COMPRESSION PARAPLEGIA…Onset varies according to the underlying cause, but usually gradual.
Age: All ages
Symptoms depend on the site of compression, nature of compressive agent and whether the compression is extradural, intradural, extramedullary or intramedullary or whether it is sudden or gradual. Sensory symptoms develop first followed by the motor symptoms.
Root pain is the first symptom which is felt over the spine radiating along the distribution of the spinal nerve. This pain may be constant or intermittent, unilateral or bilateral and is of burning or constricting in nature. This is aggravated by coughing, sneezing, jolting and other movements of the spine. Pain may pass down the arms or legs or may be of girdle distribution like a band around the chest or trunk. In transaction of the cord sensory loss occurs at and below the level of lesion, but in hemisection of the cord on the same side as lesion fine touch, tactile localisation, discrimination, vibration sense etc. will be lost due to lesion of tract of Goll and Burdach but on the opposite side there will be loss of pain and temperature sensation which is due to lesion of spinothalamic tract. When there is intramedullary lesion dissociated sensory loss will be present just like syringomyelia.
Motor symptoms include weakness unsteadiness, heaviness or stiffness of the lower limbs. At first there is a tendency to drag the legs and gradually complete paralysis develops. Lower limbs are only involved when the lesion is located below C, commonly below Ti. Girdle sensation like a constriction or tight band may be present due to irritation of the anterior horn cells above the level of lesion. When the compression is acute or there is vascular occlusion flaccid paralysis develops. On the other hand gradual compression gives rise to spastic paralysis. Sphincteric disturbances are usually late in appearance. Autonomic symptoms also develop and are variable.
(i) Nutrition of muscles may remain normal but in longstanding cases there may be disuse atrophy. Due to local compression of the anterior horn cells there may be localised segmental wasting of muscles.
(ii) Motor power is lost, either completely (paralysis) or to a lesser extent (paresis).
(iii) In cases with acute onset there is flaccidity of muscle (flaccid paraplegia) due to neural shock stage but after the shock stage is over spasticity sets in. In cases with gradual onset, spasticity develops from the very beginning. There is clasp-knife rigidity of the extensor group of muscles and lower limbs are held in extension. This is solely due to integrity of the extra pyramidal tract which is still not destroyed. This is called “paraplegia in extension”. Gradually the extrapyramidal tracts are also compressed and damaged when the lower limbs are held in flexion state due to activity of the local spinal reflex arc maintaining the flexor tone. This stage is called “paraplegia in flexion. Though it is mainly due to this, wasting, atrophy, fibrosis of muscles due to disuse may also contribute to some extent for its development. Flexor spasm will also be seen. This is a very important sign of spinal compression. At the site of compression due to irritation of anterior horn cells girdle sensation will be seen. This will indicate site of lesion one segment below the level of girdle sensation.
(iv) Co-ordination test though difficult to perform in presence of paralysis yet at times it may be possible. There may be evidences of spinal or cerebellar incoordination due to effect of compression on the ascending spinocerebellar or posterior column tracts.
(v) Involuntary muscle movements are usually absent but sometimes due to weakness there may be tremulousness. At the level of compression sometimes fasciculation may be present.
Compression of the dorsal nerve roots may give rise to hyperaesthesia which is followed by anaesthesia and analgesia. Ascending sensory tracts may be compressed producing dissociated sensory loss in cases of intramedullary compression. Pain and thermal sensations are impaired due to lesion of the spinothalamic tract; fine touch, tactile localization and discrimination, appreciation of posture, passive movement and vibration sense are lost due to lesion of the tracts of Gol1 and Burdach. At and below the level of lesion, all modalities of sensations are lost but due to irritation of the lowest viable segment by the dead segment a zone of hyperaesthesia or hyperalgesia may develop. This always indicates the level of lesion to be located one segment below it. Effects of pyramidal and posterior column lesion on the side of compression and spinothalmic tract lesion on the side opposite to the romnression constitute Brown-Sequard syndrome.
Abdominal reflexes vary according to the site of lesion. Cremasteric reflexes may be lost if the lesion involves L1 segment. Plantar reflexes may be extensor in type due to involvement of pyramidal tract. Deep reflexes below the level of compression will be brisk but those at the level of lesion will be lost while those above the level of lesion will remain normal. Sphincters are involved lately and there may be precipitancy in micturition. retention or automatism of bladder according to the site of involvement.
There may be excessive sweating below the level of compression or sometimes oedema of the lower limbs due to loss of Venomotor tone.
It shows tenderness due to local disease or due to irritation of the dorsal roots. There may be deformity of spine or sometimes rigidity of the sacrospinalis.
In long-standing cases some trophic changes develop such as bed sores, ulcers, clubbing of toes, pigmentary changes in skin, oedema, cyanosis and various others.
When patient is able to walk a characteristic gait is seen. Patient stands with a broad base and walks with the help of a stick with circumduction of both the lower limbs, called double circumduction gait.
Sometimes due to associated hypertonicity of the adductors, cross legged or scissors gait is also seen.. Again when both the two lower limbs are very much spastic they are dragged forwards which is called digitigrade gait. There may be non specific limping gait.
1. X-ray of spine may show Pott’s disease, fracture, dislocation, osteoporosis, spondilytis, secondary deposits, etc.
2. CT scan, MR images may be of help in special circumstances like craniocervical abnormalities. MRI is gradually replacing myelography.
3. Myelography shows the level of obstruction.
4. CSF: Below the level of compression the following changes may be seen which are collectively known as Froin’s loculation syndrome.
(i) Low tension.
(iii) Increased protein.
(iv) Spontaneous clot formation on standing.
(v) Increased mononuclear cells.
(vi) Queckenstedt’s test is positive.
5. Bone marrow examination may reveal metastatic deposits, myeloma cells etc.
Localisation of the Level of Lesion
This may be done by the following-
1. Root pain: Radicular pain according to the specific dermiatome supply will give a clue to the site of lesion.
2. Girdle sensation or sense of constriction according to dermatome supply will indicate the site of lesion below the segment.
3. Zone of hyperaesthesia and hyperalgesia will indicate the site of lesion one segment below this zone.
4. Change in reflex: Loss of reflex indicates local lesion in that segment. Tendon Reflexes below the affected segments will be brisk and above the affected segment will remain normal. Abdominal and cremasteric reflexes are very helpful.
5. Atrophy of muscle in a segmental distribution indicates lesion in that segment.
6. Tenderness over the spine or spinal gibbus may help in localizing the affected segment. For cervical vertebrae add one; for upper six thoracic vertebrae add two; for next three thoracic vertebrae add three; first and second lumber segments rest against tenth thoracic vetebra; third and fourth lumber segments lie against eleventh thoracic vertebra; fifth lumber segment lies against 12th thoracic vertebra; all sacral and coccygeal segments rest against first lumber vertebra.
7. Sensory loss according to dermatome supply will also help. There will be analgesia and anaesthesia at and below the site of lesion.
8. Area of sweating in segmental distribution will indicate the level of lesion.
9. Behaviour of bladder function will also help. Automatic bladder indicates lesion above the lumbosacral segments, precipitancy or retention indicates lesion at the sympathetic parasympathetic segments respectively.
10.X-ray of the spine (AP and lateral) shows destruction, fracture of spine, etc. which will indicate the site of spinal lesion.
11. Myelography will show the exact level of obstruction. But it should be done last of all.
12. Discography, CT scan and MRI will also be required in special circumstances.
13. Lumbar puncture and Froin’s syndrome will indicate spinal block above the site of puncture.
DIFFERENTIAL DIAGNOSIS OF COMPRESSION PARAPLEGIA
The jerks are lost, dissociated sensory loss is present. Trophic changes are also seen.
Subacute combined degeneration of Spinal cord
Bone marrow is megaloblastic, achylia gastrica is present and macrocytic anemia is seen. Evidences of lesion of posterior column and pyramidal tracts are present.
Chronic motor neurone disease
Widespread fasciculation is present, no sensory loss or sphincteric changes are seen.
Remission and relapse of symptoms, temporal pallor of optic disc, nystagmus, tremor, characteristic CSF changes are present.
Chronic meningomyelitis (Syphilitic)
Argyll Robertson pupil is present, VDRL test is positive in CSF and in blood.
There may be spastic paraplegia only. CT scan is diagnostic.
(a) Urinary retention, infection and calculi formation
(b) Chronic constipation.
(c) Bed sores
(d) Permanent contracture of limbs and silent fractures.
The underlying cause is to be treated as far as practicable. Physiotherapy should be done in some cases. Passive physiotherapy is helpful to avoid contracture. When there is paraplegia in flexion or extension Diazepam, Baclofen will be beneficial.
Until automatic bladder is established, it is necessary to catheterize the bladder. Infection should be promptly controlled.
Constipation is to be avoided by giving enema. Manual removal of faeces is also required.
Pressure points is to be protected, water bed or ripple mattresses are useful. Patient should be turned every 2-4 hours.
Bedsores if develops can be treated surgically. General health and morale of the patient is to be uplifted. Rehabilitation on
wheel chair or other devices can be considered. Surgery is helpful whenever required.
This is be carefully considered so that patients can use orthopaedic appliances and gradually become active member of the family and gradually of the society.
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