We have used two different experimental models to examine the relation
ship between local cerebral blood flow and metabolism in hydrocephalus
. In our first experiments local cerebral blood flow (LCBF) and local
cerebral glucose utilization (LCGU) were measured by quantitative auto
radiographic methods in adult rats rendered hydrocephalic, though asym
ptomatic, by the injection of kaolin intracisternally at 3 weeks of ag
e and in control animals. There were no significant differences in LCG
U or LCBF in any of the 29 areas of grey matter examined, including la
yer IV of the cerebral cortex. Scanning across the cerebral cortex rev
ealed an appreciable fall in LCGU and LCBF towards the inside and the
outside of the mantle in control animals. Hydrocephalus had no signifi
cant effect on this ''transmantle'' pattern of reduction in cortical m
etabolism towards the periphery, but in contrast, significantly enhanc
ed the reduction in cortical blood flow in 7 out of the 10 cortical re
gions examined. Hence, in this model of asymptomatic hydrocephalus the
re is relative uncoupling of LCBF and LCGU in the inner and outer laye
rs of the cerebral mantle. In a study performed in congenitally hydroc
ephalic H-Tx rats at 10, 20 and 28 days we found that uptake of deoxyg
lucose was impaired in hydrocephalic rats compared with their non-hydr
ocephalic siblings. Small changes were seen at 10 and 21 days, but sta
tistically significant changes were seen only at 28 days. A small redu
ction in LCBF was observed in all regions at 10 days, with statistical
ly significant differences between control and hydrocephalic rats in a
uditory and parietal cortex. By 21 days, reductions of between 25% and
70% in local cerebral blood flow were observed in all regions, with s
tatistically significant differences in visual, auditory and parietal
cortex. At 30 days, a statistically significant difference was found b
etween controls and hydrocephalic rats in pens, caudate nucleus and vi
sual, auditory, parietal and sensorimotor cortex. This second study in
dicates that decreases in local cerebral blood flow precede decreases
in cerebral metabolism and occur before the appearance of obvious symp
toms. Our experiments suggest that in hydrocephalus a decrease in tiss
ue perfusion precedes any impairment of cerebral glucose metabolism an
d may occur before the appearance of any gross symptoms.