Cervical Myelopathy Flashcards

1
Q

Definition/Description

A

Cervical myelopathy refers to compression on the cervical spinal cord. Any space-occupying lesion within the cervical spine with the potential to compress the spinal cord can cause cervical myelopathy. Cervical myelopathy is predominantly due to pressure on the anterior spinal cord with ischaemia as a result of deformation of the cord by anterior herniated discs, spondylitic spurs, an ossified posterior longitudinal ligament or spinal stenosis

The spontaneous course of myelopathy is characterised either by long periods of stable disability followed by episodes of deterioration or a linear progressive course. The presentation of a cervical myelopathy varies in accordance with the severity of the spinal cord compression as well as its location

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2
Q

Clinically relevant anatomy

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A complex system of ligaments serves to stabilise and protect the cervical spine. For example, ligamentum flavum extends from the anterior surface of the cephalic vertebra to the posterior surface of the caudal vertebra and connects to the ventral aspect of the facet joint capsules. A ligament that is often involved in this condition is the posterior longitudinal ligament.

It is situated within the vertebral canal, originating from the body of the axis, where it is continuous with the tectorial membrane, and extends along the posterior surfaces of the bodies of the vertebrae until inserting into the sacrum

Chronic cervical degeneration is the most common cause of progressive spinal cord and nerve root compression. Spondylotic changes can result in stenosis of the spinal canal, lateral recess, and foramina. Spinal canal stenosis can lead to myelopathy, whereas the latter two can lead to radiculopathy

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3
Q

Epidemiology

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Cervical spondylotic myelopathy is the most common disorder of the spinal cord in persons older than 55 years of age.Radiologic spondylotic changes increase with patient age - 90% of asymptomatic persons older than 70 years have some form of degenerative change in the cervical spine.

Cervical spine myelopathy resulting from sagittal narrowing of the spinal canal and compression of the spinal cord is present in 90% of individuals by the seventh decade of life.[10] Both sexes are affected equally. Cervical spondylosis usually starts earlier in men (50 years) than in women (60 years). It causes hospitalisation at a rate of 4.04 per 100,000 person-years.

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4
Q

Causes

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Static factors
A narrowing of the spinal canal size commonly results from degenerative changes in the cervical spine anatomy (cervical spondylosis) such as disc degeneration, spondylosis, stenosis, osteophyte formation at the level of facet joints, segmental ossification of the posterior longitudinal ligament and yellow ligament hypertrophy, calcification or ossification. Patients with a congenitally narrow spinal canal (<13mm) have a higher risk for the development of symptomatic cervical myelopathy

Dynamic factors
Due to mechanical abnormalities of the cervical spine or instability.

Vascular and cellular factors
Spinal cord ischemia affects oligodendrocytes, which results in demyelination exhibiting features of chronic degenerative disorders. Glutamatergic toxicity, cell injury and apoptosis may also occur.

Cord compression is thought to be a combination of static compression and intermittent dynamic compression from cervical motion (flexion/extension)

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5
Q

Characteristics and Clinical Presentation

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Cervical myelopathy can cause a variety of signs and symptoms. Onset is insidious, typically in persons aged 50-60 years.

The symptoms usually develop slowly. Because of the lack of pain, there may be an interval of years between the onset of disease and first treatment. Early symptoms of this condition are ‘numb, clumsy, painful hands’ and disturbance of fine motor skills.

Weakness and numbness occur in a non-specific/non-dermatomal pattern. As spinal cord degeneration progresses, lower motor neuron findings in the upper extremities, such as loss of strength, atrophy of the interosseous muscles and difficulty in fine finger movements, may present.

Additional clinical findings may include neck pain and stiffness (decreased ROM, especially extension), shoulder and scapular pain, paresthaesia in one or both arms or hands, signs of radiculopathy, Babinski and Hoffman’s sign, ataxia and dexterity loss.

Typical neurological signs of long-tract involvement are exaggerated tendon reflexes (patellar and Achilles), presence of pathological reflexes (e.g. clonus, Babinski and Hoffman’s sign), spastic quadriplegia, sensory loss and bladder-bowel disturbance.

Once the disorder is diagnosed, complete remission to normality never occurs and spontaneous temporary remission is uncommon. In 75% of the patients, episodic worsening with neurological deterioration occurs, 20% have slow steady progression, and 5% experience rapid onset and progression

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6
Q

Common Symptoms

A

Distal weakness
Decreased ROM in the cervical spine, especially extension.
Clumsy or weak hands
Pain in shoulder or arms
Unsteady or clumsy gait
Increased reflexes in the lower extremities and in the upper extremities below the level of the lesion.
Numbness and paresthesia in one or both hands
Radiculopathic signs

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7
Q

Clinical Examination

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The diagnosis of CSM is primarily based on the clinical signs found on physical examination and is supported by imaging findings. According to Cook et al, selected combinations of the following clinical findings are effective in ruling out and ruling in cervical spine myelopathy. Combinations of three of five or four of five of these tests enable post-test probability of the condition to 94–99%:

gait deviation
\+ve Hoffmann’s test
inverted supinator sign
\+ve Babinski test
age 45 years or older
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