Compression of the spinal cord

The spinal cord is compressed due to a number of causes ranging from diseases of the vertebral column, spinal tumors and inflammation of the meninges. In compression the lumen of the spinal canal is reduced resulting in injury at the site of compression either directly or indirectly due to interference of its blood supply. Except for trauma the symptoms of compression appear slowly.

Causes of compression

(a) Disease of the vertebral column

1. Tubercular disease of the spine.

2. Secondaries from malignancy somewhere in the body.

3. Spondylosis with protrusion of intervertebral discs.

4. Primary neoplasms arising from vertebrae – sarcoma, myeloma, osteoma.

5. Syphilitic osteitis, Paget’s disease

6. Fracture dislocation of spine due to trauma.

(b) Spinal tumors

1. Extramedullary – Meningioma, neurofibroma, sarcoma, lipoma, chordomas, metastatic deposits.

2. Intra medullary – Gliomas, ependymomas, spongioblastomas, medulloblastomas, leukaemic, deposits, secondaries.

(c) Meningeal inflammation

1. Pachymeningitis – Syphilitic, pyogenic infection, tuberculosis.

2. Spinal arachnoiditis.

3. Parasitic cysts – Echinococcus, cysticercus cysts.

compression of spinal cord


These are variable and depend to a large extent on the nature of compression – whether extradural, extramedullary or intramedullary.

The onset is usually gradual especially in cases of spinal tumour where there is involvement of one limb to start with. The first symptoms are root pains in the distribution of one or more spinal roots. These are in the form of soreness and tingling sensation and increase by coughing and sneezing.

Involvement of spino thalamic tracts leads to impairment of pain, heat and cold on opposite side of the body while compression of posterior spinal roots at the level of the lesion causes hyperaesthesia and hyperalgesia of the corresponding cutaneous areas. The upper level of sensory loss is below the segmental level of site of compression.

There is loss of posture, passive movement and vibration sense and generally it is more upon one side. Motor symptoms vary depending as to which part of cord has been effected.

When anterior roots or anterior horns of grey matter are affected there is wasting of muscles along with absent or diminished reflexes (Lower motor neurone lesion) while symptoms of upper motor neurone (spastic weakness of limbs, exaggerated deep tendon reflexes, absent abdominal and cremasteric reflexes) result due to compression of pyramidal tracts.

Sphinctres as a rule are not involved in early stages of compression but later on precipitancy or difficulty in micturition followed by retention occurs. Constipation may be present. In late stage incontinence may develop.

The spine may show localized pain or tenderness. Movements of spine are limited and there may be deformity.

Localization of segmental level

The main features of spinal compression are:

1. Motor symptoms which include lower motor neurone picture (wasting, atrophic paralysis, diminished or absent tendon reflexes) in the area supplied by the segments of cord compressed.

2. Features of upper motor neurone lesion (spastic paralysis with exaggeration of deep tendon reflexes. Plantars extensor) on one or both limbs below the level of compression.

3. Hyperaesthesia and hyperalgesia at level corresponding to the segment compressed. Sensory loss below the segmental level of the site of compression.

4. Autonomic disturbances like excessive sweating on the parts of body below the level of lesion.

Upper cervical region (C3-4) compression in this region causes marked pain in the neck and occiput intensified by movements of neck. Early symptoms include pain, paraesthesiae and weakness in the upper limb. Involvement of the spinal tract and nucleus of fifth nerve may cause relative analgesia and thermoanasthesia over the face.

There may be paralysis of 9th, 10th and 11th cranial nerves. Wasting may occur in both upper limbs. Involvement of phrenic nerve or its nucleus leads to diminution in movements of diaphragm. As comprçssion progresses patient develops motor weakness of all the four limbs (upper motor neurone).

Fifth cervical segment (C5) spastic paralysis of the upper and lower limbs (Quadriplegia) atrophic paralysis of muscles (Deltoid, rhomboids, biceps, brachialis and supinator) supplied by this segment. Biceps (C5-6) and supinator (C5-6) reflexes are either diminished or lost. Inversion of the radial reflex. Triceps reflex may be preserved or exaggerated.

Seventh cervical segment (C7). There is paraplegia. Triceps and extensors of wrists and fingers are involved. Triceps jerk is lost while other reflexes of upper limb are preserved.

Eighth cervical (C8) and first dorsal segment (Dl)

Spastic paralysis of the trank and lower limbs. There is atrophic paralysis of flexors of wrist and fingers and small muscles of the hands. Tendon reflexes in upper limb are normal while that in lower limbs are exaggerated. Paralysis of ocular symptathetic may occur.

Mid dorsal region. Atrophic paralysis of muscles (intercostals upper and lower rectus abdominis) supplied by the segments involved.

Spastic paralysis of muscles of abdomen and lower limbs. Epigastric reflex (D6-8) lost.

Ninth and tenth dorsal segments (D9-1O). There is spastic paraplegia. Lower halves of abdominal recti are paralysed. Upper abdominal reflexes are present while lower are lost.

Twelfth dorsal and first lumbar segment (D12-L1) spastic paralysis of lower limbs. Abdominal reflexes are preserved while cremasteric reflex (L1-2) is lost.

Third and fourth lumbar segment (L3-4) spastic paraplegia with atrophic paralysis of quadriceps and adductors of hips. Knee jerks may be lost or diminished. Ankle jerks are exaggerated with plantars extensor.

First and second sacral segments (S1-2) Flexion of hip, adduction of thigh, extension of knee and dorsiflexion of foot are preserved while all other movements of lower extremities are involved. There is wasting of glutei, calf muscles, anterior tibial and peronei as well as small muscles of foot. Knee jerks are present while ankle and plantar reflexes are lost.

Third and forth sacral segments (S3-4). There is no paraplegia but paralysis of external sphincters leading to retention of urine and faeces. Anal and Bulbocavemous reflexes are lost while reflexes of the lower limbs are normal.

Cauda equina. Paralysis of muscles below the knee distribution depending upon the nerve involved. Involvement of lower sacral nerve roots gives rise to saddle shaped anaesthesia over the butocks and back of thighs. Compression of upper sacral and fifth lumbar produces sensory loss over foot and posterior and outer aspect of leg.

Ankle jerks may be diminished or lost. Knee jerks are present. Plantar reflexes may not be elicitable. Involvement of bladder and bowel is usually late.

Diagnosis of spinal compression shall be governed by level of compression and its segmental level. It is imperative to decide whether the lesion is extra dural, extra meduallary or intra medullary.

Various clinical signs shall decide regarding localization of segmental lesion and the nature of that lesion. Once a diagnosis has been established, its further management shall depend on the duration as well as disturbance or severity of the disease process.

Earlier the diagnosis is made and treatment instituted at an early stage prognosis is good but in certain conditions like secondaries in spine, prognosis, invariably shall be poor.

error: Content is protected !!