PHYS THER
Vol. 87, No. 9, September 2007, pp. 1233-1242
DOI: 10.2522/ptj.20060150
A Pragmatic Neurological Screen for Patients With Suspected Cord Compressive Myelopathy
Chad E Cook,
Eric Hegedus,
Ricardo Pietrobon and
Adam Goode
CE Cook, PT, PhD, MBA, OCS, FAAOMPT, is Assistant Professor, Department of Community and Family Medicine, and Director of Outcomes Measures, Department of Surgery, Center for Excellence in Surgical Outcomes, Duke University, Durham, NC 27710 (USA)
E Hegedus, PT, DPT, MS, OCS, is Assistant Professor, Department of Community and Family Medicine, Duke University
R Pietrobon, MD, PhD, MBA, is Associate Professor, Department of Surgery, Center for Excellence in Surgical Outcomes, Duke University
A Goode, PT, DPT, is Assistant Professor, Department of Community and Family Medicine, Duke University
Address all correspondence to Dr Cook at: chad.cook{at}duke.edu
Submitted June 1, 2006;
Accepted April 26, 2007
 |
Abstract
|
|---|
Physical therapists commonly use screening tests to identify upper motoneuron lesions such as cord compressive myelopathy (CCM), the presence of which necessitates appropriate medical referral. Signs and symptoms of CCM include sensory and ataxic changes of the lower extremities, poorly coordinated gait, weakness, tetraspasticity, clumsiness, spasticity, hyperreflexia, and primitive reflexes. Clinical tests and measures such as Hoffmann sign, clonus, Lhermitte sign, the grip and release test, the finger escape sign, the Babinski test, and the inverted supinator sign have historically been used as screens for CCM. For effectiveness as a screen, a clinical test or measure should demonstrate high sensitivity. Diagnostic accuracy studies have shown that clinical tests and measures for CCM often display low sensitivity, indicating that a negative finding may falsely suggest the absence of a condition or disease that actually is present. To counter the low levels of sensitivity, screening should include a combination of a thorough patient history, recognition of and appropriate referral for cauda equina symptoms, and clusters of any pertinent contributory tests and measures.
 |
Introduction
|
|---|
Physical therapists examine patients with neurological symptoms in which accurate and effective differentiation is necessary. Neurological disorders can be classified into lower motoneuron (LMN) lesions resulting from damage to the alpha motoneuron, which may occur with spinal cord compression, or upper motoneuron (UMN) lesions resulting from damage to the descending inputs on the alpha motoneuron.1 Both LMN and UMN lesions typically are present in concert. Radiculopathy and myelopathy are examples of LMN and UMN lesions that present similar signs and symptoms. Radiculopathy is considered a LMN lesion in which chemical or nerve root compression causes nerve root pain.2 Myelopathy is a UMN lesion resulting from sagittal narrowing of the spinal canal.3
Because findings of myelopathy frequently overlap with radiculopathy, conscientious attention and appropriate testing is paramount.4,5 Careful examination and evaluation are necessary to rule out a disorder so that appropriate physical therapy intervention may begin. The purpose of this perspective is to recommend the use of selective combinations of screening tools to identify patient history, demographics, and appropriate symptoms of cord compressive myelopathy (CCM).
Spinal cord pathologies such as CCM differ depending on the form and location of the lesion. Multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS) are 2 conditions that present competing signs and symptoms with CCM but differ in a number of ways. Individuals with MS often will exhibit abnormal cranial nerve testing and a positive jaw reflex, whereas individuals with CCM will exhibit neither.6 Amyotrophic lateral sclerosis affects both the UMNs and LMNs and demonstrates no changes in sensation.3 Cervical, thoracic, and lumbar CCM secondary to chronic degenerative changes are much more common forms of dysfunction, present in 90% of people by the seventh decade of life.7 The exact prevalence or incidence of progression from degenerative changes to myelopathy is unknown,7 although cervical CCM is the most common form of spinal cord dysfunction in a person over the age of 55 years.6
Clarification of the form of spinal cord lesion is essential because surgical treatment has been shown to retard the effects of CCM when it is diagnosed in an expeditious manner.8,9 Failure to accurately and efficiently identify patients with CCM can result in progression of symptoms that are no longer effectively treated with conservative or surgical interventions.10 Additionally, failure to recognize CCM may result in treatment approaches that are contraindicated and may place the patient at further risk of disease progression.10
Physical therapists commonly use a neurological screen (NS), often termed an "upper-quarter screen" or a "lower-quarter screen," as a component of a physical therapist examination. The NS is a method used to understand the source of a patient's symptoms, to differentiate between UMNs and LMNs,4,5,11,12 and to determine whether a patient is appropriate for physical therapy management.11 Generally, tests and measures used during an NS are performed at the beginning of the physical examination as a screening test.13
Screening tests should be inexpensive and relatively accurate and should cause little morbidity during application.14 Screening tests are designed to assist the clinician in ruling out selected diagnoses or impairments, should demonstrate high sensitivity during preclinical stages, and should be used with disorders that have high prevalence.14–16 When a test demonstrates high sensitivity, the likelihood of a false negative is low because the test demonstrates the ability to identify accurately those who truly have the disease or impairment, thus demonstrating the ability to "rule out" a condition.16 The low rate of false negatives minimizes the mistake by the clinician of identifying a patient as "normal" when the patient may indeed have the pathology—in this case, CCM. Tests with high sensitivity correctly identify those who truly have the disease by providing a measurement value exclusive to this population.
 |
The Necessity of Screening
|
|---|
Despite the importance of screening for conditions such as CCM, recent evidence suggests that less than 5% of primary care physicians routinely examine for these findings during their initial screen.17 Even when provided with guidelines for management of patients with acute spine pain, physicians demonstrate poor concordance toward examination using guideline-recommended approaches.18,19 In a review of 6 different international guidelines for management of spine pain, all guidelines recommended a specific screen for detection of "red flags" such as CCM.20 Although the 6 international guidelines did not agree specifically on what constituted an appropriate screen, all of them suggested the importance of specific historical characteristics, laboratory findings, and outcomes from physical testing including neurological testing.20
As entry-point providers, physical therapists are increasingly placed in a position to initially screen for CCM. We know of no studies that have outlined the frequency in which physical therapists routinely screen for CCM, although conservative interventions are well documented21–23 as is treatment specifically by physical therapists.24 At present, clinical tests and measures for CCM by physical therapists and physicians lack sensitivity, a necessary element in an effective initial screen.21,25
 |
Signs and Symptoms of CCM
|
|---|
In contrast to radiculopathy and somatic referred pain, CCM involves spinal cord compression or injury and is considered a serious finding. The most commonly encountered form involves cervical spondylotic cord compressive myelopathy (cervical CCM).6,26 Cervical CCM is associated with physiological narrowing of the sagittal diameter of the spinal canal secondary to congenital or degenerative changes.26
The compression associated with cervical CCM may progress to spinal cord ischemia, leading to histopathological changes of the spinal cord, often termed "myelomalacia."27 Initial symptoms in milder cases can start with hand clumsiness or numbness, which may be unilateral at first, before gait abnormalities are noted.6,28–34 Hand clumsiness or numbness involves less sensory loss than motor dysfunction and is, in essence, an apraxia of the distal upper extremities and hands.30
Additional signs and symptoms of cervical CCM manifest as pain in the cervical, upper-quarter region or shoulder; widespread numbness; paresthesia; and sensory and ataxic changes of the lower extremities.3 Additional findings may include weakness, tetraspasticity,4 gait-related clumsiness,4 spasticity, hyperreflexia,35 and the presence of primitive reflexes.36 Other clinical findings indicative of progressive decline include acquired spastic paraparesis,6 tetraparesis, or paraparesis.27 Because the signs and symptoms often are sequential, weakness and stiffness of the legs37,38 typically precede pain and the occasional findings of bowel and bladder changes.39,40
Thoracic and lumbar CCM also can lead to serious complications.41 Within the thoracic region, myelopathic compression occurs from compression fractures,42 metastatic cancers,43 tuberculosis,43 and rheumatoid arthritis.44 A disk herniation is a possible, but rare, contributor to myelopathy in the thoracic spine.45 Because the spinal cord terminates at L1 or L2, CCM in the lumbar spine is regionally associated with spinal cord compression at the upper lumbar segments. Disk herniations are the most common contributor to CCM; nonetheless, the prevalence in the upper lumbar spine is rare, accounting for less than 2% to 3% of all herniations in the lumbar spine.46
Lower thoracic and upper lumbar signs and symptoms are similar to those found in cervical CCM. Findings may include progressive asymmetric weakness in both legs and foot drop with difficulty walking.45 Muscle fasciculations, muscle cramps, and multilevel muscle weakness also are prevalent.45 Generally, sensation changes fluctuate over time (no problems early, with progressive sensation loss over time), and reflexes provide variable information.43,45
At the conus medullaris, concurrent symptoms associated with UMN and LMN damage are possible.40 Damage to the peripheral nerves of the cauda equina, or the conus medullaris, can result in cauda equina syndrome (CES). The incidence of CES ranges from 1% to 5%, depending on the origin (ie, disk herniation, tumor) of the injurious event.40 Cauda equina syndrome involves compression or damage to the nerves of the cauda equina and may result in sciatica, low back pain, saddle and perianal hypesthesia or analgesia, reflex changes, sexual dysfunction, lower-extremity weakness, and bowel and bladder dysfunction.47 Because pathology of the lumbar spine can damage parasympathetic supply to the bowel and bladder and sensory nerves to the perineum,46 lumbar CCM can frequently demonstrate symptoms comparable to those of CES, including changes in motor function in the lower extremities and pelvis.35 Distinguishing between the 2 conditions is less essential because both conditions warrant additional medical workup and are considered serious red flag findings.
 |
Diagnosis of Myelopathy
|
|---|
Diagnostic criteria for CCM have included evidence of spinal cord abnormality based on magnetic resonance imaging (MRI) findings and dedicated clinical testing procedures.3 Magnetic resonance imaging is considered the best imaging method because it expresses the amount of compression placed on the spinal cord48 and demonstrates relatively high levels of sensitivity (79%–95%) and specificity (82%–88%) (positive likelihood ratio=4.39–7.92, negative likelihood ratio=0.06–0.27) in identifying selected abnormalities such as space-occupying tumors,8,49,50 disk herniation,51,52 and ligamentous ossification.53 The MRI provides the ability to rule out a tumor or syrinx (fluid-filled cavity that develops in the spinal cord)3 and provides detailed views of the spinal cord, intervertebral disk, vertebral osteophytes, and ligaments—all structures that potentially compress the spinal cord.26 Furthermore, MRI findings have been shown to correlate with preoperative severity of cervical compressive myelopathy and prognosis after surgery.8,49,54–56 Patients with advanced spinal cord changes often demonstrate poor outcomes after surgery, and those with only minor compression tend to demonstrate fair recovery or retardation of progression of symptoms.10
Nonetheless, MRI findings are not conclusively indicative of CCM.57 Spinal cord-related changes and subsequent symptoms from CCM overlap other types of intrinsic myelopathy, such as MS, syrinx, or ALS. Careful screening of the MRI, including the presence of T2-weighted changes, is crucial to show clear, relevant, spinal cord compression.22,58–61 False positives are common because spinal cord compression alone does not directly equate to clinical signs and symptoms.59,61 Diagnosis usually is made from a detailed history of progressive patient symptoms, weakness and hyperreflexia on examination, and clear compression of the spinal cord at an appropriate symptomatic level on the MRI scan, with or without T2-weighted changes. Because T2-weighted MRI changes usually do not abate with surgery,62 these changes are more indicative of damage than of reversible ischemia. Because a dedicated criterion standard, such as the singular use of an MRI scan to determine myelopathy, does not exist, tests designed to measure the presence of CCM always are investigated in the presence of uncertainty.63
Aside from MRI, a neuromuscular test, such as an electromyogram (EMG) or an electroneurogram, often is used to differentiate cervical CCM from carpal tunnel syndrome or other peripheral nerve problems. Because cervical CCM is a UNM syndrome, the EMG is expected to display a normal finding unless there are intervening root or peripheral nerve problems. Kang and Fan64 reported normal EMG results in 100% of patients diagnosed with cervical CCM. Evoked potentials have demonstrated the greatest assistance with the diagnosis of cervical CCM. Motor evoked potentials have a reported 70% sensitivity in the upper-extremity muscles and 95% sensitivity for muscles of the lower extremity for the diagnosis of cervical CCM.65 From an electrodiagnostic standpoint, the use of sensory evoked potentials (SEP) has demonstrated superior diagnostic ability, as Kang and Fan64 reported abnormal SEP in 19 of 20 patients diagnosed with cervical CCM.
As physical therapists increase their exposure as entry-point providers, the opportunity to identify the presence of CCM will increase, yet the use of MRI to identify CCM is still uncommon within physical therapist practice. Magnetic resonance imaging is a sensitive instrument to detect CCM, whereas we will demonstrate that most clinical tests and measures designed to screen for CCM lack sensitivity. Physical therapists require effective tests and measures that demonstrate high sensitivity to properly rule out signs and symptoms of CCM.
 |
Patient History and Clinical Tests and Measures for Myelopathy
|
|---|
Although patient history is routinely used during diagnosis of CCM,66 we know of no studies that have measured the sensitivity of patient history in diagnosing myelopathy. Nonetheless, careful attention to the patient history may provide useful information when combined with other physical findings. Patients with CCM may complain of little to no neck pain67 or of paresthesia in a nondermatomal pattern and frequently do not appreciate the underlying weakness that is present.9 Subtle changes in gait are often the first clue of the presence of CCM.9 As CCM progresses, patients may report balance disturbances, variable degrees of weakness or paralysis, and proximal muscle weaknesses.9 Findings of bowel and bladder changes39,40 associated with severe CCM should be addressed immediately.
There are a number of clinical tests and measures purportedly designed to screen for UMN lesions such as CCM. Clinical tests and measures such as Hoffmann sign, clonus, Lhermitte sign, the Babinski sign, the finger escape sign, the grip and release test, and the inverted supinator reflex9,27,68 are used traditionally to rule out the presence of CCM. Of these tests, the grip and release test, clonus, and the inverted supinator reflex have not been studied for diagnostic accuracy. The finger escape sign has been inadequately measured.
Finger Escape Sign
Hand dysfunction has been recognized as a specific sign of cervical myelopathy.69 A commonly used test for hand dysfunction is the finger escape sign, which involves the involuntary flexion and abduction within 1 minute of extended and adducted fingers when held statically.9 We are aware of one study70 that examined the sensitivity of the finger escape sign, identifying a sensitivity of 55% in a sample of 36 subjects with myelopathy.
Grip and Release Test
The grip and release test is recognized by the inability to grip and release the fist rapidly upon request.9 Although the test is considered to be a specific finding for myelopathy and has been used to rule in myelopathy for research purposes,69 we are unaware of any studies that have examined sensitivity.
Clonus
Clonus is considered a UMN lesion that appears several weeks after the presence or onset of a lesion.71 A positive clonus finding is more than 2 repetitive beats during wrist or ankle dorsiflexion movements and may be the result of a number of causes, including cerebral hemispheric or spinal cord damage.72 We know of no studies that have measured the sensitivity of clonus in ruling out CCM.
Inverted Supinator Reflex
For the inverted supinator reflex, a positive test is identified as finger flexion or triceps muscle extension during brachioradialis muscle reflex testing.68,73 A positive finding is considered a sign of an LMN lesion at the spinal level of reflex testing and of a UMN lesion such as CCM below the spinal level of testing.73 We know of no studies that have investigated the diagnostic accuracy of the inverted supinator reflex test.
The Hoffmann sign, the Lhermitte sign, and the Babinski sign have been studied for diagnostic accuracy, with varying levels of methodological quality, which may affect the diagnostic accuracy results. For example, Berger and Fannin74 reported a sensitivity of 80% in subjects with neurological dysfunction other than CCM but failed to blind test administrators to the condition of the patient or to standardize the reference used to qualify the origin of the myelopathy for comparison. Ghosh and Pradhan75 found slightly lower sensitivity values and demonstrated the strongest study design, which did include subjects with suspected CCM and appropriate blinding. Consequently, the strength of the design during study origination suggests that Ghosh and Pradhan's findings exhibited stronger internal and external validity. Other investigators76,77 found dramatically lower sensitivity values and used a study design that allowed examiner bias or used subjects who are not commonly tested using the Babinski sign. Use of diagnostic accuracy values may have limited generalizability if the spectrums of patients used for the study are not similar to those who would receive the test in clinical practice, also known as "spectrum bias."78
Babinski Sign
The Babinski sign is a commonly used clinical test for CCM and other forms of UMN lesions. A positive test is associated with a pyramidal defect and is earmarked by great toe extension, and sometimes adduction,79 during stimulus and fanning of the digits 2 through 5. Babinski sign findings are frequently used in concert with imaging to detect the presence of a UMN lesion. Findings associated with the Babinski sign are variable, and the use of this test recently has been questioned for effectiveness as a screening tool.80 Some authors81,82 have argued that the Babinski sign is difficult to differentiate from upgoing toe movement that occurs during a flexion synergy of the leg and suggested that examination of the entire leg is imperative. Failure to differentiate may result in artificially higher levels of sensitivity.
Kumar and Ramasubramanian81 described the crossed upgoing toe sign and the Allen-Cleckley sign as variations of the Babinski sign. The crossed upgoing toe sign involves resisted flexion of the opposite hip with the knee in full extension and detection of an upgoing toe on the contralateral foot. The test appears to be specific and not sensitive. The Allen-Cleckley sign appears to be a moderately sensitive test and involves flicking the second digit of the foot into extension or pressure of the distal phalange of the second digit. Other tests such as the Mendal-Bechtrew sign, Schaefer sign, Oppenheim sign, and Chaddock sign remain unstudied for diagnostic accuracy. Table 1 outlines the diagnostic values of the Babinski sign and its variations.
View this table:
[in this window]
[in a new window]
|
Table 1. Diagnostic Accuracy of the Babinski Sign and Its Variations, the Crossed Upgoing Toe Sign and the Allen-Cleckley Signa
|
|
Hoffmann Sign
The Hoffmann sign, also known as the Hoffmann reflex or the digital reflex, is commonly used to detect the presence of a UMN such as CCM.63 Like the Babinski sign, this clinical test usually is embedded within a diagnostic imaging evaluation when determining the extent of UMN damage. The test is performed by stabilizing the middle digit of the patient's hand and flicking or snapping the distal phalange into flexion, similar to a maneuver used to flick a marble. A positive test is denoted as flexion of the interphalangeal joint of the thumb, with or without flexion of the index finger and distal interphalangeal joints of the hand,70,83 and is projected to identify CCM or intracranial pathology.63
We know of 3 studies63,70,83 that have investigated the diagnostic accuracy of the Hoffmann sign. When evaluated, all studies demonstrated significant weaknesses, including blinding errors, failure to report equivocal findings, and sampling biases. Sung and Wang63 reported a sensitivity of 94%, and Wong et al70 reported a sensitivity of 82% using the Hoffmann sign during assessment of patients with cervical spine disorders. Wong et al70 tested only patients with demonstrable evidence of a UMN lesion using MRI, and Sung and Wang63 incorporated the Hoffmann sign within the diagnostic reference and did not blind investigators to the subjects conditions. Blinding apparently plays a significant role in the determination of Hoffmann sign, as Glaser et al83 reported a sensitivity of 58% when the investigators were unblinded to other clinical findings such as patient history and additional tests and measures and a sensitivity of only 28% when the investigators were blinded. This dramatic change in sensitivity based on blinding of investigators seems to suggest that a positive or a negative finding is influenced heavily by other findings within the examination. Glaser et al83 did report specificity values of 74% (unblinded) and 71% (blinded) (positive likelihood ratio=0.97–2.23, negative likelihood ratio=0.57–1.01), suggesting that the test is more specific than sensitive. Table 2 outlines the diagnostic accuracy of the Hoffmann sign.
Lhermitte Sign
The Lhermitte sign involves lower cervical flexion in sitting or standing and production of an electrical "type" response or a "pins and needles" sensation near the end range of flexion.84 Although the test was designed to measure spinal cord compression, it is commonly associated with screening for multiple sclerosis and is considered a moderately accurate tool for differentiation of spinal cord and spinal nerve trauma. We know of 2 studies35,84 that measured the diagnostic accuracy of the Lhermitte sign, and the sensitivity is markedly low (Tab. 3).
Unfortunately, all of these studies demonstrated several procedural biases that may vary the diagnostic accuracy values. Uniformly, most tests demonstrated poor-to-moderate sensitivity, which can reduce the odds of appropriately screening for myelopathy in the absence of high prevalence. These poor sensitivity results suggest that using an individual test in isolation is likely a poor selection as a screen when used early in an examination.
 |
Discussion
|
|---|
Although the clinical tests and measures for CCM are designed as screens and are frequently used early in an examination to "rule out" the presence of CCM, there are significant risks for misleading results.79 None of the tests described in this article is overtly sensitive to "rule out" CCM; thus, the presence of a negative finding should not comfort the clinician that the condition is absent.27,79,81 Many of the tests remain unstudied for diagnostic effectiveness or were tested in the presence of spectrum bias. Spectrum bias limits the usefulness of the findings because the patients who were tested are not likely to represent a population seen in traditional practice. A majority of studies are hampered by examiner bias, and the testing methods used within the studies lack differentiation from other neurological dysfunctions such as cerebral hemispheric damage.
An additional complication is that the natural history of myelopathy is poorly characterized.31,34,85,86 There are many situations in which both the patient examination and the MRI scan are indistinct or ubiquitous, in that it may be unclear on examination whether the patient has mild myelopathy and only mild-to-moderate spinal cord compression without changes on the T2-weighted MRI. Conversely, many patients demonstrate significant compression on MRI but are relatively asymptomatic.9,59,61,87 In addition, several factors associated with disease progression in myelopathy (eg, patient age, degree of spinal cord compression, preoperative function, duration of symptoms, severity of osteoarthritis, number of affected levels) have all been associated with outcome, but have not proven to be a predictor in all studies.88,89
Furthermore, there is uncertainty regarding which tests and measures are most important in ruling out CCM.66,90 Traditionally, screening for a neurologically based pathology has involved the combination of dermatome, myotome, deep tendon reflex, and pathological reflex (eg, Babinski, Hoffman) testing in the form of an upper- or lower-quarter screen.12,91–95 The presence of pathologic reflexes, hypertonic deep tendon reflexes, and sensation deficits in a nondermatomal pattern should necessitate further medical examination or imaging. Nonetheless, it is likely that clinical findings will provide inconsistent screening results, as the majority of clinical tests for CCM lack sensitivity, have been poorly tested, or involve ambiguity when tested independently of other findings. Ambiguity is likely associated with the complexity of the disorder and the weaknesses of the tests and study designs.
A pragmatic examination could reduce the risk of examination error based solely on the limitations of the tests and measures and could improve the sensitivity of the test during the early and middle portions of the natural history of myelopathy. We suggest following 3 examination guidelines during screening:
- Perform a comprehensive patient history.
- Rule out analogous symptoms associated with CES so that physical therapist examination, evaluation, and intervention may begin.
- Use a battery of clinical tests to improve the sensitivity of ruling out CCM with full recognition that a negative finding may falsely suggest the absence of a condition or disease that actually is present.
Perform a Comprehensive Patient History
Because CCM is diagnosed using clinical tests and measures, patient history, and the explicitly sensitive use of MRI, we recommend a careful and detailed patient history once the patient reaches the age of 55 years. The patient history should involve the use of standard questions, including gait-related queries and questions regarding other clinical findings associated with CCM. Thoracic spine CCM generally is associated with trauma, metastasis, or tuberculosis, and, although rare, CCM in the lumbar spine usually is associated with a herniated disk. Cervical CCM involves signs and symptoms such as lower-extremity spasticity,35 motor weakness,3,35 gait difficulties,3 and sensory changes often occurring later than motor changes.3,35 Any potentially positive finding should warrant further diagnostic workup using MRI.
Rule Out Analogous Symptoms Associated With CES
Cauda equina signs and symptoms often will overlap those of CCM. It is not uncommon to find sphincter disturbances,35 radicular pain,35 and bowel and bladder problems with both conditions.46 Moreover, because CES causing bowel and bladder dysfunction is considered an emergency that benefits from early surgical decompression,43 any associative symptoms found during the screen should prompt immediate medical referral.
Use a Battery of Clinical Tests to Improve the Sensitivity of Ruling Out CCM
Because the clinical tests and measures for CCM lack sensitivity, we suggest that they should not be used singularly and should never be used in the absence of a complete patient history. When sensitivity is poor for each given clinical test and measure, combining tests with the Boolean operator "OR" improves sensitivity. Previous authors have used a similar approach during the development of screening tools to reduce unnecessary use of radiographs. The Ottawa Ankle Rules96 and the Canadian C-spine Rule for the cervical spine97 involve guidelines during the screening examination that earmark that patient for a radiological screen (additional workup). The Ottawa rule for an ankle fracture states that a radiograph series is necessary only when there is pain near the malleoli and one or more of the following findings: (1) patient age 55 years or greater, (2) unable to bear weight for 4 steps both immediately and in the emergency room, or (3) pain with palpation of the posterior edge or tip of either malleolus. Similarly, the Canadian C-spine Rule98 makes judicious use of the Boolean operator "OR" to increase sensitivity. Both rules demonstrate high sensitivity, which effectively identifies those patients who most likely will not benefit from a radiograph series. It is worth noting that the low sensitivity values may be partially associated with the difficulty in diagnosing CCM and the ambiguity in assessment of the patient's signs and symptoms and MRI findings that make up a diagnosis.
 |
Conclusion
|
|---|
With regard to CCM, how can the primary care clinician use the best-available evidence to rule out the diagnosis so that appropriate physical therapy intervention can begin? We suggest that a careful, judicious screen involving any positive or unclear finding should prompt a referral for an MRI or equivalent imaging method. Acceptance of any positive or unclear finding will reduce the risk of late diagnosis and subsequent progression of symptoms. We have demonstrated that current clinical examination tests and measures have poor sensitivity, suggesting that a negative finding may falsely rule out CCM in patients who actually have CCM. Furthermore, such a diagnostic mistake may have devastating consequences to the "missed" patient who may have received effective and timely surgical intervention. To our knowledge, this judicious screening method is not commonly implemented in medical practice.26
Future studies should investigate the diagnostic accuracy of clustered findings and focus on improvements in methods. In addition, additional diagnostic accuracy studies with improved study designs could further identify the tests and measures that are appropriate screening tools, and such studies are warranted.
 |
Footnotes
|
|---|
Dr Cook provided concept/idea/project design, project management, institutional liaisons, and clerical support. Dr Cook and Dr Hegedus provided data collection and analysis. All authors provided writing and consultation (including review of manuscript before submission).
 |
References
|
|---|
- Purves D, Augustine G, Fitzpatrick D, et al. Neuroscience. 2nd ed. Sunderland, Mass: Sinauer Associates Inc; 2001.
- Cook CE.
Orthopedic Manual Therapy: An Evidence-Based Approach. Upper Saddle River, NJ: Prentice Hall; 2007.
- McCormick WE, Steinmetz MP, Benzel EC. Cervical spondylotic myelopathy: make the difficult diagnosis, then refer for surgery. Cleve Clin J Med. 2003;70:899–904.[Abstract/Free Full Text]
- Dvorak J. Epidemiology, physical examination, and neurodiagnostics. Spine. 1998;23:2663–2673.[CrossRef][Web of Science][Medline]
- Manifold SG, McCann PD. Cervical radiculitis and shoulder disorders. Clin Orthop Relat Res. 1999:105–113.
- Montgomery DM, Brower RS. Cervical spondylotic myelopathy: clinical syndrome and natural history. Orthop Clin North Am. 1992;23:487–493.[Web of Science][Medline]
- Dvorak J, Sutter M, Herdmann J. Cervical myelopathy: clinical and neurophysiological evaluation. Eur Spine J. 2003;12(suppl 2):S181–S187.
- Fujiwara K, Yonenobu K, Ebara S, et al. The prognosis of surgery for cervical compression myelopathy: an analysis of the factors involved. J Bone Joint Surg Br. 1989;71:393–398.[Web of Science][Medline]
- Emery SE. Cervical spondylotic myelopathy: diagnosis and treatment. J Am Acad Orthop Surg. 2001;9:376–388.[Abstract/Free Full Text]
- Yoshimatsu H, Nagata K, Goto H, et al. Conservative treatment for cervical spondylotic myelopathy. prediction of treatment effects by multivariate analysis. Spine J. 2001;1:269–273.[CrossRef][Medline]
- Govind J. Lumbar radicular pain. Aust Fam Physician. 2004;33:409–412.[Medline]
- Wainner RS, Gill H. Diagnosis and nonoperative management of cervical radiculopathy. J Orthop Sports Phys Ther. 2000;30:728–744.[Web of Science][Medline]
- Woolf AD. How to assess musculoskeletal conditions: history and physical examination. Best Pract Res Clin Rheumatol. 2003;17:381–402.[CrossRef][Medline]
- Obuchowski NA, Graham RJ, Baker ME, Powell KA. Ten criteria for effective screening: their application to multislice CT screening for pulmonary and colorectal cancers. AJR Am J Roentgenol. 2001;176:1357–1362.[Free Full Text]
- Grimes DA, Schulz KF. Uses and abuses of screening tests. Lancet. 2002;359:881–884.[CrossRef][Web of Science][Medline]
- Sackett D, Richardson W, Rosenberg W, Haynes R. Evidence-Based Medicine: How to Practice and Teach EBM. New York, NY: Churchill Livingstone Inc; 1997.
- Bishop PB, Wing PC. Knowledge transfer in family physicians managing patients with acute low back pain: a prospective randomized control trial. Spine J. 2006;6:282–288.[CrossRef][Medline]
- Bishop PB, Wing PC. Compliance with clinical practice guidelines in family physicians managing worker's compensation board patients with acute lower back pain. Spine J. 2003;3:442–450.[CrossRef][Medline]
- Gonzalez-Urzelai V, Palacio-Elua L, Lopez-de-Munain J. Routine primary care management of acute low back pain: adherence to clinical guidelines. Eur Spine J. 2003;12:589–594.[CrossRef][Web of Science][Medline]
- Staal JB, Hlobil H, van Tulder MW, et al. Occupational health guidelines for the management of low back pain: an international comparison. Occup Environ Med. 2003;60:618–626.[Abstract/Free Full Text]
- Boyce RH, Wang JC. Evaluation of neck pain, radiculopathy, and myelopathy: imaging, conservative treatment, and surgical indications. Instr Course Lect. 2003;52:489–495.[Medline]
- Matsumoto M, Toyama Y, Ishikawa M, et al. Increased signal intensity of the spinal cord on magnetic resonance images in cervical compressive myelopathy: Does it predict the outcome of conservative treatment? Spine. 2000;25:677–682.[CrossRef][Web of Science][Medline]
- Nakamura K, Kurokawa T, Hoshino Y, et al. Conservative treatment for cervical spondylotic myelopathy: achievement and sustainability of a level of "no disability." J Spinal Disord. 1998;11:175–179.[Web of Science][Medline]
- Browder DA, Erhard RE, Piva SR. Intermittent cervical traction and thoracic manipulation for management of mild cervical compressive myelopathy attributed to cervical herniated disc: a case series. J Orthop Sports Phys Ther. 2004;34:701–712.[Web of Science][Medline]
- Davis DP, Wold RM, Patel RJ, et al. The clinical presentation and impact of diagnostic delays on emergency department patients with spinal epidural abscess. J Emerg Med. 2004;26:285–291.[CrossRef][Web of Science][Medline]
- Gross J, Benzel E. Dorsal surgical approach for cervical spondylotic myelopathy. In: Camins MD, ed. Techniques in Neurosurgery. Philadelphia, Pa: Lippincott Williams & Wilkins; 1999:162–176.
- Young WF. Cervical spondylotic myelopathy: a common cause of spinal cord dysfunction in older persons. Am Fam Physician. 2000;62:1064–1070, 1073.[Web of Science][Medline]
- Chiles BW III, Leonard MA, Choudhri HF, Cooper PR. Cervical spondylotic myelopathy: patterns of neurological deficit and recovery after anterior cervical decompression. Neurosurgery. 1999;44:762–769; discussion 769–770.[CrossRef][Web of Science][Medline]
- Clark CA, Barker GJ, Tofts PS. Magnetic resonance diffusion imaging of the human cervical spinal cord in vivo. Magn Reson Med. 1999;41:1269–1273.[CrossRef][Web of Science][Medline]
- Good DC, Couch JR, Wacaser L. "Numb, clumsy hands" and high cervical spondylosis. Surg Neurol. 1984;22:285–291.[CrossRef][Web of Science][Medline]
- Kadanka Z, Bednarik J, Vohanka S, et al. Conservative treatment versus surgery in spondylotic cervical myelopathy: a prospective randomised study. Eur Spine J. 2000;9:538–544.[CrossRef][Web of Science][Medline]
- MacFadyen DJ. Posterior column dysfunction in cervical spondylotic myelopathy. Can J Neurol Sci. 1984;11:365–370.[Web of Science][Medline]
- Nurick S. The natural history and the results of surgical treatment of the spinal cord disorder associated with cervical spondylosis. Brain. 1972;95:101–108.[Free Full Text]
- Rowland LP. Surgical treatment of cervical spondylotic myelopathy: time for a controlled trial. Neurology. 1992;42:5–13.[Abstract/Free Full Text]
- Crandall PH, Batzdorf U. Cervical spondylotic myelopathy. J Neurosurg. 1966;25:57–66.[Web of Science][Medline]
- Hawkes C. Smart handles and red flags in neurological diagnosis. Hosp Med. 2002;63:732–742.[Web of Science][Medline]
- Adams RD, Victor M. Diseases of the spinal cord, peripheral nerve and muscle. In: Adam RD, Victor M, eds. Principles of Neurology. 5th ed. New York, NY: McGraw-Hill Inc; 1993:1100–1101.
- Brain WR, Northfield D, Wilkinson M. The neurological manifestations of cervical spondylosis. Brain. 1952;75:187–225.[Free Full Text]
- Cohen DB. Infectious origins of cauda equina syndrome. Neurosurg Focus. 2004;16:e2.[Medline]
- Thongtrangan I, Le H, Park J, Kim DH. Cauda equina syndrome in patients with low lumbar fractures. Neurosurg Focus. 2004;16:e6.[Medline]
- Arafat QW, Jackowski A, Chavda SV, West RJ. Case report: ossification of the thoracic ligamenta flava in a Caucasian—a rare cause of myelopathy. Br J Radiol. 1993;66:1193–1196.[Abstract/Free Full Text]
- Muto M, Muto E, Izzo R, et al. Vertebroplasty in the treatment of back pain. Radiol Med (Torino). 2005;109:208–219.[Medline]
- Arce D, Sass P, Abul-Khoudoud H. Recognizing spinal cord emergencies. Am Fam Physician. 2001;64:631–638.[Web of Science][Medline]
- Nakamura C, Kawaguchi Y, Ishihara H, et al. Upper thoracic myelopathy caused by vertebral collapse and subluxation in rheumatoid arthritis: report of two cases. J Orthop Sci. 2004;9:629–634.[CrossRef][Web of Science][Medline]
- Kleopa KA, Zamba-Papanicolaou E, Kyriakides T. Compressive lumbar myelopathy presenting as segmental motor neuron disease. Muscle Nerve. 2003;28:69–73.[CrossRef][Web of Science][Medline]
- Kostuik JP. Medicolegal consequences of cauda equina syndrome: an overview. Neurosurg Focus. 2004;16:e8.[Medline]
- Bagley CA, Gokaslan ZL. Cauda equina syndrome caused by primary and metastatic neoplasms. Neurosurg Focus. 2004;16:e3.[Medline]
- Batzdorf U, Flannigan BD. Surgical decompressive procedures for cervical spondylotic myelopathy: a study using magnetic resonance imaging. Spine. 1991;16:123–127.[Web of Science][Medline]
- Fukushima T, Ikata T, Taoka Y, Takata S. Magnetic resonance imaging study on spinal cord plasticity in patients with cervical compression myelopathy. Spine. 1991;16:S534–S538.[Web of Science][Medline]
- Ono K. Cervical myelopathy secondary to multiple spondylotic protrusions: a clinicopathologic study. Spine. 1977;2:125.
- Yousem DM, Atlas SW, Hackney DB. Cervical spine disk herniation: comparison of CT and 3DFT gradient echo MR scans. J Comput Assist Tomogr. 1992;16:345–351.[Web of Science][Medline]
- Pui MH, Husen YA. Value of magnetic resonance myelography in the diagnosis of disc herniation and spinal stenosis. Australas Radiol. 2000;44:281–284.[CrossRef][Medline]
- Mizuno J, Nakagawa H, Hashizume Y. Analysis of hypertrophy of the posterior longitudinal ligament of the cervical spine, on the basis of clinical and experimental studies. Neurosurgery. 2001;49:1091–1097; discussion 1097–1098.[CrossRef][Web of Science][Medline]
- 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.[Medline]
- Ono K, Ebara S, Fuji T, et al. Myelopathy hand: new clinical signs of cervical cord damage. J Bone Joint Surg Br. 1987;69:215–219.[Web of Science][Medline]
- Zeidman SM, Ducker TB, Raycroft J. Trends and complications in cervical spine surgery: 1989–1993. J Spinal Disord. 1997;10:523–526.[Web of Science][Medline]
- Bednarik J, Kadanka Z, Dusek L, et al. Presymptomatic spondylotic cervical cord compression. Spine. 2004;29:2260–2269.[CrossRef][Web of Science][Medline]
- Al-Mefty O, Harkey LH, Middleton TH, et al. Myelopathic cervical spondylotic lesions demonstrated by magnetic resonance imaging. J Neurosurg. 1988;68:217–222.[Web of Science][Medline]
- Chen CJ, Lyu RK, Lee ST, et al. Intramedullary high signal intensity on T2-weighted MR images in cervical spondylotic myelopathy: prediction of prognosis with type of intensity. Radiology. 2001;221:789–794.[Abstract/Free Full Text]
- Kumar VG, Rea GL, Mervis LJ, McGregor JM. Cervical spondylotic myelopathy: functional and radiographic long-term outcome after laminectomy and posterior fusion. Neurosurgery. 1999;44:771–777; discussion 777–778.[CrossRef][Web of Science][Medline]
- Matsuda Y, Miyazaki K, Tada K, et al. Increased MR signal intensity due to cervical myelopathy: analysis of 29 surgical cases. J Neurosurg. 1991;74:887–892.[Web of Science][Medline]
- Wada E, Yonenobu K, Suzuki S, et al. Can intramedullary signal change on magnetic resonance imaging predict surgical outcome in cervical spondylotic myelopathy? Spine. 1999;24:455–461; discussion 462.[CrossRef][Web of Science][Medline]
- Sung RD, Wang JC. Correlation between a positive Hoffmann's reflex and cervical pathology in asymptomatic individuals. Spine. 2001;26:67–70.[CrossRef][Web of Science][Medline]
- Kang DX, Fan DS. The electrophysiological study of differential diagnosis between amyotrophic lateral sclerosis and cervical spondylotic myelopathy. Electromyogr Clin Neurophysiol. 1995;35:231–238.[Medline]
- De Mattei M, Paschero B, Sciarretta A, et al. Usefulness of motor evoked potentials in compressive myelopathy. Electromyogr Clin Neurophysiol. 1993;33:205–216.[Medline]
- Singh A, Gnanalingham KK, Casey AT, Crockard A. Use of quantitative assessment scales in cervical spondylotic myelopathy: survey of clinician's attitudes. Acta Neurochir (Wien). 2005;147:1235–1238; discussion 1238.[CrossRef][Medline]
- Emery SE, Bohlman HH, Bolesta MJ, Jones PK. Anterior cervical decompression and arthrodesis for the treatment of cervical spondylotic myelopathy: two- to seventeen-year follow-up. J Bone Joint Surg Am. 1998;80:941–951.[Abstract/Free Full Text]
- Estanol BV, Marin OS. Mechanism of the inverted supinator reflex: a clinical and neurophysiological study. J Neurol Neurosurg Psychiatry. 1976;39:905–908.[Abstract/Free Full Text]
- Sakai N. Finger motion analysis of the patients with cervical myelopathy. Spine. 2005;30:2777–2782.[CrossRef][Web of Science][Medline]
- Wong TM, Leung HB, Wong WC. Correlation between magnetic resonance imaging and radiographic measurement of cervical spine in cervical myelopathic patients. J Orthop Surg (Hong Kong). 2004;12:239–242.[Medline]
- Deveci M, Bozkurt M, Sengezer M. Clonus: an unusual delayed neurological complication in electrical burn injury. Burns. 2001;27:647–651.[CrossRef][Web of Science][Medline]
- Mayer NH. Clinicophysiologic concepts of spasticity and motor dysfunction in adults with an upper motoneuron lesion. Muscle Nerve Suppl. 1997;6:S1–S13.[Medline]
- Boyle RS, Shakir RA, Weir AI, McInnes A. Inverted knee jerk: a neglected localising sign in spinal cord disease. J Neurol Neurosurg Psychiatry. 1979;42:1005–1007.[Abstract/Free Full Text]
- Berger JR, Fannin M. The "bedsheet" Babinski. South Med J. 2002;95:1178–1179.[Web of Science][Medline]
- Ghosh D, Pradhan S. "Extensor toe sign" by various methods in spastic children with cerebral palsy. J Child Neurol. 1998;13:216–220.[Abstract/Free Full Text]
- de Freitas GR, Andre C. Absence of the Babinski sign in brain death: a prospective study of 144 cases. J Neurol. 2005;252:106–107.[CrossRef][Web of Science][Medline]
- Hindfelt B, Rosen I, Hanko J. The significance of a crossed extensor hallucis response in neurologic disorders: a comparison with the Babinski sign. Acta Neurol Scand. 1976;53:241–250.[Web of Science][Medline]
- Whiting P, Rutjes AW, Dinnes J, et al. Development and validation of methods for assessing the quality of diagnostic accuracy studies. Health Technol Assess. 2004;8:iii, 1–234.
- Smith MS. Babinski's sign: abduction also counts. JAMA. 1979;242:1849–1850.[CrossRef][Medline]
- Glick TH, Workman TP, Gaufberg SV. Spinal cord emergencies: false reassurance from reflexes. Acad Emerg Med. 1998;5:1041–1043.[Web of Science][Medline]
- Kumar SP, Ramasubramanian D. The Babinski sign: a reappraisal. Neurol India. 2000;48:314–318.[Web of Science][Medline]
- van Gijn J. The Babinski reflex. Postgrad Med J. 1995;71:645–648.[Abstract/Free Full Text]
- Glaser JA, Cure JK, Bailey KL, Morrow DL. Cervical spinal cord compression and the Hoffmann sign. Iowa Orthop J. 2001;21:49–52.[Medline]
- Uchihara T, Furukawa T, Tsukagoshi H. Compression of brachial plexus as a diagnostic test of cervical cord lesion. Spine. 1994;19:2170–2173.[Web of Science][Medline]
- Fouyas IP, Statham PF, Sandercock PA. Cochrane review on the role of surgery in cervical spondylotic radiculomyelopathy. Spine. 2002;27:736–747.[CrossRef][Web of Science][Medline]
- Matsumoto M, Chiba K, Ishikawa M, et al. Relationships between outcomes of conservative treatment and magnetic resonance imaging findings in patients with mild cervical myelopathy caused by soft disc herniations. Spine. 2001;26:1592–1598.[CrossRef][Web of Science][Medline]
- Nakanishi T, Shimada Y, Toyokura Y. Somatosensory evoked responses to mechanical stimulation in normal subjects and in patients with neurological disorders. J Neurol Sci. 1974;21:289–298.[CrossRef][Web of Science][Medline]
- Ebersold MJ, Pare MC, Quast LM. Surgical treatment for cervical spondylitic myelopathy. J Neurosurg. 1995;82:745–751.[Web of Science][Medline]
- Kato Y, Iwasaki M, Fuji T, et al. Long-term follow-up results of laminectomy for cervical myelopathy caused by ossification of the posterior longitudinal ligament. J Neurosurg. 1998;89:217–223.[Web of Science][Medline]
- McCormack BM, Weinstein PR. Cervical spondylosis: an update. West J Med. 1996;165:43–51.[Web of Science][Medline]
- Cyriax J. Textbook of Orthopedic Medicine. Vol 1. 8th ed. London, United Kingdom: Bailliere Tindall; 1982.
- Hoppenfeld S. Physical Examination of the Spine and Extremities. Norwalk, Conn: Appleton & Lange; 1976.
- Magee DJ. Orthopedic Physical Assessment. 3rd ed. Philadelphia, Pa: WB Saunders Co; 1997.
- Winkel D, Vleeming A. Diagnosis and Treatment of the Spine. Gaithersburg, Md: Aspen Publishers; 1996.
- Yoss RE, Corbin KB, Maccarty CS, Love JG. Significance of symptoms and signs in localization of involved root in cervical disk protrusion. Neurology. 1957;7:673–683.[Free Full Text]
- Stiell IG, Greenberg GH, McKnight RD, et al. A study to develop clinical decision rules for the use of radiography in acute ankle injuries. Ann Emerg Med. 1992;21:384–390.[CrossRef][Web of Science][Medline]
- Hoffman JR, Schriger DL, Mower W, et al. Low-risk criteria for cervical-spine radiography in blunt trauma: a prospective study. Ann Emerg Med. 1992;21:1454–1460.[CrossRef][Web of Science][Medline]
- Stiell IG, Wells GA, Vandemheen KL, et al. The Canadian C-spine Rule for radiography in alert and stable trauma patients. JAMA. 2001;286:1841–1848.[Abstract/Free Full Text]

CiteULike
Complore
Connotea
Del.icio.us
Digg
Reddit
Technorati What's this?
Copyright © 2007 by the American Physical Therapy Association.