Intro cervical spine I



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Anatomy

The cervical vertebrae are the smallest of the moveable vertebrae. The 1st, 2nd and 7th have special features and will be considered separately.


The typical cervical vertebra runs from C3 to C6. It has a small but relatively broad body. The body’s anterior surface is convex transversely. The cranial surface of the body is concave transversely, convex A-P, with marked bilateral lips. The inferior surface is convex transversely and concave A-P.
Uncinate processes grow upwards from the upper aspects of the lateral parts of each vertebra (C3 to T1). Between its tip and the lower lateral surface of the vertebral body above they form the uncovertebral joints. The uncovertebral joints are present from C2-3-C7-T1. The most prominent uncinate process is found at C2-3. They start to develop at 6-9 years and are fully developed at 18 years. The medial border is formed by the disc, the lateral border by ligaments. The joint surfaces are covered with hyaline cartilage. The uncovertebral joints enhance the stability of the cervical spine. They act as a “rail” to guide flexion and extension. It limits sidebending. They are frequently affected by spondylotic changes.
The vertebral foramen is large and roughly triangular. The laminae are long and narrow.

The spinous processes are short and bifid, with the terminal tubercles often unequal in size. The transverse processes face lateral, anterior and inferior. They have a gutter on top, through which the nerve root runs. Each cervical vertebra has a transverse foramen through which the vertebral artery runs.

The superior and inferior articular processes form (when articulated), the articular pillar. The superior articular facet faces posterior and cranial, the inferior articular facet faces anterior and caudal.

The atlas


It is unique in that it lacks a body. It is a bony ring, made up of 2 lateral masses connected by a short anterior and a longer posterior arch. The anterior arch is slightly convex. The anterior tubercle serves as an attachment for the ALL. On the posterior side of the anterior arch is a small facet where the dens articulates with C1. The posterior tubercle is a rudimentary spinous process functioning as an attachment for the ligamentum nuchae. The transverse processes are very long, up to 90 mm. in males. The superior articular facets are concave and face in a medial, cranial direction. The inferior articular facets are convex and face medial and caudal.


Axis


C2 is a transitional vertebra. The dens projects vertically. It functions as an axis for C1-2 rotation. The transverse processes are small and blunt at their tips with single tubercles. The spinous processes are still bifid. The superior articular facets are concave in their bony configuration, but covered with cartilage, they are convex. The inferior articular facets are like in the mid cervical spine, facing anterior and caudal.

C7


C7 is a transitional vertebra as well, connecting the mobile cervical spine with the much more stable thoracic spine. It has a long spinous processes (although T1 is usually just as prominent), with a single tubercle at its end.

Disc


The cervical disc should not be regarded as a smaller version of the lumbar disc. It has less soft nuclear material, and the nucleus only really exists in childhood and young adulthood. By 40 years of age, there is no gelatinous nucleus anymore; rather the central region of the disc is composed of fibrocartilage. Therefore, nuclear prolapse is less likely, except in severe traumatic incidents. The annulus fibrosis is not a ring-like structure of lamellae. Rather, it is a discontinuous structure, which is made up of 2 distinct portions. The anterior annulus is crescent shaped and runs between the uncinate processes. It is well developed and thick at the midline, tapering as it approaches the anterior margin of the uncinate processes. The posterior annulus is a small structure represented by a few vertically oriented fibers located close to the median plane at the posterior aspect of the disc. It is thin, not more than 1 mm in depth. The posterolateral aspect of the disc therefore lacks the support of the annulus fibrosis.

Horizontal fissures or clefts begin developing between 9-14 years of age, until they completely transect the posterior two-thirds of the disc. This is considered to be normal anatomy of a cervical disc, which together with the absence of a substantial posterior annulus, facilitate axial rotation. The cervical disc bears less weight then the lumbar disc. As a degenerative phenomenon, lumbar discs usually herniate posterolateral. For the fissured cervical annulus it’s more common to show a generalized bar-like, posterior bulge.



Vertebral artery


The vertebral artery arises from the first part of the subclavian artery and passes upward on the longus colli to enter the foramen transversarium of C6. Occasionally it may enter the bone at the 5th, 4th or 7th cervical transverse foramen. It then ascends from C6 to C1. After emerging through the transverse foramen of C1, it winds around the articular pillar and together with the 1st cervical nerve and veins pierces the posterior atlanto-occipital membrane to enter the cranium through the foramen magnum. On the anterior side of the brainstem it joins its fellow to form the basilar artery. The vertebral arteries contribute about 11 percent of the total cerebral blood flow, the remaining 89 percent being supplied by the carotid system.
Ligaments cervical spine
Atlanto occipital joint ligaments
Joint capsule

Thin and loose. Surrounds the condyles of the occipital bones, connects them with the articular processes of the atlas.


Anterior atlanto occipital membrane

Connects the anterior part of the foramen magnum to the anterior arch of C1. It is thought to be a continuation of the ALL. May provide some A-P stability when both anterior and posterior A-O membranes are intact.


Posterior atlanto occipital membrane

Connects the posterior ring of C1 to the occiput at the foramen magnum. Broad and thin.

The anterior and posterior membranes prevent anterior and vertical displacement of C1 and C2.
Ligaments connecting C2 with occiput
Tectorial membrane

Continuation of PLL. Runs from the body of C2 up over the posterior portion of the dens and then makes a 45-degree angle in the anterior direction as it attaches to the anterior edge of the foramen magnum. It limits flexion, extension and vertical translation. Unable to prevent any anterior dislocation.


Alar ligament

A pair of ligaments attached to the dorsolateral surfaces of the tip of the dens. Each runs obliquely to the medial surfaces of the occipital condyles. They primarily limit rotation. The left one limits rotation of C1 and the head to the right, and vice versa.


Apical ligament

Connects the apex of the dens to the anterior edge of the foramen magnum. It is a fairly strong structure of elastic consistency. It contributes little to upper cervical spine stability.


Ligaments of the atlanto axial joint
Anterior atlanto axial membrane

Connects C1 to C2 anteriorly. Strengthened at mid line by a rounded cord


Posterior atlanto axial ligament

Broad thin membrane. Attaches to the posterior ring of the atlas and the axis. The posterior A- O and A-A membrane are anatomically analogous to the yellow ligament. However they are considerably different in physical properties. The yellow ligament is first present between C2-3. If present higher up, the highly elastic but still rather stiff yellow ligament would never allow the considerable amount of rotation currently present in the upper cervical spine (80 degrees). So stability is sacrificed for ROM.



Cruciate ligament

The major portion of this ligament is the transverse ligament, which is the most important ligament in the upper cervical spine. There is an ascending and a descending part, which are triangular shaped. The ascending portion attaches to the anterior edge of the foramen magnum, the descending part attaches to the body of C2. They are 3-4 mm thick. The ascending and descending part have little importance in controlling physiological motion, but they do check inferior/superior displacement of the transverse ligament.


Transverse ligament

Most important ligament in upper cervical spine, it is the number one stabilizer. It’s 7-8 mm thick. It attaches on the medial surface of the lateral mass of the atlas. It keeps the dens in contact with the anterior arch of C1. Anterior dislocation of C1 on C2 can only occur with insufficiency of the transverse ligament.


Remaining cervical spine ligaments
Nuchal ligament

Distinct band that runs from the posterior border of the occiput to the SP of C7. Anteriorly it attaches to the SP’s of the cervical vertebrae and the interspinous ligaments. Its precise role has not been identified yet. It may play an important role in the clinical biomechanics of the neck. One hypothesis is that it plays a major proprioceptive role in the functioning of the erector spinae muscles. Another hypothesis is that it provides A-P stability at C1-4 due to specific fiber attachment.


Anterior longitudinal ligament

Continuation of the ligament that runs the entire length of the spine. Well developed in the thoracic and lumbar regions. Described as a thin, translucent structure in the cervical spine. Little is known about the mechanical properties of this structure in this region of the spine.


Anatomic considerations regarding upper cervical spine stability

The O - A joint is relatively unstable. The anatomical structures providing stability are the cup shaped joints and the capsules, along with the A-O membranes. The role of the ligamentum nuchae as a stabilizer is controversial. Additional stability is gained from the tectorial membrane, the alar and apical ligaments. Dislocations of this joint are usually fatal. At C1 - 2 the facet joints are bi convex and are held together by a loose capsule designed to permit a large range of motion. Consequently, joint congruency and the joint capsules contribute little to the stability of the joint. The mechanical stability is provided through the dens and the ring formed by the anatomic structures surrounding it. These consist of the bony portion of the dens anteriorly and laterally and the transverse ligament posteriorly. All the other anatomic structures play a secondary role in the stability of this joint.

Reference


  • Mercer, Sue. Comparative anatomy of the spinal disc. Grieve’s modern manual therapy, 3rd edition. Elsevier, 2004

  • Williams P, editor. Gray’s Anatomy, 38th edition 1998. Churchill Livingstone, London.


Palpation
External occipital protuberance

Bony prominence at the middle of the occiput. Easily palpable and its size varies greatly. From here the lateral bony ridge of the occiput (linea nuchae) can be felt.



Mastoid processes

Lies beind the ear at each side of the occiput. Insertion of the SCM.



C1 transverse process

Can be palpated 1cm distal and slightly anterior to the mastoid process.



Styloid processes

Palpable right below the earlobe, between the mastoid process and the angle of the mandible. Normally very tender on palpation, so be gentle.



Transverse processes

Palpable in the lateral neck region. Located more anterior than what you would expect. Place your palpating fingers in the lateral neck region, just in front of the trapezius, and exert pressure in a medial direction.



Spinous processes C 2 - C 7

C1 does not have a spinous process. The first SP is C2. The C3-5 SP’s are difficult to palpate. C6-7 are easy to palpate. The latter two can be identified during neck extension: the SP of C6 “disappears”. It is often said that C7 has the most prominent SP, but often T1 can be more prominent. So don’t use the “most prominent SP” argument as the only reference point in identifying C7 SP.



Articular pillar

Start by palpating the SP of C2. Move one fingerswidth laterally. Gently palpate in a cranial/caudal direction, and you should feel “peaks and valleys”. The peaks are the facet joints.


Longus colli

Attaches to the anterior surface of the vertebrae from C 1 - T 3. Three - layered muscle. In the upper cervical area, start your palpation on the medial side of the SCM, in the mid/lower cervical are, start lateral from the SCM and deflect the muscle as you move medially. Be gentle when palpating the longus colli. Make sure not to compress the carotid artery when palpating. You need to palpate the muscle more medially than what you would expect at first.



Scalenus musculature

Palpable in the lateral cervical area between the upper trapezius and the SCM



First rib

Reference



  • Winkel, D. Diagnosis and Treatment of the Spine. Aspen Publishers, Gaithersburg MD 1996








Biomechanics and arthrokinematics
Approximate ROM for the Cervical Spine
Data are compiled from multiple sources. Because of the large range and variability in the data presented in the literature, the actual values listed in this table are more useful for appreciating the relative kinematics among joints, and less as a strict objective guide for evaluating movement in patients.


Joint

Flexion and Extension

Rotation

Sidebending

C0-C1

Flexion 5

Extension 10



Minimal, conjunct

5

C1-2

Flexion 5

Extension 10



35-40

0

C2-7

Flexion 35-40

Extension 55-60



30-35

30-35

Total C- Spine

Flexion 45-50

Extension 75-80



65-75

35-40

The upper cervical joints allow the head to move on the neck. The mid cervical joints position the head in space.


Coupling
Sidebending and rotation are coupled opposite in C 0 - C 1. In the mid cervical spine they are coupled to the same side.
C0 - C1

The articular surfaces of the occipital condyles are bi-convex. The superior articular surfaces of C 1 are bi - concave and face superior and medial. The long axes of the superior facets of the atlas converge anteriorly.


The joint has 2 degrees of freedom: flexion/extension in the sagittal plane and sidebending in the frontal plane. Rotation is conjunct to the opposite side of sidebending.
During flexion, both convex occipital condyles glide in the opposite direction of the movement of the occiput (posterior).
During extension, both occipital condyles glide in the opposite direction of the movement of the occiput (anterior).
During right side bending, the right C 0 moves in medial / inferior / anterior direction. The left C 0 moves in lateral / posterior / superior direction. This creates a conjunct left rotation at this level as well.
MIA has nice LPS “

C 1 - 2


The inferior articular facets of C 1 are convex, as are the superior articular facets of C 2. Due to this shape, no side bending is possible. Rotation is the main movement, while flexion / extension is fairly minor. The axis of movement during rotation of C 0 - 2 is through the dens.
A synovial joint is present between the posterior surface of the anterior arch at atlas and the anterior surface of the dens. There is also an articulation between the posterior surface of the dens and the anterior surface of the transverse ligament.
On right rotation, the right facet of C1 glides in posterior direction. The left facet glides in anterior direction. On left rotation, the opposite occurs.

During flexion, both facet surfaces of C1 roll anterior and glide posterior. The anterior arch of C1 glides in a caudal direction on the anterior surface of the dens. During extension, the opposite occurs.



C 2 - 3


C 2 is a transitional vertebra. The superior articular joint surfaces are part of the upper cervical spine, whereas the lower articular surfaces are of the mid - cervical variety.

C 2 - C 7


The articular surfaces of the superior articular facet are slightly convex and face cranial and posterior. The articular surfaces of the inferior articular facet are slightly concave and face caudal and anterior. The facet orientation in the mid cervical spine is approximately 45 degrees to the horizontal.
Flexion: the facets move up and forward

Extension: the facets move down and back

Sidebending: during right sidebending, the right facet moves down and back, the left facet up and forward.

Rotation: during right rotation, the right facet moves down and back, the left up and forward.
References

  • White AA, Panjabi MM. Clinical Biomechanics of the Spine, 2nd edition. Philadelphia, 1990, Lippincott

  • Neuman D. Kinesiology of the musculoskeletal system, 2nd edition. 2010. Mosby Elsevier

Differential Diagnosis
Fractures

Taking patients on referral even if they have been X rayed is no guarantee that there is not a fracture present. The problem is of course compounded in a direct access environment. Apart from direct trauma, there is the possibility of stress- and pathological fractures. The clinical recognition of a fracture can be very difficult and great care must be taken with patients with complaints of deep sharp pain. Among some of the clinical indicators of a fracture are the following:



  • Trauma

  • Immediate posttraumatic onset of severe pain

  • Cracking noise at time of injury

  • Posttraumatic hemarthrosis

  • Crepitus

  • Strong multidirectional spasm

  • Severe pain on compression

  • Bone tenderness

  • Pain on vibration

  • Painful weakness on isometric testing

  • Severe bruising

  • Loss of normal contour

Is there an evidence based way to determine if a patient needs a radiograph? The Canadian cervical spine CPR (JAMA 2001) helps to determine if the patient actually needs radiography.

1. Does the patient display any high risk factors that mandate radiography?


  • Patient age>65

  • Dangerous injury mechanisms: fall from > 1 meter or 5 stairs; axial load to the head; MVA >100km/hr; bike collision.

  • Paresthesiae in the extremities

2. If that is the case, radiographs are warranted. If this is not present, proceed to ROM testing. Keep in mind the following low risk factors:

  • Simple rear end MVA

  • Delayed onset of neck pain

  • Absence of midline C spine tenderness

  • Patient is ambulatory

  • Patient is able to sit in the waiting room

If that is not the case, radiographs are warranted. If this is the case though, proceed to seated ROM testing.

3. Is the patient able to actively rotate the head 45 degrees to the left and to the right? If that is not the case, radiographs are warranted.




Cervical Spinal Stenosis

Prevalence of neck pain increases in a linear fashion from age 20-60

Spondylosis, DJD is seen in 10% of 25 yrs old, and 95% of 65 yrs old

Spinal stenosis is a narrowing of the spinal canal, either central or lateral. It is associated with spondylosis. It is the most common cause of spinal cord disorders in patients >55 yrs


There are three forms of cervical spinal stenosis:

  • Degenerative: osteophyte formation, degenerative disc, hypertrophy of the ligamentum flavum

  • Congenital: present due to spinal development

  • Traumatic: single incident

Spinal canal mechanics



  • In flexion the spinal canal widens by 31%

  • In extension the spinal canal diameter decreases and narrows by 20%. The cord and roots can become pinched between disc anteriorly, and by buckling ligamentum flavum and facet osteophytes posteriorly

  • In rotation there is ipsilateral neuroforaminal narrowing, and contralateral neuroforaminal widening

Symptoms


  • Chronic and slowly progressing

  • May have focal radicular type symptoms

  • May present with spondylotic myelopathy


Treatment options for spinal stenosis

  • Pharmacology

  • Surgery

  • Conservative


Pharmacology

NSAIDs, help reduce inflammation and are more effective than placebo in back pain. Opioids should be used for patients with moderate to severe persistent pain. Neuropatic pain may be opioid resistant. Muscle relaxers are shown to reduce pain and improve function spinal pain patients. Epidural steroid injections provide up to 6 months of pain reduction.


Surgery

  • Anterior approaches report a success rate as high as 67%, 55% long term. Increased stability is noted.

  • Posterior approaches report significant immediate neurologic improvement in up to 97%, 60% long teerm success. Long term adjacent segment deterioration is noted in 40%. There is decreased success with advanced cases.

  • Factors negatively impacting surgical improvement: age>50, duration of symptoms> 1 year, involvement of multiple levels, smoking


Conservative

  • Cervical collars: no available long term evidence, some short term improvement

  • Acupuncture: lack of evidence, may provide short term pain relief

  • Physical therapy: limited quality evidence. Treat the effects of immobilization and movement restriction. Functional improvement with neuromuscular control exercises. Improved outcome measures have been reported in a case series with treatment consisting of ICT and thoracic manipulation. Traction was performed for 15-20 min at 16-24# in 24 degrees of cervical flexion. Treat the impairments within the limits of symptom exacerbation. Based on the fact that flexion increases the diameter of the spinal canal and widens it by 31%, it stands to reason to emphasize a flexion biased protocol.


Conservative treatment vs surgery

  • 1 and 10 year follow up: no significant difference

  • Recommended 3 months trial of non-operative treatment

  • Surgery recommended for moderate to severe cases with progression of neurologic symptoms

Cervical myelopathy

Cervical myelopathy is spinal cord compression in the spinal canal caused by osteophytes or disc degeneration.

  • Sensory disturbance of the hands

  • Muscle wasting of hand intrinsic muscles

  • Unsteady gait

  • Positive Hoffman’s and/or Babinski

  • Hyperreflexia

  • Bowel and bladder disturbances

  • Bilateral or quadrilateral limb paresthesiae and/or weakness

Cervical myelopathy is classified on the basis of gait dysfunction. Patients with a grade 1 CCM have upper motor neuron signs with a normal gait. Grade 1 is considered mild CCM. Grade 2-5 are characterized by worsening gait disturbances and are considered to be moderate to severe CCM. Moderate to severe CCM has a poor prognosis and is generally treated surgically. Conservative management has been recommended for patients with mild CCM.


Cook et al identified a cluster of findings useful in identifying patients with this complex diagnosis in similar patient populations. This study found clustered combinations of clinical findings that could rule in and rule out CSM


  1. Gait deviations

  2. Positive Hoffman’s

  3. Inverted supinator sign

  4. Positive Babinski

  5. Age >45 years

When 3/5 positve, CSM could be ruled in (+LR 30.9). When 1/5 positive, CSM could be ruled out (-LR 0.18)


Many PT’s look for negative findings during testing of Hoffman’s, Babinski, clonus and hyperreflexia to rule out myelopathy. However, these tests by themselves demonstrate low sensitivity and are not appropriate for ruling out myelopathy. The findings in this study are unique, as it is the first to identify a cluster of findings that not only function as a screening tool, useful for ruling out the condition of myelopathy, but also provide combinations that are confirmatory, ruling in conditions of myelopathy.
Traditionally, very little has been done in PT for cervical myelopathy management. In 2004, a case series was published (Browder et al. JOSPT), where mild cervical compressive myelopathy was treated with a combination of intermittent cervical traction and thoracic manipulation. All patients improved, although it was not quite clear if it was time, or the intervention that made the difference. However, this is a step in the right direction.
Reference

  • Browder D et al. (2004) Intermittent cervical traction and thoracic manipulation for management of mild cervical compressive myelopathy attributed to a cervical herniated disc: a case series. JOSPT

  • Cook C et al. (2010) Clustered clinical findings for diagnosis of cervical spine myelopathy. JMMT Vol 18 No 4



Neoplastic conditions

  • Age> 50 years

  • Previous history of cancer

  • Unexplained weightloss

  • Constant pain

  • Nightpain



Inflammatory or systemic disease

  • Temperature> 100 F

  • BP > 160/95 mmHg

  • Resting pulse >100

  • Resting respiration >25 bpm

  • Fatigue

Whiplash injuries

The whiplash can be either in flexion or extension. Not a diagnosis by itself. The hyperextension injury is the most disabling. Causes include MVA’s, sports injuries, direct trauma to head, neck or body, falls landing on head, trunk or shoulder. Likely lesions following a whiplash incident in the C spine include tears to the ligaments, muscles and discs, damage to the neurological, vestibular and vascular systems, occult fractures and facet joint injuries.

The main concern with treatment is with the recognition of severe damage, fractures or CNS involvement. The vertebral artery should not be tested for the first 4-6 weeks and therefore, no treatment that might threaten the artery should be given during this period.

In the early stage proceed carefully. Meadows advocates the use of a soft collar. This can be taken off when the capsular pattern disappears. This is usually after about 3 weeks. Once the capsular pattern is gone, and the vertebral artery tested, you can proceed with treating specific dysfunctions with more direct techniques.

You might consider delaying PT during the first 10 days to help settle down irritation in the CNS/sympathetic nervous system.
Whiplash recovery: 40% does well, 40% does moderately well, and 20% does poorly.
Ritchie et al. developed a whiplash clinical prediction rule to consolidate previously established prognostic factors for poor recovery from a whiplash injury. The CPR predicted 2 recovery pathways. Prognostic factors for full recovery were being less then 35 years of age and having an initial NDI score of <32%. Prognostic factors for ongoing moderate/severe pain and disability were being >35 years of age, having an initial NDI score >40%, and the presence of hyperarousal symptoms.
The median time for average person to get better is 31 days. Two percent is still disabled 1 year after injury. They present with varying degrees of pain, motion loss, headaches and emotional disturbances in the form of anxiety and depression. Management: adequate early pain management; specific rehab of motor deficits (non pain provoking); psychological intervention (decrease in psychological distress parallels decreasing pain and disability). A multidisciplinary approach seems warranted. In the presence of widespread mechanical and cold hyperalgesia, PT alone is insufficient. To reduce burnout and frustration, remember that much of the damage suffered is either irreversible or very slow to heal and essentially invulnerable to PT, at least directly.
Reference


  • Ritchie C, Hendrikz J, Jull G, El;iott J and Sterling M. (2015) External Validation of a clinical prediction rule to predict full recovery and ongoing moderate/severe disability following acute whiplash injury. Journal of Orthopedic and Sports Physical Therapy. Vol 45 No 4 242-251

  • Scientific monograph of the Quebec Task Force on whiplash-associated disorders: redefining “whiplash” and its management. Spine Vol. 20, No.8S, 1995



Cervical radiculopathy

Cervical radiculopathy is a disorder of the nerve root regardless of the cause (arthritic conditions, discogenic disorders, space occupying lesions, inflammation of the nerve root) Peak incidence is between the 4th and 5th decade. The C6-7 nerve root is most frequently involved. Ninety percent of the afflicted patients improve with conservative management. Twenty-six percent of those having surgery have a decline in status at one year follow up.

The following cluster of tests has been found to be most useful to identify cervical radiculopathy (Wainner et al. Spine 2003): ULTT +, cervical rotation to involved side< 60 degrees, Spurlings +, distraction relieves symptoms.

When two of these tests are positive there is a 21% probability of cervical radiculopathy.

Three positive tests: 65% probability, 4 positive tests: 90% probability.

Evidence for appropriate management is not great. A study by Cleland et al (JOSPT 2005) shows that a combined approach of cervical lateral glides, T spine manipulation, deep neck flexor strengthening and intermittent cervical traction is helpful. It showed that 91% of patients had decreased pain and improved function. A multimodal approach seems to work best.


Reference

  • Cleland J et al. (2005) Manual therapy, cervical traction and strength exercises in patients with cervical radiculopathy: a case series. JOSPT

  • Wainner et al. (2003) Reliability and diagnostic accuracy of a clinical exam and patient self report measures for cervical radiculopathy. Spine Vol 28









Disc lesions


Posterolateral disc prolapses as they happen in the lumbar spine are relatively rare in the cervical spine. The nucleus takes up only 15% of the available space in the disc. According to Grieve it’s more common that nerve root irritation/compression is caused by spondylotic and arthritic changes. Disc prolapses causing root signs is usually limited to the lower cervical region due to the more developed uncinate processes higher in the spine. Flexion usually limited. At times there will be a torticollis. Pain is intense and may be scapular or radiating in the arm. Traction relieves symptoms. Compression, especially in flexion will reproduce local pain and likely peripheralization. X rays are usually negative.
Central herniation: over 45 years. Bilateral and upper extremity pain with multisegmental paresthesiae, especially in the hands, which is later felt in the feet as the condition progresses. Neck flexion reproduces paresthesiae. May cause cord compression and upper motor neuron signs. Traumatic posterior prolapse following MVA is probably a fairly common condition with as many as 25-40% of these patients showing evidence of one
Reference

  • Twomey, L and Taylor, J. (1989) Joints of the middle and lower cervical spine: age changes and pathology. MTAA



Acute torticollis

Four known causes for acute torticollis:



  • Disc derangement. Patient usually wakes up in AM with deformity. Mobilization will worsen symptoms. Traction techniques with extension will help. Analogous to lateral shift in low back.

  • Facet joint dislocation

  • Spasm of sternocleidomastoid

  • Acute C2-7 facet joint impingement, with C2-3 being mostly affected, as this is a transitional vertebra. Mobilizations are highly effective.

Reference



  • Greenman P. Priniciples of Manual Medicine, 3rd edition, 2002. Lippincott, Williams and Wilkins. Philadelphia PA

Examination

Goals of history taking

To determine the kind of disorder present. Is this patient an appropriate candidate for PT?


To determine whether there are any contra indications present to further physical examination and treatment techniques
To form a baseline against which progress can be measured
To obtain a detailed description of all patients symptoms
To obtain a chronological history:


  • of the present episode. Are symptoms static/worsening/improving? Has the patient had prior treatment, and if so what kind, and what were the effects?

  • of previous episodes

  • of related medical/family history

To make an assessment of:




  • the area/structure involved

  • the nature of the problem and the stage of the problem

  • the irritability of the condition

  • the behavior of symptoms

  • aggravating /easing factors

  • the patient as a person

  • the prognosis

Special questions:




  • Recent weight fluctuation? Reason?

  • Recent X rays? Results?

  • Medication for this and/or other conditions

  • Cardinal signs/symptoms


Systemic vs. musculoskeletal signs and symptoms
Clinical signs and symptoms of systemic pain
Onset:

Recent, sudden

Does not present as a chronic problem

Description:

Knife like, stabbing, boring, deep, deep aching

Cutting, gnawing, throbbing

Bone pain
Intensity:

Related to the degree of noxious stimuli


Duration:

Constant, no change, nightpain


Pattern:

Although constant, may come in waves

Gradually progressive

Nightpain

Symptoms not relieved by rest or change in positions
Aggravating factors:

Depends on the organ involved


Relieving factors:

Usually none, but also depends on the specific problem


Associated signs and symptoms:

Fever, chills

Unusual vital signs

GI symptoms (nausea, vomiting, anorexia, unexplained weight loss, diarrhea)

Painless weakness of muscles, more often proximal, but may occur distally

Excessive perspiration

Breathlessness at rest or after mild exertion

Bowel/bladder symptoms

Skin lesions, rashes or itches not related to musculoskeletal lesions










Objective Examination
Initial observation
Deformity torticollis

Assistive devices collars, braces

Pain behavior hand over painful area

slow cautious movements

verbal and facial clues

Handshake



Structural examination

Head tilt, rotation

Forward head posture

Rounded shoulders

CT junction

Spinal curves

Muscle atrophy

Muscle hypertone


Craniovertebral scan

Performed if subjective examination suggests any possibility of craniovertebral instability or vertebral basilar insufficiency


Neurological examination

Should be performed on every patient who presents with spinal problems.


Determines what part of the nervous system is involved

Upper vs. lower motor neuron

Nerve root vs. peripheral entrapment
Are nerve root signs increased or decreased

Hyper vs. hypo

Indicates type of pathology: compression

irritation

combination

Does not indicate exact level of pathology


Cardinal plane movements

Purpose: Establish pattern of pain and limitation

Estimate range

Develop baseline for improvement


Look for patients willingness to do movements

Most painful movement done last. Try not to do residual pain carry over

Over pressure may be applied, but carefully and only if motion appears to be full and painfree.

Usually do rotation first. Chin should nearly reach plane of shoulder.

Sidebend next. Ear to shoulder.

Flexion next. Chin to chest without opening mouth, or at least within 2 fingers.

May be limited by: CT junction or upper thoracic spine problems

Adaptive shortening

Cervical disc

Extension last. Face should get close to horizontal plane.


Passive movements

Eliminates contractile tissue

Compare AROM/PROM

Check endfeel


Resisted movements

Assess strength and pain behavior


Repeated movements

Check for worsening/improving pain or increasing decreasing pain

Repeat up to 10 times
Cervical distraction and compression

Compression gradually load cervical spine

pressure through top of skull

test in neutral, flexion, extension


Distraction gradually unload cervical spine

lift up under occiput

test in neutral, flexion, extension
Quadrant test

Assess signs and symptoms by using combined movement of rotation, sidebending, flexion or extension.


Quadrants: posterior left and right

anterior left and right


Anterior quadrant: flexion with sidebending and rotation to the same side. This opens up the IVF on the opposite side.
Posterior quadrant: extension with sidebending and rotation to the same side. This closes the IVF on the same side and puts the facet on the same side in close packed position.
Spurlings test

Perform posterior quadrant test passively. If this is negative for reproduction of symptoms, carefully add vertical compression.


Sustained posture

Valuable when relevant signs and symptoms are not reproduced with active/passive/resisted movements.

Assess pain behavior with prolonged posture in flexion and extension.
Segmental mobility testing

Shoulder abduction test

Patient seated or lying. Put hand on top of head. Decrease of symptoms is indicative of C5-6 nerve root compression.


Dizziness test

Patient seated. Passively rotate head left, right. Then hold head still, while patient turns his trunk left, right. If dizziness occurs in both cases, suspect vertebral artery insufficiency. If dizziness only occurs with passive rotation of the head, suspect inner ear problems.


Palpation

NEUROLOGICAL EVALUATION

Cervical reflexes

C5 Biceps


C6 Brachioradialis

C7 Triceps

Cervical cutaneous innervation


C1 Vertex of head

C2 Posterior auricular

C3 Lateral neck

C4 Shoulder/shawl area

C5 Lateral arm

C6 Posterior thumb


C7 Posterior aspect of middle finger

C8 Posterior aspect of little finger

T1 Medial forearm

T2 Axilla


Cervical myotomes

Level Resisted movement Muscles


C1 Head flexion Rectus capitis anterior and lateralis

C2 Head extension Rectus capitis posterior

C3 Sidebend neck Scaleni

C4 Elevation shouldergirdle Levator, upper trapezius

C5 Shoulder abduction Deltoid, supraspinatus

C6 Elbow flexion Biceps

Wrist extension Extensor carpi radialis longus/brevis



C7 Elbow extension Triceps

Wrist flexion Flexor carpi radialis



C8 Thumb extension Extensor pollicis longus and brevis

T1 Finger ab/adduction Interosseous muscles

Neural tension test

Quick test for: median nerve

radial nerve

ulnar nerve


Cervical root syndromes

C 5

  • Level C 4 - C 5

  • Pain distribution: Extends outward from scapular area to anterolateral area and forearm as far as the radial side of the hand.

  • Cutaneous innervation: lateral arm

  • Reflex: biceps

  • Myotome: deltoid, biceps


C 6
  • Level C 5 - C 6


  • Pain distribution: spreads down from the front of arm to radial side of the hand, thumb and index finger

  • Cutaneous innervation: posterior thumb

  • Reflex: brachioradialis
  • Myotome: wrist extensors, biceps



C 7
  • Level C 6 - C 7


  • Pain distribution: from scapula down back of arm and forearm to index, middle and ring finger

  • Cutaneous innervation: posterior middle finger

  • Reflex: triceps

  • Myotome: wrist flexors and triceps


C 8
  • Level: C 7 - T 1


  • Pain distribution: lower scapular area, back or inner side of arm and forearm, 4th and 5th finger

  • Reflex: none

  • Cutaneous innervation: ulnar aspect of 5th finger

  • Myotome: thumb extension and finger flexion


T 1
  • Level: T 1 - T 2


  • Pain distribution: medial arm and forearm

  • Cutaneous innervation: medial arm

  • Reflex: none

  • Myotome: hand intrinsic musculature





























Craniovertebral Scan
The craniovertebral region is a critical area that may be the site of serious pathology. An acute cervical patient may have a life threatening injury requiring emergency medical attention. Before attempting to mobilize the cervical spine, two factors need to be taken into consideration. Ruling out the presence of cardinal signs and symptoms is a priority. They are considered to be extremely important as they suggest either vertebral/basilar artery insufficiency, or cervical cord compression. If such symptoms can be initiated, reproduced or aggravated by stressing the vertebral artery or by passive linear motions to the craniovertebral joints, then it’s reasonable to assume that there is possible insufficiency of the vertebral artery or that instability exists within the craniovertebral joint complex.

We think it’s prudent to test for upper cervical instability prior to testing the vertebral artery, as this involves sustained endrange rotation, which can possibly compromise the spinal cord if there would be underlying instability.


Cardinal signs and symptoms

Signs/symptoms suggestive of cervical cord compression:

  • Bilateral or quadrilateral limb paresthesiae, either constantly or reproduced/aggravated by head or neck movements.

  • Hyperreflexia

  • Clonus

  • Positive Babinski or Hoffman’s

  • Arm and leg weakness

  • Lack of coordination bilaterally


Vertebral artery

Anatomy


The vertebral artery arises from the first part of the subclavian artery and passes upward on the longus colli to enter the transverse foramen of C6. Occasionally it may enter the bone at the 5th, 4th or 7th cervical transverse foramen. It then ascends from C6 to C1. After emerging through the transverse foramen of C1, it winds around the articular pillar and together with the 1st cervical nerve and veins pierces the posterior atlanto-occipital membrane to enter the cranium through the foramen magnum. On the anterior side of the brainstem it joins its fellow to form the basilar artery, before entering the foramen magnum.
The vertebral arteries contribute about 11 percent of the total cerebra blood flow, the remaining 89 percent being supplied by the carotid system. Asymmetry in the size of the two VA’s is common. Indeed, complete interruption of blood flow in one VA may be asymptomatic as long as there is a normal configuration in the circle of Willis and adequate flow through the other VA. Symptoms will occur when the blood supply to an area is critically reduced. This will depend ultimately on a balance between compensatory and compromising factors.
Provocative positional testing is frequently used in practice. It is intended to provide a challenge to the vascular supply to the brain, and the presence of signs or symptoms of cerebrovascular ischaemia during or immediately post testing is interpreted as a positive test.
Despite endorsement by guidelines and common clinical usage, current research does not support the contention that provocative positional testing can accurately identify patients at risk for cervical artery disease. Vertebral artery testing procedures have a sensitivity and specificity that approximates zero. This indicates a high likelihood of false negative findings.
Test procedures for the vertebral artery also hold a certain risk, and screening tests will not identify all patients at risk of suffering adverse reaction to cervical manipulation. There is also disagreement on what constitutes a clinically meaningful change in blood flow on cervical movement. It should be reiterated that there is no known method for testing the intrinsic anatomy of the vertebral artery. Doppler studies (Arnold, 2004) have shown that only full range cervical rotation and a pre-manipulative hold at C1-2 stresses the vertebral artery sufficiently to demonstrate reduction of bloodflow. Therefore the Clinical Guidelines of the Australian Physiotherapy Association recommend that only rotation be used to test for VBI.
Risk factors associated with cervical arterial dysfunction

  • History of trauma to cervical spine / cervical vessels

  • History of migraine-type headache

  • Hypertension

  • High cholesterol levels

  • Cardiac disease, vascular disease, previous cerebrovascular accident or transient ischaemic attack

  • Diabetes mellitus

  • Blood clotting disorders

  • Anticoagulant therapy

  • Long-term use of steroids

  • History of smoking

  • Recent infection

  • Immediately post partum

  • Trivial head or neck trauma

  • Absence of a plausible mechanical explanation for the patient’s symptoms.


Signs/symptoms suggestive of vertebral/basilar artery insufficiency:

Early presentation:

  • Mid-upper cervical pain

  • Pain around ear and jaw

  • Head pain (front- temporo-parietal)

  • Occipital headache

  • Acute onset of pain described as "unlike any other”

Late presentation:

  • Drop attacks

  • Dizziness

  • Dysphagia (difficulty swallowing)

  • Dysarthria (speech change, either slurred or slowed)

  • Diplopia (double vision)

  • Nausea

  • Nystagmus

  • Facial lip paresthesiae/ facial numbness

  • Cranial nerve dysfunction


Differential diagnosis

  1. Vertebral artery insufficiency

  2. Alar ligament insufficiency

  3. Transverse ligament insufficiency

  4. C 1 - 2 instability

  5. Jefferson fracture

  6. Balance difficulty, due to loss of proprioception secondary to immobilization of cervical spine

  7. Symptom magnification

  8. Autonomic reactions


Craniovertebral scan

Scan performed with patient seated, minimal hands on required.



  1. Neck rotation

  2. Upper cervical sidebending

  3. Upper cervical flexion

  4. Upper cervical extension

  5. Compression

  6. Distraction


References





  1. Arnold, C. et al. (2004) Doppler studies evaluating the effect of a physical therapy screening protocol on vertebral artery blood flow. Manual Therapy

  2. Baracchini C, Tonello S, Meneghetti G, Ballotta E. (2010)Neurosonographic monitoring of 105 spontaneous cervical artery dissections A prospective study. Neurology;75:1864e70.

  3. Cassidy, J. et al. (2008) Risk of vertebrobasilar stroke and chiropractic care: results of a population based case control and case cross over study. Spine

  4. Childs, J. et al. (2005) Screening for vertebrobasilar insufficiency in patients with neck pain: manual therapy decision making in the presence of uncertainty. JOSPT Vol. 5, No. 5,

  5. Childs, J. et al.(2002) Physical Therapy for the cervical spine and TMJ. APTA Home Study Course 13.3.1,

  6. DiFabio, R. (1999) Manipulation of the cervical spine: risks and benefits. Physical Therapy Vol. 79, No. 1

  7. Grant R. Premanipulative testing of the cervical spine - reappraisal and update. Physical Therapy of the Cervical and Thoracic Spine, 3rd edition. Elsevier 2002

  8. Haldeman S, Kohlbeck FJ, McGregor M (1999) Risk factors and precipitating neck movements causing vertebrobasilar artery dissection after cervical trauma and spinal manipulation, Spine 24(8): 785

  9. Mitchell, J. (2003) Changes in vertebral artery blood flow following normal rotation of the cervical spine. Journal of manipulative and physiological therapeutics.

  10. Thiel, H. and Rix, G.(2005) Is it time to stop functional pre-manipulation testing of the cervical spine? Manual Therapy

  11. Cassidy J et al. (2009) Risk of vertebrobasilar stroke and chiropractic care. Results of a population based case control and case crossover study. Spine. 2008. Vol 33 No 45

  12. Kerry, R. and Taylor, A. Cervical Artery dysfunction: knowledge and reasoning for manual physical therapists. JOSPT;39(5)

  13. Haldmen, S and Kohlbeck, F. (2002) Unpredicability of cerebrovascular ischemia associated with cervical spine manipulation therapy: a case review of 64 cases after spinal manipulation. Spine Vol 27 Issue 1 49-55

  14. Dunning, J et al.(2012) Upper Cervical and Upper Thoracic Thrust Manipulation Versus Nonthrust Mobilization in Patients With Mechanical Neck Pain: A Multicenter Randomized Clinical Trial. JOSPT Vol 42 No 1

  15. Dunning, J and Cleland, J.(2012) Cervical and thoracic mobilization versus manipulation for mechanical neck pain. Letters to the editor-response. JOSPT Vol. 42 No 4

  16. Puentedura E et al. (20120) Safety of cervical spine manipulation: are adverse events preventable and are manipulations being performed appropriately. A review of 134 case reports. JMMT Vol 20 No 2

  17. Rushton A, Rivett D, Carlesso L, Flynn T, Hing W, and Kerry R. International Framework for Examination of the Cervical Region for potential of Cervical Arterial Dysfunction prior to Orthopaedic Manual Therapy Intervention. IFOMPT consensus document 2012

  18. Erhardt JW et al.(2015) The immediate effect of atlanto axial high velocity thrust techniques on bloodflow in the vertebral artery. A randomized controlled trial. Manual Therapy http://dx.doi.org/10/1016

  19. Macchi C, Giannelli F, Cecchi F, Gulisano M, Pacini P, Corcos L, et al. (1996) The inner diameter of human intracranial vertebral artery by color Doppler method. Italian J Anat Embryol 1⁄4 Archivio Italiano di Anatomia ed Embriologia ;101:81e7.

  20. Malo-Urries M, Tricas-Moreno M, Lucha-Lopez O, Estebanez-de-Miguel E, Hidalgo- García C, Perez-Guillen S. (2012) Vertebral and internal carotid artery flow during vascular premanipulative testing using duplex Doppler ultrasound measurements: a systematic review. Int J Osteopath Med ;15:103e10

  21. Mitchell J. (2009)Vertebral artery blood flow velocity changes associated with cervical spine rotation: a meta-analysis of the evidence with implications for professional practice. J Man Manip Ther;17:46e57

  22. Mitchell J, Keene D, Dyson C, Harvey L, Pruvey C, Phillips R. (2004) Is cervical spine rotation, as used in the standard vertebrobasilar insufficiency test, associated with a measureable change in intracranial vertebral artery blood flow? Man Ther ;9:220e7

  23. Sturzenegger M, Mattle HP, Rivoir A, Rihs F, Schmid C. (1993) Ultrasound findings in spontaneous extracranial vertebral artery dissection. Stroke;24:1910e21.

  24. Thomas L, Rivett D, Attia H and Levi C.(2015) Risk factors and clinical presence of cervical arterial dissection: preliminary results of a prospective case control study. JOSPT Vol 45 No 7

  25. Kuether TA, Nesbit GM, Clark WM, Barnwell SL. (1997) Rotational vertebral artery occlu- sion: a mechanism of vertebrobasilar insufficiency. Neurosurgery 41: 427e32. discussion 32.


Stability tests
Alar ligmanent

Patient sitting. Palpate C 2 with index finger while sidebending head to the right. Normal: should feel immediate movement of C 2 to the opposite side of sidebending.






Transverse ligament
Patient supine. Anterior movement of occiput and C 1 on C 2. Normal: C 2 should follow immediately.




Transverse plane stability.

Medial pressure on TP of C 1 while stabilizing the opposite TP. Should be no movement or crepitus (Jefferson fracture).




Upper motor neuron tests


  1. Babinski

  2. Hoffman’s. Flick patient’s middle finger. Positive when there is a flexion pattern of thumb and index finger.

  3. DTR’s

  4. Clonus



Examination
Performed when stability tests are negative and there are no upper motor neuron signs
Minimal testing recommended includes the following:

  • Sustained end range cervical rotation to the left and the right. Maintain each position with overpressure for 10 seconds 9 or less if symptoms are provoked) and on release, a period of 10 seconds should elapse to allow for any latent response to the sustained position. The patient is asked about dizziness during each test, and the eyes are observed for the presence of nystagmus

  • The position or movement that provokes symptoms as described by the patient.

  • Sustained mobilization position

Specific questioning re. production of symptoms suggestive of VBI is essential and should be done



  • Immediately before and after a cervical manipulation

  • During and immediately after a technique involving endrange rotation


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