The cord extends from Cl (its junction with the medulla) to the vertebral body of Ll (the conus medullaris). The blood supply is via the anterior spinal artery and a plexus on the posterior cord. This network is supplied
by the vertebral arteries, the thyrocervical trunk and several branches from the lumbar and intercostal vessels. Spinal cord compression The principal features of cord compression are of radicular pain at the site of compression, spastic paraparesis or tetraparesis and sensory loss which rises to the level of compression.
For example, in compression at the level of T6 a band of pain radiates around the chest wall and is characteristically worse on coughing or straining. A spastic paraparesis develops either over many months, days or hours, depending upon the underlying pathology. Numbness commencing distally in the lower limbs rises to the level of compression (the ‘sensory limb’). Compression of the cord is a potential medical emergency. It is sometimes difficult to distinguish chronic cord compression from other causes of paraparesis and tetra paresis on clinical grounds alone. This is because pain and the sensory level may be absent.
Spinal cord neoplasms
Disc and vertebral lesions
Epithelial. endothelial and parasitic cysts
Aneurysmal bone cyst
Spinal cord neoplasms
Extramedullary turnours (extradural and intradural) cause cord compression gradually over weeks to months, with local or referred root pain and a sensory level.
Intramedullary turnours (e.g. glioma) typically have a very slowly progressive course over several years. Sensory disturbances similar to syringomyelia may appear.
Disc and vertebral lesions
Central cervical disc protrusion and lumbar disc protrusion are considered.
Epidural haemorrhage and haematoma
These are rare sequelae of anticoagulant therapy, bleedingdisorders and trauma. A rapidly progressive cord lesion develops.
Spinal tuberculosis is a frequent cause of cord compression in countries where tuberculosis is common (e.g. India, Pakistan, Bangladesh and Africa). There is destruction of vertebral bodies and disc spaces, with spread of infection along the extradural space. Cord compressionand paraparesis follow (Pott’s paraplegia).
Early recognition of the syndrome is vital. Surgical exploration is frequently necessary and, if this is not performed ufficiently early, irreversible paraplegia may follow. Plain spinal films show degenerative bone disease and destruction of vertebrae by infection or neoplasm. Routine tests, e.g. chest X-ray, may indicate a primary neoplasmor infection. MRI can identify most lesions and is beginning to replace myelography. Investigations should, if possible, be done promptly in a centre equipped to carry out neurosurgical exploration. The signs of cord compression may increase after lumbar puncture. The results following the early removal of benign tumours are excellent.
Transverse myelitis This broad term is used to describe acute inflammation of the cord and paraplegia occurring with viral infection, MS and other inflammatory and vascular disorders (e.g. syphilis, radiation myelopathy, anterior spinal artery occlusion). Myelography or MRI is usually required to exclude a compressive lesion.
Anterior spinal artery occlusion Cord infarction, causing an acute paraparesis or tetra paresis (or tetraplegia) may occur in any thrombotic or embolic vascular disease (e.g. endocarditis, shock, atheroma,diabetes mellitus, syphilis, polyarteritis nodosa). It sometimes occurs during surgery to the posterior mediastinum, and follows dissection of the aorta and trauma. It occasionally occurs as an isolated event.
A mild paraparesis and sensory loss sometimes develops within several weeks to a year of radiotherapy if the cord has been damaged. Particular care is usually taken to shield the cord during radiotherapy.Metabolic and toxic cord disease Subacute combined degeneration of the cord due to vitamin BI2 deficiency (see pp. 948 and 304) is the most important example of metabolic disease causing spinal cord damage.
Cord lesions may also be seen in severe malnutrition, when they are probably due to multiple B-vitamin deficiencies.
This is an endemic, spastic paraparesis of central India caused by the toxin f3-(N)-oxalylaminoalanine. It occurs when excessive quantities of a drought-resistant pulse, Lathyrus sativa, are consumed.
Syringomyelia and syringobulbia Fluid-filled cavities within the spinal cord (myelia) and brain stem (bulbi a) are the essential features of these
A history of birth injury may be obtained and bony anomaliesat the foramen magnum, spina bifida (see p. 942), Arnold-Chiari malformation (see p. 942) or hydrocephalus (see p. 934) are often seen.
It is believed that in the presence of an anatomical abnormality at the foramen magnum, the normal pulsatile CSF pressure waves are transmitted to the delicate tissues of the cervical cord and brain stem, with secondary cavity formation. The cavity, or syrinx, is in continuity with the central canal of the cord.
The expanding cavity gradually destroys:
• Second-order spinothalamic neurones In the cervical cord
• Anterior horn cells
• Lateral corticospinal tracts
The vestibular system, trigeminal nuclei, sympathetic system and twelfth nerve nuclei may also be affected.
Patients usually present in the third to fourth decade.Pain in the upper limbs is common. This may be exacerbated by exertion or coughing. Spinothalamic (pain and temperature) sensory loss in the upper limbs leads to painless burns. Difficulty in walking may occur. The signs of a cavity in the cervical region are: AREAS OF DISSOCIATED SENSORY LOSS, i.e. pain and temperature but not touch (posterior column). These
may extend in a bizarre distribution over the trunk and upper limbs.
Loss OF UPPER LIMB REFLEXES.
WASTING of the small muscles of the hand. SPASTIC PARAPARESIS. This may initially be mild and symptomless.Neuropathic joints, trophic skin changes and ulcers may follow.
When the cavity extends through the foramen magnum into the brain stem (syringobulbia), there is atrophy and fasciculation of the tongue, nystagmus, Horner’s syndrome, hearing loss and impairment of facial sensation.
MANAGEMENT AND COURSE
The condition is intermittently progressive over several decades.
Investigation shows widening of the cervical canal on plain films and, frequently, ventricular enlargement on CT scan. An MRI scan (the investigation of choice) demonstrates the intrinsic cavity. Myelography (which is sometimes followed by deterioration) shows widening of the cord and herniation of the cerebellar tonsils through the foramen magnum. There is no curative treatment. Decompression of the foramen magnum sometimes reduces the rate of deterioration.
The patient who becomes paraplegic from any cause demands skilled and prolonged nursing care. Particular problems are discussed below.
Bladder Intermittent (or continuous) catheterization is usually necessary initially. A reflex emptying bladder develops in permanent paraplegia, avoiding the need for catheterization and some of the risks of urinary stasis, infection, and renal and bladder calculi.
Bowel Constipation and faecal impaction must be avoided.Manual evacuation is necessary following acute paraplegia, but reflex emptying later develops. Skin care The risk of pressure sores is great. Meticulous attention must be paid to cleanliness and to turning the patient every 2 hours. The sacrum, iliac crests, greater trochanters, heels and malleoli should be inspected frequently. Ripple mattresses and water beds are useful. If pressure sores develop, plastic surgical repair shouldbe considered. The lower limbs
Passive physiotherapy is helpful in avoiding contractures. Severe spasticity (with spasms either in flexion or extension) may be helped by dantrolene sodium, baclofen or diazepam.
The general health and morale of the patient should be considered carefully and regularly. Any intercurrent infection (urinary or respiratory) is potentially hazardous and should be recognized and treated early, as chronic renal failure is the single most common cause of death in paraplegia.
Rehabilitation Many patients with traumatic paraplegia or tetraplegia return to partial self-sufficiency and a wheelchair existence. Specialist advice from a skilled rehabilitation unit is necessary. Lightweight, specially adapted wheelchairs are often recommended. The patients have demanding practical, psychological and social needs but with guidance and help can often return to an active role in society.
Other causes of cord lesions
• Motor neurone disease
• Familial or sporadic paraparesis
• Non-metastatic manifestation of malignancy
Rarities, e.g. sarcoidosis (see p. 687), Behcet’s syndrome