Page 141 - Edited - Webster HEAD AND NECK - part 2-Merge PDF

HN 329

OTHER EVENTS AND NEURAL INJURY

A. LIFE IN UTERO

It is worth remembering that certain essential reflex mechanisms develop relatively late in intra-
uterine life - and even after birth. Thus, the swallowing reflex is not effective until about the 28th week of
gestation, and the reflex control of body temperature is imperfect even at 40 weeks (the normal foetal age at
birth). Factors such as these determine the management and care of premature infants and even those which
are born at the normal body weight and time.

Birth injuries must be distinguished from congenital malformations. The latter are a consequence of
disturbed developmental processes, about which little is known and even less can be done, save ante-natal
screening and the offer of abortion. Birth injuries are what the name implies: injuries sustained by the, in. fant
during labour. These may involve peripheral nerves (see below) or the brain. Modern obstetric practice has
reduced their incidence markedly, but not eliminated them completely.

The most serious long-term consequence of perinatal brain injury is cerebral palsy, the most
common form of which is spastic diplegia (Little's disease) - a double hemiplegia in which the lower limbs are
usually more seriously affected than the upper (in which case there is a classical "scissors gait" - the legs cross
in front of each other during walking) - accompanied by a variety of "higher function" deficits ranging from
mental retardation to dysphasias, dyslexia, dyspraxia, agnosias, etc. In some cases of cerebral palsy, there is no
true paralysis - only "higher order" disturbances, and/or choreo-athetosis. The causes of cerebral palsy are
almost certainly multiple. About 10% are probably genetic. The remainder are associated with intra-uterine
and immediate postnatal life, and with the mechanics of birth. These can be conveniently summarized as:

1. Anoxia. Prolonged low oxygen tensions cause diffuse degenerative changes in the developing brain.
Whether a prolonged and difficult labour (which undoubtedly does cause foetal anoxia) is alone sufficient to
account for cerebral palsy is moot - most babies are bluish at birth, but rapidly turn bright pink as they take first
stock of their estate. It seems likely that (a) prolonged period(s) of intra-uterine anoxia during pregnancy
(is) are more significant in this context.

2. Kernicterus (Greek: ·"kernel" - i.e. nucleus - and "jaundiced") is the result of poor management (even
non-detection) of Rhesus factor incompatibility between mother and foetus. Foetal (and infant's) red blood
cells are destroyed at such a rate that bile products (specifically bilirubin) are deposited even in its brain, and
1
especially in the basal ganglia, the hippocampus and the eighth cranial nerve . The neurological damage is
serious, and the consequences include motor problems (choreo-athetosis), deafness, and mental retardation.

B. BIRTH

1. Intracranial haemorrhage. Considering the mechanisms of birth and the way the skull is pushed and
pulled about (the edges of the squamous bones of the cranial vault, which are not fused along their sutures - see
SIV 12 - are often pushed over one another and remain so for 24 to 48 hours after birth) it is surprising that
any of us are here at all. Extreme deformities of the foetal cranium, in which it moulds roughly to the shape of
a bullet (point at the vertex of the skull) tense the falx cerebri which thereby tugs the tentorium
cerebelli upwards. The tentorium may tear, rupturing the straight sinus, or its junction with the great cerebral
vein, and producing a foetal subdural haematoma or a subarachnoid haemorrhage. Precipitate delivery, in which
the head is compressed in the birth canal and then suddenly expands as it leaves the vagina, can also cause
venous rupture and subdural haematoma or subarachnoid haemorrhage. (Tearing of one of the larger intracranial

1 Note: Bilirubin is found in serum conjugated with albumin and therefore does not usually cross the blood-brain barrier. Thus
simple jaundice in adults does not incur neurological penalties. (Liver failure is another matter.) In humans, the blood-brain
barrier is virtually mature at birth: many infants show a transient jaundice in the first week of postnatal life, as they dispose of
surplus erythrocytes/foetal haemoglobin more rapidly than the liver can conjugate and excrete the degradation products, but
they do not develop kernicterus. The reasons for the development of kernicterus are unclear: perhaps it starts to develop in
utero, as Rh incompatibility develops, and before the blood-brain barrier is intact or the liver able to conjugate bilirubin to
albumin? Who knows? Ask a doctor.

\NewCMedPhysSc\27 HN 327 Oth&Neurinj.