Degenerative Spinal Disorders

Basic anatomy Definition Epidemiology Etiology Degenerative disc disease Lumbar spine stenosis Spondylolisthesis.

The Vertebral column consists of 33 vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral (fused to form the sacrum), and 4 coccygeal (the lower 3 are fused)

Descending in the cord, the spinal nerves become more oblique in their course.

Spinal cord proper ends at L2 and the remaining spinal nerves, seeking their intervertebral foramen of exit form the cauda equina.

At S2 the subarachnoid space ends

The vertebrae articulate with each other by 2 types of joints:

1. Facet joints: synovial joints between the superior and inferior articular processes.

2. Intervertebral disk: cartilagenous joint between the vertebral bodies. It acts as a shock absorber.

The intervertebral disc is composed of

a. Annulus Fibrosus:Tough outer layer composed of

layers of parallel fibers that criss-cross to the next layer. It is thinner posteriorly.

b. Nucleus Pulposus:It is a fibrocartilagenous layer that

has a high water content (80%). It is the part that acts as a shock absorber.

Degenerative spinal disorders are a group of conditions that involve a loss of normal structure and function in the spine.

Epidemiology About 90% of population suffer from back pain

at some point and 30% of these will develop leg pain due to lumber spine pathology.

25% of people develop chronic low back pain. usual age of presentation: 30s to 50s

These common disorders are associated with the normal effects of aging, but also may be caused by infection, tumors, muscle strains, or arthritis. Pressure on the spinal cord and nerve roots associated with spinal degeneration may be caused by disc displacement or herniation; spinal stenosis, a narrowing of the spinal canal; or osteoarthritis, cartilage breakdown at spinal joints.

Protrusion, herniation, or fragmentation of an intervertebral disc beyond its borders with potential compression of a nerve root, the cauda equina in the lumbar region, or the spinal cord at higher levels.

  With aging, certain biochemical and structural changes occur in the intervertebral discs. There is an increase in the ratio of keratan sulfate to chondroitin sulfate, and the proteoglycans lose their close association with the disk collagen. The disc also loses its water-binding capacity and the water content decreases down to 70%. The vertebral end plates also becomes thinner and more hyalinized. This degree of disk degeneration is considered a normal part of aging.

With more advanced degeneration, dense disorganized fibrous tissue replaces the normal fibrocartilaginous structure of the nucleus pulposus, leaving no distinction between the nucleus and anulus fibrosus. Development of anular tears weakens the anulus and allows nucleus to protrude into the defect. Tears that extend through the outer anulus induce ingrowth of granulation tissue and accelerate the degenerative process. Advanced degeneration can lead to gas formation or calcification within the disk. Also, fissures develop in the cartilaginous end plates, and regenerating chondrocytes and granulation tissue form in the area.

Desiccation - loss of disk water Prolapsed disc – herniation of nucleus pulposus

througha tear in annular fbrosus Disk bulge - circumferential enlargement of the

disk contour in a symmetric fashion Protrusion - a bulging disk that is eccentric to

one side but < 3 mm beyond vertebral margin Herniation - disk protrusion that extends more

than 3 mm beyond the vertebral margin Extruded disk - extension of nucleus pulposus

through the anulus into the epidural space Free fragment - epidural fragment of disk no

longer attached to the parent disk

Directions: * Posterolateral: most common. * Lateral: traps nerve root. * Central: compresses cauda equina. Causes: * 80 % traumatic (sudden sever

strain). * 20 % degenerative (without tear).

Presentation: 1. Low back pain 2. Sciatica 3. Parasthesia 4. Weakness

Examination: 1. Inspection: scoliosis, loss of

lumber lordosis, muscle spasm & atrophy & dystrophic skin changes.

2. Focal tenderness. 3. Lumber back movement

restriction ( due to pain ).

Examination cont. 4. Special tests: * Straight leg raising: pain in <60 deg. a) Bragaard sign: pain increase with

dorsiflxion of foot. b) Crossed leg sign: elevation of the good leg

elicit pain in the other one. * Naffzigar test: pain increases with manual

compression on both jugular veins simultaneously. * Valex test: pain increases upon pressing the

buttocks or the sciatic n.

5. Neurological deficit: * L3/L4 prolepses: 1. Weakness of quadriceps muscle. 2. Diminished sensations over ant. Thigh

& medial aspect of lower leg. 3. Decreased or absent knee jerk. * L4/L5 prolapse: 1. Weak drsiflexion of foot. 2. Parasthesia in lateral foot & small toes. 3. No reflex changes.

* L5/S1 prolapse: 1. Weak planter flexion. 2. Parasthesia in lateral foot &

small toes. 3. Absent ankle jerk.6. Buttocks: Assess for gluteal atrophy,

anal sensation & sphincter function.

L5-S1 prolapsed disc: S1• Pain along the posterior of the thigh, radiating to the

heel.• Occasionally, weakness of the planter flexion.• Sensory loss in the lateral foot.• Absent ankle reflex. L4-L5 prolapsed disc: L5• Pain along the posterior-posterolateral aspect of the

thigh, radiating to the foot dorsum and the great toe.• Weakness of the foot and toe dorsiflexors.• Reflex changes unlikely.• Paraesthesia and numbness of the dorsum of the foot

and the great toe. L3-L4 prolapse: L4• Pain in the ant. Thigh.• Quadriceps wasting.• Weakness of the quadriceps and dorsiflexors of the

foot.• Diminished sensation over the ant thigh, knee and med

aspect of the lower leg.• Reduced knee reflex.

MRI: most commonly used, shows the size, configuration, position of the disc, and any nerve root or thecal compression.

Lumber myelography. (rarely used now)

High quality CT scan (rarely used now)

Magnetic resonance imaging scans of a thirty-two-year-old subject who never had low-back pain or sciatica

BODEN S. D. J Bone Joint Surg 1996:78:114-24

Compression of theacal sac below L1/L2 level causes a sort of lower motor neuron lesion bilaterally.

Symptoms: 1. Leg pain: bilaterally. 2. Parasthesia. 3. Sphincter paralysis: loss of sensation from

urinary bladder, urethral sensation & anal sensation.

4. Sexual disturbance: impotence.

Signs: 1. Sensory loss: saddle sensation. 2. Motor loss: foot drop usually with

complete loss of power in dorsi & plantar flexion of both feet.

3. Absent ankle jerks on both sides.

1) MRI: a) MOST SENSITIVE METHOD. b) Demonstrates disc disease.

2) CT- scan: a) Detects disc protrusion &

demonstrates the extent of n. root compression.

b) Hypertrophy of facet joints. c) Assess diameter of spinal canal

( done also on lateral x-ray).

3) Plain lumbosacral x-ray: a) Narrowing of disc space ( chronic cases) b) Calcification. c) Degenerative change, ostyophytes. d) Scoliosis. e) Loss of lordosis. f) Associated spondilolithaisis.

4) Other methods: Myelogram, post myelogram CT.

DDx. : 1. Referred low back pain. 2. Degenerative disease. 3. Lumber canal stenosis. 4. Spinal tumor. 5. Trauma. 6. Isolated neuropathy. 7. Infectious process. 8. Congenital anomalies.

Site: Most commonly at C5/6> C4/5> C6/7 > C3/4.

Types: 1. Lateral prolapse: presses on

corresponding n. root causing neck pain, parasthesia & radicular pain. Since each cervical spinal root emerges above it’s vertebra, disc prolapse compresses the corresponding n.

2. Central prolapse: Compresses n. root, the spinal cord & the ant. Spinal artery & vein.

Causes: 1. LMNL at the same level. 2. UMNL at the levels below

( Myelopathy): results in spastic gait, loss of fine movement of hand, sphincter affection, loss of superficial abdominal reflexes, increased tone & reflexes in lower limbs & upward planter reflex.

Plain X-ray. Post myelogram CT. MRI (most important ).

Surgical treatment: Posterior approach: if > one level involved or

with diffuse stenosis. Anterior approach: in single level involvement.

Types:1. Congenital: early fusion, thick short pedicles.

2. Acquired: hypertrophied facet joints.

Factors sharing in canal stenosis: 1) Hypertrophy of facet joints. 2) Thickening of ligamentum flavum. 3) Disc bulge.

Narrowing of the lumbar spinal canal.

Verbiest, 1949 Altough lumbar canal

stenosis and lumbar disc prolaps can be found in the same patient,they each produce distinct clinical entity.

According to diameter of the canal: 1. Central stenosis. AP diameter is

normally 12-16 mm. Mild (<12mm). Moderate (<10mm). Severe (<8mm). 2. Lateral recess stenosis: Lat.

Diameter is about 4 mm normally. If it is < 2 mm then it is stenosed.

Levels affected: L4/5> L3/4> L5/S1. Clinical features: 1- Pain: radiating diffusely into the legs,

exacerbated by walking or standing. it may have a burning quality and relieved by setting.

2- the patient often complains of a subjective feeling of weakness and a diffused ‘numbness’ and ‘tingling’ radiating down the limb.

3-sphincter problems may occur in severe stenosis

Physical findings:examination of lower limb and back

often reveals little or no abnormality. but muscular atrophy, depressed ankle jerk, sensory desturbance and weakness may occur only in the most severe cases.

Vascular claudication: 1. Skin changes. 2. More calf pain. 3. Relieved by standing still or

sitting. 4. More on walking upstairs.

5. Peripheral pulses are diminished. 6. Claudication distance decreases.

High quality CT scanning. MRI. (BEST ).

Conservative treatment:The clinical features of LCS do not

respond favorably to conservative treatment.

Surgical Treatment: Wide Lamectomy with root

decompression.

Results & Complications: Improvement in 90 %. Persistent pain in 10 %. Instability. Surgery will improve claudication

distance but may or may not improve pain.

Spondylolisthesis refers to forward displacement of one vertebra over another, usually of the fifth lumbar over the body of the sacrum, or of the fourth lumbar over the fifth.

Spondylolisthesis is graded according to how far the vertebral body moves forward on the one below (Grade 1 = 25%, Grade 2 = 50%, Grade 3 = 75%).

refers to a cleft or break in the pars interarticularis of the vertebra. It is found in about 6% of adults, mostly in males, 93-95% occur at L5, and most are bilateral.

The etiology is uncertain, but the current theory is that it represents a stress fracture from repeated trauma to the spine.

The pars defect divides the vertebra into an anterior part (vertebral body, pedicles, transverse processes, and superior articular facet) and a posterior part (inferior facet, laminae, and spinous process). The anterior part slips forward, leaving the posterior part behind. As a result, the spinal canal elongates in its anteroposterior dimension, so that spinal canal stenosis is uncommon with isthmic spondylolisthesis. Grade I spondylolisthesis is often asymptomatic, but with progressive anterior subluxation, the intervertebral disk and the posterior-superior aspect of the vertebral body below encroach on the superior portion of the neural foramen. The foramen is also elongated in a horizontal direction and may have a bilobed configuration. Exuberant fibrocartilage at the pars pseudarthrosis can further compromise the neural foramen and cause nerve root compression.

Occurs mostly in older age group, usually over 60 years old, and it is more common in women at the level of L4-L5. It develops when there are severe degenerative changes and excess motion of the facet joints. Subluxation at the facet joints allows forward or posterior movement of one vertebra over another. A degenerative spondylolisthesis narrows the spinal canal, and symptoms of spinal stenosis are common. Hypertrophic facet arthrosis is a frequent cause of foraminal narrowing.

Diagnosis: hx (back pain and leg pain, waddling gait, “tight hamstring syndrome”), PhE

Investigations:1-plain lumbar spine X-ray2- MRI to demonstrate the degree

of nerve compression.

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