Ganong's Review of Medical Physiology, 23rd Edition

572 SECTION VI Cardiovascular Physiology
Flow (mL/min)
1.6
1.2
0.8
0.4
0
FIGURE 34–3 CSF formation and absorption in humans at
various CSF pressures. Note that at 112 mm CSF, formation and absorption
are equal, and at 68 mm CSF, absorption is zero. (Modified and
reproduced with permission from Cutler RWP, et al: Formation and absorption of
cerebrospinal fluid in man. Brain 1968;91:707.)
PROTECTIVE FUNCTION
The most critical role for CSF (and the meninges) is to protect
the brain. The dura is attached firmly to bone. Normally, there
is no “subdural space,” with the arachnoid being held to the
dura by the surface tension of the thin layer of fluid between the
two membranes. As shown in Figure 34–4, the brain itself is
supported within the arachnoid by the blood vessels and nerve
roots and by the multiple fine fibrous arachnoid trabeculae.
The brain weighs about 1400 g in air, but in its “water bath” of
CSF it has a net weight of only 50 g. The buoyancy of the brain
in the CSF permits its relatively flimsy attachments to suspend
it very effectively. When the head receives a blow, the arachnoid
slides on the dura and the brain moves, but its motion is gently
checked by the CSF cushion and by the arachnoid trabeculae.
The pain produced by spinal fluid deficiency illustrates the
importance of CSF in supporting the brain. Removal of CSF during
lumbar puncture can cause a severe headache after the fluid
is removed, because the brain hangs on the vessels and nerve
roots, and traction on them stimulates pain fibers. The pain can
be relieved by intrathecal injection of sterile isotonic saline.
HEAD INJURIES
Absorption
Formation
0 68 100 112 200
Outflow pressure (mm CSF)
Without the protection of the spinal fluid and the meninges,
the brain would probably be unable to withstand even the minor
traumas of everyday living; but with the protection afforded,
it takes a fairly severe blow to produce cerebral damage.
The brain is damaged most commonly when the skull is fractured
and bone is driven into neural tissue (depressed skull
fracture), when the brain moves far enough to tear the delicate
bridging veins from the cortex to the bone, or when the brain
is accelerated by a blow on the head and is driven against the
skull or the tentorium at a point opposite where the blow was
struck (contrecoup injury).
FIGURE 34–4 Investing membranes of the brain, showing
their relation to the skull and to brain tissue. (Reproduced with
permission from Wheater PR et al: Functional Histology. Churchill Livingstone, 1979.)
THE BLOOD–BRAIN BARRIER
The tight junctions between capillary endothelial cells in the
brain and between the epithelial cells in the choroid plexus effectively
prevent proteins from entering the brain in adults
and slow the penetration of some smaller molecules as well.
An example is the slow penetration of urea (Figure 34–5). This
uniquely limited exchange of substances into the brain is referred
to as the blood–brain barrier, a term most commonly
used to encompass this barrier overall and more specifically
the barrier in the choroid epithelium between blood and CSF.
Passive diffusion across the tight cerebral capillaries is very
limited, and little vesicular transport takes place. However,
there are numerous carrier-mediated and active transport systems
in the cerebral capillaries. These move substances out of
as well as into the brain, though movement out of the brain is
generally more free than movement into it.
PENETRATION OF SUBSTANCES
INTO THE BRAIN
Outer table
of skull
Trabecular
bone
Inner table
of skull
Dura mater
Subdural
(potential)
space
Arachnoid
Subarachnoid
space
Arachnoid
trabeculae
Artery
Pia mater
Perivascular
spaces
Brain
Water, CO 2 , and O 2 penetrate the brain with ease, as do the
lipid-soluble free forms of steroid hormones, whereas their