..
of purulent bacterial meningitis, nuchal rigidity.
5–7
It is likely in
this case that the episode of meningitis produced the brain
destruction (resulting in the clinical signs indicating loss of brain
function) by the mechanism of either or both the increase in
intracranial pressure producing herniation
8
or the altered
cerebral blood flow from vasculitis.
9,10
Although the brain had
been destroyed during his acute illness, medical intervention
over the subsequent nearly two decades allowed the intracranial
changes to take place that were revealed at the time of autopsy.
Given that there was no brain to grow and enlarge the skull, the
head was microcephalic, and the calvarium was thickened.
Although, by definition, brain death entails no internal carotid or
vertebrobasilar artery blood flow, external carotid artery flow continued and permitted the dense calcification of the dura and replacement of adjacent brain parenchyma by ossification and focal areas of lose collagenous tissue. The finding that the interior of the specimen consisted mainly of mummified grumous material (with intermixed calcium deposits, clumped hemosiderin pigment, and focally mineralized cell processes)
and only a few foci of connective tissue indicates that blood flow
was insufficient over the two decades for macrophages to arrive
and remove most of the debris. This appearance of mummifica-
tion is very different from the pathologic changes reported
following meningitis in which death and autopsy occur a short
period after the onset of the bacterial meningitis.