Em. Massicotte et Mr. Del Bigio, Human arachnoid villi response to subarachnoid hemorrhage: possible relationship to chronic hydrocephalus, J NEUROSURG, 91(1), 1999, pp. 80-84
Object. The origin of chronic communicating hydrocephalus following subarac
hnoid hemorrhage (SAH) is not well understood. Fibrosis of the arachnoid vi
lli has been suggested as the cause for obstruction of cerebrospinal fluid
(CSF) flow, but this is not well supported in the literature. The goal of t
his study was to determine the relationship between blood, inflammation, an
d cellular proliferation in arachnoid villi after SAH.
Methods. Arachnoid villi from 50 adult patients were sampled at autopsy. Al
l specimens were subjected to a variety of histochemical and immunohistoche
mical stains. The 23 cases of SAH consisted of patients in whom an autopsy
was performed 12 hours to 34 rears post-SAM. Fifteen cases were identified
as moderate-to-severe SAW, with varying degrees of hydrocephalus. In compar
ison with 27 age-matched non-SAM controls, the authors observed blood and i
nflammation within the arachnoid villi during the Ist week after SAH. Great
er mitotic activity was also noted among arachnoid cap cells. The patient w
ith chronic SAH presented with ventriculomegaly 2 months post-SAM and exhib
ited remarkable arachnoid cap cell accumulation.
Conclusions. The authors postulate that proliferation of arachnoidal cells,
triggered by the inflammatory reaction or blood clotting products, could r
esult in obstruction of CSF flow through arachnoid villi into the venous si
nuses. This does not exclude the possibility that SAH causes generalized fi
brosis in the subarachnoid space.