C • DISLOCATIONS OF THE VERTEBRAL COLUMN
137
the only or main cause of paraplegia and tetraplegia and that immediate decompression
will rectify the damage. It is ignored that the mechanism of spinal cord injury following
fracture-dislocations differs fundamentally from that of a slow-growing tumour or
tuberculous process of the spine. A vertebral injury producing instantaneous clinical
symptoms of complete or partial paralysis is the result of the acute impact of violence
on the neural elements themselves, causing concussion, contusion, laceration or transec-
tion of the cord. This mechanism is always associated with damage to the vascular supply
at, below and above the site of the trauma. In this connection, it must be remembered
that, although most severe damage of the spinal cord and roots often occurs in individuals
with normal diameter of the spinal canal, this occurs even more readily in individuals with
an abnormally narrow spinal canal. In recent years, attention has been drawn to this
congenital abnormality of the vertebral column by several authors (Verbiest, 1962; Ehni,
1965; Hinck & Suchdev, 1966; Hancock, 1967).
Secondly, narrowing of the vertebral canal by protruding bone or intervertebral disc
alone, as demonstrated by X-rays, or in combination with a subarachnoidal block found
immediately after injury, is only too readily accepted as conclusive evidence of the
concept of compression, regardless of whether the neurological lesion is complete or
incomplete. It must be stressed at once that neither X-ray findings nor the presence of a
complete or partial block in the acute stage, are in themselves evidence of compression
as the cause of paraplegia or tetraplegia. For it is a well-known fact that, in spite of
X-ray evidence of a severe fracture-dislocation with marked narrowing of the spinal
canal, the clinical symptoms may be either minimal or even entirely absent, as the
spinal cord has miraculously escaped injury. Striking examples of this fact have been
previously published (Guttmann, 1954; Meinecke, 1964 and others. See also Figs. 50,
53> 54> 59, 65, 67).
Thirdly, the initially complete block is of no diagnostic value at this stage (Guttmann,
1 949)5 as it is due to temporary oedema or some bleeding into the subarachnoid space
which will clear up in due course. Conversely, in spinal injuries resulting in severe
damage or transection of the cord, the complete block is due to merging and firm fixation
of dura and arachnoidea with the disrupted tissues of the cord and/or the protruding
bone which has caused the cord injury. Personal observations at post mortem and those
of other workers have frequently confirmed these findings and proved the futility of
exploratory or decompressive laminectomy in complete transverse cord lesions with
areflexia lasting longer than 24 or 48 hours. This is now generally accepted by surgeons
with extensive experience in this field. On the other hand, it was found that considerable
recovery of severe cord or cauda equina symptoms may occur in spite of a persistent
block and unreduced fracture-dislocation (Figs. 58 and 69). Myelography has also been
employed in the acute stage of traumatic paraplegia but has not been found a reliable
indicator of the need for decompression.
Many surgeons, especially in the U.S.A., Canada, and in some European continental
and eastern countries, still carry out immediate or early decompressive laminectomy in
complete and incomplete traumatic transverse lesions of the cord following spinal
fracture, regardless of whether there is a sub-arachnoidal block or not, the concept being
the prevention of further damage. Moreover, this operation is also advocated in in
complete lesions which do not show or have stopped recovery and even while recovery
