The primate cranial base: ontogeny, function and - Harvard University

D.E. Lieberman et al.]
PRIMATE CRANIAL BASE 129
Some researchers (Scott, 1958; Giles et al.,
1981; Enlow, 1990) suggest that changes in
cranial base angulation occur interstitially
within synchondroses through a hinge-like
action. If so, flexion would result from increased
chrondrogenic activity in the superior
vs. inferior aspect of the synchondrosis,
while extension would result from increased
chrondrogenic activity in the inferior vs. superior
aspect of the synchondrosis. Experimental
growth studies in macaques, which
labeled growth using flurochrome dyes,
show that angulation also occurs through
drift in which depository and resorptive
growth fields differ on either side of a synchondrosis,
causing rotations around an
axis through the synchondrosis (Michejda,
1971, 1972a; Michejda and Lamey, 1971;
Giles et al., 1981). All three synchondroses
are involved in prenatal angulation (Hofer,
1960; Hofer and Spatz, 1963; Sirianni and
Newell-Morris, 1980; Diewert, 1985; Anagastopolou
et al., 1988; Sperber, 1989; van
den Eynde et al., 1992); however, the extent
to which each synchondrosis participates in
postnatal flexion and extension is poorly
known, and probably differs between humans
and nonhuman primates. The SOS,
which remains active until after the eruption
of the second permanent molars, is
probably the most active synchondrosis in
generating angulation in primates (Björk,
1955; Scott, 1958; Melsen, 1969). The MSS
fuses prior to birth in humans (Ford, 1958),
but may also be important in nonhuman
primates (Scott, 1958; Hofer and Spatz,
1963; Michejda, 1971, 1972a; but see Lager,
1958; Melsen, 1971; Giles et al., 1981). Finally,
the SES fuses near birth in nonhuman
primates, and remains active only as a
site of cranial base elongation in humans
during the neural growth period (Scott,
1958; Michejda and Lamey, 1971). Other
ontogenetic changes in the cranial base angle
(not necessarily involved in angulation
itself) include posterior drift of the foramen
magnum (see above), inferior drift of the
cribriform plate relative to the anterior cranial
base (Moss, 1963), and remodeling of
the sella turcica, which causes posterior
movement of the sella (Baume, 1957; Shapiro,
1960; Latham, 1972).
A few experimental studies provide evidence
for the presence of complex interactions
between the brain and cranial base
synchondroses that influence variation in
the cranial base angle. DuBrul and Laskin
(1961), Moss (1976), Bütow (1990), and Reidenberg
and Laitman (1991) all inhibited
growth in the SOS in various animals
(mostly rats), causing a more flexed cranial
base, presumably through inhibition of cranial
base extension. In most of these studies,
experimentally induced kyphosis of the
basicranium was also associated with a
shorter posterior portion of the cranial base,
and a more rounded neurocranium (see below).
Artificial deformation of the cranial
vault also causes slight but significant increases
in cranial base angulation (Antón,
1989; Kohn et al., 1993). However, no controlled
experimental studies have yet examined
disruptions to the other cranial base
synchondroses. In addition, there have been
few controlled studies of the effect of increasing
brain size on cranial base angulation.
In one classic experiment, Young
(1959) added sclerosing fluid into the cranial
cavity in growing rats, which caused
enlargement of the neurocranium with little
effect on angular relationships in the cranial
base. Additional evidence for some degree
of independence between the brain and
cranial base during development is provided
by microcephaly and hydrocephaly, in
which cranial base angles tend to be close to
those of humans with normal encephalization
(Moore and Lavelle, 1974; Sperber,
1989).
Important differences in cranial base angulation
among primates exist in terms of
the ontogenetic pattern of flexion and/or extension,
which presumably result from differences
in the rate, timing, duration, and
sequence of the growth processes outlined
above. Jeffery (1999) suggested that, prenatally,
the basicranium in humans initially
flexes rapidly during the period of rapid
hindbrain growth in the first trimester, remains
fairly stable during the second trimester,
and then extends during the third
trimester in conjunction with facial extension,
even while the brain is rapidly increasing
in size relative to the rest of the cranium
(see also Björk, 1955; Ford, 1956; Sperber,