Cervical Spondylotic Myelopathy (11.08.2010)

CERVICAL SPONDYLOTIC CERVICAL SPONDYLOTIC MYELOPATHY MYELOPATHY

Dr. A.S. PattajoshiDr. A.S. PattajoshiPost Doctoral Post Doctoral

Department of Neurosurgery, Department of Neurosurgery, S.C.B. Medical College, CuttackS.C.B. Medical College, Cuttack

Anatomical review of cervical spine : Highly mobile segment of the spinal column. Maintain a gentle lordotic curve at rest. Balance point between flexion and extension

runs through centre of C2 body and odontoid at rest.

Functionally constitute two segment1) Atlantoaxial complex2) Subaxial complex

INTRODUCTIONINTRODUCTION

Joint space are flattened and horizontal with posterior and inferior inclination.

Stability of the cervical spine depends upon ligament structures and paraspinal muscles.

The average spinal canal diameter between C3 & C7 in a normal adult is 17 to 18 mm.

The normal range of movement for - Flexion - 450

- Extension - 540

- Lateral bending - 400

- Rotation - 700

Anatomical review of cervical spine contd…Anatomical review of cervical spine contd…

DefinitionDefinition• Cervical spondylosis is a general term

encompassing a number of degenerative conditions

– Degenerative disc disease (DDD)– Spinal stenosis– With or without degenerative facet joints– With or without the formation of osteophytes– With or without a herniated disc

• One single component as a diagnosis is rare

The beginning of pathogenesis is due to- Accumulation of repeated movement,

stress and strain on the osseo-ligamentous structure.

Genetic factors Developmental factors Most commonly affected motion

segment is C6-C7 followed by C5-C6 and less upon C4-C5.

Pathogenesis of CSMPathogenesis of CSM

Molicular changes and effect on disease process

• Beginning of the spondylosis results in loss of water content and changes in the relationship of the glucose aminoglycansS and other polymers in the disc which leads to loss of volume of the disc and subsequent alteration of biomechanical characteristics.

Pathogenesis contd…Pathogenesis contd…

PathogenesisPathogenesis

• The process is thought to begin in the annulus fibrosus with changes to the structure and chemistry of the concentric layers

• Over time, these layers suffer a loss of water content and proteoglycan, which changes the disc’s mechanical properties, making it less resilient to stress and strain.

Changes in the disc initiate the cascade of changes in cervical spondylosis.

Degeneration of the facets and ligaments and reactive bony changes follow the primary discogenic pathology.


Mechanism of Canal Narrowing :

Spondylotic change begin at one level

Degeneration of disc

Segmental flexion deformity at the level

Abnormal movement at the level

Reactive spur formation Hypertrophy of lig flavum Facet hypertrophy

Anterior encroachment Posterior encroachment

SPINAL CANAL STENOSIS


OsteophytesOsteophytes

Mechanism of Progression of the diseaseBeginning of the pathogenesis at lower level C5/6, 6/7

Fusion of joint space & Motion at the level

More and more stress Laxity of the annulus

at higher level & the longitudinal ligaments

change in character of movement transmission of altered

dynamics of motion through the pedicles to facet joints leading to facet joint degeneration.

Retro / anterolisthesis

Progression of degeneration


Other variety of cervical spondylosis OPLL – ossified posterior longitudinal ligament DISH – diffuse idiopathic skeletal hypertrophy In OPLL – there occurs preferential

accumulation of calcium in the posterior longitudinal ligaments which extends vertically for a variable distance.

In DISH – there occurs exuberant accumulation of anterior osteophytes and calcification along the vertebral bodies.

Pathogenesis Contd…Pathogenesis Contd…

Clark, Robinson/1956/120 patients Neurological examinations did not return to

normal after patient became symptomatic. Motor changes tend to persist Sensory & sphinctor changes tend to be

transient. Slow/steady progression in 20%. Rapid onset of symptoms with lengthy period

of stability – 5%. Slow & steady progression punctuated by new

episode – 50%. Stabilised between episodes – 25%.

Natural history Natural history

Symon & Lavender in 1963, 2 gr. of pts. Myelopathy with stenosis Stenosis without myelopathy 1st gr.- Initial episode followed by a period of

neurological stability or improvement.> 10 yrs history – episodic deterioration with progressive deficit followed by period of stabilisation or improvement. No steadily progressive deterioration.

2nd gr. - Did not develop symptoms.

Natural history contd…Natural history contd…

Lees & Turners statement : It was a generally benign disorder. In which

disability develops in an initial phase & later remains static except in older patients in whom it may progress.

Symon & Lavendor 1967 : 67% had a steadily progressive course

challenging the motion that the disease is episodic in nature with a relatively benevolent course.


Phillips (1973) : Patient symptomatic < 1 yr 50% improve

with collar. Patient symptomatic 1-2 yr 40% improve Patient symptomatic > 2 yr No improvement


Depends upon Clinical level Degree of compression Number of levels involvedPrincipal clinical symptoms are Decrease range of motion Pain Neurological deficits

Clinical ManifestationClinical Manifestation

Pathogenesis of decrease range of motion Decrease volume of the disc Accumulation of osteophytes Change in consistency of the ligamentous

and capsular structures. Ankilosis of the phacet joint

Clinical Manifestation contd…Clinical Manifestation contd…

Pathogenesis of pain : Inflammation and reaction to the

osseoligamentous change. Irritation or compression of nerve roots or

dural structures. Compression results from - disc herniation- onco-vertebral joint hypertrophy- foraminal stenosis from facet hypertrophy.


Character of the pain : Radicular or non-radicular Axial or apendicular in distribution Axial and proximal non-radicular pain are

consequence of degenerative changes causing biomechanical strain of ossioligamentous structure, inflammation and muscle fatigue.

The axial pains is typically in the posterior cervical region which can extend cephalad to the sub-occipital and occipital parietal region.

Pain can radiate to the interscapular and scapular regions. Can lateralise to suprascapular and trapizious proximal arm and anterior chest region.


Due to radiculopathy or myelopathyPathogenesis of Myelopathy Direct compression of the cord by the

prolapse disc. Ischaemic injury secondary to vascular

disease. Repetitive spinal cord microtrauma

associated with neck movements.

Pathogenesis of Neurological Pathogenesis of Neurological deficitdeficit

Spinal canal compromiseSpinal canal compromiseStatic factors

• Intervertebral disc bulging• Dorsal vertebral body osteophytes• OPLL• Uncovertebral & facet joint

hypertrophy• Ligamentum flavum & facet joint

capsule laxity & infolding

Spinal canal compromiseSpinal canal compromiseDynamic factors

• Flexion compresses spinal cord against protruded disc & osteophytes

• Extension narrows spinal canal by buckling of ligamentum flavum & facet joint capsule

• Extension shortens & thickens spinal cord making it more susceptible to compression

Gait abnormality (broad based, stooped, hesitant).

Hand symptoms Urgency Neck pain

Gait abnormality pre date upper ext. symptoms.Bowel incontinents is relatively there.

Usual mode of presentationUsual mode of presentation

Lower motor neuron findings at the level of prolapse.

UMN findings below the level. Lhermitti sign Increase DTR Impaired propriation Slow, stiff opening and closing of hands Weakness & atrophy if disease is long

standing. Spasticity

Neurological findingsNeurological findings

Myelopathy hand (spastic dysfunction, deficient pain sensation).

Amyotrophic myelopathic hand (atrophy of intrinsic, extrinsic muscles, mild or no sensory disturbance, extension of finger weakness).

Numb & clumsy hand ( proprioception vibration, minimal motor findings little sensory deficits).

Hand findings in cervical Hand findings in cervical myelopathymyelopathy

Transverse lesion syndrome(Corticospinal spinothalamic dorsal column) Most frequent type Spasticity severe Frequent sphinctor involvement Represent end stage of disease

Syndrome related to Syndrome related to cervical spondylosiscervical spondylosis

Motor System Syndrome(Corticospinal, anterior horncell) No sensory impairment Severe spasticity in 75%

Central cord syndrome Useless hand Painful parasthesia or dysesthesia Lhermitte’s sign in 50%

Syndrome related to cervical Syndrome related to cervical spondylosis Contd…spondylosis Contd…

Brown Sequired Syndrome Ipsilateral corticospinal tract Contralateral spinothalamic tract

Brachialgia & Cord Syndrome Upper limb pain Long tract involvement

Syndrome related to cervical Syndrome related to cervical spondylosis Contd…spondylosis Contd…

Symptoms and physical findings in CSM are shared with many diseases.

Asymptomatic cervical spondylosis is very common for which detailed clinical examination is needed to exclude other differential diagnosis.

Differential diagnosisDifferential diagnosis

Entrapment peripheral neuropathy Lung apex tumor Thoracic outlet syndrome Multiple sclerosis Amyotrophic lateral sclerosis SACD Chiari malformation Vertibrobasilar insufficiency

Differential diagnosis contd…Differential diagnosis contd…

X-ray of cervical spine : Lateral view – to access spinal canal

diameter. Oblique view – for foraminal stenosis Flexion extension view – to see gross

instabilityCT : Direct measurement of the canal diameter CT myelo gives information about

Intervertebral foramen, nerve root impimgement, compression of thecal sac.

Imaging and Imaging and investigations in CSMinvestigations in CSM

MRI : Superior soft tissue imaging. Helps excluding other causes of myelopathy. Gives detail information of osseoligamentus

structure of the spine. Extent of disc desication presence of

reactive changes in end plates. Accumulation of fluid in the facet joints are

clearly seen in MRI study.

Imaging and investigations in Imaging and investigations in CSM Contd…CSM Contd…

MRI contd… The area of increased T2 signal in the spinal

cord at the area of greatest compression represents – odema, inflammation, gliosis, vascular ischaemia, myelomalacia.

Surgical outcome is not good in patients who exhibit T2 hyperintensity.


Electrophysiological study : Helps differentiating CSM from

peripheral entrapment neuropathy, brachial plexus abnormality or a radiculopathy.


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Cervical Spondylotic Myelopathy (11.08.2010)