Cervical Arthritis, Cervical Spondylotic Myelopathy by Pablo Pazmino MD


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This video explains Cervical Stenosis and Cervical Spondylosis/Arthritis. When stenosis begins to affect the spinal cord this is called Cervical Spondylotic Myelopathy. This video highlights the history, epidemiology, and treatment options both conservative and surgical. If you or someone you know needs to be seen in regards to Cervical Stenosis/Arthritis feel free to look us up online www.beverlyspine.com or www.santamonicaspine.com OR call toll free 1-8SPINECAL-1

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  • Cervical Arthritis, Cervical Spondylotic Myelopathy by Pablo Pazmino MD

    1. 1. Pablo Pazmi ño, MD
    2. 2. Orthopaedic Surgery American Academy of Orthopaedic Surgeons Clinical Faculty Olympia Medical Center Cedars Sinai Medical Center Century City Doctors Hospital <ul><li>Education </li></ul><ul><ul><li>The University of California, Los Angeles </li></ul></ul><ul><ul><li>The University of Michigan, Ann Arbor </li></ul></ul>
    3. 3. <ul><li>History </li></ul><ul><li>Epidemiology, Natural History </li></ul><ul><li>Pathophysiology </li></ul><ul><ul><li>Pathoanatomic Theories </li></ul></ul><ul><ul><li>New Theories </li></ul></ul><ul><li>Diagnosis </li></ul><ul><ul><li>Symptoms </li></ul></ul><ul><ul><li>Exam Findings </li></ul></ul><ul><li>Studies </li></ul><ul><li>Treatment </li></ul><ul><ul><li>Non Operative </li></ul></ul><ul><ul><li>Decision Making Process </li></ul></ul><ul><ul><li>Operative </li></ul></ul><ul><li>Cases </li></ul>Dr. V.A.H. Horsley (1857-1916)
    4. 4. <ul><li>Cervical Spondylosis: Progressive degenerative changes that develop slowly over time, this alters the spinal biomechanics from the loss of shock absorption properties of intervertebral discs. This leads to secondary changes in surrounding structures. </li></ul><ul><li>Dysfunction  Instability  Stabilization (Marginal Osteophytes) </li></ul>
    5. 5. Type I: Cervical Radiculopathy: Cmprsn +Inflammation of Spinal Nerve with symptoms that correspond to the level involved Type II: Cervical Myelopathy: Cord involvement Type III: Axial Joint Pain (Mechanical neck pain, “discogenic pain”, facet syndrome, painful instability
    6. 6. <ul><li>Sex: Radiographic changes are more severe in men than in women. </li></ul><ul><li>Cervical Spondylosis present in 50% of population at 50 years of age. Kellgren Ann Rheum Dz 1958 </li></ul><ul><li>Irvine et al defined the prevalence of Spondylosis using radiographic evidence. Lancet 1965 </li></ul><ul><ul><li>♂ prevalence was 13% in the third decade  100% by age 70 years. </li></ul></ul><ul><ul><li>♀ prevalence ranged from 5% in the fourth  96% > 70 years. </li></ul></ul><ul><ul><li>In 1992, Rahim and Stambough noted that spondylotic changes are most common in those older than 40 years. Eventually, more than 70% of men and women are affected Orthop Clin North Am 1992 </li></ul></ul><ul><ul><li>By age 60-65 95% of nonsymptomatic men and 70% of asymptomatic women develop at least one degenerative change on Xray Gore Spine 1986 </li></ul></ul><ul><li>Moore and Blumhardt series, 23.6% of patients presenting with nontraumatic myelopathic symptoms had CSM. Spinal Cord 1997 </li></ul><ul><li>CSM is the most common cause of nontraumatic spastic paraparesis and quadriparesis. </li></ul>
    7. 7. <ul><li>This study found that No patient ever returned to normal state </li></ul><ul><li>75% Had episodic worsening/progression </li></ul><ul><li>20% Slow steady progression </li></ul><ul><li>5% Rapid onset followed by lengthy disability </li></ul><ul><li>Motor changes tended to persist and progress with time </li></ul><ul><li>Sensory/bladder changes were transient </li></ul><ul><li>Soft collar improved gait and Nroot syx for 50% pts </li></ul><ul><ul><ul><li>Clark E, Robinson PK Cervical Myelopathy: a complication of cervical spondylosis Brain 56:79:483-70 (120 patients) </li></ul></ul></ul>
    8. 8. <ul><li>Patients develop Stepwise degeneration with periods of stability between exacerbations. </li></ul><ul><li>45% of patients with non myelopathic symptoms have good resolution after onset, the remaining 55% continue to have moderate long term morbidity </li></ul><ul><ul><ul><li>Lees Turner BMJ 63:2:1607 (44pts/ CSM 3-40yrs) </li></ul></ul></ul>
    9. 9. <ul><li>Found Overall Poor outcome of Nonsurgical Management of CSM </li></ul><ul><li>The study looked at 43pts </li></ul><ul><li>23 Medical treatment: Decrease in ability to perform ADLs, worsening of Neurologic symptoms </li></ul><ul><li>20 Surgical treatment: Decreased neurologic symptoms,overall pain, and improved functional status </li></ul><ul><li>Sampath P et al Spine 2000: 25:670 </li></ul>
    10. 10. <ul><li>Gowers (1892) He first noticed the changes associated with Cervical Spondylosis . He called these “Vertebral Exostoses” and thought they were exceedingly rare and their chief characteristic was chronicity. </li></ul>
    11. 11. October 24,1892 20 YO “builder who under the influence of alcohol, fell off his van on to the road striking his right shoulder.” Over 2month this man gradually lost control of legs and sphincters Dr Horsley performed the First Laminectomy of 6 th Cervical Vertebra. Oct 1892 During surgery he saw the Spinal cord was compressed by a ridge projecting backwards from the body of the vertebra. After surgery the patient had a Complete recovery by September of that year
    12. 12. <ul><li>Cervical spondylosis and cord impingement was originally described by Stookey in 1928 </li></ul><ul><li>He attributed compression of the cord by “extradural chondromas” cartilaginous nodules . Which he thought was similar to these enlargements seen on ears </li></ul><ul><li>It was not until 1934 Peet, MM and Echols, DH showed that these “chondromas” were actually disc protrusions </li></ul>Lord Brain, F.R.S., D.M., F.R.C.P. (1895-1966)
    13. 13. <ul><li>In 1952 Lord Brain was the first person who recognized myelopathy and radiculopathy as a clinical disorder </li></ul>
    14. 14. <ul><li>Association between a narrowed, spondylotic cervical spinal canal and the development of CSM has previously led to the formulation of a relatively simple pathoanatomic concept that a narrowed spinal canal causes compression of the enclosed cord, leading to local tissue ischemia, injury, and neurological impairment. </li></ul><ul><li>However, this simple mechanism fails to explain the entire spectrum of clinical findings observed in CSM, particularly the development of significant neurological signs in patients without evidence of static spinal cord compression. </li></ul>
    15. 15. Mechanical Factors Static Canal Stenosis Severity Cmprsn Dynamic Changes Flexion Changes Extension Role of Ischemia Pathological Evidence Central gray and medial white most severely affected Relative sparing of anterior columns Progression with severity Lateral CSpinal Tracts most vulnerable Ant Horn Cells less infarction Extensive Infarct Gray and White with AP Cmpr<20% Cellular and molecular mechanisms Free radical mediated cell injury Cation-mediated cell injury (Na + /Ca ++ ) Glutamatergic toxicity/cell injury Apoptosis
    16. 16. <ul><li>Biomechanical </li></ul><ul><li>Shear/ Stretch related, Dynamic Stenosis, Pincer Effect, Euler’s Theorum </li></ul><ul><li>Shear /Stretch Principle (Out of Plane Loading </li></ul><ul><li>Poisson’s Effect </li></ul><ul><li>Dentate Tension Theory </li></ul>
    17. 17. <ul><li>Anteriorly  disc degeneration and osteophytes ,PLL </li></ul><ul><li>Anterolaterally  uncovertebral joint, and facet hypertrophy </li></ul><ul><li>Posteriorly  Ligamentum flavum buckling </li></ul><ul><li>Parke WW. Spine 1988 </li></ul><ul><li>Bernhardt et al JBJS 1993 </li></ul>Progressive cervical spondylotic changes result in circumferential narrowing of the cervical canal
    18. 18. <ul><li>The normal cervical canal diameter from C3 to C7 in Caucasians is 17-18 mm (< Asians) </li></ul><ul><li>Cervical cord varies little in size from C1 to C7, measuring approximately 10 mm in diameter (range, 8.5-11.5 mm). </li></ul><ul><li>2/3 unoccupied by the spinal cord from C1 to C3 </li></ul><ul><li>¼ C4 to C7. Payne, Brain ’57 </li></ul><ul><li>Normal spinal canal can accommodate the development of spondylotic changes CSM is more likely to develop in a congenitally narrowed </li></ul>
    19. 19. Cord compression ratio remains<0.4 Smallest AP Diam/Largest Trans Fujiwara JBJS BR ‘89
    20. 20. <ul><li>The transverse area of the spinal cord was measured to determine the severity of cervical cord compression and was related to prognosis with surgical intervention. </li></ul><ul><li>Transverse area ≠ preoperative neurologic status </li></ul><ul><li>Transverse area ≈ response to surgery after decompression </li></ul><ul><li>≥ 30 mm2, functional recovery was favorable. </li></ul><ul><li>≤ 30 mm2 a poor response </li></ul><ul><li>Penning L, AJR Am J Roentgenol 1986. </li></ul>
    21. 21. <ul><li>With an anteroposterior compression ratio < 20% extensive infarction of all the gray matter occurred. </li></ul><ul><li>Ogino et followed 9 patients with CSM were observed clinically, radiographically, and, at time of death, neuropathologically. </li></ul>Histological Changes
    22. 22. <ul><li>1. Early involvement of the corticospinal tracts </li></ul><ul><li>2. Later destruction of anterior horn cells, demyelination of lateral and dorsolateral tracts </li></ul><ul><li>3. Relative preservation of anterior columns and dorsal regions of dorsal columns (Involved Severe CSM). </li></ul><ul><li>Ogino H, Spine 1983;8:1-15. </li></ul>
    23. 23. <ul><li>Less severe myelopathy Changes confined largely to the lateral funiculi </li></ul><ul><li>More severe myelopathy Involvement of the medial gray area and ventral aspect of the dorsal columns ( including gliosis and anterior horn cell dropout.) </li></ul>
    24. 24. <ul><li>Advanced CSM. </li></ul><ul><li>Anterior columns and the subpial axons in the dorsal columns were relatively preserved </li></ul><ul><li>Breig A, J Neurosurg 1966 </li></ul>
    25. 25. <ul><li>Histopathologic observations support the concept of ischemic injury to gray matter and medial white matter </li></ul><ul><li>Oligodendroglia may be particularly vulnerable to ischemic injury, accounts for </li></ul><ul><ul><li>Demyelination in chronic CSM </li></ul></ul><ul><ul><li>Demyelination of the corticospinal tracts is one of the first pathologic changes in CSM </li></ul></ul><ul><ul><li>Ogino H Spine 1983 </li></ul></ul>First proposed by Lord Brain in 1948
    26. 26. Dynamic Stenosis Pincer Effect Euler’s Theorum Shear /Stretch Principle (Out of Plane Loading Poisson’s Effect Dentate Tension Theory
    27. 27. <ul><li>1) Clinical studies of cervical mobility in patients with CSM, </li></ul><ul><li>2) Histopathological studies of spinal cord tissue from CSM patients </li></ul><ul><li>3)Biomechanical studies : an improved understanding of the material properties and biomechanical behavior of spinal cord tissue under various physiological and pathological conditions. </li></ul>
    28. 28. <ul><li>Functional canal diameter may be reduced to a critical level or less White and Panjabi </li></ul><ul><li>Flexion,cord lengthens (more anterior path) resulting in axial tension and, potentially, ischemia. </li></ul><ul><li>In the presence of anterior osteophytes, the spinal cord can be stretched over the anterior bars. </li></ul>
    29. 29. <ul><li>Progressive encroachment on the spinal canal by ventral and dorsal anatomic structures may first lead to spinal cord compression that occurs only transiently during physiological cervical range of motion . </li></ul><ul><li>The appearance of clinical signs and symptoms arising from this condition has been described as “dynamic stenosis.” </li></ul><ul><li>With progressive narrowing of the spinal canal, dynamic stenosis evolves into static compression of the spinal cord and leads to CSM. </li></ul><ul><li>Burnhardt et al JBJS 1993 </li></ul>
    30. 30. <ul><li>Extension </li></ul><ul><li>1. Ligamentum flavum buckles inward,which results in the maximal reduction in cross-sectional area of the cervical canal. </li></ul><ul><li>2. Spinal cord shortens, and its cross-sectional area increases. </li></ul><ul><li>Combination places the cord at significant risk in extension. </li></ul><ul><li>A pincer effect : spinal cord is compressed in extension between the posteroinferior margin of one vertebral body and the lamina or ligamentum flavum of the next caudal level. </li></ul>
    31. 31. <ul><li>Euler’s Theorum </li></ul><ul><li>Spinal cord ( a viscoelastic cylinder) when compressed from the sides, exhibits net tissue creep, bulging axonal membranes, and fluid flow to the free ends of the cylinder </li></ul><ul><li>Longitudinal Tension forces are created within the neuraxis perpendicular to the plane of compression. </li></ul>
    32. 32. <ul><li>A ventral compression force (stenosis) results in increased axial cord tension and fissuring on the side opposite the compression </li></ul>“ Out-of-plane loading” Shear
    33. 33. <ul><li>Mild compressive deformation of the spinal cord resulted in viscoelastic stretch when the ventral-dorsal diameter < 20-30% </li></ul><ul><li>Axial tension forces exceeded the material properties of the tissue and resulted in the tearing of axial fibers </li></ul>
    34. 34. <ul><li>Common materials become narrower in cross section when they are stretched. </li></ul><ul><li>Inter-atomic bonds realign with deformation. </li></ul><ul><li>Stretching of honeycomb by vertical forces, illustrates the concept. </li></ul><ul><li>Normal “in-plane” strain can result in “out-of-plane” stresses. This is called Poisson’s effect, and it accounts for lateral contraction accompanying longitudinal extension. </li></ul>Poisson’s Effect: Most materials resist a change in volume (as (determined by the bulk modulus) more than they resist a change in shape (shear modulus)
    35. 35. <ul><li>The addition of forces from a ventral spondylotic bar results in maximal stress in the lateral funiculi as the cord is pulled laterally (flattened) by the dentate ligaments (tighten in flexion, anchored by dural root sleeves and dural ligaments). </li></ul><ul><li>Flexion of the neck increases dural tension and should be avoided in the conservative treatment of CSM. </li></ul><ul><li>Both anterior and posterior extradural surgical operations can diminish dentate tension, which may explain their usefulness in CSM. </li></ul>
    36. 36. <ul><li>The role of the dentate ligaments in this model provides an explanation </li></ul><ul><li>1) Characteristic histological findings of the less severe cases of CSM </li></ul><ul><li>2) Explains why histopathological changes can be found remote from the point of compression </li></ul>
    37. 38. <ul><li>At the lower cervical and upper thoracic spine, where the amount of flexion tends to be greatest, the spinal cord stretches up to 24% of its length with a corresponding increase in length of the spinal cord of 17.6 mm at the level of the cervicothoracic junction during flexion </li></ul><ul><li>The increased stretching occurring locally at the cervicothoracic </li></ul><ul><li>junction translates into a significant increase in strain and stress in the white matter and a higher stress in gray matter </li></ul><ul><li>Reid J Neur 1960 </li></ul>
    38. 39. <ul><li>Look how much the spinal cord moves with flexion of the neck </li></ul><ul><li>Notice the strain on the nerves as well </li></ul>
    39. 41. <ul><li>Impairment of intracellular energy metabolism increases neuronal vulnerability to glutamate which, even at nl concentrations can damage neurons. </li></ul><ul><li>This mechanism of slow excitotoxicity thought to be involved in neuronal death in chronic neurodegenerative diseases </li></ul><ul><li>Riluzole, a glutamate antagonist, has therapeutic efficacy in human ALS </li></ul>
    40. 42. <ul><li>Free radicals released from activated microglia may initiate MN injury by increasing the susceptibility of the MN AMPA/kainate receptor (white matter injury) and NMDA (anterior horn injury) to the toxic effects of glutamate. </li></ul><ul><li>Bunge RP Adv Neurol 1993. Fehlings, M Spine 1998 </li></ul>
    41. 43. <ul><li>Show similar pathophysiology of cell injury with traumatic and ischemic injury to the CNS </li></ul><ul><li>Both: Delayed anterior horn cell loss, gliosis </li></ul>
    42. 44. <ul><li>Amyotrophic lateral sclerosis </li></ul><ul><li>Extrinsic neoplasia (metastatic tumors) </li></ul><ul><li>Hereditary spastic paraplegia Intrinsic neoplasia (tumors of spinal cord parenchyma) </li></ul><ul><li>Multiple sclerosis </li></ul><ul><li>Normal/Low pressure hydrocephalus </li></ul><ul><li>Spinal cord infarction </li></ul><ul><li>Syringomyelia </li></ul><ul><li>Vitamin B12 deficiency </li></ul><ul><li>SCIWORA syndrome </li></ul><ul><li>Spinal cord tumor </li></ul><ul><li>Cerebral hemisphere lesion             </li></ul>
    43. 45. <ul><li>Lhermitte’s sign </li></ul><ul><li>Paresthesias: Global non dermatomal </li></ul><ul><li>Fine motor control </li></ul><ul><li>Clumsy or weak hands </li></ul><ul><li>Handwriting </li></ul><ul><li>Zippers/Buttons </li></ul><ul><li>Leg weakness or stiffness (Chair/Stairs) Proximal>>Distal LExtr </li></ul><ul><li>Chronic suboccipital headache </li></ul><ul><li>Suboccipital and may radiate to the base of the neck and the vertex of the skull. </li></ul><ul><li>Changes bowel/bladder (severe, Rare) </li></ul>
    44. 46. <ul><li>Asymptomatic </li></ul><ul><li>Intermittent neck and shoulder pain </li></ul><ul><li>1/3 present with headache </li></ul><ul><li>>2/3 present with unilateral or bilateral shoulder pain. </li></ul><ul><li>A significant amount of these patients also present with arm, forearm, and/or hand pain. </li></ul><ul><li>Radicular signs </li></ul><ul><ul><li>Often not dermatomal. More pain proximally in their limbs, while paresthesias dominate distally. </li></ul></ul>
    45. 47. <ul><ul><li>Radiculopathy ,most commonly 6th 7th roots from C5-6 or C6-7 spondylosis, </li></ul></ul><ul><ul><li>Patients usually present with pain, paresthesias, weakness, or a combination of these symptoms. </li></ul></ul><ul><ul><li>Pain usually is in the cervical region, upper limb, shoulder, and/or interscapular region. </li></ul></ul>
    46. 48. <ul><li>First described by Pierre Marie and Chatelin in 1917. </li></ul><ul><li>Lhermitte reported on this symptom in 1920, and in 1924 </li></ul><ul><li>A sudden electrical sensation down the neck and back triggered by neck flexion </li></ul><ul><li>27% of patients CSM Crandall Batzdorf J Nsx 66:25:57-66 </li></ul><ul><li>A lesion in the posterior columns of the cervical spinal cord is the cause of Lhermitte's sign in multiple sclerosis . Anatomic-radiologic basis of Lhermitte's sign in multiple sclerosis J. A. Gutrecht Archives Neurol Aug 93 </li></ul>Les douleurs à type discharge éléctrique consécutives à la flexion cephalique dans la sclérose en plaques. Un cas de la sclérose multiple. Revue neurologique, Paris, 1924
    47. 49. <ul><li>Upper motor dysfunction </li></ul><ul><ul><li>Hyperactive deep tendon reflexes </li></ul></ul><ul><ul><li>Ankle and/or patellar clonus </li></ul></ul><ul><ul><li>Increased Tone/Spasticity ( especially of the lower extremities, bladder wall  frequency and nocturia ) </li></ul></ul><ul><ul><li>Pathological reflexes are also present . </li></ul></ul><ul><ul><li>Babinski sign </li></ul></ul><ul><ul><li>Hoffman sign. </li></ul></ul><ul><ul><li>Pectoralis muscle reflex. </li></ul></ul><ul><ul><li>Jaw jerk may distinguish an upper cervical cord compression from lesions that are above the foramen magnum. </li></ul></ul>
    48. 50. <ul><li>Weakness is most commonly seen in the triceps and/or hand intrinsic </li></ul><ul><li>Muscle atrophy in the following muscles: supraspinatus, infraspinatus, deltoid, triceps, and the first dorsal interosseus muscle. Proximal motor weakness, most commonly in the iliopsoas followed by the quadriceps femoris </li></ul><ul><li>Gait stiff or spastic gait </li></ul><ul><li>Sensory abnormalities variable pattern Loss of vibratory sense or proprioception in the extremities can occur (feet) </li></ul><ul><li>Spinothalamic sensory loss may be asymmetric. </li></ul><ul><li>Romberg test stands with the arms held forward </li></ul><ul><li>and the eyes closed (test for position sense; loss of balance consistent with posterior-col dysfunction. </li></ul>
    49. 51. <ul><li>Babinski’s extension of the big toe and fanning of the other toes in response to stroking the sole of the foot </li></ul>
    50. 52. <ul><li>Hyperextension and lateral rotation toward the symptomatic side </li></ul><ul><li>Works by narrowing the ipsilateral neural foramina during lateral flexion and rotation, while the initial extension aggravates posterior disk bulging. </li></ul><ul><li>While this maneuver has a low sensitivity for cervical radiculopathy, it has a specificity of nearly 100%. </li></ul>Roy Glenwood Spurling American neurosurgeon, born September 6, 1894, Centralia, Missouri; died February 7, 1968, La Jolla, California. Spurling’s Maneuver for Radiculopathy 1935 Practical Neurological Diagnosis, with Special Reference to Problems of Neurosurgery
    51. 53. <ul><ul><li>Only valuable if it is associated with other upper motor neuron–related findings. </li></ul></ul><ul><ul><li>The Hoffman sign : Hand at rest, stabilize the proximal phalanx between the examiner's index and middle finger. With the examiner's thumb distal middle finger is flicked  reflex contraction of the thumb and index finger </li></ul></ul><ul><ul><li>The sensitivity of this examination maneuver may be increased by examining the patient during multiple full flexion or extension of the neck (Dynamic Hoffman sign). </li></ul></ul>Ohne Zusammenfassung
    52. 54. <ul><li>Finger-escape sign. The patient holds his fingers extended and adducted. In patients with cervical myelopathy, the two ulnar digits will flex and abducted usually in less than 1 minute. Ono K JBJS ‘87 </li></ul>
    53. 55. <ul><li>Inverted radial reflex. Tapping the distal brachioradialis tendon produces a hypoactive brachioradialis reflex plus hyperactive finger flexion, this is a positive radial reflex. </li></ul><ul><li>This correlates with cord and C5 root lesions that produce spasticity distal to the compression and a hypoactive response at the level of the root/ant horn cells. </li></ul>
    54. 56. Grip-and-release test. Normal adults can perform rapid complete grip and release to full finger extension 20 times in 10 seconds. This not only becomes slower but, in advanced cases, exaggerated wrist flexion occurs with attempted finger extension and exaggerated wrist extension occurs with finger flexion.
    55. 57. <ul><li>Vladimir Mikhailovich Bekhterev 1902 </li></ul><ul><li>This reflex involves the lateral and medial pectoral nerves (innervation from the C-5 through T-1 roots). </li></ul><ul><li>Tapping of the tendon of the pectoralis major in the deltopectoral groove </li></ul><ul><li>In the normal state, contraction may be felt, but gross contraction and movement are not seen. </li></ul><ul><li>A hyperactive response causes adduction and internal rotation of the shoulder </li></ul>
    56. 58. It suggests compression in the upper cervical spine (C2-C4). Concept that compression of the spinal cord above the level of the innervating roots of the reflex should prevent the normal descending inhibition of the spinal reflexes, resulting in hyperreflexia. It does not exclude coexisting compression at lower levels
    57. 59. <ul><li>The main clinical features are localized wasting and weakness of the extrinsic and intrinsic hand muscles, but not accompanied by either sensory loss or spastic quadriparesis. </li></ul><ul><li>Ono K, Ebara S, Fuji T: Myelopathy hand. New clinical signs of cervical cord damage. J Bone Joint Surg Br 1987; 69 (2): 215-219 </li></ul>
    58. 60. <ul><li>Plain film </li></ul><ul><ul><li>(AP), </li></ul></ul><ul><ul><li>Lateral :Overall sagittal alignment (lordosis versus kyphosis) </li></ul></ul><ul><ul><li>Flexionextension: Instablility, a compensatory subluxation one or two levels above the stiffer levels. </li></ul></ul><ul><ul><li>Oblique views: foraminal narrowin due to uncovertebral joint spurring </li></ul></ul><ul><li>CT/ CT Myelography better definition of bone spurs and OPLL. The exact degree of cord deformation in the transverse plane </li></ul><ul><li>MRI Indications: Persistent neck or arm pain (present </li></ul><ul><li>for more than 2 or 3 months), neurologic findings, or a worsening symptomatic picture warrants neuroradiologic investigation. If evidence of myelopathy is present on physical examination, </li></ul><ul><li>Electromyographic–nerve conduction : carpal tunnel syndrome, ulnar cubital tunnel syndrome, or thoracic outlet syndrome. </li></ul><ul><li>Electrodiagnostic modalities may also help elucidate the confusing </li></ul><ul><li>clinical presentations of amyotrophic lateral sclerosis, multiple sclerosis, </li></ul><ul><li>and severe peripheral neuropathy. </li></ul>
    59. 61. <ul><li>Myodil Column Displacement </li></ul><ul><ul><li>Central and Lateral Filling defects, Root sheath obliteration </li></ul></ul>
    60. 62. <ul><li>Conservative </li></ul><ul><li>Surgical </li></ul><ul><li>Complex decision making </li></ul>
    61. 63. <ul><li>Patients with neuroradiologic evidence </li></ul><ul><li>of spinal cord compression but no symptoms or signs of myelopathy should generally be observed. </li></ul><ul><li>Exception would be a patient with such severe compression that even low-energy trauma (rear-end motor vehicle impact or a fall) result in SCI </li></ul>
    62. 64. <ul><li>Natural history of cervical myelopathy for most patients is slow deterioration over time . Typically, this is in a stepwise fashion with variable periods of stable neurologic function. </li></ul><ul><li>Extent of myelopathy is reflected predominantly by physical examination findings (balance deficits, gait, motor weakness, long-tract signs, and changes in function=motor) </li></ul>
    63. 65. <ul><li>If the patient is in a plateau period without recent exacerbation, nonoperative treatment may be indicated. </li></ul><ul><li>Reevaluation every 6 to 12 months to look for deterioration of neurologic function or a change in symptoms may be appropriate. </li></ul>
    64. 66. <ul><li>The amount of pain experiencing </li></ul><ul><li>Degree of change of fcn that can be tolerated, </li></ul><ul><li>Evaluation of symptoms. </li></ul><ul><li>Severity of compression evident on neuroradiologic studies (Worsening: cord area, cord atrophy, myelomalacia kyphotic deformity) </li></ul><ul><li>Ex Rapid neurologic deterioration </li></ul><ul><li>should undergo earlier operative intervention. </li></ul><ul><li>Positive Prognositic Factors </li></ul><ul><li>Larger transverse area of the cord, </li></ul><ul><li>Younger patient age </li></ul><ul><li>Shorter duration of symptoms </li></ul><ul><li>Single rather than multiple levels of involvement. </li></ul><ul><li>Fujiwara J Bone Joint Surg Br 1989;71: 393-398. Koyanagi T, Hirabayashi K, Spine 1993 </li></ul>
    65. 67. <ul><li>Address 3 goals </li></ul><ul><li>1. Pain relief </li></ul><ul><li>2. Improved Function </li></ul><ul><li>3. Prevention of recurrence </li></ul>
    66. 68. <ul><li>1. Pain relief </li></ul><ul><li>PT, Rehabilitation, Medication, Injection therapy, Manipulation all differ in approaches. </li></ul><ul><li>2. Improved Function </li></ul><ul><li>CSM major physical capacity deficits </li></ul><ul><li>Disuse </li></ul><ul><li>Change in endurance/aerobic fitness </li></ul><ul><li>Each pain episode increases fear </li></ul>
    67. 69. <ul><li>3. Prevention of recurrence </li></ul><ul><li>“ Cycling down” : Disuse leads to decreasing physical capacity which makes the now less protected area subject to overload from even less stress of the initial injury. Chronic reinjury and recurrence. </li></ul><ul><li>Develop protective mechanisms: Condition, strengthen muscles acting around spinal construct. Forms basis of PT. Intensive exercise program of >3mo effective Manniche Lancet ‘88 ,Pain ‘91 </li></ul><ul><li>Repeated PT, Manipulation is generally unsuccessful in treating chronic cond. </li></ul>
    68. 70. <ul><li>Disease Education </li></ul><ul><li>Information (Re: resp pain, anatomy,ergonomics,Wt rdxn, Lifestyle changes) Nutritional, Activity avoidance </li></ul><ul><li>Rest </li></ul><ul><ul><li>Shorter periods of bed rest 2d are as good as longer 7d periods. Prolonged  Negative N balance, deconditioning, loss of BMD, Strength </li></ul></ul><ul><ul><li>Modalities: Hot packs, Cryotherapy, US, Traction, Massage (Psychological and physical benefit) </li></ul></ul><ul><ul><li>Isometrics: Static muscle training (Prevent loss of muscle tone, resistance to atrophy) Lat Dorsi, Rhomboid, Sh Abd, Trapezius (4 supporters neck and shoulder girdle). Cervical Flexor, ext, lat bend, rotator musculature Daily for 1 week, then Aerobic conditioning </li></ul></ul><ul><ul><li>Aerobic Conditioning: Beneficial effect on pain, Weight reduction will decrease spinal loading. Avoid impact aerobics. Focus treadmill/stationary bicycle. Max 30 min 3x/wk </li></ul></ul>
    69. 71. <ul><ul><li>Flexibility Exercises: Maintenance of adequate ROM. Upper back, trunk, shoulders and neck during aerobic phase. Active and AAROM </li></ul></ul><ul><ul><li>No passive ROM or manipulation </li></ul></ul><ul><ul><li>Progressive Resistive Exercises: Change from static to dynamic training. </li></ul></ul><ul><ul><li>Medication </li></ul></ul><ul><ul><li>Nsaids, Narcotics, Muscle Relaxants, Antidepressants </li></ul></ul>
    70. 72. <ul><ul><li>Injection Therapy </li></ul></ul><ul><ul><li>Trigger Point, Selective Nerve Root block </li></ul></ul><ul><ul><li>Manipulation </li></ul></ul>
    71. 73. <ul><li>Can be expected to halt progression in deterioration of neurologic function and may improve motor, sensory, and gait </li></ul><ul><li>disturbance. </li></ul><ul><li>The degree of recovery depends largely on the severity of at the time of intervention. Fujiwara J Bone Joint Surg Br 1989;71: 393-398. Koyanagi T, Hirabayashi K, Spine 1993 </li></ul>
    72. 74. <ul><li>Decompression of Neural elements </li></ul><ul><li>Stabilization of unstable segments </li></ul><ul><li>Ablation of painful articulations via fusion </li></ul>
    73. 75. <ul><li>Progressive Neurologic signs or symptoms </li></ul><ul><li>Presence of Myelopathy for >6 months </li></ul><ul><li>Canal/Vertebral Body diameter approaching 0.4 Law Bernhardt ICL 1995 </li></ul><ul><li>Severe Spinal cord compression Bohlman ’97 </li></ul><ul><li>Cord Signal Changes with any signs CSM recommend earlier intervention before permanent deficits arise </li></ul><ul><li>Atlantoaxial Instability (RA) 1/3-1/2 Vertical Migr dvlp LTS/5yrs  N Hx Death </li></ul><ul><li>Subaxial Segmental Instability </li></ul><ul><li>Difficulty Walking </li></ul><ul><li>Loss of Balance </li></ul><ul><li>Bowel / Bladder Incontinence </li></ul><ul><li>Neck Pain (absence of neural deficit) less defined {Intractable correlated with radiologic studies} </li></ul>
    74. 76. <ul><li>Anterior Options </li></ul><ul><li>Single/Multiple anterior diskectomies with fusion and/or corpectomy (ACDF) </li></ul><ul><li>Strut fusion techniques with or </li></ul><ul><li>without the use of anterior instrumentation. </li></ul><ul><li>Posterior Options </li></ul><ul><li>Single/multilevel laminectomy </li></ul><ul><li>Laminoplasty </li></ul><ul><li>Laminectomy plus fusion procedures. </li></ul>
    75. 77. <ul><li>Factors to be considered </li></ul><ul><li>Number of involved levels </li></ul><ul><li>Overall sagittal alignment </li></ul><ul><li>Direction of compression </li></ul><ul><li>Presence of instability </li></ul><ul><li>Clinical symptoms. </li></ul><ul><li>Weigh Advantages and Disadvantages Ant vs Post </li></ul><ul><li>(1) Approach-related, </li></ul><ul><li>(2) Decompression-related </li></ul><ul><li>(3) Graft related, </li></ul><ul><li>(4) Long-term. </li></ul>
    76. 78. <ul><li>Anterior Approach </li></ul><ul><li>Direct decompression </li></ul><ul><li>Stabilization with arthrodesis </li></ul><ul><li>Correction of deformity </li></ul><ul><li>Axial lengthening of spinal column </li></ul><ul><li>Good axial pain relief </li></ul><ul><li>Posterior Approach </li></ul><ul><li>Less loss of motion </li></ul><ul><li>Not as technically demanding </li></ul><ul><li>Less bracing needed </li></ul><ul><li>4. Avoids graft complications </li></ul>
    77. 79. <ul><li>Anterior </li></ul><ul><li>1. Technically demanding </li></ul><ul><li>2. Graft complications (dislodgment, fracture, and severe settling into the cancellous VB) </li></ul><ul><li>3. Need for postoperative bracing limitations </li></ul><ul><li>4. Loss of motion </li></ul><ul><li>5. Vertebral artery, Dysphagia, Upper airway compromise </li></ul><ul><li>Posterior </li></ul><ul><li>Indirect decompression </li></ul><ul><li>2. Preoperative kyphosis and/or instability </li></ul><ul><li>Late instability </li></ul><ul><li>Adjacent segment degeneration </li></ul><ul><li>Laminectomy procedures :increased risk of postlaminectomy kyphosis, swanneck deformity, or instability with late neurologic deterioration. </li></ul><ul><li>Laminoplasty techniques decrease these risks, but add the potential complication of inadvertent closure of the opened lamina with recurrent stenosis. </li></ul><ul><li>7. Inconsistent axial pain results </li></ul>
    78. 81. <ul><li>Yonenobu et al prefer the anterior approach for patients with pathologic changes at one or two levels and posterior surgery for those with involvement at three or more levels. </li></ul><ul><li>Yonenobu K, Fuji T, Ono K, Okada K, Yamamoto T, Harada N: Choice of surgical treatment for multisegmental cervical spondylotic myelopathy. Spine 1985;10:710-716. </li></ul>
    79. 82. <ul><li>42 yo High school Math teacher </li></ul><ul><li>Slip and fall onto right side of body while at work in October 2005 </li></ul><ul><li>C/o neck pain and radiating Right arm pain 8/10 </li></ul><ul><li>Now on temporary disability </li></ul><ul><li>Rx Vicodin Robaxin </li></ul><ul><li>Pex </li></ul><ul><ul><li>Painful Rom : Flexion 5 deg, ext 10 </li></ul></ul><ul><ul><li>Spurlings + Right side </li></ul></ul><ul><ul><li>Reflexes: Diminished Rt biceps 1+ </li></ul></ul><ul><ul><li>Hoffmans negative </li></ul></ul><ul><ul><li>Motor sensory normal </li></ul></ul>
    80. 84. Axial C5-6 2 3 4 5 6
    81. 85. <ul><li>Doing well </li></ul><ul><li>Feels resolution of neck pain improvement right arm pain </li></ul><ul><li>Off all narcotic Rx </li></ul>
    82. 86. <ul><li>73 yo female neck and arm pain </li></ul><ul><li>2 nd opinion: 1 st rec ACDF </li></ul><ul><li>Failed conserv therapy </li></ul><ul><li>Tried Lyrica, Tegretol </li></ul><ul><li>Worsening pain </li></ul><ul><li>+Lhermittes’s </li></ul><ul><li>Neck and arm pain with extension and rotation to right </li></ul><ul><li>Denies B/Bladder </li></ul><ul><li>Pmhx Trigem Neuralgia, TMJ sx,Osteoperosis </li></ul><ul><li>PEx </li></ul><ul><ul><li>Weak Bilat Shoulder abduction, wrist flexion </li></ul></ul><ul><ul><li>Absent Tri,Bi,Brad reflexes,Lextemities </li></ul></ul><ul><ul><li>+Bilat Hoffmans </li></ul></ul><ul><ul><li>+Spurlings to Right and Left </li></ul></ul>
    83. 88. 2 4-5 4 5 6 5-6
    84. 89. <ul><li>s/p ACDF C45 C56 </li></ul>
    85. 90. <ul><li>59 yo male </li></ul><ul><li>s/p Two level ACDF C 5-6 6-7 </li></ul><ul><li>Now with significant axial neck pain </li></ul><ul><li>Had a Pain modulating unit inserted with no improvement in syx </li></ul><ul><li>Weakness: Wrist E/F, Finger E/F, Bi,Tri </li></ul><ul><li>+Hoffmans </li></ul><ul><li>2+ Reflexes Brad Bi Tri Patellar Achilles </li></ul>
    86. 92. 4
    87. 94. <ul><li>C 3,4,5 Laminoplasty:Plating, Rib graft </li></ul><ul><li>Bilateral foraminotomies C6-7 C7-T1 </li></ul>
    88. 95. <ul><li>Resolution of Axial neck pain </li></ul><ul><li>Resolution of Lextremity pain </li></ul><ul><li>Immediate Improvement in Upper Extremity Strength </li></ul><ul><ul><li>Wrist F/E </li></ul></ul><ul><ul><li>Finger F/E </li></ul></ul><ul><ul><li>Biceps </li></ul></ul><ul><ul><li>Triceps </li></ul></ul>
    89. 99. <ul><li>Brazilian Now with significant axial neck pain, instability, wearing a brace </li></ul><ul><li>Had a previous ASF,HWR,PSF, decompression </li></ul><ul><li>Weakness: Wrist E/F, Finger E/F, Bi,Tri, Interossei </li></ul><ul><li>+Hoffmans </li></ul><ul><li>2+ Reflexes Brad Bi Tri Patellar Achilles </li></ul>
    90. 104. Hoffmans + Gait Weakness Prox Neck Pain Hyper reflexic Myelo Hand Babinski
    91. 110. <ul><li>Laminoplasty Oct 2005 C4-7 </li></ul>
    92. 114. <ul><li>Patient underwent a laminoplasty </li></ul><ul><li>Patient has done well and since returned to work as an accountant 3 months afterwards </li></ul>
    93. 115. <ul><li>Surgery should be a last resort, when conservatives measures fail. </li></ul><ul><li>In some cases surgery needs to be done sooner than later, or even urgently, depending on the physical exam, history, neural deficits, and size of the herniation. </li></ul>
    94. 117. <ul><li>All our procedures are peformed </li></ul><ul><li>in a minimally invasive manner. </li></ul><ul><li>All patients receive a plastics closure and are followed closely afterwards </li></ul>
    95. 118. <ul><li>Payne EE, Spitlani JD. An anatomicopathologic study of 70 specimens (using a special technique) with particular reference to the problem of cervical spondylosis. Brain 1957;80:571-96 </li></ul><ul><li>Parke WW. Correlative anatomy of cervical spondylotic myelopathy. Spine 1988;13:831-7 </li></ul><ul><li>Penning L, Wilmink JT, van Woerden HH, Knol E. CT myelographic findings in degenerative disorders of the cervical spine: Clinical significance. AJR Am J Roentgenol 1986;146:793-801. </li></ul><ul><li>Panjabi M, White AD. Biomechanics of nonacute cervical spinal cord trauma. Spine 1988;13:838-42. </li></ul><ul><li>Ogino H, Tada K, Okada K, et al. Canal diameter, anteroposterior compression ratio, and spondylotic myelopathy of the cervical spine. Spine 1983;8:1-15. </li></ul><ul><li>Nurick S. The pathogenesis of the spinal cord disorder associated with cervical spondylosis. Brain 1972;95:87-100. </li></ul><ul><li>J Neurol Sci. 1967 May-Jun;4(3):607-8 The Rt. Hon. The Lord Brain, F.R.S., D.M., F.R.C.P. (1895-1966). </li></ul><ul><li>Bunge RP, Puckett WR, Becerra JL, et al. Observations on the pathology of human spinal cord injury. A review and classification of 22 new cases with details from a case of chronic cord compression with extensive focal demyelination. Adv Neurol 1993;59:75-89. </li></ul><ul><li>Choi DW. Excitotoxic cell death. J Neurobiol </li></ul><ul><li>Lord Brain, M. Wilkinson. Cervical Spondylosis and other disorders of the cevical spine. 1967. </li></ul><ul><li>Irvine DH, Foster JB, Newell DJ: Prevalence of cervical spondylosis in a general practice. Lancet 1965 May 22; 14: 1089-92 </li></ul><ul><li>Holt S, Yates PO: Cervical spondylosis and nerve root lesions. Incidence at routine necropsy. J Bone Joint Surg Br 1966 Aug; 48(3): 407-23 </li></ul><ul><li>Rahim KA, Stambough JL: Radiographic evaluation of the degenerative cervical spine. Orthop Clin North Am 1992 Jul; 23(3): 395-403 </li></ul><ul><li>Fujiwara K, Yonenobu K, Ebara S, Yamashita K, Ono K: The prognosis of surgery for cervical compression myelopathy: An analysis of the factors involved. JBJS BR 1993 </li></ul><ul><li>Koyanagi, Toyama Y, Fujimura Y: Predictability of operative results of cervical compression myelopathy based on preoperative </li></ul><ul><li>computed tomographic myelography. Spine 1993;18:1958-1963. </li></ul>
    96. 119. <ul><li>Thank you for your time. </li></ul><ul><li>If you know someone who could benefit from a consultation for Neck Pain, Neck Arthritis or Cervical Spondylotic Myelopathy please refer them to our online website or call toll free to schedule an appointment </li></ul><ul><li>1-8SPINECAL-1 </li></ul><ul><li>www.beverlyspine.com </li></ul><ul><li>www.santamonicaspine.com </li></ul>