Brain Infections 05 - Clinical Case Summary
Brain Infections 05 - Clinical Case Summary
Brain Infections 05 - Clinical Case Summary
SummaryHistory
11 month old male with recent gastroenteritis treated with multiple antibiotics. Fever persisted along with adenoviral lymphadenitis, increasing irritability and depressed level of consciousness. An initial head MR was obtained. Over one month developed status epilepticus & HLH (hemophagocytic lymphohistiocytosis); a second MR was obtained 3 weeks later.
Exams Performed
MR flair; MR T1-w post contrast; MR diffusion; MR susceptibility (SWI)
Prior sequence impressions
MR flair
1. There are minimal changes of leptomeningeal reaction or leptomeningeal infection (possibly viral). The patient has been treated with antibiotics making CSF cultures negative. Differential includes immune overshoot response to the documented GI adenoviral infections (cytokine storm/SIRS) versus actual infectious leptomeningitis.
MR T1-w post contrast
1. Negative post contrast T1-w head MR coronal.
MR diffusion
1. Regional, mainly parietal and ventral upper brain stem subpial edema and sulcal protein leak without contrast leak consistent with a humeral immune response. But, whether this represent partially treated leptomeningitis or a abnormal systemic immune response remains indeterminate.
2. Three small subcortical sites of positive MR diffusion are present consistent with cytogenic injury; basis is indeterminate.
MR susceptibility (SWI)
1. Negative MR susceptibility imaging
1. There are minimal changes of leptomeningeal reaction or leptomeningeal infection (possibly viral). The patient has been treated with antibiotics making CSF cultures negative. Differential includes immune overshoot response to the documented GI adenoviral infections (cytokine storm/SIRS) versus actual infectious leptomeningitis.
MR T1-w post contrast
1. Negative post contrast T1-w head MR coronal.
MR diffusion
1. Regional, mainly parietal and ventral upper brain stem subpial edema and sulcal protein leak without contrast leak consistent with a humeral immune response. But, whether this represent partially treated leptomeningitis or a abnormal systemic immune response remains indeterminate.
2. Three small subcortical sites of positive MR diffusion are present consistent with cytogenic injury; basis is indeterminate.
MR susceptibility (SWI)
1. Negative MR susceptibility imaging
Overall impression
1. Evidence of focal hyperacute leptomeningeal changes is consistent with viral leptomeningitis, partially treated pyogenic leptomeningitis, or immune-based (SIRS) type of meningeal inflammation.
2. Be on the lookout for immune overshoot (cytokine storm/SIRS) whenever adenoviral and E Coli infection is documented clinically.
2. Be on the lookout for immune overshoot (cytokine storm/SIRS) whenever adenoviral and E Coli infection is documented clinically.
Lessons to be learned
1. Partially treated bacterial leptomeningeal infections are always difficult to diagnose, since CSF cultures are often unrevealing. It is also difficult to differentiate viral leptomeningeal infections and reactive, immune-based, changes from partially treated pyogenic leptomeningitis.
2. Adenoviral and E-coli infections anywhere can be complicated by immune overshoot problems.
3. When leptomeningeal findings are present in conjunction with subcortical MR diffusion sites of restriction, follow-up imaging is likely to be more revealing for appreciating the full extent of brain injury. In this case the follow-up MR and the clinical testing confirmed the cause as an immune-based encephalopathy with both SIRS (systemic immune response syndrome) and HLH (hemophagocytic lymphohistiocytosis).
2. Adenoviral and E-coli infections anywhere can be complicated by immune overshoot problems.
3. When leptomeningeal findings are present in conjunction with subcortical MR diffusion sites of restriction, follow-up imaging is likely to be more revealing for appreciating the full extent of brain injury. In this case the follow-up MR and the clinical testing confirmed the cause as an immune-based encephalopathy with both SIRS (systemic immune response syndrome) and HLH (hemophagocytic lymphohistiocytosis).