I decided to post the actual results of Emma’s most recent MRI for those who want specific things to pray for. I also wanted to convey the urgency of certain prayers. If you read through the report, there are several new finding as well as information that is “developing.” Well, all the findings are “developing,” but this post is to communicate the more urgent and critical concerns. Basically, it translates as the following: Although the infection is clearing, Emma’s brain has seen more damage even since we’ve been on the best course of treatment which isn’t necessarily abnormal, but also not entirely expected. The severity of the infection took everyone by surprise. I think the main thing I want to convey, however, is that this is expected to not only continue at this point, but could also worsen. You can Google “wallerian degeneration,” for more information. There are other factors (some of which you can read about below) and things that are occurring, but this seems to be the main one. Fair warning…the report below is, well, a lot especially if you start looking up definitions for more information. The notes from the neurologists (not posted here) are even more extensive and perhaps better to post, but I could not access them via laptop [where I’ve been writing from] for some reason.
Emma is also at risk of clotting, stroke, seizure, respiratory failure, and other scary unknowns; all of which the neurologist said will be a risk for the unforeseeable futures except the stroke. In addition, she is also at risk of [and being closely monitored for] hydrocephalus (the abnormal buildup of cerebrospinal fluid which causes increased pressure and brain damage) especially with the severity of the infection. This would be very bad as there is no actual cure, just treatment with a shunt or endoscopic third ventriculostomy (ETV) by way of neurosurgery.
There is actually quite a bit more, but it all along the same lines as far as present and future risks as things develop…so…THINGS TO PRAY FOR!
Emma’s brain MRI from 2/20/26
FINDINGS:
Overall, there is evidence of interval improvement of
intracranial infectious manifestations. There is persistent but
decreased degree and extent of the multifocal regions of
restricted diffusion in the supratentorial compartment involving
extra-axial fluid spaces, deep cerebrum, and ventricles,
consistent with persistent but decreased meningitis with purulent
debris, ventriculitis, and cerebritis. Multifocal residual small
areas of parenchymal reduced diffusivity primarily affect the
basal ganglia; in the same regions there there is evolving
necrosis with increased regions of T2 FLAIR suppression,
increased T1 shortening, and tissue loss in the interim. Areas of
intrinsic T1 hyperintense signal along the periphery of the
affected regions, with faint enhancement are more conspicuous
than on prior exam. Scattered foci of susceptibility signal drop
out are seen within these regions have not significantly
changed. However, there is a new focus of susceptibility in the
left thalamus consistent with interval microhemorrhage in this
area. Reduced diffusivity in the posterior limb internal capsules
and cerebral peduncles likely reflects pre-Wallerian
degeneration, slightly increased.
Interval enlargement of the supratentorial ventricles, now
prominent and mildly enlarged, nonspecific but at least in part
due to volume loss. Content layering along the occipital horns is
now showing susceptibility signal dropout with intrinsic high T1
signal intensity suggestive of blood products. There is
persistent restricted diffusion along the ependymal surface of
the temporal horns of the bilateral lateral ventricles, with a
focus within the right atrium. A component of pus/ventriculitis
is likely still present. Areas of restricted diffusion more
evident along occipital lobes and medial cranial fossa, are again
seen. There is more signal suppression in the middle cranial
fossa fluid spaces on the T2 FLAIR sequence, which may indicate
reduced purulent debris in this area in the interim.
There is persistent pachymeningeal/leptomeningeal enhancement,
particularly over the parietooccipital regions and posterior
fossa. There is leptomeningeal enhancement along the medulla as
well as enhancement of the cranial nerves. These findings were
most likely present on prior MRI but limited evaluated due to
motion.
Stable prominence of the subarachnoid spaces overlying, occipital
lobes and anterior temporal lobes bilaterally, with areas of
curvilinear restricted diffusion and enhancement, and curvilinear
regions of susceptibility concerning for regions of residual
subarachnoid purulent debris and potentially small vascular
thrombosis, similar prior. There is also stable prominence of the
retrocerebellar CSF spaces, with similar areas of curvilinear
restricted diffusion. Dural venous sinuses enhance throughout.
Intraorbital contents are grossly stable and unremarkable apart
from possible mild perioptic edema.
There is opacification of the developing paranasal sinuses.
Mastoid air cells and middle ear cavities are clear.
IMPRESSION:
1. Interval improvement of intracranial infectious findings
consistent with favorable treatment response, as described.
Evolving encephalomalacia/necrosis in the deep cerebrum, most
pronounced in the basal ganglia.
2. Mild interval enlargement of the lateral ventricles. Content
layering along the occipital horns is suggestive of blood
products, however a component of pus/ventriculitis is likely
still present.
3. Persistent areas of enhancement along the supratentorial and
infratentorial subarachnoid spaces and leptomeninges, consistent
with meningitis.
Leave a Reply