile encephalopathy. The main reason being non-inclusion of this subject in curriculum. This study was intended to understand all the possible MRI findings in acute febrile encephalopathy, correlate it with clinical findings and try to extract as much information as possible from the MRI images including the probable aetiology. The added knowledge of MRI will ultimately aid in management and prognostication of these cases.

Funding: No funding sources

Conflict of interest: None declared

Ethical approval: The study was approved by the Institutional Ethics Committee

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