Cervical Myelopathy Differential Diagnosis


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Cervical Cord Compression
Journal of Orthopaedic & Sports Physical Therapy
Monica Sasaki, MPT, FAAOMPT

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Cervical Myelopathy Differential Diagnosis

  1. 1. Journal of Orthopaedic & Sports Physical Therapy Official Publication of the Orthopaedic and Sports Physical Therapy Sections of the American Physical Therapy Association Cervical Cord Compression Secondary to Ossification of the Posterior Longitudinal Ligament Monica Sasaki, MPT, FAAOMPT 1 Study Design: Resident’s case problem. fied, appropriate and efficient re- Background: A 52-year-old Chinese male with a 10-year history of gradually worsening right hip ferral to specialists and appropri- stiffness, weakness, and pain was referred to physical therapy by his orthopedist, who made a ate medical care can then be diagnosis of developmental dysplasia of the right hip, with possible Legg-Calve-Perthes disease. facilitated. A hypothesis-driven ap- The patient reported multiple falls over the last several years and a gradual onset of low back pain with an onset of ‘‘electricity’’ down both legs. The patient also reported mild numbness in both proach to evaluation and the gath- forearms and the right hand over the previous several months. This resident’s case problem ering of evidence to identify or illustrates how a physical therapist recognized the presence of an atypical musculoskeletal rule out a musculoskeletal pathol- pathology through the use of hypothesis-driven clinical reasoning and detailed physical examina- ogy is an essential skill for the tion. physical therapist as the roles and Diagnosis: Examination of the patient’s lumbar and cervical spine and hips revealed joint responsibilities of physical thera- dysfunctions. Neurological testing revealed hyperreflexia. Special testing revealed lower extremity pists on health care teams expand. clonus with a positive Babinski sign with gait disturbances. The patient was referred back to his The patient in this resident’s primary physician and then to a neurologist and neurosurgeon. An MRI revealed cervical myelopathy due to ossification of the posterior longitudinal ligament from C3/C4 to C5/C6. The case problem presented with an patient then underwent a C3 through C7 laminectomy. initial medical diagnosis that was Discussion: It is always imperative that sound clinical reasoning be used when performing unrelated to the final diagnosis of physical therapy evaluations, regardless of the referral status of the patient. Patients with cervical myelopathy secondary to nonmusculoskeletal pathology may seek physical therapy services and it is the physical therapist’s ossification of the posterior longi- responsibility to complete a thorough examination and refer to specialists when appropriate. tudinal ligament. This is a poten- J Orthop Sports Phys Ther 2005;35:722-729. tially serious pathology that can Key Words: cervical spine, myelopathy, neck, spine, spinal cord result in permanent neurological dysfunction if not identified early. Many physical therapists treat indi- O ne of the primary goals of the American Physical viduals with acute and chronic Therapy Association is to promote ‘‘physical therapists as cervical pathologies and it is im- autonomous practitioners to whom patients/clients have portant to identify pathologies that unrestricted direct access as an entry point into the require referral to a specialist. health care delivery system.’’1 Direct access laws allow In 1838, Key was the first to physical therapists to work as independent practitioners who are able to report compression of the spinal evaluate and treat patients without a physician’s referral. Thirty-nine cord by an ossified liga- states in the United States now allow some form of direct access.1 It is ment.9,10,21,27,30,31 Later in Japan essential that physical therapists use a systematic approach to evaluation in 1960, Tsukimoto described the to ensure that proper care and services are provided to their patients. A pathology with autopsy find- detailed interview and physical examination, as well as utilization of ings.9,10,27,31 Terayama then intro- special questions, are all necessary to assist the therapist in implicating duced the term ossification of the or ruling out sinister and/or nonmusculoskeletal pathology. If identi- posterior longitudinal ligament (OPLL) in 1964.21,27 Due to the 1 Staff Physical Therapist, California Pacific Medical Center, San Francisco, CA. rapidly increasing number of cases This resident’s case problem was completed in fulfillment of the requirements of the Kaiser Permanente Hayward, PT Fellowship in Advanced Orthopedic Manual Therapy. identified in Japan, the Ministry of Address correspondence to Monica Sasaki, California Pacific Medical Center, Department of Physical Public Health and Welfare of Ja- Medicine and Rehabilitation, 2360 Clay Street, San Francisco, CA 94115. E-mail: mjsasaki@comcast.net pan appointed a special study 722 Journal of Orthopaedic & Sports Physical Therapy
  2. 2. group, the Investigation Committee for Ossification detailed physical evidence gathering, recognized the of the Posterior Longitudinal Ligament, to research presence of an atypical musculoskeletal pathology the disease in 1974.23,27,31 and facilitated referral to specialists to attain an OPLL is characterized by the development of appropriate diagnosis and enhance the care of the cortical bone made up of lamellar bone with devel- patient. oped Haversion canals with or without marrow fat.23 The ossification is located along the posterior margin of the vertebral body, in the posterior longitudinal Patient Characteristics and History ligament, and is most commonly found in the mid cervical spine (C3-C5).7,27 The diagnosis of OPLL is usually made by its appearance on plain radiographs, A 52-year-old Chinese male was referred to physical conventional tomography, or computerized tomog- therapy by his orthopedist with a diagnosis of devel- raphy.27,29 The resultant cord compression is best opmental dysplasia of the right hip and possible visualized through magnetic resonance imaging Legg-Calve-Perthes disease. He presented with a 10- (MRI).7,13,29 year history of gradually worsening right hip stiffness, OPLL is one of the most common causes of weakness, and pain. Over the previous 2 to 3 years, myelopathy in Asians.17,28 The disease has a preva- the patient reported multiple falls, which he attrib- lence of 1.9% to 4.3% in Japan and 0.01% to 1.7% in uted to hip stiffness and decreased balance. He the United States and Europe.12 It is most commonly reported a gradual onset of low back pain over the diagnosed between the fifth and seventh decades of previous 4 years, with an onset of ‘‘electricity’’ down life, most frequently between the ages of 50 and 60 both legs approximately 1 year ago. Upon question- years.12,27,29,30,31 Prevalence in males is twice that in ing, the patient reported mild numbness in both females.7,27,29,30,31 forearms and the right hand over the past several This case illustrates how a physical therapist, with months. The body chart depicts the patient’s symp- the use of hypothesis-driven clinical reasoning and toms (Figure 1). R E S I D E N T’ S CASE PROBLEM FIGURE 1. Body chart indicating areas of symptoms. J Orthop Sports Phys Ther • Volume 35 • Number 11 • November 2005 723
  3. 3. The patient worked full time as a supervising feet, cervical cord compression was considered. The maintenance technician. He had reduced his physical initial working hypothesis following the patient inter- activities over the past 2 to 3 years secondary to his view was spinal cord involvement with a concomitant symptoms. He walked 0.75 to 1.5 km 4 to 5 times a hip component, possibly osteoarthritis. The initial week for regular exercise. He stopped playing basket- physical therapy evaluation included a cervical spine ball and tennis regularly secondary to leg weakness examination, as well as an assessment of the lumbar approximately 2 to 3 years ago. Squatting and stairs spine and the right hip. This was due to the patient’s aggravated his current symptoms of lower extremity report of bilateral upper and lower extremity symp- weakness. He required upper extremity support from toms and the hypothesis of spinal cord compression. furniture and railings to return from squatting and A neurological examination, which included motor, ascend and descend stairs safely. Standing 20 to 30 sensory, and reflex testing was also performed that minutes and walking approximately 1.5 km would included tests to implicate central involvement, in- aggravate his symptoms of weakness and low back/ cluding clonus, Babinski, and Hoffman’s signs. hip pain. Once aggravated, his symptoms would slowly decrease after sitting 5 to 15 minutes or lying Tests and Measures down. The patient was trying to control his symptoms Observation/Inspection The patient presented with a with avoidance of activity and modifying activities by decrease in lumbar lordosis with the pelvis held in a incorporating rest breaks in sitting or lying. His sleep mild posterior tilt. A spinal shift or side bend was not was uninterrupted and he awoke in the morning with present on visual inspection. During stance both an improvement in pain, but with mild stiffness in knees were locked in extension, providing lower the low back and hip. His symptoms appeared to extremity stability. worsen as the day progressed. Gait The patient exhibited an antalgic gait pattern. The patient had a history of hypoglycemia and He was observed to lock his right knee in hyperexten- hyperlipidemia. He was taking Nabumetone or sion and use a shortened stance phase on the right. Relafen for pain with minimal improvements in Due to a mild right foot drop, he compensated with a overall pain level. Relafen is a nonsteroidal anti- steppage pattern (excessive hip and knee flexion) inflammatory drug that exhibits analgesic, antipyretic, and with mild hip circumduction during the swing and anti-inflammatory properties. He denied any phase of the right lower extremity to consistently unexplained weight loss or gain. Imaging studies clear the right foot. included radiographs of the right hip, which revealed Motion Testing Active motion testing of the lumbar an abnormal contour of the femoral head. To clarify spine, cervical spine, and right hip revealed limited the information previously provided, the patient was range of motion. Lumbar flexion was screened by asked questions related to potential spinal cord com- visual observation, with the patient reaching mid shin pression, including whether he had ever experienced with his fingertips. Extension was limited to approxi- his reported numbness and/or tingling in both upper mately 15° by visual observation with the patient extremities and/or lower extremities at the same time reporting mild central low back pain at approxi- and any specific gait disturbances. The patient re- mately L5. Right and left side bending was limited to ported bilateral lower extremity ‘‘electricity’’ and 7.6 cm between the fingertips and the lateral tibial- weakness at the same time, as well as ‘‘tripping over femoral joint line, as measured with a tape measure. his feet.’’ His difficulty consistently clearing the right Right side bending resulted in a ‘‘pulling’’ sensation foot resulted in multiple falls over the previous in the right lumbar region. several months. He denied problems with urinary Cervical range of motion was assessed utilizing initiation and/or bowel control. techniques described by Norkin and White.23 Cervical The patient’s goals were to gain strength in his legs spine flexion was measured with a tape measure with and to decrease the frequency of pain and falls. a distance of 2.5 cm from the chin to the sternal notch. A goniometer was used to measure extension DIAGNOSIS and rotation. Extension measured 45°, with pain in the left upper trapezius region, while right rotation Working Hypothesis was limited to 60°, with pain in the right upper trapezius region. Left rotation was painless at 70°. The patient presented with chronic low back and Using goniometric techniques described by Norkin right hip pain with lower extremity weakness that was and White,23 hip flexion was 120° bilaterally; right moderate in severity and minimal in irritability. His hip internal rotation was limited to 10°, and left hip symptoms of leg/back pain and weakness were easily internal rotation was limited to 20°. aggravated but relieved quickly, within minutes with Neurological Testing Reflex testing with 6 repetitive rest. Based on the history and the patient’s response taps over the tendon revealed hyperreflexia of the to special questioning, which included bilateral upper patellar, Achilles, biceps, triceps, and finger flexors and lower extremity symptoms and tripping over his tendons bilaterally.16 Motor testing using manual 724 J Orthop Sports Phys Ther • Volume 35 • Number 11 • November 2005
  4. 4. Table. Summary of initial working hypotheses with supporting data. Data Refuting Working Hypotheses Supporting Data Hypotheses Central cord involvement • Bilateral symptoms, positive UMN signs: positive (cord compression/cervical myelopathy) Babinski, 4- to 5-beat clonus bilateral ankles • Bilateral UE/LE hyperreflexia: patellar, achilles, biceps, triceps, finger flexors • Frequent falls, abnormal gait due to foot drop Lumbar stenosis • Bilateral symptoms, aggravating factors: standing/walking • Positive UMN signs • LE weakness: 3/5 extensor hallucis, 4/5 quadriceps, 3+/5 • Hyperreflexia peroneals • UE signs and symptoms • Gradual onset of symptoms Hip OA (as a concomitant condition) • Right hip pain and limited motion influencing patient’s • Positive UMN signs ability to stand, walk, and squat • Hyperreflexia • Decreased hip internal rotation (10°) • UE signs and symptoms Suspected nonmusculoskeletal • Gradual onset of symptoms with progressive decrease in (ie, MS, ALS, spinal tumor) strength and decline in function • Distribution of symptoms in upper and lower extremity • Frequent falls secondary to LE weakness Abbreviations: ALS, amytrophic lateral sclerosis; LE, lower extremity; MS, multiple sclerosis; OA, osteoarthritis; UE, upper extremity; UMN, upper motor neuron. muscle testing revealed 4/5 strength of the flexor withdrawal on the right. Hoffman’s sign, tested quadriceps (reflective of L3 and L4 nerve roots) in the upper extremity with a flick of the nail of the bilaterally.3,15 Testing of the extensor hallucis (reflec- middle finger,8 was negative bilaterally. tive of L5 nerve root) revealed 3/5 strength on the Joint Play (Accessory Motion) Testing Passive accessory right and 4/5 on the left. Testing indicated 3/5 movement was assessed in the lumbar and cervical strength of the peroneals (reflective of L5 and S1 spine, using the movement scale described by nerve roots) bilaterally.3,15 Finger flexors and triceps Maitland.16 Central posterior-to-anterior (PA) pres- (reflective of C7 nerve root) strength was 4/5 bilater- sure at L4 and L5 indicated limited mobility with ally.3,15 Superficial sensation was assessed with a local tenderness. Unilateral PA pressure at L5 and S1 toothpick, comparing right to left over specific also indicated limited mobility with local tenderness. dermatomes.15,16 The patient reported decreased Unilateral PA pressure at C6 to T3 indicated limited mobility throughout. sharp sensation at the left groin region (reflective of L1 nerve root). All other areas were symmetrical. Neurodynamic Testing The straight leg raise test Possible Differential Diagnosis performed in supine with the knee extended was Following the physical examination, the working limited to 50° bilaterally without reproduction of hypothesis was spinal cord involvement with superim- R E S I D E N T’ S symptoms.15 The prone knee bend test assessed in posed right hip osteoarthritis. Lumbar stenosis was prone by passively flexing the knee was limited to still a possibility along with a nonmusculoskeletal 115° bilaterally without reproduction of symptoms.15 pathology (eg, multiple sclerosis, amyotrophic lateral Passive neck flexion was assessed in supine without sclerosis, etc). Spinal cord involvement was supported complaints.15 by the positive clonus and Babinski tests, in addition Special Tests Lower extremity clonus was tested with to the positive findings on the neurological exam. the knee flexed at 45°. The ball of the foot was The Table includes a summary of the initial working grasped by the examiner and the ankle was quickly hypotheses following the physical examination and CASE passively dorsiflexed.2 Upper extremity clonus was the data supporting and refuting each hypothesis. tested with quick passive wrist extension with the elbow supported in 90° of flexion.2 Five-beat clonus Outcomes was observed for the right ankle and 4-beat clonus PROBLEM for the left. No clonus was noted in the upper The patient’s status and examination findings were extremities. The Babinski reflex was tested in supine, discussed with his primary care physician. One week with stimulation of the sole of the foot from the later, the patient was referred to a neurologist who midpoint of the heel, then distally and laterally along suspected cervical spondylosis with myelopathy. The the outer border of the foot, then medially to the MRI (Figure 2), which was ordered by the neurolo- ball of the foot, with a blunted, pointed object.2,8 The gist, showed diffuse spondylosis with multilevel areas patient exhibited a positive test bilaterally, including of central lateral recess and neural foraminal stenosis J Orthop Sports Phys Ther • Volume 35 • Number 11 • November 2005 725
  5. 5. extending from C3/C4 to C5/C6, with associated to severe stenosis with degenerative disc disease, L3-4 myelomalacia of the spinal cord due to cord compres- mild stenosis, and L4-5 mild to moderate stenosis. He sion and spinal stenosis. The patient was then re- then underwent an L1-L4 lumbar laminectomy. One ferred for a neurosurgical consultation. He reported week after discharge home, the neurosurgeon fol- to the neurosurgeon that he could no longer carry lowed up with the patient by telephone. The patient heavy objects and could not hold urine, resulting in reported that his preoperative leg pain was com- ‘‘dribbling’’ if he waited too long. The neurosurgeon pletely gone and his walking was slightly better. He found decreased pinwheel sensation from the neck did however, notice bilateral thigh numbness that he down and observed an extremely slow, unsteady was not aware of prior to the surgery. wide-based gait pattern. He interpreted the MRI In total, this patient consulted with 3 specialists results as C3-4, C4-5, C5-6, and C6-7 disc osteophyte who addressed the issues documented in his initial complex, likely due to ossification of the posterior physical therapy evaluation. He improved with respect longitudinal ligament. He also noted increased signal to his upper extremity symptoms but continued to intensity within the spinal cord at C4/5 due to either exhibit residual gait disturbances that were addressed gliosis or edema within the spinal cord. The with medications and later by a multilevel lumbar neurosurgeon’s diagnosis was cervical myelopathy laminectomy. due to OPLL. He recommended urgent surgery to decompress the spinal cord. The patient under went a C3 through C7 laminectomy with the additional removal of a hypertrophied yellow ligament (ligamentum flavum) approximately 1 month after the initial neurosurgery consultation. The delay in surgery was due to the patient declining immediate intervention, per the neurosurgery notes. Postoperatively, the patient was able to ambulate with a walker prior to discharge home. Four days after discharge, the neurosurgeon followed up by telephone with the patient. His daughter reported that he was walking with improved balance compared to his preoperative status and he no longer complained of his preoperative arm symp- toms. Five weeks after the surgery, the patient was re- ferred to physical therapy at another facility for rehabilitation. He continued to exhibit gait distur- bances, lower extremity weakness, and hyperreflexia. He completed 5 therapy sessions, which focused on lower extremity strengthening, stretching, and gait training. He was also fitted for an ankle foot orthosis at that time. The patient was then referred to a physiatrist for functional and spasticity evaluation. The physiatrist found a stiff-knee gait pattern with decreased step length. He noted decreased selective motor control with decreased strength bilaterally in the iliopsoas (4/5), quadriceps (4/5), hamstrings (4/5), tibialis anterior (3/5), gastrocnemius (3–/5), triceps (4/5), and finger flexors/intrinsics (4/5 on the right). Reflexes were found to be abnormal, but the levels were not specified. Sensory loss was found to be patchy with levels not specified. The physiatrist’s impression was a spastic gait pattern. He recom- mended a trial of Baclofen to decrease the muscle spasms. The patient continued to report leg pain that limited his ability to walk. He underwent an MRI of FIGURE 2. Magnetic resonance imaging (MRI) showing cervical the lumbar spine, which demonstrated L1-2 moderate cord compression. 726 J Orthop Sports Phys Ther • Volume 35 • Number 11 • November 2005
  6. 6. DISCUSSION Consistent with OPLL, the patient was in his fifth decade, was of Asian descent, and reported bilateral This resident’s case problem shows the importance upper and lower extremity symptoms, a spastic gait of sound clinical reasoning with hypothesis genera- pattern, and bladder dysfunction. The physical thera- tion during the patient interview to guide a thorough pist suspected cord compression based on answers to patient examination. When the interview and physical questioning during the patient interview. She imme- examination findings did not fit a typical muscu- diately focused on the special questions discussed loskeletal pathology and tests for central nervous previously and on the testing for hyperreflexia, system involvement were positive, the patient was clonus, and upper motor neuron involvement. The immediately referred to specialists for further investi- diagnosis was confirmed with MRI, which demon- gation. strated a C3-4, C4-5, C5-6, C6-7 disc osteophyte A key question in the management of this patient complex with cord compression. The type of OPLL was identifying the factors, which led to a delay in was not determined or stated in the neurosurgery diagnosis. The patient did not seek immediate med- documentation. ical attention when his symptoms initially arose or Along with OPLL, one may also see ossification of when his symptoms began to progress. He felt that the anterior longitudinal ligament and/or his weakness was due to cutting back on his activities. ligamentum flavum (yellow ligament).30,31,32 This pa- tient did demonstrate hypertrophy of the yellow Furthermore, the patient did not divulge all of his ligament, which was removed during surgery. symptoms, including bilateral lower extremity weak- The patient demonstrated several features com- ness with electricity sensations and loss of urinary monly seen with OPLL; however, it is difficult to control, to his primary physician or his orthopedist. define a typical clinical presentation for OPLL. This He only disclosed his main complaint of right hip is due to the fact that ossification of the ligament and low back pain. His primary care physician did does not necessarily result in cervical myelopathy. A not perform upper motor neuron testing. given patient may be asymptomatic or present with The etiology of OPLL is unknown, but a number sensory and/or motor disturbances in the upper of risk factors have been associated with the disorder. and/or lower extremity, with or without bladder Because of the high prevalence found in Asian dysfunction, abnormal reflexes, or gait distur- countries, researchers believe there may be a genetic bances.12,19,24,31 In those studies involving subjects as well as a dietary component (high salt, low meat with confirmed diagnoses of OPLL24,27 the most intake) associated with OPLL.11,12,20,32 Higher serum common symptoms were cord signs, which were estrogen levels, along with a history of diabetes defined by Ono24,27 as bilateral lower extremity mo- mellitus have also been associated with tor and sensory disturbances. OPLL.11,29,31,32 Other risk factors include a high body The treatment for OPLL ranges from conservative mass index, hyperinsulinemia, hypoparathyroidism, to surgical management.7,18,30 There are no specific low enteral calcium absorption, fluoride intoxication, studies that have reviewed the efficacy of conservative and abnormal blood levels of retinal and retinal- treatment. However, Tsuyama31 stated that almost binding protein.4,11,25,27,29,30,31 70% of patients responded favorably to conservative There are 4 types of OPLL, which are defined by management, identified as traction, bed rest, neck R E S I D E N T’ S the distribution of ossification: continuous, segmen- braces, avoidance of hyperextension, and physical tal, mixed, and circumscribed.6,27,31 Continuous therapy, for which no specific details were listed. OPLL has the appearance of ossification extending Tsuyama31 postulated that neurological symptoms are over several vertebral bodies. Segmental OPLL occurs caused by a combination of pressure from the ossified with ossification behind each vertebral body sepa- mass and dynamic irritation of the cord by abnormal rately. Mixed OPLL is a combination of both continu- bony prominences and suggested that conservative ous and segmental. Circumscribed OPLL occurs techniques would decrease the dynamic irritants. The when the ossification corresponds to an interver- patient in this study did not receive any of these CASE tebral disc level. conservative treatments. This may be due to the fact Individuals with OPLL may be asymptomatic or that he did not seek care in the early stages of the may have symptoms consistent with spinal cord com- disorder. By the time he was diagnosed, his physician pression.18,22,30 The onset of symptoms is often insidi- determined that his only treatment option was sur- ous or can present after minor trauma.14 The PROBLEM gery. ossification can result in significant myelopathy and is Surgical management includes a number of tech- often characterized by a spastic gait pattern, abnor- niques, with the choice of technique depending on mal deep tendon reflexes, muscle atrophy/weakness the distribution of ossification and the physician’s below the area of compression, disturbances of fine preference. The approach can be either anterior movements of the hand, and bladder dysfunc- and/or posterior and may or may not include fusion tion.7,18,19 of vertebral levels. Techniques include the following: J Orthop Sports Phys Ther • Volume 35 • Number 11 • November 2005 727
  7. 7. posterior decompressive laminectomy, laminoplasty APTA vision, mission and goals. Available at: http:// with or without posterior fusion; anterior fusion; www.apta.org/Govt_Affairs/state/directaccess/State3. Ac- vertebrectomy with microsurgical resection of the cessed July 1, 2004. 2. Chusid JG, deGroot JL. Correlative Neuroanatomy. 12th ossified posterior longitudinal ligament and autograft ed. East Norwalk, CT: Appleton & Lange; 1988. fusion from the iliac crest; anterior cer vical 3. Cyriax JH. Textbook of Orthopaedic Medicine Vol. 1: discectomy with microsurgical resection of the ossi- Diagnosis of Soft Tissue Lesions. London, UK: Bailliere fied posterior longitudinal ligament and autograft Tindal; 1975. fusion; medial corpectomy, which is the removal of 4. De Bandt M, Meyer O, Fuster JM, Kahn MF. Ossifica- the vertebra with removal of the ossified posterior tion of the posterior longitudinal ligament, diffuse, longitudinal ligament, and fusion with a fibular graft; idiopathic skeletal hyperostosis, abnormal retinol and retinol binding protein: a familial observation. and multilevel anterior corpectomy/fusion followed J Rheumatol. 1995;22:1395-1398. by posterior fusion.5,7,10,17,31 This patient underwent 5. Epstein NE. Circumferential cervical surgery for ossifica- a C3-C7 posterior decompressive laminectomy with tion of the posterior longitudinal ligament: a removal of a hypertrophied yellow ligament. This was multianalytic outcome study. Spine. 2004;29:1340- consistent with surgical interventions discussed in the 1345. literature. 6. Epstein NE. Ossification of the posterior longitudinal ligament in evolution in 12 patients. Spine. 1994;19: 673-681. CONCLUSION 7. Gaucher A, Dellestable F, Blum A, Pere P, Regent D. As the role of physical therapy changes, it is Ossification of the posterior longitudinal ligament in the cervical spine. Arthritis Rheum. 1993;36:273-276. imperative that physical therapists use sound clinical 8. Hoppenfeld S. Orthopaedic Neurology: A Diagnostic reasoning when performing physical therapy evalua- Guide to Neurologic Levels. Philadelphia, PA: Lip- tions to ensure that we are providing appropriate pincott Williams & Wilkins; 1977. medical care. Our role of diagnostician will only 9. Kameyama T, Hashizume Y, Ando T, Takahashi A, become more important to the practice of physical Yanagi T, Mizuno J. Spinal cord morphology and therapy in the future. Patients with nonmusculo- pathology in ossification of the posterior longitudinal skeletal pathology may seek physical therapy services ligament. Brain. 1995;118 (Pt 1):263-278. 10. Klara PM, McDonnell DE. Ossification of the posterior and it is our responsibility to complete a thorough longitudinal ligament in Caucasians: diagnosis and examination and refer to specialists when appropri- surgical intervention. Neurosurgery. 1986;19:212-217. ate. The patient discussed in this resident’s case 11. Kobashi G, Washio M, Okamoto K, et al. High body problem was a clear example of the importance of mass index after age 20 and diabetes mellitus are clinical reasoning and good physician-therapist com- independent risk factors for ossification of the posterior munication. The primary care physician followed up longitudinal ligament of the spine in Japanese subjects: quickly and referred the patient for further testing a case-control study in multiple hospitals. Spine. 2004;29:1006-1010. and to the appropriate specialists. 12. Koga H, Sakou T, Taketomi E, et al. Genetic mapping of Physical therapists often find themselves in the ossification of the posterior longitudinal ligament of the position of being a patient advocate, facilitating spine. Am J Hum Genet. 1998;62:1460-1467. appropriate and efficient referrals to the primary 13. Koyanagi I, Iwasaki Y, Hida K, Imamura H, Abe H. care physician and appropriate specialists. Beyond Magnetic resonance imaging findings in ossification of typical orthopedic testing for common musculo- the posterior longitudinal ligament of the cervical spine. skeletal conditions, the physical therapist needs to J Neurosurg. 1998;88:247-254. 14. Koyanagi I, Iwasaki Y, Hida K, Imamura H, Fujimoto S, remain current and skilled in special questions and Akino M. Acute cervical cord injury associated with neurological testing to differentiate possible sinister ossification of the posterior longitudinal ligament. pathology. With the thorough understanding of Neurosurgery. 2003;53:887-891; discussion 891-882. musculoskeletal assessment physical therapists possess, 15. Magee DJ. Orthopedic Physical Assessment. 2nd ed. we can play a vital role on the health care team. Philadelphia, PA: W. B. Saunders Company; 1992. 16. Maitland GD, Banks K, English K, Hengeveld E. Maitland’s Vertebral Manipulation. 6th ed. Oxford, UK: ACKNOWLEDGMENTS Butterworth Heinemann; 2001. The author would like to thank Carol Jo Tichenor, 17. Maroun FB, Makino AP, Tong TR, et al. Cervical PT, MA and Nancy Woelffer, MPT for their support myelopathy secondary to ossification of the posterior and assistance with reviewing and editing the manu- longitudinal ligament in a Caucasian patient. Can J Neurol Sci. 1993;20:329-332. script, and Ivan Matsui, PT for his consultation. 18. Matsunaga S, Kukita M, Hayashi K, et al. Pathogenesis of myelopathy in patients with ossification of the posterior longitudinal ligament. 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  8. 8. 20. Matsunaga S, Yamaguchi M, Hayashi K, Sakou T. 27. Resnick D. Diagnosis of Bone and Joint Disorders. 4th Genetic analysis of ossification of the posterior longitu- ed. Philadelphia, PA: W. B. Saunders; 2002. dinal ligament. Spine. 1999;24:937-938; discussion 28. Schmidt MH, Quinones-Hinojosa A, Rosenberg WS. 939. Cervical myelopathy associated with degenerative spine 21. Nagashima C. Cervical myelopathy due to ossification disease and ossification of the posterior longitudinal of the posterior longitudinal ligament. J Neurosurg. ligament. Semin Neurol. 2002;22:143-148. 1972;37:653-660. 29. Singh H, Khanna V, Sivasankar R, Mothukuri R. Ossifi- 22. Nakanishi T, Mannen T, Toyokura Y, Sakaguchi R, cation of posterior longitudinal ligament. MJAFI. Tsuyama N. Symptomatic ossification of the posterior 2004;60:284-286. longitudinal ligament of the cervical spine. Clinical 30. Trojan DA, Pouchot J, Pokrupa R, et al. Diagnosis and findings. Neurology. 1974;24:1139-1143. treatment of ossification of the posterior longitudinal 23. Norkin CC, White DJ. Measurement of Joint Motion: A Guide to Goniometry. Philadelphia, PA: FA Davis Com- ligament of the spine: report of eight cases and litera- pany; 1985. ture review. Am J Med. 1992;92:296-306. 24. Ono K, Ota H, Tada K, Hamada H, Takaoka K. Ossified 31. Tsuyama N. Ossification of the posterior longitudinal posterior longitudinal ligament. Spine. 126-138;2:126- ligament of the spine. Clin Orthop Relat Res. 1984;71- 138. 84. 25. Ono K, Yonenobu K, Miyamoto S, Okada K. Pathology 32. Wang PN, Chen SS, Liu HC, Fuh JL, Kuo BI, Wang SJ. of ossification of the posterior longitudinal ligament and Ossification of the posterior longitudinal ligament of the ligamentum flavum. Clin Orthop Relat Res. 1999;18-26. spine. A case-control risk factor study. Spine. 1999;24: 26. Physicians’ Desk Reference 2005. 59th ed. Montvale, 142-144; discussion 145. NY: Thompson PDR. R E S I D E N T’ S CASE PROBLEM J Orthop Sports Phys Ther • Volume 35 • Number 11 • November 2005 729