Management of a patient with chronic low back pain and multiple health conditions using a pain mechanisms-based classification approach.

[

case report

]

Journal of Orthopaedic & Sports Physical Therapy® Downloaded from www.jospt.org at Otterbein University on June 1, 2014. For personal use only. No other uses without permission. Copyright © 2014 Journal of Orthopaedic & Sports Physical Therapy®. All rights reserved.

CRAIG P. HENSLEY, PT, DPT, OCS, FAAOMPT1 • CAROL A. COURTNEY, PT, PhD, FAAOMPT, ATC2

Management of a Patient With Chronic Low Back Pain and Multiple Health Conditions Using a Pain Mechanisms– Based Classification Approach

L

ow back pain (LBP) is one of the most common disorders encountered by physical therapists.35 While many individuals improve, some fall into a chronic pain condition that leads to reduced quality of life and high medical costs.44 Poor health and comorbidities are associated with chronic LBP.18,22,69 Among patients with chronic kidney failure, those with poor balance, weakness, hypertension, bone disease, and cerebrovascular disease were most TTSTUDY DESIGN: Case report.

TTBACKGROUND: Pain can lead to a significant

reduction in quality of life. A pain mechanisms– based classification scheme has been outlined to improve management of patients with pain, but studies describing its use are limited. Evidence for physical therapy interventions in those with chronic pain and multiple health conditions is also lacking. This case report describes management of a patient with chronic pain and multiple health conditions.

TTCASE DESCRIPTION: A 29-year-old man

presented with a 3-year history of low back pain and 11-month history of lower extremity paresthesia. Current health conditions included left-sided hemiparesis secondary to a stroke, pancreatic kidney transplant, left-sided blindness, and osteoporosis secondary to hyperparathyroidism. Inability to walk to school, sit through class, and pain-related sleep disruption were the primary activity and participation restrictions. Outcome measures included the numeric pain rating scale, global rating of change, Oswestry Disability Index, and pain medication usage. A score of 12 on the Leeds assessment of neuropathic symptoms and

signs (LANSS) pain scale indicated the presence of neuropathic pain, but other pain mechanisms were also hypothesized to be present. A plan of treatment was designed to improve patient goals considering these pain mechanisms.

TTOUTCOMES: The patient was seen for 20

visits over 6 months. Ten months after the initial evaluation, the patient’s Oswestry Disability Index scores improved by more than 50% and the patient achieved all initially stated goals without pain medication.

TTDISCUSSION: A pain mechanisms–based

approach assisted in the management of a patient with chronic pain and multiple health conditions. Using this approach may enhance clinical decision making when managing individuals with chronic pain.

TTLEVEL OF EVIDENCE: Therapy, level 4.

J Orthop Sports Phys Ther 2014;44(6):403-414. Epub 25 April 2014. doi:10.2519/jospt.2014.4861

TTKEY WORDS: central sensitization, comorbidities, physical therapy

likely to develop chronic LBP, purportedly due to an inactive lifestyle.22 Recently, sensitization of nociceptive pathways has been demonstrated in those with chronic pancreatitis compared to healthy controls.12 Further, small-fiber polyneuropathy, common in type 1 diabetes, has been suggested to contribute to pain syndromes.51,52 Clinical studies of individuals with LBP often exclude potential participants with multiple medical conditions to control confounding variables. This leaves a void in the literature regarding physical therapy management in those with LBP and multiple health conditions. Furthermore, pharmacological management of individuals with LBP and multiple medical conditions may be limited, due to adverse drug reactions that predispose these patients to chronic LBP. The “Guide to Physical Therapist Practice”2 has suggested that categorization based on signs and symptoms should be a primary goal of the diagnostic process. Such classification has been utilized in the management of LBP.25 Some researchers36,76 have suggested that a pain mechanisms–based pain diagnosis be made to assist in directing treatment. The neurophysiological mechanisms responsible for the generation and maintenance of pain are divided into separate catego-

University of Chicago Medicine, Chicago, IL. 2University of Illinois at Chicago, Chicago, IL. The Office for the Protection of Research Subjects at the University of Illinois at Chicago reviewed and approved this case report. The authors certify that they have no affiliations with or financial involvement in any organization or entity with a direct financial interest in the subject matter or materials discussed in the article. Address correspondence to Dr Craig P. Hensley, University of Chicago Medicine, MC1081, W107, 5841 South Maryland Avenue, Chicago, IL 60637-1470. E-mail: [email protected] t Copyright ©2014 Journal of Orthopaedic & Sports Physical Therapy® 1

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TABLE 1

case report

]

Clusters of Symptoms and Signs Differentiating Pain Mechanisms–Based Classification* 62-64

Category/Description

Pain Pattern

Example Interventions

Nociceptive: pain that is predominantly driven by activation of peripheral nociceptive sensory fibers

1. P ain localized to the area of injury/dysfunction 2. C lear, proportionate mechanical/anatomic nature to aggravating/easing factors 3. U sually intermittent and sharp with movement/mechanical provocation; may be constant dull ache/throb at rest 4. A bsence of: a. P ain in association with other dysesthesia b. N ight pain/disturbed sleep c. Antalgic postures/movement patterns d. P ain variously described as burning, shooting, sharp, or electric-like

1. Posture education 2. S tretching of hip flexors and pectoralis muscles 3. J oint mobilization to hip, lumbar, and thoracic spines 4. Motor control exercises for the trunk and lower extremities 5. S trengthening for the trunk and lower extremities 6. B ack brace

Peripheral neuropathic: pain attributed to a lesion or dysfunction in the dorsal horn or cervicotrigeminal nucleus or peripheral nerve

1. P ain referred in a dermatomal or cutaneous distribution 1. Soft tissue mobilization to trigger points in hamstrings 2. H istory of nerve injury, pathology, or mechanical compromise 2. N erve gliding/stretching exercises 3. P ain/symptom provocation with mechanical/movement tests 3. L umbar spine joint mobilization that move/load/compress neural tissue

Central sensitization: amplification of neural signaling in the central nervous system that elicits pain hypersensitivity

1. D isproportionate, nonmechanical, unpredictable pattern of pain provocation in response to multiple/nonspecific aggravating/easing factors 2. P ain disproportionate to the nature and extent of injury or pathology 3. S trong association with maladaptive psychological factors 4. D iffuse/nonanatomic areas of pain/tenderness on palpation

1. C ognitive behavior treatment a. Pain physiology education b. Problem-solving strategies c. G oal setting d. Attention diversion e. Activity pacing f. Maintenance 2. C ardiovascular exercise 3. S trength training 4. Manual therapy

*Listed are the theoretical presentations of pain physical therapists encounter, divided into 3 classes, and interventions used to address each.

ries.62,76 One scheme, outlined in TABLE 1, divides pain into central sensitization,62 peripheral neuropathic pain,63 and nociceptive pain.64 Patients may demonstrate a combination of these pain mechanisms.61-64 Nociceptive pain in musculoskeletal tissue occurs when group III and IV fibers are activated in response to noxious chemical, mechanical, or thermal stimuli.76 Peripheral neuropathic pain refers to pain arising from trauma, compression, inflammation, or ischemia in a peripheral nerve, dorsal root ganglion, or dorsal root.76 With severe or repetitive injury, nociceptive input to the central nervous system may generate neuroplastic changes at spinal and supraspinal levels, hence the term central sensitization. Thus, the experience of pain can be “centrally mediated,” and treatment directed only at peripheral tissues may be ineffective. A characteristic of central sensitization is

the expansion of symptoms,6 which can be regionally localized, as in spine-related leg pain,53 or widespread, as in fibromyalgia,1 where pain sensitivity is pervasive. Furthermore, elevated levels of psychosocial distress, including depression, hypervigilance, catastrophization, and fear avoidance, have been associated with centrally mediated pain conditions.23,39,41 While exact differentiation between pain mechanisms may not be possible through clinical examination, potential indicators may be identified and treatment directed accordingly. For example, neuropathic pain is addressed pharmacologically by prescribing medications such as gabapentin, which has been shown to be effective in decreasing heightened pain processing.17 Alternatively, pain education programs have targeted psychological factors that may be linked to elevated pain processing or a central sensitization response.48,49,57 Discriminative validity to

justify usage of a pain mechanisms–based approach has been demonstrated,61 but evidence of its effectiveness in physical therapy outcomes is limited.28 The purpose of this case report was to describe the management of a patient with chronic LBP and multiple health conditions using a pain mechanisms– based approach.

CASE DESCRIPTION

T

he patient was a 29-year-old man (height, 145 cm; weight, 48 kg; body mass index, 22.9 kg/m2) who presented with chronic LBP and bilateral numbness, tingling, and pain in his lower extremities. He provided consent for publication of his case and signed an informed-consent form. The Office for the Protection of Research Subjects at the University of Illinois at Chicago reviewed and approved this case report.

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History of Present Condition Three years prior, the patient was a backseat passenger in a car that was hit from behind during a motor vehicle accident. His LBP began approximately 30 minutes after the collision. Magnetic resonance imaging of his lumbar spine, taken on the day of injury, revealed 2 disc bulges, per patient report. Following the injury, the patient received physical therapy and chiropractic care on multiple occasions. Treatment consisted of stretching, strengthening, yoga, joint mobilization, hot packs, and electrical stimulation for pain, all with no relief. He had taken multiple pain medications and received an epidural steroid injection in his lumbar spine that also provided no benefit. Since the accident, he felt as though his LBP severity and irritability had gradually worsened, with no pain-free periods. Eleven months prior to the initial evaluation, while standing and watering plants, his legs “went out” and he fell to the ground, with pain in the posterior thighs. Later that day, he began experiencing intense numbness and tingling in his posterior thighs while sitting. Followup with neurology resulted in a second lumbar spine magnetic resonance imaging scan (FIGURE 1), demonstrating biconcavity of the thoracic/lumbar end plates, suggestive of secondary hyperparathyroidism. He was sent to the primary author for management. The patient denied additional falling episodes, but his thigh symptoms were increasing in severity and frequency. He denied any previous episodes of LBP or leg pain prior to the motor vehicle accident. A pain diagram was completed by the physical therapist (FIGURE 2).

Medical History, Screening, and Medication The patient reported uncontrolled type 1 diabetes since the age of 7. This led to multiple health conditions, including hypertension, hyperlipidemia, hypoglycemia, seizures, chronic kidney failure, stroke with left hemiparesis 5 years prior to the initial evaluation, and blindness in

FIGURE 1. Midsagittal T1 magnetic resonance image of the lumbar spine revealing biconcave end plates secondary to hyperparathyroidism throughout the lower thoracic and lumbar spines.

his right eye. He owned a walking stick but did not use it. Two years prior to evaluation, he had a pancreas and kidney transplant. Finally, 11 months prior to initial evaluation, he was diagnosed with osteoporosis secondary to hyperparathyroidism. A dual X-ray absorptiometry scan revealed T scores below –2.5 in his hip, lumbar spine, and forearm. He denied headaches, dizziness, visual disturbance, bowel/bladder dysfunction, saddle paresthesia, fevers, night sweats, or change in symptoms with or after eating. To screen for depressive symptoms, the Whooley questions were administered.74 The Whooley questions are 2 items from the Patient Questionnaire of the Primary Care Evaluation of Mental Disorders that screen for depressive symptoms: (1) “During the past month, have you often been bothered by feeling down, depressed, or hopeless?” and (2) “During the past month, have you often been bothered by little interest or pleasure in doing things?” The patient answered no to both questions. A “no” response to both questions indicates a decreased likelihood of depression based on previous findings (positive likelihood

FIGURE 2. Body pain diagram detailing location, severity, irritability, nature, aggravating and easing factors, 24-hour pattern, and allodynia in the lumbar spine area (black shaded region). P1, pain 1 (black shaded area). P2, pain 2 (gray shaded area in posterior thighs).

ratio = 2.2; negative likelihood ratio = 0.07).74 The patient had an extensive list of medications (TABLE 2), many with side effects, including reduction of bone mineral density and paresthesia. The patient



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[ TABLE 2

case report

] lings in a house with stairs. He had not worked for several years but was taking classes 5 hours a day, 5 days a week to become a paralegal. He walked 2.2 km to attend class, which required taking 3 or 4 rest periods to manage his LBP. He stood frequently in class to decrease leg symptoms. He had not been participating in recreational activities because of his LBP. He also denied anxiety, smoking, alcohol consumption, or illicit drug use. He noted that his daily attention was primarily focused on his pain. He anticipated pain with activities of daily living (ADLs).

Medication List

Category/Medication, Dose Pain Hydrocodone, 325 mg, 1 to 2 tablets every 4 h Tramadol, 100 mg, 4 times per d Journal of Orthopaedic & Sports Physical Therapy® Downloaded from www.jospt.org at Otterbein University on June 1, 2014. For personal use only. No other uses without permission. Copyright © 2014 Journal of Orthopaedic & Sports Physical Therapy®. All rights reserved.

Lidoderm patch Gabapentin, 100 mg, 3 times per d Bone mineral density Calcitonin, daily spray Ergocalciferol, 50 000 units every 2 wk Actonel, 35 mg, weekly Reclast solution

Goals

Tissue antirejection CellCept, 500 mg, 3 times per d

The patient’s goals were to walk to school without needing rest periods, to sit for at least 60 minutes, and to initiate an exercise program.

Tacrolimus, 1 mg, 2 times per d Other Docusate (stool softener), 100 mg every 12 h Metoclopramide (antiemetic), 10 mg, 3 times per d Omeprazole (proton-pump inhibitor), 20 mg, daily

Outcome Measures

Simvastatin (cholesterol inhibitor), 5 mg, daily

Several outcome measures were utilized (TABLE 3). The modified Oswestry Disability Index (ODI) was chosen as the primary outcome measure. The ODI is composed of 10 items scored from 0 to 5. Item scores are summed and divided by the total possible number of points (50) to express the overall score as a percentage from 0% to 100%, with higher scores indicating greater disability. The ODI has demonstrated strong psychometric properties,19 with a threshold of 50% improvement as a valid measure for defining success.26 The numeric pain rating scale16 and global rating of change scale31 were also used. The numeric pain rating scale is an 11-point scale on which patients rate their pain from 0 (no pain) to 10 (worst pain imaginable).33 It has been shown to have concurrent and predictive validity for pain intensity.33 A 2-point change on the numeric pain rating scale is clinically meaningful in those with LBP.16 The global rating of change scale is a 15-point scale ranging from –7 (a very great deal worse) to +7 (a very great deal better) on which patients indicate their subjective perceived changes in condition.31 It has been validated and used extensively in research as an outcome measure.37 Scores

Aspirin, 81 mg, daily

TABLE 3

Outcomes Visit/Week

Outcome NPRS (rest/activity)

1/1

3/3

7/6

12/12

17/17

19/19

20/20

Weeks 24 and 46

10/10

10/10

7/10

6/6

10/10

10/10

9/9

6/6

ODI*, %

77

…

60

20

60

28

26

20

GRC

…

…

0

+5

…

…

…

+5

Gait, km

0.2

…

2

2.4

0.2

2.4

2.4

2.4

Sitting, min

15

…

15

45

60

60

60

60

Sleep disturbance from pain (wake events per night)

2-3

…

2-3

0

2-3

0

0

0

Pain medications

4

…

4

0

0

0

0

0

Bridges

0

12

50

…

0

…

50

…

No

No

Allodynia

Yes

No

SLR test (left/right)

60°/50°

…

Balance, s (tandem/ single leg)

0/0

…

60°/50° 80°/80° 10/10

…

Yes

No

No

…

82°/82°

82°/82°

82°/82°

…

…

…

…

…

Abbreviations: GRC, global rating of change; NPRS, numeric pain rating scale; ODI, Oswestry Disability Index; SLR, straight leg raise. *Modified ODI percentage score.

denied any medication changes in the 3-month period prior to the onset of leg paresthesia.

Social History There was excellent support at home. He lived with his mother, father, and 2 sib-



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of +5 or better have been used to represent a successful outcome and have been associated with at least a 50% change in the ODI.26 Pain medication usage was also monitored by asking the patient if the prescribed medications recorded at the initial evaluation were being used. If the patient stated “no,” the new frequency of use and dosage of each drug were noted.

TABLE 4 Objective Assessment

Findings

Sitting/standing posture

•D ecreased lumbar lordosis, increased thoracic kyphosis • Forward shoulders

Functional activities Observational gait analysis

• Increased LBP in L terminal stance at 101 m (90 s) • Increased lumbar extension during terminal stance (L greater than R) • Decreased B hip extension (L greater than R) • Compensated Trendelenburg on L

Grasp pen from floor

• Increased LBP flexing at both lumbar/thoracic spines • Minimal flexing at hips and knees • Maintaining neutral spine with flexion at hips/knees prevented onset of LBP

Physical Examination TABLE 4 details the physical examination.

Assessment of lumbar flexion was avoided because of the patient’s advanced osteoporosis and potential risk of fracture. Positioning the patient in supine immediately worsened his LBP, secondary to contact between his spine and the mat, regardless of leg position. Accordingly, lower extremity range of motion was assessed in sidelying. Allodynia, the report of pain with application of a nonnoxious cutaneous stimulus,20,76 was present in the lumbar region (FIGURE 2) and was measured statically (light touch) and dynamically (light brushing). The Leeds assessment of neuropathic symptoms and signs (LANSS) pain scale was used to assess for the presence of neuropathic pain.7 This scale assesses for neuropathic symptoms such as spontaneous pain and dysesthesia, and includes objective tests for allodynia and pinprick threshold, which may be present in both centrally mediated and peripheral neuropathic pain.20,32,38,40 The scores for the 7 items are summed for a composite score of 0 to 24, with a score of 12 or more indicating neuropathic pain (sensitivity and specificity of 83% and 87%, respectively).7 The scale has been shown to be reliable and valid.7 During the evaluation, once a score of 12 was obtained, the test was terminated.

Evaluation The patient presented with a 3-year history of worsening, constant LBP, a more recent history of bilateral lower extremity paresthesia, and multiple health conditions that likely interacted to reduce his

Physical Examination

Balance Romberg

• 30 s, eyes open and closed

Tandem

• Unable to complete task with eyes open

Single leg

• 1 s on R, unable to complete on L, eyes open

Neurological exam Coordination

• Intact with rapid arm movement, finger to nose, heel to shin, and B toe tap

Patellar/Achilles reflexes

• Absent B

Myotomes L2: hip flexors (supine)

• At least 3/5

L3: quadriceps

• 4/5 R, 3+/5 L

L4: ankle dorsiflexors

• 4–/5

L5: extensor hallucis longus

• 4/5

S1: unilateral heel raise

• 1 R, 0 L

Upper motor neuron tests

• Babinski, Hoffmann, clonus: negative

Sensation (static mechanical stimuli)55

• Allodynia (pain) in lumbar region; intact lower extremities

Proprioception55

• Intact in lower extremities Table continues on page 408.

overall quality of life. Although the LBP and lower extremity paresthesia were potentially related, the history and behavior of symptoms differed.

Evidence for Nociceptive Pain There was some evidence that supported a nociceptive source of pain in this patient. Worsening of symptoms occurred with specific movements (walking and lifting with poor mechanics) and was relieved when movements were altered. However, there was no clear mechanical nature to all of the aggravating factors. The pain was not localized to the area of injury and was constant. The patient experienced dysesthesia, had night pain

that disturbed his sleep, and reported burning, all of which are inconsistent with Smart’s criteria for nociceptive pain.64 Thus, a nociceptive component seemed unlikely to be the predominant pain mechanism.

Evidence for Neuropathic Pain The following evidence supported a neuropathic source of pain: the patient’s prior history of cerebrovascular accident and diabetes, both of which may lead to neuropathic pain; his score on the LANSS pain scale; and his positive response to gabapentin, a known pharmaceutical treatment for neuropathic pain.17 In addition, a positive straight leg



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[ raise was present, which is a criterion for peripheral neuropathic pain, according to the classification system of Smart et al.63 However, no deficits in static cutaneous mechanical detection threshold were found during the neurological exam, and the distribution of symptoms was not in a dermatomal pattern, decreasing the likelihood that the patient’s symptoms stemmed from the lumbar spine as peripheral neuropathic pain.

Evidence for Central Sensitization The patient’s presentation fit all 4 criteria outlined by Smart et al62 for central sensitization. The patient reported a nonmechanical aspect to his pain presentation. He reported constant, severe LBP aggravated by most activities, including sitting, standing, walking, performing ADLs, and sleeping, which was inconsistent with a nociceptive source of pain. His LBP seemed disproportionate to the nature and extent of the injury and pathology, and had worsened in the 3 years since the motor vehicle accident, despite multiple interventions. While the patient did not report depression or anxiety, there was a strong association with maladaptive psychological factors, as the patient directed attention to his LBP repetitively and expected pain with most ADLs. Attention to77 and expectation of39 pain and hypervigilance (repetitive and automatic prioritization of pain)41 have been implicated in the amplification of pain transmission. Finally, allodynia was present in the lumbar spine region with tactile stimulation. The presence of allodynia strongly supports a centrally mediated pain mechanism.20,76 While lower-limb paresthesia may be associated with neuropathic pain such as radiculopathy, the neurological exam did not demonstrate a clear pattern of nerve root pathology.4 Pseudoradicular limb pain, a centrally mediated spread of symptoms6 from chronic LBP, was also hypothesized. Pseudoradicular pain can mimic actual nerve root pathology and share characteristics of peripheral neuropathic pain,24 such as positive neu-

case report TABLE 4

]

Physical Examination (continued)

Objective Assessment

Findings

Straight leg raise test with bubble inclinometer13

• 6 0° L, 50° R • Reproduced ipsilateral posterior thigh pain, numbness, and tingling, B

Range of motion50 Cervical/thoracic spine

• Within normal limits (thoracic flexion not tested)

Lumbar (no overpressure due to severity of LBP) Lateral flexion/rotation

• Within normal limits (increased LBP at end range)

Extension

• 90% limited; increased LBP

Flexion

• Not tested

Hip (tested in sidelying) Flexion

• 100° B

Extension

• Severely limited (L greater than R)

Rotation/abduction

• Within normal limits

Knee/ankle

• Within normal limits

Passive accessory joint motion (prone) Thoracic vertebra

• Limited anterior glide, T6-T12; firm end feel

Lumbar vertebra

• Limited anterior glide; increased LBP, L1-L5; pain end feel

Hip

• Limited anterior, posterior, caudal B; firm end feel

Muscle length50 Iliopsoas/rectus femoris

• Limited, L greater than R

Pectoralis major and minor

• Limited, L greater than R

Muscle performance Hip abduction55

• 4/5 R, 3+/5 L

Abdominal/multifidi in quadruped56

•W eak multifidi contraction • Marked rectus abdominis contraction; no contraction of transversus abdominis

Abbreviations: B, bilateral; L, left; L2-S1, lumbar-sacral myotomes; LBP, low back pain; R, right.

ral provocation tests (eg, the straight leg raise test). Positive neural provocation tests may be an indicator of central sensitization.68 The patient’s health conditions might also have contributed to his chronic pain. Central nervous system disorders, including stroke, have been associated with chronic pain.10 Small-fiber neuropathy that occurs with diabetes has been implicated in centrally mediated pain syndromes, such as fibromyalgia.51,52,71 The patient reported no pain in the upper body, and palpation of typical tender points in this region did not elicit pain, which suggested that central sensitization was regional and not widespread.59 Central sensitization was hypothesized to be the patient’s predominant pain

mechanism. Given that persistent sensory input might have been responsible for this centrally mediated pain, nociceptive input from the lumbar spine could have served as a peripheral driver of such pain, along with psychosocial factors and health conditions that further increased central sensitization. The patient’s lower extremity paresthesia was potentially a component of central sensitization that was pseudoradicular in nature. Given the chronicity and complexity of the patient’s multiple problems, both immediate changes and a return to a painfree lifestyle were not expected. However, we felt that a detailed rehabilitation program tailored to the patient, addressing hypothesized pain mechanisms in accordance with the International Clas-



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TABLE 5

Interventions and Regimens

Visit

Assessment

In-session Treatment and Education

Reassessment

Home Exercise Program

1

See TABLE 4

• F racture and fall risk, pain physiology education •C ognitive behavior treatment

…

•A bdominal hollowing and multifidi isometric contractions in standing/sitting: 10 sets of 5-s hold, 4 times per d • Modified tandem balance: 8 sets of 30 s

2

See TABLE 4

•A nterior glide on proximal femurs, grade 4+*: 1 min each •H ip flexor stretch in half kneel: 5 min

• Gait†: 1 min 38 s

•H ip flexor stretch: 30 s, 20 times per d • Tandem balance: 8 sets of 10 s

3

• • • •

S upine lying; no increase in LBP G ait†: 1 min 38 s B ridge*: 12 L umbar joint mobility: L1-L3, LBP past resistance; L4-L5, LBP before resistance of tissue felt

•H ip joint mobilization •H ip flexor stretch •A nterior glide to L1-L3, grade 3; L4-L5, grade 2: 1 min each

•N o change in gait or bridge

• L unge with abdominal hollowing and multifidi contractions: 2 sets of 15, 5 times per wk • Bridge: 2 sets of 10, 5 times per wk • Sidelying hip abduction: 2 sets of 10, 3 times per wk

4

• • • •

G ait†: 1 min 38 s B ridge†: 12 T andem balance: 10 s, eyes open S LB: 5 s, eyes open

•W rapped bed sheet around waist • E ducated patient to purchase back brace

•G ait†: 5 min 51 s • Bridge†: 19

•S LB: 10 sets of 5-10 s • Hip abduction: 2 sets of 15

5

• • • •

G ait (with brace): 12 min, no increased pain S LB: 10 s B ridge†: 22 with brace L umbar joint mobility: no change from visit 3

•A nterior glide at L1-L2, grade 3+

•B ridge: 28 with brace

• Lunges, bridges, hip abduction: 2 sets of 20

6

•G ait† (no brace): 3 min 8 s •B ridge (no brace): 27

•A nterior glide, T4-T12, grade 4+ •P ectoralis stretching, 5 × 30 s

• Gait†: 3 min 57 s

•P ectoralis stretching: 30 s, 20 times per d • Lunges, bridges, hip abduction: 2 sets of 25

7

•B ridge (no brace): 50 •S oft tissue mobilization, mid posterior • L umbar ROM: extension 50% improved, rotathigh: 5 min tion and sidebend intact • L umbar and thoracic joint mobility: improving movement, anterior glide at L4† •S LR‡: no change from visit 1 •P alpation to mid posterior thigh‡

•S LR‡: 70° L, 65° R

•C hest flys, rows, triceps push-downs, biceps curls: blue Thera-Band, 2 sets of 15 • Alternating UE16 lifts in quadruped: 2 sets of 15 each

Table continues on page 410.

sification of Functioning, Disability and Health model,34 could improve activity and participation restrictions, including walking, sitting, and sleeping tolerance, allowing the patient to finish school and join the work force. For this to occur, several interventions were planned to address specific pain mechanisms, which are presented in TABLE 1. To address the nociceptive component, for example, we expected that improving muscle and joint flexibility, motor control, balance, and strength and educating on posture would decrease peripheral nociceptive drivers and potentially aid in reducing central sensitization. Also, a reduction in pain medication to decrease the risk of adverse drug reactions was considered an important goal. Finally, long-term

follow-up was necessary to ensure carryover and prevention of future flare-ups of symptoms, as patients with chronic pain have frequent recurrences.45

Intervention The patient was seen for 20 visits over a 6-month duration. The assessment and interventions for each treatment session are outlined in TABLE 5, with further description in the APPENDIX (available online). The patient verbalized and demonstrated an understanding of each individual intervention and agreed to the plan of care.

Pain Mechanisms Considered in Patient Management The present case was managed using

a biopsychosocial-oriented rehabilitation program that primarily addressed central sensitization,49 including many strategies of cognitive behavior treatment (CBT). These included cognitive restructuring, activity pacing, attention diversion, problem-solving strategies, goal setting, graded exposure, and maintenance.57 Education on pain physiology was used initially to address cognitive restructuring of pain perception.48,57 Given his biomechanical/motor control deficits, we discussed how activity pacing (eg, stop walking before onset of increased pain) was also important in decreasing peripheral nociception. Problem-solving strategies and goal setting were discussed, with the primary objectives of improving activity and de-



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[

case report

]


TABLE 5

Interventions and Regimens (continued)

Visit

Assessment

In-session Treatment and Education

Reassessment

Home Exercise Program

8

•S LR‡: no change from visit 1

•S oft tissue mobilization, mid posterior thigh: 5 min • T ibial nerve glides, 30

•S LR‡: 70° L, 65° R

• • • •

9


•D istraction: SLR29 position, 1 min, grade 3

•S LR‡: 70° L, 71° R

•A lternating LE lifts: 2 sets of 20 • Remove alternating UE lifts

10

•S LR‡: 61° L, 65° R

•D istraction: SLR, 1 min, grade 3+

•S LR†: 70° L, 72° R

•A lternating LE lifts: 2 sets of 25 • Tandem gait: 50 ft, 5 times per d • Remove tandem balance

11-12


•S elf-mobilization: SLR “stretch”: 30

•S LR‡: 75° bilaterally

•S LR stretch: 30, 4 times per d • Alternating LE lifts: 2 sets of 30

13-16

•S LR‡: 80° bilaterally

• • • •

• SLR: no change

• Knee-to-chest stretch: 30 s, 20 times per d

17-18

• • • • •

• T ranscutaneous electrical nerve stimulation to low back, 20 min •P ain physiology education

• No change

•A bdominal hollowing and multifidi isometric contractions in standing/sitting: 10 sets of 5-s hold, 4 times per d

•P ain physiology education

…

• Continue with exercise program as of visit 16

S LR: 82° bilaterally A llodynia, lumbar spine S upine lying† G ait (without brace)†: 1 min 59 s L umbar AROM: extension,† 10% of normal range •S LB and rotation†: normal ROM

19-20 • • • •

S upine lying, no increase in pain S LR: 82° B ridge: 50 L umbar ROM: 10% limited into extension; flexion not tested; otherwise normal

A nterior glide, grade 3+, L4 T ransverse glide, grade 3, L3-L4 U nilateral knee-to-chest stretch, 4 min L 4-S1 prone distraction, grade 3

T ibial nerve glides: 30, 4 times per d Staggered heel raises and unilateral squats: 2 sets of 15 Alternating LE lifts (quadruped)16: 2 sets of 15 Remove lunges

Abbreviations: AROM, active range of motion; L, left; LBP, low back pain; LE, lower extremity; R, right; ROM, range of motion; S1, sacrum; SLB, single-leg balance; SLR, straight leg raise; UE, upper extremity. *Grade and technique of manual therapy, from Maitland et al.43 † Reproduced LBP. ‡ Reproduced leg pain, numbness, and tingling.

creasing participation restrictions. The patient chose “walking to school” as his primary participation restriction, and his goal was to walk 2.2 km to school without stopping. Several strategies were offered, including using a back brace and exercising to improve flexibility, endurance, strength, and balance. Fracture and fall risk were discussed due to his osteoporosis and balance deficits. This was considered to be imperative to prevent further injury and focus the patient on problems other than pain. Emphasis on posture, strength, and motor control deficits also served to divert his attention away from pain. Further, we educated the patient about why it was critical for him to use his walking stick.

The exercise program was conducted using graded exposure. Activation of deep stabilizing abdominals and multifidi was initiated while sitting upright.56 We progressed this muscle recruitment pattern to more complex exercises within the patient’s tolerance, including bridge and lunge exercises. As pain diminished, the importance of a maintenance program was discussed. In addition to CBT, joint mobilization was used to decrease central sensitization.21 Joint mobilization has been demonstrated to decrease spinal nociceptive hyperexcitability, indicating that the effects of this intervention are, in part, centrally mediated.67 The patient was initially unable to tolerate manual

therapy applied to his lumbar spine, thus treatment was directed at the hip until allodynia in the lumbar spine subsided. Once allodynia subsided, joint mobilization was commenced at the lumbar spine. Joint mobilization was also used to decrease stiffness and alter joint mechanics.15 It was hypothesized that the patient’s limited hip extension might accentuate nociceptive input from the spine, thereby contributing to his chronic pain. Joint mobilization is theorized to decrease stiffness and alter joint mechanics.15 Thus, joint mobilization was initiated at the hip, along with hip flexor stretching to improve hip extension, with the goal to improve gait.73 The patient’s kyphotic thoracic spine and tight pec-



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toralis muscles were hypothesized to be shifting his center of gravity anteriorly, increasing risk of falls and likelihood of chronic LBP.47 Therefore, stretching of the pectoralis muscles11 and thoracic joint mobilizations43 were added. Though joint mobilization has been considered to be unsafe in those with osteoporosis, a reasonable margin between failure load in vitro and applied posterior-to-anterior mobilization in vivo in the thoracic spine has been demonstrated.65 The patient’s gait tolerance had not improved by the fourth treatment session. Because the patient expected that a back brace would help, it was hypothesized that a lumbar support might improve symptoms.8 A bed sheet, tied securely in a knot covering the lumbar spine, was used as a trial back support. The patient’s gait time immediately improved from 90 seconds to approximately 6 minutes. By the following treatment session, the patient had purchased an over-the-counter back brace (ACE Brand Deluxe Back Stabilizer; 3M, St Paul, MN) and was instructed to wear the brace when walking outside his home. By the seventh treatment session, 6 weeks following initial consultation, the patient’s walking continued to improve, but his lower extremity paresthesia was unchanged. No change in pain medication frequency or dosage had taken place. The paresthesia was reproduced at the posterior mid thigh with palpation. Soft tissue mobilization directed to trigger points perceived to be present in the hamstrings was performed, and the patient’s straight leg raise improved immediately after treatment. At the 11th treatment session, the patient was educated in the straight leg raise stretch, with 30 repetitions performed in the clinic, with positive results. This exercise was therefore added to his exercise program. Strength and balance training exercises were performed to improve weakness and motor control. Weight-bearing exercises were performed to improve bone health.9 To target cardiovascular health, in accordance with the American College

of Sports Medicine guidelines, the patient was walking 30 minutes per day, 5 times per week, once his LBP was controlled.27

OUTCOMES

O

utcomes are presented in TABLE 3. By visit 12, the patient and his physician discharged all pain medication. At the 17th treatment session, 17 weeks after initial consult, the patient’s LBP had returned insidiously. He had attempted wearing his brace but could not tolerate it touching his lumbar region. Allodynia had recurred in the lumbar spine region, and his ambulation time regressed to baseline level. Transcutaneous electrical stimulation and ice were applied separately surrounding his allodynic area within the parameters for pain14 in the prone position without improvement, possibly due to a negative interaction with long-term opioid use.60 The patient was again educated on the physiology of a pain flare-up with chronic LBP.45,57 He was also encouraged to continue exercise within tolerance. His exacerbation of LBP began to resolve 2 weeks later, by the 19th treatment session. A month later, at his 20th treatment session, the patient was ambulating to school, sitting for 1 hour, and sleeping through the night. At that time, 6 months after his initial consultation, he was discharged with a final exercise program and independent with self-management. At 1 and 4 months after discharge, the patient was contacted by phone. He stated that no changes had occurred since his last visit and he was continuing his exercise program. The patient was pleased with his outcome and felt no further physical therapy intervention was necessary.

DISCUSSION

T

his case report describes the management of a patient with chronic LBP and multiple health conditions. A pain mechanisms–based classification scheme was used to aid in

clinical decision making. Classifying pain has been advocated as a means of directing treatment at the source of symptoms (neurobiological mechanism).54,76 Ultimately, nociceptive pain and central sensitization were the proposed pain mechanisms involved. We hypothesized that nociceptive input from the lumbar spine was driving ongoing LBP and facilitated central sensitization. We considered the patient’s lower extremity paresthesia to be pseudoradicular in nature24 and centrally mediated. Many patients with chronic pain disorders, such as LBP, share multiple pain mechanisms.61-64,66 Considering that heightened central pain processing causes expansion and amplification of pain, directing treatment at central sensitization as the primary mechanism while addressing mechanical drivers of nociceptive input seemed appropriate. Certain psychosocial factors were likely facilitating centrally mediated pain. It has been suggested in the literature that there is an association between central sensitization and maladaptive behaviors/thoughts.58,62 While the patient denied depression or anxiety, he directed attention to his pain and expected pain with ADLs, both of which have been implicated in enhancement of pain transmission.39,41,77 Nijs et al49 suggested that, before initiating a thorough treatment regime, patients’ counterproductive thoughts and behaviors should be challenged. Indeed, the results of a recent systematic review indicated the positive effects of neuroscience education on pain, disability, catastrophizing, and physical performance.42 A cognitive behavioral approach along with other interventions was used to discuss these maladaptive thoughts/behaviors and to guide the patient’s exercise program and was successful in improving pain and ODI scores. In a publication reporting an intervention similar to the present one, Rundell and Davenport57 used CBT to treat a patient with chronic LBP and maladaptive behaviors, although central sensitization was not mentioned.



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[ The patient’s health conditions might have contributed to his chronic pain. Central sensitization may be a component of chronic visceral disorders.75 In particular, small-fiber neuropathy present with diabetes has been associated with central pain syndromes.51,52 Further, central nervous system disorders, like stroke, have been implicated in chronic pain.10 These factors may limit the ability of interventions that target pain modulation and explain why the patient may continue to have pain, despite multiple previous medical and rehabilitation interventions. There is a void in the literature in regard to the treatment of patients with LBP and multiple medical comorbidities, despite the fact that poor general health is a significant predictor for developing disabling LBP.17 Further, in those under hemodialysis for chronic kidney failure, muscle strength and balance deficit were among the strongest variables associated with chronic LBP.22 It has recently been demonstrated that a nonspinal comorbidity did not affect outcomes in those with LBP.46 However, that study examined those with an acute LBP episode, and more than 85% of the patients had only 1 significant comorbidity. Physical therapists can play a critical role in managing individuals with multiple medical problems. Many patients with multiple health conditions consume medication to manage respective diseases. This leaves a window for adverse drug reaction to take place with the addition of pain medication. Therefore, it is critical to develop sound physical therapy pain management strategies for this cohort. We suggest future research to optimize physical therapy treatment strategies to prevent and treat musculoskeletal problems in those with medical comorbidities. Long-term follow-up was critical for a positive outcome. As has been demonstrated in those with LBP,45 this patient had a recurrence of symptoms. Weakness and motor control deficits of the transversus abdominis and multifidi have been suggested as possible contributing factors.3 Cortical changes derived from

case report

]

multiple factors, including pain memory and altered perceptions of pain threat, have been strongly implicated in the recurrence of pain.3 Intermittent increases in the patient’s pain can markedly alter disability,45 as in the present case. During these intermittent flare-ups, it is not uncommon for pain medication usage to increase.45 Without long-term physical therapy follow-up, patients may develop prolonged, severe symptoms again and resort back to pain medication, which increases the medical costs associated with evaluation and treatment. In managing those with chronic LBP, follow-up visits at specific intervals should be scheduled near the end of the episode of care and clear guidance provided to contact the physical therapist if symptoms recur.

Limitations This case report has several limitations. We did not use validated self-reports for assessing maladaptive behaviors, such as the Fear-Avoidance Beliefs Questionnaire72 or Pain Catastrophizing Scale.70 Using these measures, if found to be elevated, would have validated our treatment approach of CBT. Use of ultrasound imaging to assess muscle function of the abdominal and lumbar muscles might have been helpful in the rehabilitative process of this patient.30 Finally, the addition of thermal quantitative sensory testing might have been beneficial in determining the presence of neuropathic pain.5 However, equipment required for objective measurement of thermal sensation is often not readily available in clinical settings.

CONCLUSION

T

his case report demonstrates that a pain mechanisms–based approach may contribute to the effective evaluation and management of a patient with chronic LBP and multiple health conditions. Future research should focus on the utilization and efficacy of a pain mechanisms–based approach in those with musculoskeletal pain to improve quality of care and outcomes. t

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APPENDIX


Description of a sample of manual therapy and therapeutic exercises utilized in this case. Sets and repetitions are provided in TABLE 5. Exercise SLR with distraction29

Description • Patient position: supine with side being treated closest to edge of table near therapist. Side closest to therapist is lifted in SLR position, ankle dorsiflexed, while other leg is resting on the table • Therapist position: staggered stance, hand closest to patient on plantar foot, applying force into dorsiflexion; other hand wraps around the knee, maintaining knee extension • Mobilization: therapist applies a force away from the patient’s hip in traction

SLR stretch

• In sitting, dorsiflex ankle, extend knee, and flex cervical spine

Illustration

journal of orthopaedic & sports physical therapy | volume 44 | number 6 | june 2014 | C1


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[

case report

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APPENDIX


Exercise Staggered heel raises

Description • Stand in staggered stance and raise heels off the ground. The table can be used for support

Illustration

Quadruped lower extremity lifts • Position on all 4 extremities. Flex 1 hip with the knee straight to align with spine. Return and repeat on opposite leg

Abbreviation: SLR, straight leg raise.

C2 | june 2014 | volume 44 | number 6 | journal of orthopaedic & sports physical therapy


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Chronic low back pain patient and spouse.

An integrated approach to the examination and treatment of a patient with chronic low back pain.

Classification of nonspecific low back pain. I. Psychological involvement in low back pain. A clinical, descriptive approach.

Health utilities for chronic low back pain.

A study of National Health Service management of chronic osteoarthritis and low back pain.

Chronic back pain. A common sense approach.

Acute low back pain management in primary care: a simulated patient approach.

Classification of Chronic Back Muscle Degeneration after Spinal Surgery and Its Relationship with Low Back Pain.

Predictors of self-management for chronic low back pain.

Abdominal aortic aneurysm in a patient with low back pain.

Personality traits in patients with acute low-back pain. A comparison with chronic low-back pain patients.

Multiple myeloma and low back pain.

Lumbar disc screening using back pain questionnaires: oswestry low back pain score, aberdeen low back pain scale, and acute low back pain screening questionnaire.

Medical approach to low back pain.

Low back pain patient subgroups in primary care: pain characteristics, psychosocial determinants, and health care utilization.

Low back pain in young athletes. A practical approach.

Pain intensity measurement in chronic low back pain.

Discography's role in low back pain management.

Therapeutic ultrasound for chronic low-back pain.

Corticosteroid injections for chronic low back pain.

Probability of multiple myeloma in patients with low back pain.

TENS for chronic low back pain.

TENS for chronic low-back pain.

Acupressure for chronic low back pain: a single system study.