Diagnosis of Intermittent Vascular Claudication in a Patient With a Diagnosis of Sciatica.

Key Words: Differential diagnosis, Sciatica, Vascular claudication.

In the United States, back pain is the second most frequently reported reason that people seek medical care, it is the second leading cause of lost time from work, and it results in more lost productivity than any other medical condition.[1] Approximately 85% of back pain involves the lower back, and about 12% of people with low back pain also have sciatica.[1]

In 1934, Mixter and Barr[2] reported that sciatica was caused by a herniated disk impinging on a lumbar nerve root. They also described a surgical technique to remove a portion of the disk and subsequently resolve the symptoms. Many causes of sciatica exist, however, and many causes of leg pain and paresthesia can mimic sciatica. Some of the other conditions that can produce or mimic sciatica are herpes zoster and postherpetic neuralgia,[3,4] endometriosis of the sciatic nerve,[5,6] bacterial endocarditis,[7] soft tissue tumors in the pelvis,[8] diabetic neuropathy (diabetic radiculopathy, proximal motor neuropathy, amyotrophy, Bruns-Garland syndrome),[9-11] psoas muscle abscess,[12] Sjogren syndrome,[13] ischemia of the sciatic nerve,[14] and peripheral vascular disease.[15]

Arterial insufficiency of the distal aorta, iliac, or femoral arteries is commonly associated with lower-extremity (LE) aching, cramping, numbness, tightness, or fatigue and, therefore, may mimic sciatica.[14-18] The symptoms are most common in the calf but also occur in the thigh, buttocks, or low back region if the occlusion is proximal.[16,18-22] Patients with arterial stenosis are more likely to be heavy smokers than are people without stenosis.[19,23] Other risk factors for stenosis are age (increased risk with age greater than 40 years), gender (men are at greater risk), hypertension, diabetes, obesity, sedentary lifestyle, and a family history of coronary heart disease.[23,24]

The most common site for atherosclerosis in people under the age of 40 years is the aortoiliac junction.[23] Occlusion at this junction may produce muscle weakness, numbness, paresthesia, paralysis, cold and pale legs with decreased or absent peripheral pulses, and intermittent claudication of the lower back, gluteal muscles, quadriceps femoris muscle, or calves.[20] The symptoms typically appear after walking the same distance each time and resolve with rest, even standing still.[16-19] The walking distance that produces symptoms will usually decrease over time. Peripheral vascular disease involving a peripheral vessel, such as the iliac or femoral artery, will usually produce symptoms in one extremity, whereas aortic stenosis may produce symptoms in both extremities as well as the buttocks or low back.[19,20]

An important component of an initial orthopedic evaluation is to differentiate the etiology of a patient's pain as being neuromusculoskeletal in origin versus being visceral in origin. Screening for disease is important for several reasons:

1. Many visceral diseases mimic orthopedic symptoms, and a delay in diagnosis and appropriate treatment may lead to morbidity or mortality.

2. Many people over the age of 60 years seek orthopedic physical therapy, and this age group is at a greater risk for visceral pathology and disease.

3 The current managed care environment has reduced the amount of time that primary care physicians spend with their patients and has made it more difficult to refer patients to specialists and to refer them for diagnostic testing, which may lead to a delay in diagnosing disease.

4. Patients who are referred for outpatient physical therapy have high blood pressure, anemia, thyroid problems, cancer, diabetes, kidney disease, liver disease, or heart disease at a frequency rate that varies between 1 and 15 patients with a particular visceral disease per 100 outpatients.[27]

5. Patients who are referred for outpatient physical therapy have a family history of cancer, heart disease, diabetes, or stroke at a frequency rate that varies between 15 and 29 patients with a particular family history per 100 outpatients.

The purpose of this case report is to illustrate the importance of a thorough screening to rule out diseases that may mimic musculoskeletal symptoms. The report points out the importance of a thorough history, a medical screening questionnaire, and a comprehensive examination.

Case Description

Patient

A 41-year-old Caucasian woman was referred for physical therapy with a diagnosis of sciatica from her primary care physician. She was initially evaluated by another therapist whose assessment was "right upslip with right anteriorly rotated ilium and a left posteriorly rotated ilium." Left radicular signs and symptoms were also noted. The patient received only the evaluation and was subsequently referred to another therapist (JCG) due to problems scheduling the patient for a return visit. A brief re-evaluation was initiated to confirm the first therapist's findings and to become familiar with the patient and her symptoms. After discovering that the patient was complaining of bilateral LE weakness every time she walked half a block, that she denied leg pain, and that all LE nerve tension tests were negative, I decided to perform an extensive history and orthopedic examination before beginning any form of treatment.

The patient complained of bilateral LE weakness, commenting, "Every time I walk half a block, my legs [left greater than right] feel like they're going to collapse on me." The patient reported minimal (3/10: 0=no pain, 10=worst pain imaginable) pain in the region of her left sacroiliac joint and left buttock, with periodic numbness below her left knee and into the foot, which she noted after walking (Fig. 1). She also reported sensations of cold and then heat along the anterolateral aspect of the left thigh during walking and periodic cramps in her right calf muscle. Her symptoms were aggravated by walking, and they were relieved by rest, including standing still. She reported that the pain was not worse at night. She reported that the pain started suddenly, without trauma, 2 months prior to her referral for physical therapy. During the first week of her symptoms, the patient was able to walk-up to half a mile (0.8 km). She reported having no LE pain, bowel or bladder dysfunction, shortness of breath, chest pain, or arm pain. No plain radiographs, magnetic resonance imaging, computerized tomography scan, bone scan, or vascular studies had been performed prior to her physical therapy evaluation.

[Figure 1 ILLUSTRATION OMITTED]

One month prior to the onset of her symptoms, the patient had a mild low back injury, with pain concentrated at her left buttock. The pain was minimal in intensity after 1 month. Four years previously, she had been in a motor vehicle accident in which her upper back was injured. She received 6 months of physical therapy, and the symptoms resolved. She reported having no previous history of LE injuries, surgery, or symptoms.

General Health

The patient completed a general medical screening questionnaire at the time of her initial evaluation with her first physical therapist (Fig. 2). The results of this questionnaire suggested that the patient did not have any history or symptoms of visceral pathology or disease. During my evaluation of the patient, she was given a comprehensive medical screening questionnaire (Fig. 3). This latter questionnaire consisted of 84 questions, compared with the former questionnaire with 30 questions. The results of the comprehensive questionnaire showed evidence of possible disease or dysfunction in both the pulmonary and cardiovascular systems of the patient. The patient marked "no" for a history of heart disease on the first questionnaire, and she marked "yes" for a family history of heart disease on the second questionnaire. This latter question was not on the first questionnaire. On follow-up questioning, she said that her grandfather died at age 59 years of a myocardial infarction (MI), her grandmother died at age 31 years of an MI, her father died at age 59 years of an MI, and her mother, now aged 63 years, had a massive MI 5 years previously.

[Figures 2-3 ILLUSTRATION OMITTED]

Diet and Smoking Habits

The purpose of investigating the patient's diet was to determine whether poor nutritional habits may be contributing to her symptoms. Daily ingestion of caffeine (coffee, tea, or soda), for example, has been shown to increase the urinary loss of calcium, magnesium, sodium, and potassium.[28,29] Calcium and magnesium are important minerals for maintaining optimal health and function in bone, muscle, and nerve. Smoking has many well-known adverse health effects, including cancer, osteopenia, accelerated degenerative disk disease, and cardiovascular disease.[24,30-32] The patient drank 3 cups of nondecaffeinated coffee a day, drank 1 glass of tea a day, and had smoked a pack of cigarettes a day for the past 26 years. She reported that she did not take any vitamins or dietary supplements.

Functional Status

The patient's major functional limitation was her inability to walk more than a block. She walked at work, and her only form of physical exercise outside of work was walking. Her goal was to be able to walk again for 2 miles (3.2 km).

Examination

The following examination was performed to confirm or rule out involvement of the lumbar spine and the sciatic nerve or lumbar nerve roots as a source of the patient's complaints and limited ability to walk.

Lumbar active range of motion. The purposes of taking these measurements were to evaluate the patient's willingness to move through full active range of motion (ARUM) and to identify any limitations in range of motion (ROM) or reproduction of pain or other symptoms and note any deviations from the primary plane of motion. Both contractile and noncontractile tissues were stressed. The patient was examined while standing with her feet a shoulder width apart and pointed in their normal comfortable direction and with her knees extended. She was instructed to slowly move in the requested direction, keeping her knees straight, until she felt that she could go no farther due to tightness, pain, or a reproduction of other symptoms (temperature changes, numbness, cramps). The directions were forward bending, backward bending, side bending, and rotation. She moved in each direction twice. The patient demonstrated full lumbar AROM without reproduction of her symptoms.

Lumbar passive range of motion. The purpose of taking these measurements was to examine the patient's passive range of motion (PROM) in an effort to determine whether the symptoms were arising from a noncontractile tissue associated with the lumbar spine and pelvis. In addition, these measurements allowed the therapist to examine the patient's willingness to let her spine move through a full ROM and to identify any limitations in ROM (gross as well as segmental) as well as reproduction of pain or other symptoms. Because PROM always exceeds AROM, it is important to stress a muscle, ligament, or joint to its end ROM during PROM, even though the AROM is pain-free. These measurements were obtained with the patient kneeling (hips in 0 [degrees] of flexion, knees bent 90 [degrees]) with the buttocks supported by a treatment table. This position helped to stabilize the pelvis and allowed for uninhibited motion of all the lumbar segments, especially L5-S1. During a standing PROM examination of the lumbar spine, it is difficult to stabilize the pelvis. During a sitting PROM examination of the lumbar spine, the flexion of the lumbar spine will limit the ROM of the L5-S1 segment, which means that segment will not be tested through its full ROM.

The patient was instructed to completely relax without helping or resisting the motions performed by the therapist. Each position was held for at least 5 seconds at the end of the available ROM if the patient did not report pain or discomfort. Only one repetition was performed in each direction. The directions were backward bending, side bending, and rotation.-Forward bending was tested in a sitting position for better stabilization of the pelvis. Combined motions of extension, side bending (ipsilateral), and rotation (contra-lateral) were also performed in a kneeling position. In my opinion, these motions compress the disk, facet joint (cartilage, menisci), and nerve roots in the intervertebral foramen on the concave side of the side-bending motion and stretch the disk, facet joint capsule, muscles, and ligaments on the convex side of the side-bending motion. The patient demonstrated full lumbar PROM without reproduction of her symptoms.

Lumbar spine muscle testing. The purpose of this examination is to rule out spinal muscle tissue as a source of the pain or symptoms. This test was skipped because the lumbar ARUM and lumbar PROM tests did not reproduce the patient's symptoms. I decided to spend the remaining time available for the evaluation performing test procedures that were more likely to reproduce the patient's symptoms.

Special tests of the lumbar spine. The purpose of the lumbar compression and heel-drop tests was to help rule out the lumbar spine as a source of the patient's symptoms. Lumbar compression was produced through the patient's shoulders while she was seated with the therapist standing behind her. The procedure was performed with the patient in an erect sitting posture, in a slouched position (lumbar flexion), and with exaggerated lumbar lordosis (lumbar extension). The therapist produces a compressive force with his or her hands pushing down on the patient's shoulders for up to 10 seconds in each posture. Reproduction of the patient's low back pain or LE symptoms is considered a positive test. Various structures (disks, vertebrae, nerve roots, facet joints, and ligaments) are stressed in the 3 different postures. The theory is that if pain occurs in all 3 postures, then the disks or vertebrae are involved because these are the only tissues that are stressed in all 3 postures (Ola Grimsby, Ola Grimsby Institute Residency Program, San Diego, Calif). The heel-drop test is performed in a standing position. The patient rises up onto his or her toes and then quickly drops all of the body weight onto the heels. The patient is instructed to keep his or her knees straight. If no pain or other symptoms occur, then the procedure is repeated with the body weight dropping a little quicker. The test is considered positive if there is a reproduction of low back pain or LE symptoms. This test may produce pain in individuals with symptomatic diskogenic disease, facet joint arthropathy, lumbar foraminal stenosis, vertebral compression fractures, spondylolysis (acute or unstable fracture), or spondylolisthesis (Ola Grimsby, Ola Grimsby Institute Residency Program, San Diego, Calif). In this patient, lumbar spine compression in the 3 different postures and the standing heel-drop test were all negative.

Lower-extremity strength testing. The purposes of this test were to examine the patient's willingness and ability to exert maximum isometric resistance against an external force and to confirm or rule out. lumbar nerve root or sciatic nerve compression. Muscle testing was performed as a screening examination. I instructed the patient to resist, "as hard as you can," the motion that I induced. The following muscles were tested with the patient in a seated position: iliopsoas, quadriceps femoris, hamstring, anterior tibialis, and extensor hallucis longus. The seated position was used, modified for some muscles as described by Kendall and McCreary,[33] to facilitate the examination, save time, and minimize the number of positional changes the patient would have to make during the evaluation. Triceps surae muscle strength was assessed in a one-legged stance for 10 repetitions. The patient demonstrated Normal strength (5/5) in her LEs during the isometric break-test for strength.

Sensation. The purpose of this test was to rule out sensory abnormalities that may be due to nerve root damage, peripheral neuropathy, vascular deficiencies, or systemic disease (eg, diabetes). A brief screening examination was performed on this patient to determine whether more time should be spent on sensory examination. If abnormalities are noted with light touch, then further investigation might include pinprick, temperature, vibration, or proprioception testing.

A horsehair brush was lightly stroked over the dermatomes of the LEs to detect any differences (either increased or decreased) between the LEs in the patient's perceived sensation to light touch. As I stroked one dermatome in the left leg and the same dermatome in the right leg, I asked the patient, "Does this ... feel the same as this?" She demonstrated normal sensation to light touch in her LEs.

Lower-extremity deep tendon reflexes. This test was not performed because the above tests of the nervous system were all negative, and I was conserving time to examine other tissues of the body.

Mobility of neural tissue. The purpose of this test was to rule out restricted mobility of neural structures intrinsic or extrinsic to the nerve as well as inflammation or sensitization of the lumbar spinal nerve roots or the sciatic nerve as a source of the symptoms. The straight-leg-raising (SLR) test, or Lasegue's test, was performed with the patient in a supine position.[34] I held the patient's knee in extension and allowed her ankle to relax. As I passively raised her leg, increasing hip flexion, I told the patient, "Tell me when your hamstring muscles feel tight." The hip was then passively rotated medially (internally) and adducted as the ankle was passively dorsiflexed to provide maximum tension on the neural tissues (sciatic nerve).[35] The test is considered positive if there is a reproduction of the posterior LE pain.

Cram's (bowstring) sciatic nerve tension test was also performed with the patient in a supine position.[36] The starting position was the same as for the SLR test. The leg was passively raised until the patient noted symptoms or significant hamstring muscle or neural tension, at which point the knee was flexed slightly (20 [degrees]) to abolish the symptoms and any hamstring muscle or neural tension. Next, the hip was flexed to the point that symptoms or hamstring muscle or neural tension was produced. The hip was then extended slightly to again abolish the symptoms. At this time, I produced firm digital pressure, just proximal to the popliteal fossa, against the posterior tibial nerve division of the sciatic nerve to elicit symptoms. Clinically, I have found that a sharp localized pain behind the knee indicates sensitization of the nervous system (sciatic nerve) or a mildly irritated nerve. Pain radiating to the buttock or foot, with or without paresthesia, is usually indicative of a more serious lesion to the sciatic nerve or lower lumbar spinal nerve roots. The sitting slump test was performed with the patient seated and her knee passively extended, her ankle passively dorsiflexed, her trunk in a slouched posture, and her head actively flexed to her chest (modified from Maitland[37]). A positive test results in a reproduction of leg pain or symptoms. The SLR test, Cram's test, and the sitting slump test for nerve tension were all negative.

Pulse. The purposes of palpation were to look for diminution in the pulse amplitude of the LEs and to check for asymmetry in the strength of the arterial pulse from one extremity to the other. The distal arterial pulses of the foot and ankle were examined. The purpose was not to locate the exact level of any potential vascular compromise, but to determine whether a vascular abnormality existed that would explain the patient's symptoms. The patient had a moderately diminished (grade 2/4) left dorsalis pedis pulse at rest. The right dorsalis pedis pulse at rest was normal (grade 4/4). The posterior tibialis muscle pulses were difficult to palpate on this patient and, therefore, were not graded.

Special test of the vascular system (van Gelderen bicycle test). Exercise testing is an important part of a complete evaluation in patients suspected of having occlusive vascular disease. Pulses are palpated at rest and then quickly after the patient has exercised to induce symptoms.[38] Ischemia secondary to exercise causes the peripheral arterial beds to dilate.[38,39] This dilation of the peripheral arterial beds decreases the peripheral vascular resistance, which diminishes the pulse amplitude.[38,39]

The van Gelderen bicycle test is designed to stress the LE vascular system without causing any central canal or foraminal stenosis that could be misinterpreted as intermittent neurogenic claudication.[40] The patient was instructed to cycle at a moderate pace (90 rpm) for 5 minutes or until she felt the onset, of her symptoms. Lumbar flexion (high seat height with low handle bars) was used to help minimize any effect from a neurogenic claudication, which would be exacerbated in lumbar extension and relieved by lumbar flexion. A positive test is indicated by a reproduction of some or all of the patient's symptoms in the same extremity that demonstrates a decrease in the pulse amplitude of a particular arterial branch. The test reproduced the patient's symptoms, and her legs collapsed as she stepped off the bicycle after 5 minutes. Her dorsalis pedis pulse on the left side was temporarily abolished (grade 0/4).

Evaluation

I suspected that the patient had intermittent vascular claudication secondary to occlusive vascular disease. The lumbar spine was ruled out as a source of the buttock or leg symptoms because the following tests were negative: AROM and PROM testing, lumbar compression in 3 different postures, and the heel-drop test. Sciatica or nerve root lesions were ruled out as a source of the buttock or leg symptoms because the following tests were negative: strength testing of the LEs, sensation to light touch in the LEs, SLR test, sitting slump test, and Cram's test. Vascular claudication was considered the most likely diagnosis due to the patient's history of smoking; strong family history of cardiovascular disease; LE weakness when walking the same distance each time; symptoms aggravated only by walking and not by a change in body position or posture; relief of symptoms with rest, even when standing (which helped rule out neurogenic claudication); decrease in the strength of the dorsalis pedis pulse at rest; and a positive van Gelderen bicycle test.

Plan

I referred the patient back to her physician for reevaluation to rule out occlusive vascular disease. Due to the seriousness of the diagnosis and the patient's family history of sudden death from MI, I referred her immediately. Concurrent treatment of the patient's sacroiliac joint (SIJ) and buttock was not considered because she needed to focus on obtaining a quick and accurate medical diagnosis to confirm or rule out intermittent vascular claudication. The pain in the region of the SIJ and buttock was minor during the lumbar spine evaluation and did not inhibit her functional status. In addition, the symptoms could be explained by a proximal or aortic lesion.[16,18-22] The abdominal aorta bifurcates into the left and right common iliac arteries at the level of the L4 vertebrae (anterolaterally on the left side).[41] The common iliac arteries divide into internal and external branches at the level of the lumbosacral junction, anterior to the SIJ.[41] The internal iliac artery continues to descend posteriorly to the superior margin of the greater sciatic foramen.[41]

To treat the SIJ and buttock with exercise was contraindicated because the patient was thought to have occlusive vascular disease and the exact location and degree of stenosis was unknown. Manipulation to the lumbar spine or the SIJ also is contraindicated in people with atherosclerosis.[42,43] Modalities such as ultrasound and superficial heat or cold are known to influence blood flow and would also be contraindicated.[44-47]

Outcome

The patient was subsequently seen by her primary care physician, who reported finding "poorly palpated pulses in her feet, no popliteal pulses, and probably somewhat reduced pulses over the femoral areas." His assessment was "rule out claudication." The patient was then referred to a vascular specialist. The specialist noted that the symptoms the patient described were somewhat unusual for vascular related disease. He noted that "her right femoral [area] is palpable; her left femoral [area] is palpable and slightly diminished. She also has diminution of the posterior tibial pulses bilaterally, but the dorsalis pedis pulses are intact." His impression was "asymmetric distribution of the pulses in a young lady with atypical symptoms." He ordered an angiogram to rule out a vascular etiology. Subsequently, the patient received an aortogram with runoff arteriogram. The results of this test demonstrated a "high-grade circumferential stenosis of the distal-most aorta at its bifurcation."

Aortic graft surgery was recommended to the patient. The physician also strongly recommended to the patient that she quit smoking. Two months after her physical therapy evaluation, the patient underwent angioplasty, with stents implanted into the aorta. A stent is a tiny metal structure that is mounted on the angioplasty balloon. When the balloon is inflated, the stent expands. After the balloon is deflated, the stent remains in place. It now provides a scaffolding for the newly widened artery. Within a few weeks, the endothelium, the natural lining of the artery, will grow over the metallic stent. Following the surgery, the patient reported the complete relief of all of her symptoms, including the pain in the region of her SIJ and buttock. According to the patient, these stints were supposed to last 3 to 5 years; however, the stints failed after 18 months, and the patient subsequently underwent synthetic graft surgery to her distal aorta.

Discussion

The physical therapy diagnosis in this case was reached by trying to rule out or confirm the primary diagnosis of sciatica. The possibility of a disease was found through a careful history, medical screening questionnaire, and physical examination. The "red flags" in this case were as follows: primary complaint of LE weakness and giving-out in the absence of a strong pain component, progressively decreasing distance of walking and a specific walking distance that brought on symptoms every time, extensive and severe family history of cardiac disease, symptoms with walking and stair climbing that decreased with rest (standing), cold and hot sensations in her thigh, and onset of symptoms without trauma. Physical therapists should never minimize their evaluation of a patient just because the patient is referred with a medical diagnosis and symptoms that may appear to match.

Acknowledgment

I acknowledge the support and assistance of Anne-Marie Kaiser in the preparation of the manuscript.

References

[1] Praemer A, Furner S, Rice DP. Musculoskeletal Conditions in the United States. Park Ridge, Ill: American Academy of Orthopaedic Surgeons; 1992:23-33.

[2] Mixter WJ, Barr JS. Rupture of the intervertebral disc with involvement of the spinal cord. N Engl J Med. 1934;21!:210-214.

[3] Helfgott S, Picard D, Cook J. Herpes zoster radiculopathy. Spine. 1993;18:252.5-2524.

[4] Watson C, Deck J, Morshead C, et al. Post-herpetic neuralgia: further postmortem studies of cases with and without pain. Pain. 1991;44:105-117.

[5] Dhote R, Tudoret L, Bachmeyer C, et al. Cyclic sciatica: a manifestation of compression of the sciatic nerve by endometriosis, a case report. Spine. 1996;21:2277-2279.

[6] Takata K, Takahashi K. Cyclic sciatica: a case report Spine. 1994;19:89-90.

[7] Hunder G. When musculoskeletal symptoms point to endocarditis. Journal of Musculoskeletal Medicine. 1992;9: 33- 40.

[8] Ball A, Serpell J, Fisher C, Thomas J. Primary soft tissue tumours of the pelvis causing referred pain in the leg. J Surg Oncol. 1991 ;47:17-20.

[9] Naftulin S, Fast A, Thomas M. Diabetic lumbar radiculopathy: sciatica without disc herniation. Spine. 1993;18:2419-2422.

[10] Barohn R, Sahenk Z, Warmolts J, Mendell J. The Bruns-Garland syndrome (diabetic amyotrophy): revisited 100 years later. Arch Neurol. 1991;48:1130-1135.

[11] Pascoe MK, Low PA, Windebank AJ, Litchy WJ. Subacute diabetic proximal neuropathy. Mayo Clin Proc. 1997;72:1123-1132.

[12] Haines J Jr, Chop W Jr, Towsley D. Primary psoas abscess: an often insidious infection. Postgrad Med. 1990;87:287-288.

[13] Kaplan J, Rosenberg R, Reinitz E, et al. Invited review: peripheral neuropathy in Sjogren's syndrome. Muscle Nerve. 1990;13:570-579.

[14] Lamerton AJ, Bannister R, Withrington R, et al. "Claudication" of the sciatic nerve. BMJ. 1983;286:1785-1786.

[15] Frawley JE. Clinical features of vascular insufficiency in the limbs. Aust Faro Physician. 1984;13:812-816.

[16] Sliwa J, Wiesner S, Novick A, Charuk G. Concurrent musculoskeletal pain in a patient with symptomatic lower extremity arterial insufficiency. Arch Phys Med Rehabil. 1989;70:848-850.

[17] MacNab I, McCulloch J. Backache. Baltimore, Md: Williams & Wilkins; 1990:22-25.

[18] Goodman CC, Snyder TEK. Differential Diagnosis in Physical Therapy. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1995:77-146.

[19] Boissonnault WG, Bass C. Pathological origins of trunk and neck pain, part II: disorders of the cardiovascular and pulmonary systems. J Orthop Sports Phys Ther. 1990;12:208-215.

[20] Goodman CC. The cardiovascular system. In: Goodman CC, Boissonnault WG, eds. Pathology: Implications for the Physical Therapist. Philadelphia, Pa: WB Saunders Co; 1998:263-353.

[21] Halperin JL, Creager MA. Arterial obstructive diseases of the extremities. In: Loscalzo J, Creager MA, Dzau VJ, eds. Vascular Medicine: A Textbook of Vascular Biology and Diseases. Boston, Mass: Little, Brown and Co Inc; 1992:835-865.

[22] Fairbairn JF II. Clinical manifestations of peripheral vascular disease. In: Juergens JL, Spittell JA Jr, Fairbairn JF II, eds. Peripheral Vascular Disease. Philadelphia, Pa: WB Saunders Co; 1980:3-15.

[23] Krajewski LP, Olin JW. Atherosclerosis of the aorta and lower extremity arteries. In: Young JR, Olin JW, Bartholomew JR, eds. Peripheral Vascular Diseases. 2nd ed. St Louis, Mo: Mosby; 1996:208-224.

[24] Hooi JD, Stoffers HE, Kester AD, et al. Risk factors and cardiovascular diseases associated with asymptomatic peripheral arterial occlusive disease: The Limburg PAOD Study. Scand J Prim Health Care. 1998;16:177-182.

[25] Kerr EA, Mittman BS, Hays RD, et al. Managed care and capitation in California: How do physicians at financial risk control their own utilization? Ann Int Med. 1995; 123:500-504.

[26] Davis K, Schoen C. Assuring quality, information, and choice in managed care. Inquiry. 1998;35:104-114.

[27] Boissonnault WG, Koopmeiners MB. Medical history profile: orthopaedic physical therapy outpatients. J Orthop Sports Phys Ther. 1994;20:2-10.

[28] Massey L, Wise K. Effects of dietary caffeine on mineral status. Nutritional Research. 1984;4:43-50.

[29] Bergman EA, Massey LK, Wise KJ, Sherrard DJ. Effects of dietary caffeine on renal handling of minerals in adult women. Life Sci. 1990;47:557-564.

[30] Lash TL, Aschengrau A. Active and passive cigarette smoking and the occurrence of breast cancer. Am J Epidemiol. 1999;149:5-12.

[31] Egger P, Duggleby S, Hobbs R, et al. Cigarette smoking and bone mineral density in the elderly. J Epidemiol Community Health. 1996;50:47-50.

[32] Battie MC, Videman T, Gill K, et al. Smoking and lumbar intervertebral disc degeneration: an MRI study of identical twins. Spine. 1991;16:1015-1021.

[33] Kendall FP, McCreary EK. Muscles: Testing and Function. 3rd ed. Baltimore, Md: William & Wilkins; 1983:129-183.

[34] Kosteljanetz M, Bang F, Schmidt-Olsen S. The clinical significance of straight-leg raising (Lasegue's sign) in the diagnosis of prolapsed lumbar disc: interobserver variation and correlation with surgical finding. Spine. 1988;13:393-395.

[35] Butler D, Gifford L. The concept of adverse mechanical tension in the nervous system, part 1: testing for "dural tension." Physiotherapy. 1989;75:622-629.

[36] Cram RH. A sign of sciatic nerve root pressure. J Bone Joint Surg Br. 1953;35:192-195.

[37] Maitland CD. The slump test: examination and treatment. Australian Journal of Physiotherapy. 1985;31:215-219.

[38] Roon AJ. The history and physical examination of the patient with peripheral vascular disease. In: Miller DC, Roon AJ, eds. Diagnosis and Management of Peripheral Vascular Disease. Menlo Park, Calif: Addison-Wesley Publishing Co Inc; 1982:1-16.

[39] Cox JM. Low Back Pain: Mechanism, Diagnosis, and Treatment. 5th ed. Baltimore, Md: Williams & Wilkins; 1990:257-308.

[40] Dyck P, Doyle JB Jr. "Bicycle test" of van Gelderen in diagnosis of intermittent cauda equina compression syndrome: case report. J Neurosurg. 1977;46:667-670.

[41] Williams PL, Warwick R, Dyson M, et al. Gray's Anatomy. 37th ed. New York, NY: Churchill Livingstone Inc; 1989:662-858.

[42] Kleynhans AM, Terrett AG. The prevention of complications from spinal manipulative therapy. In: Glasgow EF, Twomey LT, Scull ER, Kleynhans AM, eds. Aspects of Manipulative Therapy. 2nd ed. New York, NY: Churchill Livingstone; 1985:161-175.

[43] Hartman LS. Handbook of Osteopathic Technique. 2nd ed. New York, NY: Chapman & Hall; 1985:23-27.

[44] Knight KL. Cryotherapy: Theory, Technique, and Physiology. Chattanooga, Tenn: Chattanooga Corp; 1985:33-42.

[45] Michlovitz SL. Cryotherapy: the use of cold as a therapeutic agent. In: Michlovitz SL, ed. Thermal Agents in Rehabilitation. Philadelphia, Pa: FA Davis Co; 1986:73-98.

[46] Michlovitz SL. Biophysical principles of heating and superficial heat agents. In: Thermal Agents in Rehabilitation. Philadelphia, Pa: FA Davis Co; 1986:99-118.

[47] Ziskin MC, Michlovitz SL. Therapeutic ultrasound. In: Michlovitz SL, ed. Thermal Agents in Rehabilitation. Philadelphia, Pa: FA Davis Co; 1986:141-176.

JC Gray, PT, OCS, FAAOMPT, is a clinical specialist in orthopedic manual therapy practicing at Sharp Rees-Stealy, San Diego, Calif. He is a member of the faculty of the Ola Grimsby Institute, San Diego, Calif. Address all correspondence to Mr Gray at 13364 Corte Playa Cancun, San Diego, CA 92124-1539 (USA)([e-mail]).

This article was submitted June 30, 1997, and was accepted February 18, 1999.