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CHAPTER 10
of the Stoke Mandeville group of workers (Frankel
et
a/., 1969), the late instability was
only 4 (0-65 per cent). These figures of low late instability speak for themselves. Some
surgeons try to prove instability of a reduced fractured vertebra by control-X-rays in
extensive retro- and forward flexion of head and neck at an early stage. I consider this as
much an unnecessary as it is an hazardous procedure, for a fibrous or not yet fully mature
bony union may be easily broken by such extreme movements. This control, unless
indicated by the development or progression of neurological symptoms, should not be
carried out before 3-4 months after alignment of fracture-dislocations. Bedbrook (1971)
from his extensive experience came to the conclusion 'we should never say that a fracture
dislocation is unstable under at least eight weeks, and probably between eight and twelve
weeks'. In McSweeney's view the majority of neck injuries are stable after 4 months.
Another subject of dispute is the term 'Hyperextension Injuries', generally accepted
for certain fracture-dislocations, in particular of the cervical spine due to facial or frontal
injuries, which, however, was recently criticized by Roaf (1971) as being inaccurate.
True hyperextension of both vertebrae and spinal cord may actually occur in vertical
direction as a result of excessive skull traction by pull-weights which are too heavy
(iatrogenic hyperextension) (Figs. 44, 45). However, the mechanism of certain cervical
fractures and fracture-dislocations resulting from a fall or blow on the forehead or face,
for instance, following diving into shallow water, is, in fact, that of a retro-hyperflexion
of the head and cervical spine, with or without rotation. The violent retroflexion of head
and neck forces the spinous and articular processes of the mid-cervical vertebrae (C4-C6)
together, and these, now acting as a fulcrum, cause a separation between the vertebral
body and the adjacent lower intervertebral disc, which results in dislocation. According
to the intensity and speed of the driving force, the separation may still continue and rupture
the anterior longitudinal ligament. Moreover, the posterior ligament may then be dis–
lodged from the vertebral body below, become buckled up and thus, squeezing the spinal
cord backward against the lower vertebra, cause partial or complete transection of the
cord. This squeezing effect also explains the spinal cord damage often found in segments
well above and below the fractured vertebra. This mechanism of cervical fracture, first
described by Taylor & Blackwood (1948), explains well the spinal cord damage com–
monly called hyperextension injury, but which is actually due to a retroflexion injury of
the spine. In some cases with this type of injury occurring in ankylosing spondylitis of
the cervical spine, the separation was not found between the body and its adjacent
cartilagenous tissues but the vertebral body itself was ruptured and broken in two
(Guttmann, 1966) (Fig. 57).
In contrast to the mechanism just described, the mechanism responsible for another
type of cervical injury is caused by ventro-hyperflexion of the head and neck. In such
an event the acting force will not cause a fulcrum at the spinous and articular processes
but, on the contrary, will force together two adjacent vertebral bodies at the level of the
maximal stress and may drive the anterior-inferior edge of the upper vertebra into the
body of the vertebra below, split it into two and may avulse part of it forward or down–
ward (commonly called tear-drop burst fracture). The posterior part of the fiactured
body will be displaced backward into the spinal canal and crush the spinal cord (Fig. 51).
In both mechanisms, however, the spinal cord above the fulcrum produced by the
