Spinal tumours are conveniently classified, from both the pathological and clinical points of view, into those which occur outside the spinal theca (extradural), those which occur within the theca but outside the cord itself (intradural extramedullary) and those oc- curring within the cord (intramedullary).
The tumours most commonly encountered are the following.
1 Extradural.
a Secondary deposits in the spine – by far the most common.
b Primary vertebral bony tumours (e.g. osteo- clastoma, myeloma).
c Lymphomas (Hodgkin’s disease, non-Hodg- kin’s lymphoma).
2 Intradural extramedullary.
a Meningioma.
b Neurofibroma.
3 Intramedullary (rare).
a Glioma.
b Ependymoma.
c Others, such as haemangioma.
Clinical features
The three groups of spinal tumours listed above each tend to have a fairly distinctive clinical picture.
• The extradural tumours are usually fast growing and malignant; they therefore give a picture of rapidly progressive cord compression leading to paraplegia, although symptoms of root irritation (see later in this chapter) may also be present.
• The intradural extramedullary tumours are usu- ally slow growing and benign. Initially, there is irritation of the involved nerve roots; pain occurs in the localized area of nerve distribution, which is often aggravated by recumbency and by factors such as coughing, sneezing or straining, which raise the CSF pressure. There may be hyperal- gesia in the affected cutaneous segment. Motor symptoms due to anterior root pressure are not a feature if only one nerve segment is involved, as most major muscle groups are innervated from several segments; however, if more than one seg- ment is affected, there may be localized flaccid paralysis.
As the tumour increases in size, cord com- pression takes place. There may be features of
the Brown-Séquard syndrome (see earlier in this chapter). Further compression results in com- plete paraplegia of the spastic type with increased tendon jerks and extensor plantar response, to- gether with overflow retention of urine and severe constipation.
Cauda equina tumours produce a lower motor neurone lesion: flaccid paralysis with diminished reflexes and paralysis of the anal and bladder sphincters with incontinence.
• The intramedullary tumours may be accompanied by pain, but much more frequently give a picture very similar to that of syringomyelia. Progressive destruction of the cord produces bilateral motor weakness below the lesion and, as the crossed spi- nothalamic tracts are the first to be involved, there may be dissociation of sensory loss below the le- sion, with abolition of pain and temperature but with persistence of vibration and position sense until later on in the progress of the disease.
Differential diagnosis
Spinal tumours are relatively uncommon and are great impersonators of other diseases; indeed, a cor- rect diagnosis made ab initio is something of a rarity.
The root pain, if it occurs in the thoracic or abdominal segments, is often mistaken for intrathoracic or intra- abdominal disease; if the pains radiate to the leg, they may be at first diagnosed as a prolapsed disc or in- termittent claudication. The intramedullary lesions closely simulate syringomyelia and it may be difficult at first to differentiate them from disseminated scle- rosis or other intraspinal lesions.
Special investigations
• MR has become the definitive investigation and gives almost anatomically perfect imaging of spi- nal tumours.
• X-rays of the spine may show obvious bony de- posits within the vertebral bodies. In other cases, pressure erosion from the enlarging tumour may scallop the posterior aspect of the vertebral body, erode one or more vertebral pedicles or enlarge the intervertebral foramen. Occasionally, calcifi- cation is seen within a meningioma.
• Lumbar puncture. Cytological examination of the CSF, together with its protein content and CSF pressure measurement, may be useful. The pro- tein in the CSF is nearly always raised above the normal 0.4 pg/L and may indeed be grossly el- evated with yellow (xanthochromic) fluid, which
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The spinemay actually clot in the container. Queckenstedt’s test4 may show either no rise or else a very slow rise and fall of the CSF pressure on jugular com- pression, indicating a complete or partial block within the spinal canal.
• A radiculogram, in which radio-opaque water-sol- uble contrast medium is injected into the theca, will confirm the presence of a space-occupying le- sion and localize its position accurately.
Treatment
A laminectomy (or vertebral body excision and bone grafting) is required to confirm the pathological
4Hans Heinrich Queckenstedt (1876–1918), physician, Leipzig, Germany. He described his test while serving in the German Army; he was killed accidentally 2 days before the Armistice.
nature of the tumour and also to decompress the cord.
Wherever possible, the tumour is completely excised;
this is usually confined to the benign meningiomas and neurofibroma, in which case complete recovery can be anticipated. In the malignant tumours, radio- therapy is usually the only practical treatment and the prognosis is poor.
Additional resources
Case 36: A spinal abnormality in a newborn child Case 37: Back injury
General Surgery Lecture Notes, Thirteenth Edition. Harold Ellis, Sir Roy Y. Calne and Christopher J. E. Watson. © 2016 John Wiley & Sons, Ltd. Published 2016 by John Wiley & Sons, Ltd.
Companion website: www.lecturenoteseries.com/surgery
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Although there is no regeneration of divided tracts in the central nervous system (CNS), injured peripheral nerve fibres may recover to a varying extent, depend- ing on the severity of the trauma.
Classification
Nerve injuries are commonly the result of laceration, stretching (traction) or compression (crush) injuries.
There are three types of injury.
1 Neurapraxia. Damage to the nerve fibres without loss of continuity of the axis cylinder; this is analo- gous to concussion in the CNS. The conduction along the fibre is interrupted for only a short pe- riod of time. Recovery usually commences within a few days and is complete in 6–8 weeks.
2 Axonotmesis. This is injury to the axon and my- elin sheath without disruption of the continu- ity of its perineural sheath. The axon distal to the lesion degenerates (Wallerian degeneration1) and regrowth of the axon occurs from the node of Ranvier2 proximal to the injury. As the sheath is intact, the correct axon will grow into its origi- nal nerve ending. The rate of regeneration is
approximately 1 mm/day; therefore, the time to recovery depends upon the distance between the injury and end organ.
3 Neurotmesis. This is actual physical disruption of the peripheral nerve. Regeneration will take place provided the two nerve ends are not too far apart, but functional recovery will never be com- plete.
Following the complete disruption of neurotme- sis, the distal part of the severed nerve undergoes Wallerian degeneration. The medullary sheath is depleted of myelin and the axon cylinders vanish;
the empty endoneural sheaths remain as tubules composed of proliferating neurilemmal cells. The proximal end of the nerve degenerates up to the first uninjured node of Ranvier. New axis cylin- ders proliferate from this point and grow into the empty neurilemmal tubules. However, there is no selection of tubules for the appropriate axon; the distal growth is governed solely by the position of the nerve fibres. Thus, with most mixed nerves, there is likely to be considerable wastage owing to regenerating fibres growing into endings which will be functionless, such as motor nerve fibres growing into sensory nerve endings, and vice versa. Even when a motor nerve grows into a motor nerve end- ing, it may not supply the original muscle and the patient will have to relearn the affected movement.
A peripheral nerve contains a large number of in- dividual fibres, so it is quite possible in a nerve in- jury for some fibres to suffer from neurapraxia, oth- ers axonotmesis and others neurotmesis. However, a distinction between the first two and the last may be quite clear in that, if the nerve is found to be sev- ered at surgical exploration, neurotmesis must have occurred.
Peripheral nerve injuries
Learning objectives
✓ To know the different types of nerve injury and their prognosis.
✓ To be able to recognize the patterns of neurological deficit that occur with injury to all the main nerves in the upper and lower limbs.
1Augustus Waller (1816–1870), a general practitioner in London, UK, for 10 years before working as a physiologist in Bonn, Germany, Paris, France, and Birmingham, UK.
2Louis Ranvier (1835–1922), Professor of Histology, Paris, France.
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Peripheral nerve injuriesPartial nerve injury may occur as the result of pres- sure or friction, for instance from a crutch, a tightly applied plaster cast or a tourniquet, as well as from closed injuries or open wounds.