Disorders of the Cervical Spine

Prepared by Farrah Camille E. Amik, PTRP

I. CERVICAL SPINE
A. Anatomy and Biomechanics
 7 Vertebrae & 5 IV discs
 C1 – Atlas
 C2 – Axis (Dens/odontoid – Epistropheus)
 C2 – C7 articulate anteriorly through IV discs and uncovertebral joints (Joints of Luschka); posteriorly through the zygapophyseal joints
 Occipito-Atlanto-Axial
o Oc-C1-C2
o Synovial joints only; no IV discs
o Biconcave ring – C1
o Convex – condyles of occiput
o C1 ring & condyles are anchored to C2 via dens
o Oc attached to C2 – alar ligaments, apical and upper arm of cruciform ligament
o C1 bound to C2 odontoid – transverse arm of cruciform ligament
o Flexion (10 deg) &extension (25 deg) (Oc-C1)
o Axial rotation (45 deg) (C1-C2)
 Lover cervical spine (C3-C7)
o IV disc
 ¼ of cervical height
 2:5 disc-vertebral body ratio
 Avascular; only outer annulus is vascularized
 Thicker anteriorly than posteriorly – lordotic posture
 allows for a greater degree of motion
 2 components:
 Annulus Fibrosus
- External component
- Multiple lamellae (Type I & II collagen)
- fiber direction of the annular lamellae alternates, with each consecutive layer, oriented opposite to the adjacent fibers
- accommodate angular motion -> stability against torsion and shear
 Nucleus Pulposus
- Semifluid gel
- Water 46-60%
- Compressive loading
- Slowly replaced by fibrocartilage (aging)
 Separated from VB by endplates
 Endplates
 hyaline & fibrocartilage -> permeable surface -> passage of nutrients
o Ligaments
 Anterior Longitudinal Ligament (ALL)
 Anterior vertebral body & discs
 Limits cervical extension
 Posterior LongitudinalLigament
 Post. Disc and VB
 Taut during flexion
 Superficial Ligamentum Nuchae
 Dense, midline band from OC to spinous process of C7
o C3-C6 – zygopohyseal joints are angled at 45 degrees; steeper angle for C7 (vertebra prominence)
 Neural Elements
o Spinal Cord
o Dorsal and ventral roots (Bell majendie law)
o Spinal nerves
 Exit the spinal canal through the intervertebral foramen
o Dorsal and ventral rami
 C1-C4 ventral rami – cervical plexus
 C5-T1 ventral rami – brachial plexus
II. CERVICAL SPINE DISORDERS
A. Axial Pain and Symptom Referral
 Cervical Spondylosis
o Degenerative change affecting 5 articulations
 IV discs
 Bilat. Zygopophyseal joints
 Biat. Uncovertebral joints of Luschka
o Pathophysiology
 Desiccation and loss of disc height -> approximation of uncovertebral joint & disruption of Zygo. Jt. Biomechanics
o Clinical Manifestation:
 Uncovertebral & zygopophyseal hypertrophy
 Osteophyte formation
 Annular disruption
 Ligamentum flavum hypertrophy
 Pain – not all with degenerative changes; 95% experience it at age 65
 Referred Pain
 brain is unable to decipher the true pain origin secondary to convergence at the level of the spinal cord and thalamus
 experienced as deep, diffuse, and poorly localized
 IV disc and zygapophyseal joints – pain generators
 IV Disc
- Degenerative disc dse – mc @ C5-C6; C6-C7 2nd
- Due to increased segmental motion
 - Disc injury may be acute traumatic / degenerative – produce local and referred sx
- Outer 1/3 of AF houses nerve endings – stimulated during injury
- Annular defect -> migration of nuclear material -> stimulate outer annulus, dura mater, PLL, DRG, or spinal nerve -> inc.
inflammatory mediators
- Herniation
 Herniation/Protrusion
 Extrusion
 Sequestration
- Clinical Manifestation:
 Pain referral on scapular region – C3-C4
 Upper limb pain referral – C5-C6
 Pain referral ant. Chest wall – C6-C7
 Zygapophyseal Joint
 Active pain generator (degenerative/traumatic)
 whiplash injury
 may also produce zygapophyseal jt fractures, intra-articular hemorrhage, and capsular tears
 C2-C3 most frequently symptomatic, C5-C6 2nd


B. Radiculopathy
 Pathologic compressive processes affecting the nerve root
 Etiology:
o Acute disc herniation
o Degenerative Foraminal Stenosis
o Trauma
o Tumor
 Epidemiology:
o M.C. involve C7 & C6 (esp. C7); followed by C5 & C8
o Younger than 55 yo – radiculopathy from disc herniations
o Older than 55 yo – degenerative foraminal or central canal stenosis
 Pathophysiology
o Compression (IV disc (MC), zygapophyseal or uncovertebral, or combined) -> Herniation (soft – more acute injury nucleus displacement; hard
– calcified and spondylotic ridge) into different directions (ant – less common d/t ALL) -> impinge or hit nerves
o Disc Herniation
 Location
 Intraforaminal
- Acute radiculopathy affecting the nerve root exiting thru the respective foramen
- Compression at C4-C5 will affect?
 Posterolateral
- Between lateral edge of PLL and Uncinate process
 Central Disc Herniation
- Passes thru PLL
- Result to central canal compromise and SC compression
- Occur in later stages of cervical degeneration – uncovertebral hypertrophy blocks lateral disc material migration
o Clinical Manifestation:
 Pain
 Weakness
 Paresthesia / sensory motor deficit – (dermatomal and myotomal)
 Cervical and UE pain that began with trauma
 Coughing, sneezing, or Valsalva maneuver worsen sx
 Pseudoangina pectoris
o PT Assessment:
 MBT
 AROM cervical
 ST:
 Distraction Test
 Foraminal Compression Test
- Spurling’s Test
 Maximum Cervical Compression Test
 Jackson’s Compression Test
 Shoulder Abduction Test (Bakody’s)
- C4-C5
 MMT
 DTR
o Non-Surgical Treatment
 Cervical collars
 Rest
 Manipulation
 Therapeutic exercise
 Calliet’s
  NSAIDs
 Epidural injections - severe
o Surgical Treatment:
 Cervical spine decompression
 Laminoforaminotomy
C. Myelopathy
 Injury to SC due to severe compression
 Average age onset is at 50 yo
 M>F
 Typically insidious, some acute onset c/s a preceding traumatic event
 Clinical Manifestation:
o numbness and paresthesia in the distal limbs and extremities
o weakness LE > UE
o Intrinsic hand mm wasting
o Cervical axial pain
o Flexion bias
o Bladder function disturbance (S2-S4)
o Unilateral or bilateral radicular pain
o Pain and temperature disturbances (LST tract) “glove stocking” distribution
o Proprioception and vibratory deficits (post. Column)
o UMNL signs (Hoffman, Babinski, brisk reflex)
 Pathophysiology:
o initial deterioration -> disc space narrowing -> loss of normal lordosis -> osteophyte formation -> static period that can last several years ->
stenotic compromise of central canal and spinal cord
 Other Etiology
o dynamic stressors
o vascular insufficiency
o ischemia
o instability
o ossification of PLL
 Assessment:
o Palpation ofneck for tenderness
o ST:
 Lhermitte’s Sign
 Finger Escape sign
 Grip and release Test
o Sensory assessment
o Vibratory Testing
o Reflexes
o Romberg Test
 Treatment:
o Non-operative:
 Physical therapy
 Cervical Orthosis
o Surgery:
 Pts c severe or progressive sx
 Failed conservative measures
 Anterior Cervical Diskectomy
 Cervical Intervertebral Disk Herniation (CIDH)
 Diskectomy c fusion at appropriate level
 Removal offending structures
 PLL ossification or degenerative spondylosis (osteophyte)
 Corpectomy
 Anterior decompression by removing vertebral body along with the IVD
 Segment is then fused with fibula allograft or bone cage
 Laminectomy
 Posterior decompression
 c/s posterior fusion or laminoplasty
D. Cervical Sprain
 Overstretching or tearing injuries of the ligaments
 Etiology:
o External forces towards the neck or sustained faulty posture or positioning
 Pathophysiology:
o Occur at the extremes of motion or in association of violent muscle contractions. It may occur to any ligaments traversing the cervical spine
as well as capsular ligaments surrounding facet joints.
 Clinical Manifestations: 
o Pain
o Stiffness
o LOM with NO NEUROLOGIC or osseous injury
 Differential Diagnosis:
o Cervical strain
 Pharmaceutical mx:
o NSAIDS
 PT Manangement: 
o Rest
o Cryotherapy
o Follow up tx – Superficial heat
o Isometric exercises
o Gentle Stretching
E. Cervical Strain
  Musculotendinous injury produced by an overload injury resulting from excessive forces imposed on cervical spine
 Etiology:
o external forces towards neck or sustained faulty posture or positioning
 Clinical Manifestation:
o Pain
o Stiffness
o LOM
o Mm spasm
o Increase pain in active contraction and passive stretching
 Differential Diagnosis: Cervical Sprain
o Medical Mx: NSAIDs
 PT Mx:
o Use of cervical collar for support will facilitate symptom subsiding within 3-7 days
o Gentle stretching
o Isometric exercise
 Follow up tx:
o superficial heat
o Resistance exercise
F. Cervicogenic headaches
 constellation of symptoms that represent the common referral patterns of cervical spine structures
 Pathophysiology:
o N. roots, spinal nerves, dorsal root ganglia, uncovertebral jts, IVD, facet jts, muscles, and ligaments – possible affected sites
o “Convergence Theory”
 Epidemiology:
o W>M
o Zygapophyseal Joint – C2-C3
o IV Disk – C2-C3, C3-C4, C4-C5
 Etiology:
o Degenerative changes
o Direct trauma
o No underlying biomechanical insult
 Clinical Manifestation:
o HA - unilateral and stemming from the posterior occipital region
o Pain referral on the vertex of scalp, ipsilateral anterolateral temple, forehead, midface, or ipsilateral shoulder girdle
o Lasts for a few hours up to a few weeks
o Less excruciating and non-throbbing
 PT Assessment:
o NPS
o AROM – commonly reduced
o MMT
G. Whiplash Syndrome
 Hyperflexion-hyperextension
 3 components:
o Whiplash event:
 biomechanical effect incurred by the occupants of one vehicle
 Rear-end collisions
 Inertial response
o Whiplash Injury:
 Impairment, or injured structure, resulting from the whiplash event
 passive movement – no mm stabilization
 Straining/spraining and compression of structures
 anterior disk, anterior longitudinal ligament, posterior disk or annulus, and cervical zygapophyseal joints
 typically heal over a relatively short period
o Whiplash syndrome:
 set of symptoms arising from the whiplash injury
 neck pain & headaches – mc
 followed by shoulder girdle pain, upper limb paresthesia, and weakness
 dizziness, visual disturbances & tinnitus – LC
 recover within the first 2 to 3 months after the injury, and after 2 years
III. MECHANICAL INTERVENTION, THERAPEUTIC EXERCISE, AND MODALITIES
A. Mechanical Therapy
 McKenzie Exercises
o Extension
o Centralization vs peripheralization
 William’s Exercises
o Flexion
 Postural Correction
o Mirror method
o Breathing
o Stretching
o Core Strengthening
o Pelvic Positioning
 Stretching
o adaptively shortened structures
o daily stretching program
B. Mobilization/Manipulation
 Reduction of spinal derangements
 Discourage spinal mobilization based on palpation
 Communicate with patient regarding pain provocation
 Grades of Passive Movement to Restore Spinal Motion
 o Grade 1
 Small oscillations at beginning of of ROM
o Grade 2
 Large oscillations on resistance free ROM
o Grade 3
 Large Oscillations at 50% jt. resistance
o Grade 4
 Small oscillations at 50% jt resistance
C. Collars
 Soft Collars
 Rigid Collars
D. Modalities
 Cryotherapy/Ice – Acute
 Heat – Sub-acute/Chronic
o US - Phonophoresis
o IRR
o HMP
 Others
o TENS
o Iontophoresis
o Shockwave
E. Traction
 Apply manual first then mechanical
 Max post elongation is at 24 deg of flexion
 Mechanical – uniform/static or intermittent force
 Static - more acutely inflamed, if the patient’s symptoms are easily aggravated by motion, or if the patient’s symptoms are related to disc
protrusion
 Recommended initial force – 8-10 pounds
 15 lbs – mm stretching
 25 lbs – vertebral separation
F. Stabilization
 Strengthening neck flexors and scapular stabilizers
 Calliet’s
G. Work Ergonomics
 Avoid symptom aggravating positions
 recommended positioning at the desk or computer station is usually prescribed with approximately 90 degrees of hip, knee, and elbow flexion
 distance from the computer monitor is an arm’s length measurement
 upper third of the computer screen should be situated at eye level
H. Massage
 debilitating muscle guarding or soft-tissue pain persists
 use of massage should likely be limited to the more acute injury phase – decrease dependency