Disorders of the cervical spine Flashcards

1
Q

What is cervical spondylosis?

A

Cervical spondylosis is a chronic degenerative osteoarthritis affecting the intervertebral joints in the cervical spine.

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2
Q

How does cervical spondylosis occur?

A

The primary pathology is usually age-
related disc degeneration, which is followed by marginal osteophytosis (osteophyte formation adjacent to the end plates of the vertebral bodies) and facet joint osteoarthritis.

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3
Q

How does cervical spondylosis lead to radiculopathy?

A

The resultant narrowing of the intervertebral foramina can put pressure on the spinal nerves leading to radiculopathy. Symptoms of radiculopathy include dermatomal sensory symptoms (e.g. paraesthesia, pain), and myotomal motor weakness.

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4
Q

How does cervical spondylosis lead to myelopathy?

A

If the degenerative process leads to narrowing of the spinal canal, this may instead put pressure on the spinal cord leading to myelopathy. This is a less common outcome than radiculopathy, and may manifest as global muscle weakness, gait dysfunction, loss of balance and/or loss of bowel and bladder control. These symptoms arise due to compression and dysfunction of the ascending and descending tracts within the spinal cord.

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5
Q

What is a Jefferson’s fracture?

A

A fracture of the anterior and posterior arches of the atlas vertebra (C1).

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6
Q

How does a Jefferson’s fracture present?

A

The fracture causes the C1 vertebra to burst open like a broken Polo mint.

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7
Q

What is the mechanism of injury of a Jefferson’s fracture?

A

The mechanism of injury is axial loading e.g. diving into shallow water,
impacting the head against the roof of a vehicle, or falling from playground
equipment. Patients may present to the Emergency Department supporting their head with their hands.

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8
Q

What does a Jefferson’s fracture lead to?

A

Fortunately, the ‘bursting open’ of the bone fragments reduces the likelihood of impingement on the spinal cord. This fracture therefore typically causes pain but no neurological signs.
Occasionally, however, there may be damage to the arteries at the base of the skull leading to secondary neurological sequelae e.g. ataxia, stroke, or Horner’s syndrome.

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9
Q

What is Horner’s syndrome?

A

Horner’s syndrome is damage to the sympathetic trunk leading to miosis
(decreased pupil size), partial ptosis (drooping eyelid), anhidrosis (decreased sweating on the affected side of the face) and enophthalmos (sunken appearance of the eyeball).

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10
Q

What is a Hangman’s fracture?

A

The axis vertebra (C2) is fractured through the pars interarticularis (the region between the superior and inferior articular processes).

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11
Q

What is the mechanism of injury of a Hangman’s fracture?

A

The mechanism of injury is usually
forcible hyperextension of the head on
the neck; historically by ‘hanging’ and
more recently in road traffic collisions.
This fracture is unstable and requires
treatment. Similar to a Jefferson’s fractures of the C1 vertebra, the fracture configuration tends to expand the spinal canal, thereby reducing the risk of an associated spinal cord injury.

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12
Q

How are fractures of the odontoid process caused?

A

They can be caused by either flexion
or extension injuries. The most commonly seen mechanism is an elderly patient with osteoporosis falling forwards and impacting their forehead on the pavement. This hyperextension injury of the cervical spine can result in a fracture of the odontoid peg. Alternatively, sometimes these fractures are caused by a blow to the back of the head resulting in a hyperflexion injury e.g. falling against a wall when balance is compromised (such as when intoxicated).

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13
Q

What is whiplash injury?

A

A forceful hyperextension-hyperflexion injury of the cervical spine. The cervical spin has high mobility and low stability (as they are inversely related in joints), making it very prone to whiplash.

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14
Q

What is the classical mechanics of a whiplash injury?

A

The classical mechanism is the patient’s car being struck from the rear leading to an acceleration-deceleration injury as follows:
* At the time of impact, the vehicle suddenly accelerates forward. About 100ms later, the patient’s trunk and shoulders follow, induced by a similar
acceleration of the car seat.
* The patient’s head, with no force acting on it, remains static in space. The result is forced extension of the neck, as the shoulders travel anteriorly under the head. With this extension, the inertia of the head is overcome, and the head then accelerates forward.
* The neck then acts as a lever to increase forward acceleration of the head, forcing the neck into flexion.
* The hyperextension followed by hyperflexion leads to tearing of cervical
muscles and ligaments. Secondary oedema, haemorrhage and inflammation may occur. The muscles respond to injury by contraction (spasm), with surrounding muscles being recruited in an attempt to splint the injured muscle. This spasm causes pain and stiffness.

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15
Q

What will a patient with whiplash injury complain of?

A

Patients may complain of arm
pain and paraesthesia as a result of injury to the spinal nerves during the whiplash movement of the cervical spine. Patients may also develop shoulder injuries due to holding the steering wheel at the time of collision. Lower back pain also develops acutely in 40-50% of patients with acute whiplash.

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16
Q

What can develop secondary to whiplash injury and why?

A

Chronic myofascial pain syndrome can sometimes develop as a secondary tissue response to disc or facet-joint injury. There is a surprisingly high prevalence of chronic pain that results from whiplash injury, although secondary gain (e.g. financial compensation) may lead to prolongation of symptoms in a number of patients.

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17
Q

Why can there be injury to the cervical cord in a whiplash injury?

A

Sometimes whiplash can result in injury to the cervical cord, despite there being no accompanying bony fracture. The cervical spine is highly mobile and the ligaments and capsule of the joints are weak and loose. Hence, there can be significant movement of the vertebrae (e.g. subluxation or dislocation) at the
time of impact, with return to the normal anatomical position afterwards. Soft tissue swelling may be the only visible feature on imaging.

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18
Q

What is a protective factor against spinal cord injury?

A

A protective factor against spinal cord injury is that the vertebral foramen is large relative to the diameter of the cord. The normal diameter of the cervical spinal canal is 17-18 mm. The average diameter of the spinal cord in the cervical region is 10mm.

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19
Q

Who are cervical disc prolapses most common in?

A

Cervical disc prolapse with associated compression of nerve roots or spinal cord most commonly develops in the 30 to 50 year-old age group.

20
Q

What is the mechanism of a cervical intervertebral disc prolapse?

A

A tear develops in the annulus fibrosus of the disc, and the nucleus pulposus protrudes from the disc, with impingement onto an adjacent nerve root or the spinal cord. Sometimes sequestration occurs in which an extruded segment of nucleus pulposus separates from the main body of the disc and enters the spinal canal where it is ultimately resorbed over a period of weeks, with resolution of symptoms.

21
Q

What is different about the intervertebral discs in the cervical spine compared to the lumbar spine?

A

The discs in the cervical spine are not very large. However, there is also little space available for the exiting nerves (unlike in the lumbar spine) so even a small cervical disc herniation may impinge on the nerve and cause significant pain.

22
Q

How are cervical intervertebral disc prolapse?

A

Cervical intervertebral disc prolapse may be spontaneous in origin or may be related to trauma and neck injury.

23
Q

What are the symptoms associated with cervical intervertebral disc prolapse?

A

Symptoms are dependent on the site of the prolapse. Paracentral prolapse may impinge on a spinal nerve leading to radiculopathy whereas a canal-filling
prolapse may lead to acute spinal cord
compression.

24
Q

In the cervical spine, which root is compressed in a disc herniation?

A

The exiting nerve root (there is no traversing nerve root)

25
Q

What is cervical myopathy?

A

Cervical myelopathy is spinal cord dysfunction due to compression of the cord. It is caused by narrowing of the spinal (vertebral) canal.

26
Q

What causes cervical myelopathy?

A

A common cause is degenerative stenosis of the spinal canal caused by cervical spondylosis (degenerative osteoarthritis). This most commonly
affects 50 – 80 year olds. ‘Cervical spondylotic myelopathy’ (i.e. myelopathy secondary to cervical spondylosis) is the result of degenerative changes which
develop with age, including ligamentum flavum hypertrophy or buckling, facet joint hypertrophy, disc protrusion and osteophyte formation. One or all of these changes contribute to an overall reduction in canal diameter which may result in cord compression.

27
Q

What are other causes of cervical myelopathy?

A

Other causes of cervical myelopathy include congenital stenosis of the spinal canal (which is often asymptomatic until adulthood when age-related secondary degeneration starts to occur), cervical disc herniation, spondylolisthesis, trauma, tumour
and rheumatoid arthritis affecting the cervical spine.

28
Q

When does a patient start to experience symptoms associated with cervical myelopathy?

A

The symptoms are due to compression of the long tracts in the spinal cord. The normal diameter of the cervical spinal canal is 17-18 mm. The average diameter of the spinal cord in the cervical region is 10mm. When the diameter of the spinal canal falls below
12-14mm, myelopathic symptoms may be experienced.

29
Q

What is the classical presentation of cervical myopathy?

A

The classical presentation is loss of balance with poor coordination, decreased dexterity, weakness, numbness and in severe cases paralysis. Pain is a symptom in
many patients but it is important to remember that it may be absent; the absence of pain often leads to a delay in diagnosis. In older patients, cervical myelopathy often manifests with a rapid deterioration of gait and hand function.

30
Q

What do upper cervical lesions lead to?

A

Upper cervical lesions tend to cause a loss of manual dexterity with difficulties in writing and nonspecific alteration in arm weakness and sensation. Patients may demonstrate dysdiadochokinesia - impaired ability to perform rapid alternating
movements.

31
Q

What do lower cervical lesion lead to?

A

Lower cervical lesions tend to lead to spasticity [increased muscle tone, sometimes with clonus] and loss of proprioception in the legs. Patients commonly say that their legs ‘feel heavy’ and experience reduced exercise tolerance. They typically have gait disturbance and may suffer multiple falls.

32
Q

What are the signs of an exaggerated response to stimulation and how do they occur?

A

Normally the signals in the long tracts dampen the spinal reflexes, so a person does not overreact to stimuli. When the long tracts become damaged, however, these protective capabilities are less effective, and the patient may demonstrate an exaggerated response to stimulation, as seen in a positive Hoffman’s or Babinski sign.

33
Q

What is the Hoffman’s test?

A

The doctor holds the patient’s
middle finger at the middle phalanx and flicks the finger nail. If there is no movement in the index finger or thumb after this motion, the patient has a negative Hoffman’s sign (normal). If the index finger and thumb move, the patient has a positive Hoffman’s sign (abnormal).

34
Q

What is the Babinski sign?

A

The lateral side of the sole of the foot is stroked with a blunt instrument from the heel towards the toes. Normally in children over the age of approximately 2-3 years and adults, the response is flexor in that the toes flex downwards towards the sole (plantarflex). In a positive (abnormal) Babinski sign, the hallux dorsiflexes and the toes fan out. This suggests damage to the long tracts of the spinal cord.

35
Q

What is L’Hermitte’s phenomenon?

A

The sensation of intermittent electric shocks in the limbs, exacerbated by neck flexion. It is classically associated with cervical myelopathy.

36
Q

What can occur in cervical myelopathy if the compression is severe?

A

Late in the disease, when compression is severe, if surgical decompression is not performed the symptoms may progress to sphincter dysfunction and quadriplegia (paralysis of all four limbs)

37
Q

A patient develops myelopathy of the cervical spine at the level of C5 (with a C4 neural level – the lowest intact level of sensation and function), what do the likely symptoms and signs will include:

A

Pain: Neck pain
Motor weakness: Weakness of shoulder abduction and external (lateral) rotation (C5) and weakness of all myotomes distally, including the trunk and the lower limbs
Sensory: Paraesthesia from the shoulder (C5 dermatome) distally, trunk and lower limbs.

38
Q

What the most common causes of thoracic cord compression?

A

Vertebral fractures (with bony
fragments in the spinal canal) and tumours in the spinal canal.

39
Q

Why are metastases to the thoracic spine very common?

A

The incidence of any cancer during a
person’s lifetime is 1 in 2. 50-60% of patients with cancer will have skeletal metastases at death and the spine is the second most common site for skeletal metastases (most common = pelvis).

40
Q

What are the symptoms of thoracic cord compression?

A

Symptoms of spinal cord compression
from this metastasis would therefore
include pain at the site of the lesion
(thoracic spine), spastic paralysis of all of the muscles in the legs, paraesthesia in the dermatomes distal to the site of
cord compression (i.e. from a few
centimetres below the umbilicus
distally), and loss of sphincter control.

41
Q

If the tumour was at T5, how would the presentation change?

A

In addition to the symptoms above, there would be weakness of the intercostal muscles from the 5th intercostal space distally, leading to reduced chest expansion on inspiration and the patients predominantly relying on diaphragmatic breathing (phrenic nerve C3,4,5). The distribution of the paraesthesia would be from just below the nipples distally. [The patient would also still exhibit weakness of all the
muscles in their legs and loss of sphincter control.]

42
Q

What are the three ways pathogens can reach the bones and tissues of the spine?

A
  • Haematogenous
  • Direct inoculation during invasive spinal procedures (e.g. lumbar puncture, epidural or spinal anaesthesia)
  • Spread from adjacent soft tissue infection
43
Q

How does haematogenous spread occur?

A

Haematogenous spread from a septic focus elsewhere in the body is the most common route and typically occurs via the arterial supply to the vertebral bodies, but can also occur through retrograde (backwards) venous flow.

44
Q

What is infection of the intervertebral disc called?

A

Spondylodiscitis or disci tis

45
Q

Who is spondylodiscitis most common in?

A

It most commonly occurs in immunocompromised patients e.g. those with diabetes, HIV and patients on steroids. In adults, the intervertebral disc is avascular and it is thought that organisms are therefore initially deposited in the vertebral body, via its segmental artery, leading to bony ischaemia and infarction. Necrosis of the bone then allows direct spread of organisms into the adjacent disc space, epidural space and
adjacent vertebral bodies.

46
Q

Spread of infection into the spinal canal can lead to neurological damage, what are the mechanisms via which this occurs?

A
  • Septic thrombosis leading to ischaemia
  • Compression of neural elements by abscess / inflammatory tissue
  • Direct invasion of neural elements by inflammatory tissue
  • Mechanical collapse of bone leading to instability, particularly in chronic
    infections