In this article we will discuss about:- 1. Introduction to Compression of the Spinal Cord 2. Clinical Features of Compression of the Spinal Cord 3. Diagnosis 4. Investigation Strategies 5. Treatment.
Introduction to Compression of the Spinal Cord:
Compression of the spinal cord may be due to causes in vertebral column, meninges and in the spinal cord itself.
Important causes of compression of the spinal cord are:
(1) In the Vertebral Column:
(a) Trauma causing vertebral fracture, vascular damage or whiplash injury due to acute stretch-damage of the spinal cord.
(b) Protruded I.V. disc.
(c) Metastatic new growth— commonly prostatic, bronchus and breast carcinomas.
(2) In the Meninges:
Meningioma, neuro-fibroma, lymphomas, leukaemias, epidural abscess, tuberculosis or syphilitic meningitis.
(3) In the Spinal Cord:
Gliomas, ependymal or malignant metastasis.
The effects on the spinal cord may be due to direct pressure effect or by causing local oedema duetto venous obstruction. Ischaemia may occur due to occluded blood supply.
If the compression is relieved early, recovery is possible, but if the nerves or nerve-cells are damaged due to prolonged pressure or ischaemic changes chance of recovery is remote.
Clinical Features of Compression of the Spinal Cord:
In acute traumatic injury paralysis occurs rapidly, otherwise in most cases cord compression produces gradual and progressive appearance of signs and symptoms.
In cases of injury or metastasis the onset is acute, especially if the blood supply is occluded. Local new growths are usually slow growing. These may be extra medullar (i.e. growing from structures outside spinal cord) or intramedullary (i.e. growing from structures within the spinal cord). Disc protrusion is a common cause of cord compression.
New growths or disc prolapse’ may either cause pressure on nerve roots or on the spinal cord directly or may cause occlusion of arterial blood supply, resulting in loss of function of structures involved. If the cause can be removed before permanent neuronal damage has occurred, considerable functional recovery may be possible. Hence early diagnosis is most important.
Suspicious symptoms are local pain, aggravated by coughing, sneezing or movement of the spine.
There may be root pains and local discomfort over the spine. The clinical features will depend on the level of lesion. Numbness, paraesthesia, cold or hot sensations may be felt. Motor paralysis may gradually be noticed. Segmental localisation is most important to find out the level of lesion.
Involvement of posterior root gives sensory deficits in the particular segment. If motor root is involved LMN lesion of the same segmental distribution will occur. Affection of one half of the spinal cord will result in Brown-Sequard syndrome. If descending motor fibres are affected, there is UMN paralysis below the segment of the lesion. Bladder and bowel control may be affected.
Therefore, segmental landmarks should be carefully learnt and remembered- Quadriparesis or quadriplegia may occur when the lesion is above fifth cervical segment. Lesion at this level causes UMN type of paresis of all four limbs.
If the lesion is situated between fifth cervical and first thoracic segment of the spinal cord, there will” be segmental sensory deficit of upper limb with LMN type of lesion, while the lower limb will have spasticity due to UMN lesion.
If the lesion is situated above twelve thoracic segment, there will be spastic paraplegia associated with sensory level in appropriate level. However, it should be remembered that a tumour or haematoma in the region of falx cerebri (e.g. meningioma) may also cause spastic paraplegia.
As the spinal cord ends at the level of first lumbar vertebra, lesions below this; level cannot compress the cord but may only affect the spinal roots resulting in root lesion. If the tumour is large enough, it may damage the cauda equina as a whole resulting in so-called “cauda equine” syndrome.
From Table 12.1, it is possible to correlate the segmental levels of cord, roots and vertebra. Seventh cervical spine is also a good landmark as from this level spines of each vertebra can be located. It is also to be noted that seven cervical vertebrae contain eight segments and eight pairs of cervical roots emerge almost horizontally. C1 has no sensory root. In infancy, lower tip of cord ends at the level of L4, while in adults it is L1. Lower the segment of cord, longer the root and exit is also obliquely and downwardly oriented.
Each segment of the spinal cord has a pair of sensory and motor-root which joins on either side to form the nerves which emerge out of intervertebral foramina on either side of vertebral column. Each nerve root has a cutaneous territory of supply through posterior root which is called a “dermatome”. Thirty-one pairs of spinal nerves have overlapping areas of sensory supply.
Section of one particular sensory root does not produce much recognisable sensory impairment. However, pressure on a particular sensory root causes typical pain sensation i.e. “root pain”. When two or three segments of cord are affected, definite bands or areas of sensory impairment will be manifested. Localisation of sensory disturbances of any segment can be diagnosed at which the highest level of sensation is impaired if there is a band of hypo- or hyper-aesthesia.
If two sides are not equally involved loss of sensory level is asymmetrical. When spinothalamic tract is affected, loss of pain and temperature sensation occurs at specific level. As pain fibres cross at a lower level than heat and touch fibres, the loss of these modalities will vary with same lesion. The “pointer sensory” levels are to be noted for rapid bed-side diagnosis.
Sacral neoplasms may be difficult to detect. There is no root pain but vague sacral discomfort may be present. Coxalgia is often a pointer. These patients come late to the neurologist and too late to the neurosurgeon.
The crux of the diagnosis lies in the fact that lesion of plexus or peripheral nerve causes different kinds of sensory impairment than produced by lesions of the segments or roots.
The skeletal muscles are also supplied in segmental fashion through motor roots and each segmental unit is called a “myotome”.
Similar to myotomes and dermatomes; segmental supply of all internal organs are also supped by the spinal segments. These are called “enterotomes” but this is not clinically so easy to localise.
Motor Segmental Diagnosis:
Each segment of the cord has lower motor neuron cells clustered in the anterior horns. Skeletal muscles receive their nerve supply from anterior-horn cells on segmental basis while mots skeletal muscles receive their supply through two or three motor roots, depending on the size of the muscles.
In complete transverse lesion of the cord all voluntary movements of skeletal muscles at end below the lesion are lost. At the segmental level, LMN lesion will cause loss of tone and reflexes as well as wasting of segmental muscles. Below the level it shows UMN type of paralysis. However, if the lesion is acute there will be flaccid paralysis during the stage of spinal shock and spasticity may occur later, when some recovery is taking place.
Assessment of the wasting of skeletal muscle should be carefully made. Wasting is often overlooked as there may be hypertrophy of the neighbouring muscles. Deep reflexes and plantar response should be tested to localise the level of damage.
Above the level of lesion the reflexes are normal, while at the level of damage reflexes are reduced or lost. Below the level of lesion reflexes are exaggerated unless there is spinal shock. Plantar response will be extensor in case of UMN lesion.
Any lesion affecting one half of the spinal cord may damage pyramidal tract, spino-thalamic tract as well as posterior column of the cord of the involved side. This is known as Brown-Sequard syndrome. Pyramidal lesion on the side of lesion causes weakness with spasticity on the side of lesion but pain and temperature sensation is lost on the opposite side.
The upper level of-the loss of pain and temperature sensation on the opposite side will be a few segments below the level of lesion, as fibres which are involved at the site of entry into the cord causes a band of analgesia and thermo-anaesthesia on the same side just below the lesion.
Involvement of the posterior column is not always present, but when it is affected, loss of position and vibration sense occurs on the same side of the lesion.
Diagnosis of Compression of the Spinal Cord:
Only about 10% of spinal tumours are intramedually consisting of ependymoma and gliomas. The remaining extramedullary tumours may be intradural or extradural. Secondaries are also usually extradural.
When pain is the chief presenting feature, it may be diagnosed as rheumatism, colitis, G.B. disease, hepatitis or renal pain. A good neurological examination, assessment of muscular wasting and determination of any sensory loss only reveal the diagnosis.
Hints on Localisation:
(1) History should be taken carefully especially regarding injury, fall and any symptoms of bladder dysfunction as well as sexual incapacity.
(2) Note if the patient has real root pains, girdle pain, hyperalgesia, hyperaesthesia or sensory loss at any level.
(3) Tenderness over the spines is also suspicious.
(4) Wasting of muscles and its segmental distribution, if any, is noteworthy.
(5) Determine the deep reflexes carefully. The jerks are lost at the level of lesions and may be exaggerated below the level of lesion, unless there is spinal shock.
(6) Plantar response, abdominal reflexes and cremasteric reflexes should always be tested.
(1) Motor neuron disease — Wasting of muscles, fasciculation, absence of sensory loss and no sphincter disturbances are characteristic.
(2) Sub acute combined degeneration — There are lesions of pyramidal tract and posterior column of cord, associated with macrocytic anaemia, achylia gastrica, megaloblastic bone marrow.
(3) Syringomyelia — The deep jerks may be lost associated with dissociated sensory loss, tropic skin changes and congential defects, e.g. pes cavus etc.
(4) Multiple sclerosis – Remission and relapse of symptoms, nystagmus, intention tremor, ataxia and temporal pallor of optic disc are characteristic.
(5) Syphilitic meningomyelitis – A.R. pupil, VDRL test and CSF findings are helpful.
(6) Parasagittal intracranial tumour — may cause spastic paraplegia.
Investigation Strategies of Compression of the Spinal Cord:
(1) CSF — studies may be helpful. High protein content with normal glucose and cell count are strongly suggestive features. CSF may be xanthochromic. Queckenstedt’s test may be positive.
(2) X-ray of the spine should always be taken; the part to be studied depends on clinical data. It may show evidence of caries spine, possible disc lesion or metastatic deposits.
A very significant finding is flattening of pedicles and increased interpedencular distances, due to expanding lesions in the spinal canal. Tumours of nerve roots cause erosion and widening of I.V. foramina.
Treatment of Compression of the Spinal Cord:
(1) Surgical treatment may be considered where possible. Intramedullary tumours are difficult to excise, hence only irradiation therapy may have to be done. Decompression provides temporary relief from pain and possibly some functional improvement.
(2) Decompression of spinal cord surgically followed by irradiation may be done in cases of epidural spinal metastasis.
(3) Steroids may also be used in high doses in short courses to relieve pain.
(4) Certain tumours, e.g. meningioma can be removed successfully with considerable functional recovery. Similarly, disc problems can be surgically well managed.
(5) Symptomatic treatment to relieve pain, reduce spasticity and control of bladder infection is important.