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it was felt that the increased motor symptoms were due to oedema or some haemorrhage
aifecting the anterior roots only which would be absorbed in due course. From 12 May
1954,19 days after injury and 15 days after deterioration, I was satisfied that the decision
not to operate, when the clinical symptoms increased, was correct. The motor function
in the toes and feet on the right gradually returned followed by functional recovery of
the same muscles as well as the extensor digitorum and peronei on the left side. Bladder
control gradually returned. X-rays of 14 June 1954 showed re-expansion of the com
pressed vertebra and good alignment of the broken-off lateral part, and the fractured
pedicles of the fourth lumbar vertebra had become fixed again. In due course, further
recovery of muscle function occurred and the patient was discharged home six and a half
months after injury, able to walk without support of any kind, and he took up employ
ment very soon afterwards (Guttmann, 1954).
(3) Development of paraplegia after free interval
An extremely rare incidence is the gradual development of paraplegia after a more or
less long free interval following acute injury to the back without causing damage to the
vertebra and without immediate cord or cauda equina symptoms, in a person with an
already existing though asymptomatic pathology of the cord, such as tumour or haeman-
gioma. There is only one case of benign tumour amongst our material where a paraplegia
developed after a free interval following injury to the back.
A man, aged 22, was involved in a car accident on i November 1959 when the car
hit a lamp-post. He was shaken and experienced pain in his back but got out of the car
and walked. He was taken to the nearest hospital where no pathological clinical signs of
cord involvement was found, nor did X-ray examination of the spine reveal any vertebral
injury. He was sent home and went to bed, but he woke up at 6 a.m. because of increasing
pain in his back. Some time later, he had paraesthesia in both legs and at 11 a.m. became
paralysed and was unable to pass urine. He was taken to the nearest hospital, where a
lumbar puncture showed a complete block and myelography a stop at T8 level. The
clinical signs were those of an almost complete paraplegia below T8 with sparing of the
posterior columns only. At operation on 2 November 1959 a localized neuro-fibroma
was found lying in front of T8 level; 'the cord had obviously been damaged and the
appearances were suggestive of an anterior spinal artery thrombosis'. The tumour was
removed completely but the severe though incomplete paraplegia persisted; the reflexes
in the legs did not return for at least 4 weeks and—alas—he developed pressure sores
on both heels and sacrum and urinary infection. He was transferred to Stoke Mandeville
on 18 December 1959, where the sores were healed, and, in due course, he made some
motor and sensory recovery but developed a marked spastic paraparesis. He was dis
charged on 31 January 1961 and has returned for check-ups ever since. The spasticity
was greatly relieved in due course by bilateral iliopsoas myotomy and lengthening of the
Achilles tendons. He runs a hairdressing saloon and is married.
Another case of gradually progressive paraplegia following free interval after a back
injury was a young boy of 16 in whom an operation and epidural haemangioma was
found which had bled.
