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Acute Mechanical Low Back Pain Waddell, after critical review of these studies, reached several interesting conclusions. “Social class” in Waddell’s discussion reflects occupation (manual rather than clerical labor) and social disadvantage (e.g., poor medical care). The prevalence of back pain appears to be slightly higher in those patients who perform more manual types of labor. It is unclear which particular aspect of work, social disadvantage (e.g., poor medical care), lifestyle, attitudes, or behavior influences this “social class” finding. Back pain does have a greater impact on people in heavy manual labor jobs. They are more likely to stay off work and stay off longer than “clerical” laborers. This may be a reflection of the effect of their back pain (i.e., patient cannot lift the heavy loads required at work) or may reflect the medical advice given to them by their physicians (stay off work because of the possibility of aggravating the back pain with resumption of heavy labor). The examiner should evaluate and rule out potential emergent causes of LBP during history and physical examination. Careful history and review of systems may detect nonmusculoskeletal origin of LBP. Our approach to the work-up of LBP is to first rule out emergent or nonmusculoskeletal causes of LBP. Once this is done, the appropriate examinations and tests are performed to confirm or rule out mechanical, nerve root, tumor, infectious, traumatic, systemic, or inflammatory etiology. Predictors of Return-to-Work Status of Patients with Back Pain (Chronicity) Cats-Barril and Frymoyer (1991) followed 250 patients to evaluate which of numerous factors best predicted who was still off work (no return to work) after 6 months. They found the best predictors, in order of decreasing accuracy, were 1. Job characteristics: work history, occupation, job satisfaction, satisfaction with policies and benefits. 2. Patient beliefs about whether back pain was compensable, party at fault, and legal involvement (social factors). 3. Past hospitalization for back pain. 4. Educational level. Workplace and social factors were by far the most powerful influences on chronicity (84% accurate in predicting who will be chronically disabled). These were more predictive than type of injury, health behavior, or other factors. Evaluation of Patients with Low Back Pain A thorough history and examination allows an accurate working diagnosis to be made in 90% of patients with LBP. Be wary of constant pain unrelated to activity or position, nocturnal pain, pain refractory to treatment, or concomitant constitutional symptoms (Table 9–1). History should also include questioning of nonmusculoskeletal symptoms (e.g., colic symptoms, penile discharge) (Table 9–2). General History 1. Demographic information a. Age i. Younger—often discogenic pain. ii. Older—stenosis, osseous, lateral disc herniation. b. Gender i. Male—discogenic, ankylosing spondylitis, Reiter’s syndrome more common. ii. Female—osteoporosis, fibromyalgia. c. Occupation i. Specific physical duties—possible increased incidence of back injury with repetitive lifting, twisting, vibration. ii. Emotional, work-related stresses—if significant, monitor for nonorganic component to pain. iii. Lack of job satisfaction—high correlation with time off work. iv. Last date patient worked—the longer the interval off work, the lower the likelihood of return to work. v. Feasibility of finding “light” or “clerical” duty at work—we have had much more success with rapid return to work having our patients sit at a desk 8 hours a day (often in a very boring setting), rather than having them stay at home. vi. Time left to retirement. 2. Recreational sports History of Present Illness 1. Onset of pain a. When did episode begin? b. How did pain begin? i. Spontaneously (a) Sudden onset. (b) Gradual onset. ii. Traumatically (a) Motor vehicle, work-related, nonlegal setting. (b) Mechanism—flexion, extension, twist, lift, fall, sneeze, cough, strain, other. c. Motor vehicle accidents i. Types of cars involved. ii. Direction of impact. iii. Extent of vehicle damage—however, significant injury can occur with minor damage to vehicle. iv. Seat belt used? Lap belt versus shoulder harness—flexion injuries with lap belts, torsional injuries with harness. v. Loss of consciousness. vi. Did head hit windshield, or did chest hit steering wheel? vii. Specific location of immediate pain, if any. viii. Visit to emergency department? Diagnostic and therapeutic measures performed. d. Work-related injuries i. Details of specific injury. ii. Litigation pending. iii. Compensation for time off work. e. Sports-related injuries i. Sports involving torsion (e.g., golf, racquet sports, baseball)—higher incidence of discogenic pain. ii. Sports involving repetitive hyperextension (e.g., gymnastics, dance, crew)—greater loading of posterior elements (e.g., spondolysis, facet syndrome). iii. Details of specific injury. 2. Time course of pain a. Intensity of pain—use of visual analog pain scale may be helpful i. Overall improvement or worsening overall: quantitate with visual analog pain scale or have patient assign a numerical or percent value to pain. ii. Response to specific treatment. b. Recurrences: frequency and duration. 3. Location of pain a. Pain diagram is helpful (have patient draw on pain diagram) i. Structural lesions. ii. Possibility of functional component. b. Ask about area of most intense pain—back versus leg: right, left, or bilateral? i. Primarily back pain—think of annular tear, facet syndrome, local muscular pathology, bony lesion. ii. Primarily distal lower extremity pain—think of lateral or extruded herniated nucleus pulposis (HNP), stenosis, nerve lesion. c. How has location changed over time and in response to specific treatments? 4. Relationship of pain to daily routine a. What positions increase the pain? i. Prone—pain is increased with facet pain, lateral HNP, systemic process. ii. Sitting—increased with annular tear, paramedian HNP. iii. Standing—increased with central stenosis, facet syndrome, lateral HNP. b. Is there pain on arising from a seat? A positive answer is typical of discogenic pain. c. How does walking affect the pain? i. How far can the patient walk? Is the distance variable (lumbar stenosis) or constant (vascular claudication)? ii. Is there more pain with uphill or downhill walking? (a) Patients with spinal stenosis or facet pain have less pain while walking uphill because the lumbar spine is flexed, which increases foraminal and central canal space. (b) Discogenic symptoms decrease while walking downhill because the lumbar spine is extended and discs are unloaded. iii. Is it more comfortable to walk holding a wagon or carriage or in a flexed posture? A positive answer is typical of stenosis. d. How is the pain affected by time of day? i. Is the patient awakened from sleep? Consider a systemic process if so. ii. Is there morning stiffness? Of what duration? Discogenic patients are stiff for 20 to 30 minutes, whereas rheumatic patients may be stiff for 2 hours. iii. Does the pain increase or decrease as the day progresses? The response helps guide treatment. e. Is pain intensified by coughing, sneezing, laughing, or Valsalva maneuver? In which location? i. Suggests disc disease or, rarely, an intraspinal tumor. ii. Reproduction of distal pain strongly supports discogenic pain. f. What activities is the patient unable to perform? g. Do any positions or maneuvers relieve the pain or other symptoms? 5. Associated neurologic symptoms a. Location of anesthesia, hypoesthesia, hyperesthesia, paresthesias i. Regional. ii. Dermatomal. iii. Sclerotomal. iv. Nonphysiologic. b. Does the patient note weakness? i. Differentiate inability to perform a task owing to pain from actual weakness. ii. Has the patient noted a dragging foot, buckling knee, difficulty with stairs or curbs? Suggestive of myotomal, plexus, cord, or non-physiologic process. c. Has the patient noted bladder, bowel, or sexual dysfunction? If so, consider cauda equina syndrome. d. Does the patient have associated upper extremity, central nervous system, or brain stem symptoms? 6. Diagnostic studies a. Patient should be requested to bring in all images and reports. b. Patient should report the results of unavailable studies. 7. Response to prior treatments—ask for specifics (answer helps guide treatment) a. Bedrest—may be of limited benefit in stenosis. b. Medications i. Benefits. ii. Side effects. c. Modalities i. Superficial heating and cooling. ii. Electric stimulation. iii. Ultrasound. iv. Transcutaneous electrical nerve stimulation (TENS). d. Manual or mechanical therapy i. Centralization techniques—passive and active extension, shift correction. Positive response suggests discogenic pain. ii. Traction. iii. Stretching. iv. Mobilization. (a) Relief with specific facet mobilization suggests facet disease. (b) Mobilization may also treat other causes of pain (e.g., segmental dysfunction). v. Manipulation may treat facet pain and other sources of lumbar spine pain. vi. Rapid response to facet manipulation suggests a facet syndrome. e. Exercises i. Flexibility. ii. Strengthening and stabilization. iii. Aerobic conditioning. f. Education in proper body mechanics. g. Corset or bracing. h. Biofeedback. i. Soft tissue injections i. Trigger points. ii. Tendon. iii. Ligament. j. Spinal injections i. Anesthetic phase relief or steroid phase relief. ii. Fluoroscopy and/or contrast used? k. Percutaneous rhizolysis. l. Acupuncture. m. Surgery i. Specific procedure and date performed. ii. Immediate change in symptoms and/or signs. iii. Long-term change in symptoms and/or signs. iv. Complications. Medical History 1. Prior and current medical conditions a. Diabetes. b. Hypertension. c. Cardiac disease. d. Cancer. e. Infections. f. Rheumatologic diseases. g. Gastrointestinal disorders (tolerance for non-steroidal anti-inflammatory drugs [NSAID] use). 2. Present medications and drug allergies. 3. Operations, injuries, and previous hospitalizations, with names, addresses, phone numbers of all practitioners involved in patient’s care. 4. Review of systems, asked selectively a. Constitutional symptoms i. Weight loss. ii. Loss of appetite. iii. Fever or night sweats. iv. Chills. v. Fatigue. vi. Night pain. b. Integument—rheumatologic disorders (e.g., rashes, psoriasis). c. Lymph nodes i. Malignancy. ii. Infection. d. Hematopoietic system i. Anemia. ii. Bleeding. e. Endocrine system—symptoms suggestive of i. Diabetes. ii. Thyroid dysfunction. f. Eyes i. Visual loss. ii. Inflammation. g. Mouth i. Pain. ii. Ulcerations. h. Bones, joints, muscles i. Pathologic fractures. ii. Peripheral or cervicothoracic joint symptoms. iii. Muscle pain or weakness. i. Breasts i. Pain. ii. Lumps. iii. Discharge. j. Respiratory system i. Pain. ii. Shortness of breath. iii. Cough. k. Cardiovascular system i. Chest pain. ii. Palpitations. iii. Orthopnea. iv. Dyspnea on exertion. v. Intermittent claudication. vi. Distal skin lesions. vii. Edema. l. Gastrointestinal system i. Dysphagia. ii. Nausea. iii. Vomiting. iv. Hematemesis. v. Jaundice. vi. Change in bowel habits. vii. Bowel incontinence. m. Genitourinary system i. Urologic (a) Nocturia. (b) Dysuria. (c) Hematuria. (d) Pyuria. (e) Urinary frequency. (f) Retention. (g) Incontinence. ii. Gynecologic (a) Number of full-term pregnancies. (b) Last menstrual period (currently pregnant?). (c) Are menses regular or irregular? (d) Date and results of last pelvic examination and Papanicolaou smear. (e) Back or lower extremity pain associated with menses. n. Nervous system i. Cranial nerves. ii. Movement disorders. iii. Coordination. iv. Convulsions. v. Mental status. Family History 1. Familial conditions. 2. Family members with chronic pain syndromes and/or spine pain. 3. Family members on disability. Social History 1. Open-ended: “Tell me about your family.” 2. Marital status—impact of condition on relationship and vice versa. 3. Children—impact of condition on relationship and vice versa. 4. Substance abuse history a. Alcohol intake. b. Smoking history. c. Illicit drug usage. 5. Social and economic status a. Extent of education. b. Special financial problems. Physical Examination of the Lower Back Several excellent texts on spinal examination are available, including Hoppenfield’s Physical Examination of the Spine and Extremities (1976), Hoppenfield’s Orthopaedic Neurology (1988), and Reider’s The Orthopaedic Physical Examination (1999). Some general guidelines should be followed in the examination of a patient with back pain. Observation and/or Palpation
Range of Motion of Lower Back and Hip Joints Muscle Strength (Table 9–3)
Tendon Reflexes, Pathologic Reflexes Sensory Testing Nerve Tension Signs Nerve Tension Tests Straight-Leg Raises Test (see Fig. 9–5) Lasègue Test (see Fig. 9–6) Crossed Straight-Leg Raises Test (see Fig. 9–7) Bowstring Sign (see Fig. 9–8) Slump Test (see Fig. 9–9) Femoral Nerve Stretch Test (see Fig. 9–10) Rectal Examination (Sphincter Tone) Five signs that suggest nonorganic pathology (Waddell signs) 1. Superficial or nonanatomic tenderness to palpation 2. Simulation sign 3. Distraction sign 4. Regional sensory or motor disturbance 5. Overreaction Other Important Areas That Should Be Examined Simultaneously Figures 9–12 to 9–14 and Tables 9–4 and 9–5 illustrate lumbar disc levels, neurologic levels, and associated motor, sensory, and reflex findings. We also employ the single-leg hyperextension test (stork test, Fig. 9–15) to evaluate for possible spondylolysis in children performing repetitive spine flexion and extension. Imaging for Low Back Pain Plain Films (Fig. 9–16) The Agency for Health Care Policy and Research guidelines for plain films for LBP:
Clinical Pearls for Low Back Pain Disc Herniation Over 95% of lumbar disc herniation occurs at the L4–5 level (L5 signs) or L5-S1 level (S1 signs). Seventy-five percent of lumbar herniated discs spontaneously resolve within 6 months. Leg pain and paresthesias are more symptomatic than the back pain. Only 5 to 10% of patients with persistent sciatica require surgery. Patients with a documented symptomatic herniated lumbar disc treated with surgery have a 10-times-higher risk of developing subsequent disc herniation compared with the general public. Acute disc herniation is usually characterized by sudden onset of low back discomfort and radicular pain into the leg. Facet Joint (Posterior Element) Pain Fifteen to 40% of chronic LBP is due to facet joint pain. The facet joints of the spine are the interfaces where the posterior elements of one spinal segment contact the posterior elements of the next. Like other synovial joints, they can become inflamed. With lumbar facet syndrome, pain is typically aggravated by lumbar extension (which compresses the posteriorly located joint) and is relieved by lumbar flexion (which separates the joint surfaces). The diagnosis is clinical (no specific imaging or examination studies) and is one of exclusion. Pain often occurs acutely with extension and rotation of the lumbar spine. The pain usually presents as nonradiating lumbar spine pain (at times radiating to the buttock, rare to radiate below the knee). Approximately 80% of patients with facet syndrome have evidence of prior disc disease. Facet syndrome has no localizing neurologic symptoms associated with its presentation. Sudden attacks of LBP is more suggestive of facet joint involvement. Steadily increasing pain is more common with disc lesions. A dramatic response to facet manipulation suggests facet syndrome clinically. Contrast-enhanced facet injections that give relief during the anesthetic phase are diagnostic for facet syndrome. Spondylolysis, Spondylolisthesis, and Pars Interarticularis Injuries Definitions Spondylolysis occurs most commonly in young children who perform repetitive flexion and extension of the spine (e.g., gymnasts). SPECT scanning often confirms a stress fracture of the pars interarticularis (spodylolysis). Spondylolysis Spondylolisthesis Degenerative Lumbar Spinal Stenosis Spinal stenosis classically presents with neurogenic claudication The presentation is usually a slowly progressive increase in back and radicular symptoms that occur with walking variable distance. You must rule out vascular claudication. Degenerative lumbar stenosis is a common cause of disabling back pain in patients over 50. The general incidence of degenerative lumbar spinal stenosis ranges from 1.8% to 8% (DeVilliers and Booysen 1976). Lumbar stenosis is caused by reduction of the space available for nerve elements due to filling of the spinal canal with hypertrophic tissue. The process begins with degeneration of facet joints and intervertebral disks, resulting in narrowing of the neural foramina and spinal canal. Associated spinal instability (defined as more than 3 mm of motion between vertebrae on dynamic lateral radiographs) or a congenitally narrowed spinal canal may exacerbate the stenosis. Arnoldi et al (1976) classified lumbar stenosis as congenital, acquired, or combined. The term central stenosis is used when compression of the dural sac is the main component. Lateral stenosis refers to compression of the nerve root in the lateral recess, in the neural foramen, or lateral to the neural foramen (Kirkaldy 1978). Three types of spinal canals have been described: round, ovoid, and trefoil. Trefoil canals have the smallest cross-sectional area and are associated with the highest incidence of symptomatic lumbar stenosis (Bolender et al 1985). The most common pathophysiology noted is that as the nerve roots of the lumbar spine traverse the lateral recesses, they are encroached on by hypertrophic facet joints, infolded ligamentum flavum, and a bulging annulus fibrosis. The degenerative stenosing process may also be accompanied by the development of segmental spinal instability. We recommend employing preoperative prone and supine lumbar radiographs to evaluate for possible segmental instability. Documented segmental instability on dynamic views is an indication for concomitant intertransverse bone grafting with the decompression. Clinical Presentation of Spinal Stenosis Most patients at initial presentation have a long-standing history of lumbar back pain with progression of lower-extremity pain (neurogenic claudication complex). Amundsen et al (1995) reported that the most common symptoms in lumbar spinal stenosis were back pain (95% prevalence) neurogenic claudication (91%), leg pain (71%), and weakness (31%). In 70% of their patients the back pain and leg pain were equally distributed. There are usually few associated physical findings with spinal stenosis. Amundsen et al (1995) reported sensory changes in 51% of patients, reflex changes in 47%, lumbar tenderness in 40%, reduced spinal mobility in 36%, positive straight-leg raising in 24%, and weakness in 23%. Post-exercise examination (e.g., stair-climbing or walking) may reveal greater motor weakness than a static exam. The key to correctly diagnosing degenerative lumbar spinal stenosis is to recognize the classic neurogenic claudication history. Patients with neurogenic claudication classically complain of pain, weakness, numbness, tingling, or cramping in 1 or both legs. These symptoms occur with walking or standing; sitting or leaning forward alleviates at least some of the symptoms. Cycling, which involves forward flexion, is also usually tolerated by patients with lumbar stenosis. Differential Diagnosis It is also essential, given the paucity of physical findings, to rule out other conditions that may present with low back and/or lower extremity symptoms. Patients with vascular claudication will have diminished pulses, evidence of peripheral vascular disease, and relief with rest rather than forward flexion. Other conditions that should be considered include peripheral neuropathy, which presents as dysesthesias and paresthesias rather than activity and position-related changes, and arthritis of the hip, which often presents with buttocks pain but should exhibit hip irritability on internal rotation and abduction. Conditions such as aortic aneurysm, knee arthritis, pelvic or sacral pathology, cervical myelopathy, amyotrophic lateral schlerosis, demyelinating disease, depression, or retroperitoneal tumors should be ruled out. Diagnostic Modalities Plain lumbar spine films are employed to exclude tumor, fracture, infection, etc. In patients with signs and symptoms consistent with spinal stenosis, MRI or post myelographic CT scans are needed to confirm neural element compression. On myelogram, nerve root entrapment in the lateral recess or central canal stenosis is demonstrated by the level of cutoff of contrast material. Herno et al (1994) found that myelographic evidence of complete cutoff of contrast material (severe stenosis) correlated with a better surgical outcome. Riew et al (1998) concluded that post-myelographic CT is superior to MRI as a single study for the preoperative planning of decompression for lumbar spinal stenosis. Electrophysiologic studies are rarely useful in the evaluation of lumbar stenosis. Natural history of Non-operative Treatment Johnsson et al (1992) studied the progression of symptoms over a 4 year period in 32 patients with lumbar stenosis who refused or were not medically cleared for surgery. 70% of patients were unchanged at 4-year follow-up. Of the remaining 30%, half were better, half worse. The results of the prospective Maine Lumbar Spine Study part 3 (Atlas et al 1996) demonstrated superior outcomes at 1 year for operative treatment of symptomatic lumbar stenosis compared with non-operative treatment. The operative patients maintained their superior status at 3 years. Non-operative Treatment of Lumbar Stenosis We recommend use of the algorithm employed by Hilibrand and Rand (1999) (Fig. 9–26) for the non-operative treatment of degenerative lumbar spinal stenosis. NSAIDS are part of the initial management unless contraindicated. Physical therapy is employed using a modification of the standard low-back exercise program. Postural exercises in flexion are combined with pelvic stabilization and aerobic conditioning. Bicycle exercise is recommended because the slight forward flexion is typically well-tolerated by these patients. A back brace fashioned in slight forward flexion may also be useful, but long-term brace wear may eventually lead to truncal deconditioning. Epidural steroid injection (ESI) is commonly used to treat patients with lumbar stenosis. Cuckler et al (1985) performed a prospective, randomized, double-blind study of epidural steroids in patients with lumbar radicular symptoms, half of whom had a diagnosis of lumbar spinal stenosis. In the spinal stenosis patients, there was no statistical difference in symptom improvement between the ESI and placebo injections at 24 hours and at 1 year. However, a similar study by Dilke et al (1973) demonstrated a statistically significant (p <0.05) improvement in short-term pain and functional measures. Hilibrand and Rand (1999) reserve the use of epidural steroid injections for mild to moderate stenosis and major medical co-morbidities for whom physical therapy and other medical treatments have not helped. Operative Treatment (Fig 9–27) Success rates for surgical treatment of lumbar stenosis have ranged from 57% to 85% (Spengler 1987; Hilibrand 1999). A thorough work-up is recommended to identify any associated degenerative pathologic changes-such as spondylosisthesis, segmental instability, or scoliosis-that might require concomitant stabilization in addition to decompression. Piriformis Syndrome (Pseudosciatica) This syndrome results from compression or inflammation of the sciatic nerve as it courses under or through the piriformis muscle in the buttock. The patient presents with pseudosciatica-buttock and leg pain. They have tenderness on piriformis muscle palpation. Fifty percent of patients have LBP; 23% have dyspareunia. To distinguish piriformis syndrome from lumbar radiculopathy, perform a nerve tension test (positive in the latter). To distinguish piriformis syndrome from sacroiliitis, review pelvic radiographs. Sclerosis or irregularity of SI joints should be evident in sacroiliitis (Table 9–8). Physical Therapy Approaches in Low Back Pain-Overview of Extension-Flexion Bias In patients with LBP and concomitant radiating leg pain, McKenzie (1981) has described a clinical phenomenon known as “centralization.” During McKenzie’s procedure, a change in pain location from peripheral (or distal) to a more proximal (or central) location is desired during the mechanical assessment and manipulative evaluation. Determination of the initial movement pattern to be used by the therapist is based on presumed pathology (e.g., discogenic versus posterior element pain), pain pattern, and successful pain centralization. Again, this underscores the importance of thorough evaluation that allows the physician to accurately categorize the malady being sent to the therapist for treatment as discogenic, posterior facet joint, or something else. Extension Bias As a very generalized guideline, the extension bias (see later) is most commonly used with discogenic pathology; symptoms decrease with repetitive extension on motion pattern testing and pain centralizes with extension. Flexion Bias Flexion bias is most commonly used in patients with posterior spine element (e.g., facet) pain. In these patients, symptoms decrease with repetitive flexion on motion pattern testing and pain centralizes with flexion. Exercise Programs for Low Back Pain Several exercise programs have been developed for acute LBP. These include those designed by McKenzie (mainly extension exercises) (1981), Williams (1937), Aston (1999), Heller (1991), and Feldenkrais (Lake 1985), and other lumbar stabilization programs, stretching regimens, and aerobic conditioning programs. McKenzie Technique The McKenzie technique is one of the most popular of the many conservative spine care programs. It is a method of diagnosis and treatment based on movement patterns of the spine (Fig. 9–30). For any spinal condition, certain movements aggravate the pain and other movements relieve the pain. Because the McKenzie method works best for acute back pain that responds to lumbar extension, mobilization, and exercises, the technique has been erroneously labeled an extension exercise program. McKenzie, in fact, advocates position and movement patterns, flexion or extension, that best relieve the patient’s symptoms. McKenzie’s method is complex and much has been written explaining its theoretical basis. In The Lumbar Spine: Mechanical Diagnosis and Therapy (1981), McKenzie classifies LBP based on spinal movement patterns, positions, and pain responses, and describes a postural syndrome, derangement, and dysfunction. Each classification has a specific treatment that includes education and some form of postural correction. A basic explanation of the method is as follows. Some stages of the lumbar degenerative cascade create symptoms because of pathoanatomic abnormalities, which can be positively altered by spinal positioning. This hypothesis has led to several forms of spinal manipulation, including chiropractic and osteopathy. The McKenzie technique is a more passive form of spinal manipulation in which the patient produces the motion, position, and forces that improve the condition. Examples of pathoanatomic alterations include a tear in the annulus and acute facet arthritis. Repeated lumbar extension may reduce edema and nuclear migration in an annular tear or may realign a facet joint in such a way as to reduce inflammation and painful stimuli. Through trial and error, the position and exercise program that best relieve the patient’s symptoms can be found (see Fig. 9–30). Cyclic range of motion exercises (usually in passive extension) are the cornerstone of the McKenzie program. These repetitive exercises “centralize” pain, and certain postures prevent end-range stress. Lumbar flexion exercises may be added later, when the patient has full spinal range of motion. Treatment is based on evaluation of pain location and maneuvers that change the pain location from referred to centralized (Fig. 9–31). Once identified, the direction of exercise and movement (such as extension) is used for treatment. Centralization, as McKenzie use the term, refers to a rapid change in perceived location of pain from a distal or peripheral location to a proximal or central one. Donelson and colleagues (1990) reported centralization of asymmetrical or radiating pain in 87% of patients during the first 48 hours of care. For a movement to eventually centralize pain, it must be performed repetitively, because the initial movement often aggravates or intensifies the pain. Centralization also occurs more rapidly if the initial movements are performed passively to end-range. Centralization most frequently occurs as a result of extension movement, occasionally from lateral movements, and only rarely with flexion. McKenzie reported that 98% of patients with symptoms for less than 4 weeks who experienced centralization during their initial assessment had excellent or good results; 77% of patients with subacute symptoms (4 to 12 weeks) had excellent or good results if their pain centralized initially. The critical clinician should always bear in mind the self-limited course typical for patients with low back pain (e.g., a 90% resolution rate at 6 weeks). The advantage of this program is that it gives patients an understanding of their condition and responsibility for maintaining proper alignment and function. Disadvantages are that the program requires active, willing participation of the patient, who must have the ability to centralize the pain; better results are obtained for patients with acute pain than for those with chronic pain, and the very complex regimen requires a therapist trained in McKenzie’s techniques to obtain the best results. Each movement is taken to its end-range repetitively as long as distal pain continues to diminish. McKenzie stresses the importance of taking the movements to the end-range permitted by the patient to accurately observe changes in the pain pattern. If distal symptoms worsen, that specific movement is discontinued. Pain locations from these maneuvers are carefully observed and recorded. Based on the clinical response to centralization, the patient is taught to perform home spinal exercises in that direction of movement (usually extension). For example, for a patient with acute pain, the self-care exercise program may include prone extension for a few seconds at a time, with sets of 10 repetitions performed every hour or two. The patient is also taught modified resting positions (for sitting, standing, and lying) and work postures that will maintain centralization and avoid peripheralization. Most patients have centralization of pain in the first 2 days or sooner. Again, treatment outcomes in “centralizers” are typically good. McKenzie classified lumbar movements that have the potential to centralize symptoms into extension, flexion, lateral bending, rotation, and side-gliding (combination of lateral bending and rotation). These may be used individually or in combination to diminish the peripheral pain. Gravity-elimination (prone) versus gravity-assisted (standing) symptom reduction further increases the number of lumbar movement combinations that the therapist must understand and possibly use in an effort to centralize symptoms. The result is that more than 40 different exercise regimens are available, and application of the appropriate regimen may require complex customization. Williams Flexion Exercises (Fig. 9–37) The goals of this isometric flexion regimen, developed in the 1930s, are to (1) widen the intervertebral foramina and facet joint to reduce nerve compression, (2) stretch hip flexors and back extensors, (3) strengthen abdominal and gluteal muscles, and (4) reduce “posterior fixation” of the lumbosacral junction. A concern with this method is that certain flexion maneuvers increase intradiscal pressure, possibly aggravating herniated or bulging discs. According to Nachemson (1981), Williams’ first exercise increases intradiscal pressure to 210% over that in a standing posture (see Fig. 9–35). Three of the six exercises increase intradiscal pressure, and these three are contraindicated for patients with acute herniated disc. Lumbar Stabilization Programs There is no evidence that early return to activity increases the likelihood of back pain recurrences. On the contrary, physically fit individuals have fewer and shorter attacks of LBP and are more tolerant of pain. With a better understanding of spinal biomechanics, specific activities, and positions that increase loads on the spine, reinjury can be avoided. Numerous studies have shown that patients with LBP can perform selected activities almost normally without increasing pain. Body mechanics that avoid painful positions are called cautious or preventive body mechanics. Body mechanics that attempt to overcome the condition with muscular effort and knowledge of body positions have led to the field of stabilization training. Back schools, which gained prominence in the 1970s, gave education and training in cautious or preventive body mechanics for routine daily activities, but they did not provide techniques for heavy laborers or for highperformance athletes, who require dynamic, ballistic body mechanics for high-level activities. Practitioners with backgrounds in martial arts or sports training and some therapists with European influences in training developed stabilization training primarily for these patients. The basic premise of stabilization training is that an individual with back pain (considered an unstable condition) can be taught to stabilize the painful pathologic condition through muscular development and movement patterns that allow painless return to a higher-than-normal level of functional activities. Stabilization training incorporates almost all aspects of conservative treatment: education, body mechanics, manual therapy, the McKenzie technique, Williams’ exercises, yoga, martial arts, work hardening, and functional restoration. The techniques of stabilization training have been extensively demonstrated in many texts and videotapes, and the techniques are used by many therapists who treat high performance athletes with back problems. The main goal of the lumbar stabilization program is to build musculature that stabilizes the torso, with cocontraction of abdominal muscles to provide a corseting effect on the lumbar spine. This concept is centered on the assumption that an injured lumbar motion segment may create a weak link in the kinetic chain, with subsequent predisposition to reinjury. This program is used in conjunction with other methods aimed at controlling acute pain (such as NSAIDs). Emphasis is on positioning the spine in a nonpainful orientation, termed the neutral spine. Stretching and range of motion exercises are then completed daily in this configuration. Supervision by an appropriately oriented trainer is advised. The second phase of treatment consists of active joint mobilization methods, including extension exercises in prone and standing positions, and alternating midrange flexion extension in a four-point stance. Simple curl-ups for abdominal muscle strengthening is progressed to dynamic abdominal raising. This includes “dead bug” exercises, using alternate arm and leg movements while supine. Diagonal curl-ups and incline board work are performed. Progression to aerobic exercise, exercise with a ball, and weight training may be added (see box later). The program endpoint is determined by maximal functional improvement, the point beyond which no further improvement in function will result from additional exercise. |
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