C- DISLOCATIONS OF THE VERTEBRAL COLUMN
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an initially complete distal paraplegia may develop ascending symptoms over a great
number of segments within a week or two. This may be due to an intradural but extra-
meduallary haemorrhage at higher level (Foerster, 1929) or a progressive, large localized
epidural haematoma. These are, however, extremely rare incidences, and amongst more
than 2,500 traumatic paraplegics and tetraplegics I have not seen a single case. Laminec-
tomy may be, at least, justified in such an event, but alas—at operation one will find, as a
rule, either signs of a spinal artery thrombosis or a haematomyelia. Frankel (1969) has
given a statistic of 7 patients of Stoke Mandeville with ascending symptoms of at least 4
segments. Six had Tn or Ti2 fractures with initial symptoms ranging from Ti2 or L4
rising to T5 and Cy/8 respectively. One patient had a fracture-dislocation of T4 and the
initial transverse lesion ascended to
Cj.
All but 2 had a subarachnoidal block, but in one
of these myelography demonstrated a block at the level of the fracture (Ti2). In this
patient with an initial lesion below L4, the lesion rose to Cy/8 and receded eventually
to Ti/T3. He was the only patient who had two laminectomies at the admitting hospital
while the lesion was rising, and the spinal cord was described as swollen and pink.
Following the second operation the lesion continued to rise and he was treated with
Heparin, following which there was no further rise. All the other patients were treated
conservatively with Heparin, Dindevan, Rhoemacrodex, Arvine and Prednisolone
respectively and in 6 cases the lesion became static at higher level, and in one case only
the symptoms went down to Tn.
(2) Progressive paralysis in incomplete lesions
Progressive paralysis may occur in a case of fracture or fracture-dislocation where initially
there has been an incomplete lesion with no or only minimal signs of cord or cauda equina
involvement. However, it must be stressed again that motor or sensory symptoms in
incomplete cauda equina lesions which have increased in the following days after injury
may recede spontaneously. Therefore, there is no hurry for immediate exploration and
the longer one observes such a case by thorough and frequent neurological control
the less often will a surgical exploration be necessary. The following case is a good
example:
A man, aged 33, was hit by a cement mixer on 23 May 1954, and sustained an incom
plete cauda equina lesion. The first X-ray revealed a severe fracture of the fourth lumbar
vertebra, apart from multiple fractures of the transverse processes of Li to L4 on both
sides. The lateral third of the right side of L4 was broken off, and there was also a fracture
of the pedicles of that vertebra making the whole vertebra extremely unstable. On
admission on 24 April 1954 he had a marked weakness of both lower limbs. Knee and
ankle jerks and plantar response were absent on both sides and there was sensory impair
ment below L3 with analgesia in 83 to 85. Bladder and bowels were paralysed. Postural
reduction and fixation on sorbo-packs was carried out with regular turnings from side to
side every two hours. Four days after admission the motor symptoms increased and gradu
ally all dorsi- and plantar-flexors of the feet and toes became paralysed. However,
having regard to the fact that there was no increase in the disturbance of sensation
surgical interference was decided against and the conservative treatment continued, as
