+Model

BJPT 322 1---8 ARTICLE IN PRESS

1 Brazilian Journal of Physical Therapy 2020;xxx(xx):xxx---xxx
2

3 Brazilian Journal of
Physical Therapy
https://www.journals.elsevier.com/brazilian-journal-of-physical-therapy

MASTERCLASS

4 The why, where, and how clinical reasoning model for

5 the evaluation and treatment of patients with low
6 back pain
7 Q2 Sean P. Riley a,∗ , Brian T. Swanson b , Joshua A. Cleland c

8 Q3 a Physical Therapy Program, Sacred Heart University, Fairfield, CT, USA

b
9 Department of Rehabilitation Sciences, University of Hartford, West Hartford, CT, USA
c
10 Physical Therapy Program, Department of Public Health and Community Medicine, Tufts University School of Medicine, Boston,
11 MA, USA

12 Received 2 July 2020; received in revised form 19 September 2020; accepted 1 December 2020

13 KEYWORDS Abstract
14 Hip; Background: There is considerable overlap between pain referral patterns from the lumbar
15 Lumbosacral region; disc, lumbar facets, the sacroiliac joint (SIJ), and the hip. Additionally, sciatic like symptoms
16 Probability theory; may originate from the lumbar spine or secondary to extra-spinal sources such as deep gluteal
17 Problem solving; syndrome (GPS). Given that there are several overlapping potential anatomic sources of symp-
18 Theoretical toms that may be synchronous in patients that have low back pain (LBP), it may not be realistic
19 that a linear deductive approach can be used to establish a diagnosis and direct treatment in
20 this group of patients.
21 Objective: The objective of this theoretical clinical reasoning model is to provide a framework
22 to help clinicians integrate linear and non-linear clinical reasoning approaches to minimize
23 clinical reasoning errors related to logically fallacious thinking and cognitive biases.
24 Methods: This masterclass proposes a hypothesis-driven and probabilistic approach that uses
25 clinical reasoning for managing LBP that seeks to eliminate the challenges related to using any
26 single diagnostic paradigm.
27 Conclusions: This model integrates the why (mechanism of primary symptoms), where (location
28 of the primary driver of symptoms), and how (impact of mechanical input and how it may
29 or may not modulate the patient’s primary complaint). The integration of these components

30

∗ Corresponding author at: Doctor of Physical Therapy Program, Sacred Heart University, 5151 Park Avenue, Fairfield, CT 06825, USA.
E-mail: rileys4@sacredheart.edu (S.P. Riley).

https://doi.org/10.1016/j.bjpt.2020.12.001
1413-3555/© 2020 Associação Brasileira de Pesquisa e Pós-Graduação em Fisioterapia. Published by Elsevier Editora Ltda. All rights reserved.

Please cite this article in press as: Riley SP, et al. The why, where, and how clinical reasoning model for the BJPT
evaluation
322 1---8
and treatment of patients with low back pain. Braz J Phys Ther. 2020, https://doi.org/10.1016/j.bjpt.2020.12.001
 +Model
BJPT 322 1---8 ARTICLE IN PRESS
2 S.P. Riley et al.

31 individually, in serial, or simultaneously may help to develop clinical reasoning through reflec-
32 tion on and in action. A better understanding of what these concepts are and how they are
33 related through the proposed model may help to improve the clinical conversation, academic
34 application of clinical reasoning, and clinical outcomes.
35 © 2020 Associação Brasileira de Pesquisa e Pós-Graduação em Fisioterapia. Published by Elsevier
36 Editora Ltda. All rights reserved.

37 Background nostic labels to direct treatment,21,22 it is also clear that 85

the current treatment-based classifications are not able 86

38 Identifying the specific anatomic source of symptoms in to classify patients 25---34% of the time23,24 and current 87

39 patients that have low back pain (LBP) may not be an movement-based classifications fare no better than general 88

40 attainable goal. The convergence of several different neuro- guidelines for patients with chronic LBP.25 89

41 logic structures in anatomic regions surrounding the lumbar Clinicians that treat patients with LBP are also inter- 90

42 spine in this patient population makes identifying the source ested in seeing if the patient’s primary complaint at any 91

43 of referred symptoms problematic. There is considerable given time is modifiable through mechanical input.26 Given 92

44 overlap between pain referral patterns from local lumbar that there are several overlapping potential anatomic and 93

45 pathoanatomic sources related to the disc and facets, and non-anatomic sources of symptoms that may be synchronous 94

46 pathoanatomic sources outside of the lumbar spine associ- in patients that suffer from LBP, it may not be realistic 95

47 ated with the sacroiliac joint (SIJ), and the hip.1---6 Based on that a linear deductive approach can be used to classify, 96

48 studies utilizing the patient’s history, physical exam findings, diagnose, and direct treatment in this group of patients. 97

49 diagnostic imaging, epidural injections, and facet blocks, One of the significant challenges for any clinical reasoning 98

50 among patients seeking care for LBP with or without leg approach in a clinical or academic setting is how to account 99

51 pain, approximately 82% have spine pathology. Still, only for the lack of certainty when combining linear (deductive) 100

52 61---65% will present with isolated spine findings.7,8 An addi- and non-linear (inductive) reasoning processes when per- 101

53 tional 12.5---17.5% of patients are likely to present with some forming clinical reasoning. Exam findings in patients that 102

54 combination of spine and hip or spine and SIJ dysfunction, have LBP are not dichotomous. They shift the probability 103

55 and 8---9% may present with hip or SIJ pathology without of something being true. We would therefore like to pro- 104

56 spine pathology.7,8 The combination of all three areas pre- pose a hypothesis-driven, probabilistic, mechanism-based 105

57 senting as pain generators appears to be less than 2%.7 approach to managing LBP that eliminates the challenges 106

58 Overall, it seems that 10---15% of cases of LBP may present related to using any single diagnostic paradigm. 107

59 with an undefined anatomic source of pain.7,8 The overall The purpose of this theoretical clinical reasoning model 108

60 prevalence of non-lumbar pathology is approximately 14.5% is to provide a framework to help clinicians integrate 109

61 for SIJ pathology, and 12.5% for hip pathology.8 linear and non-linear clinical reasoning approaches to mini- 110

62 Sciatic like symptoms may originate from the lumbar mize clinical reasoning errors related to logically fallacious 111

63 spine,9 SIJ,10 or secondary to extra-spinal sources such as thinking and cognitive biases. This model is based on the 112

64 piriformis syndrome11 or deep gluteal syndrome (GPS).12 integration of the presented evidence with the opinion and 113

65 Piriformis syndrome is reported to account for the major- clinical experience of the authors. It seeks to serve as a vehi- 114

66 ity of cases of sciatic symptoms outside the lumbar spine cle through which the clinician may integrate and apply the 115

67 from a musculoskeletal origin.13 GPS has been proposed best available evidence in a clinical context. 116

68 as a diagnosis to include anatomic structures that may

69 be involved with nerve compression outside of the lumbar ‘‘Whenever you find yourself on the side of the majority, 117

70 spine. These anatomic structures include the piriformis mus- it is time to pause and reflect.’’ ---- Mark Twain 118

71 cle, fibrous bands in gluteal muscles, the hamstring muscles,

72 the gemelli-obturator internus complex, vascular abnormal- Hypothesis generation 119
73 ities, and space-occupying lesions.12 It is estimated that
74 6---17% that present with sciatic symptoms have GPS.14
The generation of hypotheses is an iterative process that 120
75 Controversy exists regarding the anatomic source of a
begins when the clinician first meets the patient and evolves 121
76 patient’s symptoms. This is secondary to the use of different
during the examination process. The evolution occurs as 122
77 reference tests and gold standards for establishing a diag-
data are progressively gathered, organized, and prioritized 123
78 nosis in patients that experience LBP.15 The cause of the
using Bayesian reasoning. Bayesian reasoning involves the 124
79 patient’s symptoms may not be attributable to kinesiopatho-
application of probability theory to abductive and inductive 125
80 logical or pathoanatomic variables,16---18 and there is a
reasoning.27 As data are progressively collected, it shifts 126
81 high prevalence of pathoanatomic findings in asymptomatic
the probability that something is true. There is a growing 127
82 individuals.19 Additional challenges include misleading test
body of literature to support that theoretical instruction 128
83 metrics and overly complicated diagnostic labels.20 While
in Bayesian concepts improves the estimation of post-test 129
84 substantial effort has been placed on the creation of diag-
probabilities during the reasoning process.28---30 Bayesian rea- 130

Please cite this article in press as: Riley SP, et al. The why, where, and how clinical reasoning model for the BJPT
evaluation
322 1---8
and treatment of patients with low back pain. Braz J Phys Ther. 2020, https://doi.org/10.1016/j.bjpt.2020.12.001
 +Model
BJPT 322 1---8 ARTICLE IN PRESS
Clinical reasoning for patients with low back pain 3

131 soning includes the reasoning related to musculoskeletal may provide a robust and reasoned approach when applied 190

132 pain irritability.31 Musculoskeletal pain irritability is pain iteratively within and between treatment sessions. 191

133 that continues after the symptom provoking activities that

134 produced a patient’s symptoms have stopped.32 This concept
Nociplastic (central sensitization) 192
135 may be an essential consideration as the clinician plans
136 how to perform the physical exam following the medical
In the absence of red flag findings, nociplastic symptoms 193
137 history. Given that most testing is provocative, the clin-
are characterized by pain that is disproportionate, non- 194
138 ician must do the least amount of testing to attain the
mechanical, unpredictable, and diffuse.34 Patients with 195
139 greatest amount of information. If the patient has high
nociplastic symptoms often have maladaptive behaviors 196
140 symptom irritability, symptom alleviation may be the most
related to the presence of negative beliefs (fear-avoidance), 197
141 powerful tool to use at that time and defer a more compre-
lack of positive beliefs related to self-efficacy, and dyski- 198
142 hensive physical exam to a later date, while still offering
netic movement related to kinesiophobia.34 This cluster of 199
143 meaningful information regarding symptom behavior. This
findings was found to have a sensitivity of 91.8% and a speci- 200
144 hypothesis testing strategy may include using a comparable
ficity of 97.7%.34 If a patient has nociplastic mediated pain, 201
145 sign related to the patient’s primary symptoms as a bench-
it is expected that the physical exam may not significan- 202
146 mark for the hypothesis testing strategy to determine if
tly change the patient’s primary symptomatic complaints. 203
147 the hypothesis is probabilistically accurate.31 This involves
These findings strongly suggest that the patient should be 204
148 symptom modification that tests a hypothesis by determin-
educated that their pain experience may not be driven 205
149 ing if an examination procedure or intervention changes
through mechanical input, especially early during the reha- 206
150 (increases, decreases, or stays the same) the patient’s
bilitation process. The focus should be on using techniques 207
151 primary symptoms.26 Rationally, the thought that any proce-
to increase the patient’s function without increasing their 208
152 dure or intervention "caused" the modification in symptoms
symptoms. Numerous techniques have been proposed to be 209
153 can never be assumed to be completely accurate without
useful in this biopsychosocial context. A discussion of the 210
154 the risk of creating cognitive biases and logical fallacies.
assessment and management of LBP using the biopsychoso- 211
155 The principles of any treatment system for LBP may be used
cial model is beyond the intent and scope of this clinical 212
156 to generate and modify hypotheses at any given time dur-
reasoning model. Although there is evidence in support of 213
157 ing the examination process. The hypotheses, however, must
the importance of the model in determining etiological and 214
158 be tested and verified probabilistically within the context of
prognostic factor variables for managing patients with LBP, 215
159 the patient.
the optimal method of assessment and treatment utilizing 216

this approach has yet to be identified.40 The technique that 217

160 Using mechanism-based classifications: matches the patient’s and clinician’s beliefs is likely the best 218

161 identifying the why choice of intervention at any given time. If the patient does 219

not have any red flag findings or the cluster of findings con- 220

33 sistent with nociplastic symptoms, this mechanism can be 221

162 Smart et al. established the discriminative validity of three
ruled out. If the patient responds to interventions with an 222
163 classification systems for individuals that suffer from LBP
increase in symptoms related to mechanical input, nociplas- 223
164 that were derived through a Delphi consensus of clinical indi-
tic symptoms may be a secondary contributing factor, and 224
165 cators. They then used statistical modeling based on patient
nociceptive and peripheral neuropathic contributions to the 225
166 symptoms to identify predominant sources of a patient’s
patient’s primary complaints should be ruled out. 226
167 symptoms that have LBP. Through this approach, they iden-
168 tified a mechanisms-based classification for musculoskeletal
169 pain that included: 1) central sensitization;34 2) peripheral Peripheral neuropathic (referred and/or radicular) 227

170 neuropathic (radicular or referred), 35 and 3) nociceptive.36

171 The ability to identify the predominant mechanism-based Peripheral neuropathic pain has been described as pain that 228

172 classification is reliable in patients with nonspecific cervical occurs secondary to mechanical deformation or dysfunction 229

173 pain (kappa = .84 (95% CI, .65, 1.00), p < .001).37 Chimenti in a peripheral nerve.41,42 Patients with primary periph- 230

174 et al.38 have modified the work of Smart et al.33 ; by chang- eral neuropathic pain have symptoms that are referred in 231

175 ing the name of the central sensitization classification to a dermatomal or cutaneous distribution, have a history of 232

176 nociplastic, placed each mechanism in an overlapping Venn nerve injury, pathology, or mechanical compromise of the 233

177 diagram to illustrate that all three sources of symptoms may nerve with symptom provocation with mechanical testing. 234

178 occur at the same time, and have put the interaction of This cluster of findings was found to have a sensitivity 235

179 these classifications in the context of the movement sys- of 86.3% and a specificity of 96.0%.35 For patients with 236

180 tem and psycho-social factors.38 They have also linked these potential referred symptoms, hypotheses should be formu- 237

181 mechanisms to physical therapy interventions that may be lated related to the primary mechanism (why) and structure 238

182 most appropriate to address the patient’s symptoms.38 The (where) that is responsible for the symptoms. If the primary 239

183 validity of this classification has not been established in a mechanism and structure are accurate, the clinician should 240

184 clinical setting.39 This classification system may, however, be able to predict how the referred symptoms should change 241

185 be a valuable tool for generating a hypothesis related to the (increase or decrease) with alterations in position, load, 242

186 patient’s dominant mechanism-based symptoms at any given and tension through the structure. The pattern of symp- 243

187 time. Attempting to modify a patient’s symptoms, testing tom provocation and alleviation can be used to educate the 244

188 the hypothesis with an exam strategy or intervention that patient on what to avoid and to identify what may be used 245

189 should change their symptoms if the hypothesis is correct, to modulate the patient’s primary symptoms. 246

Please cite this article in press as: Riley SP, et al. The why, where, and how clinical reasoning model for the BJPT
evaluation
322 1---8
and treatment of patients with low back pain. Braz J Phys Ther. 2020, https://doi.org/10.1016/j.bjpt.2020.12.001
 +Model
BJPT 322 1---8 ARTICLE IN PRESS
4 S.P. Riley et al.

247 For patients with radicular symptoms, it becomes cru- ruling out and ruling in the SIJ as the anatomic source of the 304

248 cial to identify the potential primary structure(s) that may pathology. Once determined as an anatomic source of pain 305

249 be responsible. If the patient has a lateral lumbar shift, a or dysfunction, it should then be determined if the SIJ has 306

250 shift correction could be used to determine if the patient’s issues of hyper or hypomobility. Modifiable symptoms of SIJ 307

251 primary complaint centralizes or peripheralizes.43,44 In the hypermobility may be determined through a positive active 308

252 absence of a lumbar shift, the patient’s reports of their straight leg raise test49 or if function can be significantly 309

253 symptomatic response (increase and/or decrease) to pos- improved by generating internal force closure via muscu- 310

254 ture, position (flexion or extension), repetitive motion lar contraction50 or externally with an SIJ belt.51 Modifiable 311

255 (flexion or extension), mid-range motion, load, and tension symptoms of SIJ hypomobility may be determined via symp- 312

256 may provide valuable clues to generate hypotheses related tom provocation during compressive tests such as the SIJ 313

257 to the most likely source of the radicular symptoms at any compression test48 and the FABER test.52 314

258 given time. These hypotheses should be tested to determine Hip pathology, particularly hypomobility, is a commonly 315

259 if these variables peripheralize or centralize the patient’s identified potential anatomic source or contributing factor 316

260 radicular symptoms.45 An inability to centralize patient’s in patients with LBP.53---56 Generating a hypothesis based on 317

261 symptoms suggests a poor prognosis to non-surgical mana- the presence of hip hypomobility and testing the hypothesis 318

262 gement and may indicate the need for a referral in the case by providing an intervention that should improve hip hypo- 319

263 of non-responsive progressive symptoms.46 mobility and then reassessing the impact of the improved 320

mobility on the patient’s primary symptomatic complaint 321

264 Nociceptive may provide an easy access point to understand the role 322

of hip hypomobility as a primary or secondary driver of the 323

patient’s symptomatic complaint.57 324

265 Nociceptive pain is localized to an area of injury or
In the context of determining where the above examples 325
266 dysfunction.36 Provocation and/or alleviation are identi-
are meant to illustrate one possibility of how the patient’s 326
267 fiable and proportionate, match known mechanical and
story may unfold. In the context of identifying where, work- 327
268 anatomical distributions, symptoms are usually intermit-
ing proximally to distally while first ruling out symptom 328
269 tent and start with the onset of movement or mechanical
provocation from the lumbar spine, followed by the SIJ and 329
270 provocation.36 The quality of symptoms may be a cons-
hip, may provide the most pragmatic way to funnel the pri- 330
271 tant dull ache or a throb at rest.36 This group of patients
mary location that needs the most attention at any given 331
272 should not have pain associated with other dysesthesias,
time. In the context of the test-treat-retest model of assess- 332
273 night pain or disturbed sleep, and antalgic postures or move-
ing within and between-session change, it has been our 333
274 ment patterns. Pain described as burning, shooting, sharp,
clinical experience that it is easier to get something moving 334
275 or electric-shock-like would be more consistent with periph-
than it is to make something more stable or stronger. With 335
276 eral neuropathic symptoms.36 This cluster of findings was
hypermobile presentations, ensuring that distal hypomo- 336
277 found to have a sensitivity of 90.9% and a specificity of
bility is not contributing to proximal hypermobility before 337
278 91.0%. A more specific response to the mechanical factors
initiating interventions to improve stability may be the most 338
279 of position, load, and tension should be expected with indi-
pragmatic approach. 339
280 viduals with dominant nociceptive symptoms.

281 Using anatomic sources: identifying the where Using mechanical inputs: identifying the how 340

282 The lumbar spine, SIJ, and hip are three potential anatomic In this context, we are defining the how as the primary 341

283 sources of symptoms with the highest probability of pain mechanical input that significantly changes the patient’s 342

284 generation that should be considered during the examina- primary complaint at any given time if we are addressing 343

285 tion process in patients that have LBP. The lumbar spine nociceptive and/or peripheral neuropathic mechanisms as 344

286 is known to be the most likely primary anatomic source of the why. Independent of the cause of the symptomatic out- 345

287 the patient’s symptoms, observed approximately 2/3 of the put, the ability to change the patient’s primary symptoms 346

288 time.7,8 This should be the starting point in hypothesis test- through mechanical input suggests that the patient’s pri- 347

289 ing in the context of symptom modification testing and/or mary complaint at that time is not primarily nociplastically 348

290 interventions directed to this region. Symptom modification mediated. In this context, the patient should respond favor- 349

291 in the lumbar spine, in any portion of the active, passive, ably to modifications in load, position, and/or tension. Each 350

292 or passive accessory motion examination, indicates treat- mechanism should be considered as an aspect of an over- 351

293 ment as identified by symptom behavior but does not rule lapping Venn diagram, as all three sources of symptoms may 352

294 out distal influences from the hip or SIJ. occur at the same time, and the interaction of these fac- 353

295 In the absence of lumbar symptom modification, the pro- tors can all be considered in the context of the movement 354

296 gression of assessment from proximal to distal allows for the system. 355

297 most apparent differentiation of the pain generating struc- The influence of load may first be considered mechan- 356

298 ture, mainly if there is somatic referred pain. The lumbar ically. Load increases through compression or decreases 357

299 spine should not reproduce symptoms before progressing through distraction. Load also may be regarded as relative 358

300 distally, as SIJ dysfunction is generally identified through to changes to the patient’s position (standing versus sitting 359

301 a process of exclusion.47 Symptom provocation tests have versus laying down), relative to the presence and absence of 360

302 been well researched in this area, and the cluster described muscular contractions, or relative to the compressive forces 361

303 by Laslett et al.48 has been shown to have utility in both generated by tissues on a stretch. The influence of load is 362

Please cite this article in press as: Riley SP, et al. The why, where, and how clinical reasoning model for the BJPT
evaluation
322 1---8
and treatment of patients with low back pain. Braz J Phys Ther. 2020, https://doi.org/10.1016/j.bjpt.2020.12.001
 +Model
BJPT 322 1---8 ARTICLE IN PRESS
Clinical reasoning for patients with low back pain 5

Figure 1 The why (mechanism), where (location), how (mechanical input) clinical reasoning model.

363 considered in the context of the "where" as it relates to symptoms worsen in lumbar extension, is likely to have 386

364 known effects on anatomic structures. a positional sensitivity due to a neuroforaminal interface 387

365 The impact of the position may be explored by identify- issue rather than adverse neural tension. Thoughtful use of 388

366 ing how the patient responds to modifications in end-range change in position or tension will allow the sensitivity to be 389

367 positions, posture, mid-range, and end range motion, and discerned during testing. 390

368 mid-range and end range repetitive motion. Exploring these If the patient responds to load, tension, and posi- 391

369 variables and determining their impact on the patient’s tion, then their primary symptoms are probabilistically 392

370 primary symptomatic complaint should help the clinician dominated by nociceptive or peripheral neuropathic mech- 393

371 identify how to modify and change mechanical interventions anisms. If the patient’s primary symptoms do not respond to 394

372 to improve the patient’s primary symptomatic complaint at load, tension, or position, or stop responding to modification 395

373 any given time. Inherent in this model is the understanding of these variables, their primary symptoms are probabilisti- 396

374 that changes in position cause changes in load and tension cally being driven by a nociplastic mechanism. If this is true, 397

375 around the articular structure in question. they should respond more favorably to interventions meant 398

376 Tension refers to the stretch of tissues, including mus- to address more centrally mediated changes if the patient 399

377 cles, ligaments, capsules, and nerves. Modifications in does not have red flag findings. 400

378 tension frequently overlap with changes in position. This

379 may be explored by muscle length testing, neurodynamic Putting it all together 401
380 testing, and ligamentous stress tests. For example, if a
381 patient experiences leg symptoms in a slump test position, The performance of the physical exam to rule out serious 402
382 which is alleviated by returning the lumbar spine to exten- pathology and contributing factors by region is based on the 403
383 sion, it may indicate tension sensitivity of the nerve, or patient’s primary complaint at any given time. This com- 404
384 it may indicate a positional sensitivity to lumbar flexion. plaint may be related to alterations in body structures and 405
385 Conversely, a patient with leg symptoms in a slump, whose function, activity limitations, and participation restrictions 406

Please cite this article in press as: Riley SP, et al. The why, where, and how clinical reasoning model for the BJPT
evaluation
322 1---8
and treatment of patients with low back pain. Braz J Phys Ther. 2020, https://doi.org/10.1016/j.bjpt.2020.12.001
 +Model
BJPT 322 1---8 ARTICLE IN PRESS
6 S.P. Riley et al.

407 while considering the environment and personal factors that patient outcomes, future clinical research is needed to sup- 466

408 are attained while taking the patient’s history. The applica- port these claims. 467

409 tion of this hypothesis testing strategy may not be possible

410 in patients that have centrally mediated symptoms.26 Focus-
411 ing on symptoms in this subgroup of patients may erode the Conclusion 468
412 therapeutic alliance by creating unrealistic patient expecta-
413 tions regarding physical therapy interventions and/or result The theoretical model that we are proposing may help 469
414 in the creation of hypervigilant behaviors. Dominant cen- to conceptually integrate the many concepts and chal- 470
415 trally mediated pain must be identified early in the process lenges related to the teaching and clinical application of 471
416 of hypothesis generation. clinical reasoning in patients with LBP. A better understand- 472
417 The pain diagram may be useful in hypothesis generation ing of what these concepts are and how they are related 473
418 by allowing the patient to provide a visual representation through the proposed model may help to improve the clini- 474
419 of symptoms: local, proximal to distal, or global, including cal conversation, academic application of clinical reasoning, 475
420 symptoms that may represent a centrally mediated source and clinical outcomes. 476
421 of symptoms or red flags that need to be ruled out. Chronic
422 widespread pain, defined as ≥ 20% of coverage of the surface
423 area of a pain diagram, has been shown to be correlated to Conflicts of interest 477
424 higher anxiety scores, psycho-social stressors, significant life
425 events, and the use of a greater number of pain management
The authors report that they have no conflicts of interest. Q4 478
426 strategies.58 Very early in the exam process, this tool may
427 be valuable in helping the clinician decide to evaluate and
428 treat, evaluate and refer, or refer the patient to a more
429 appropriate practitioner to rule out conditions indicated by
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322 1---8
and treatment of patients with low back pain. Braz J Phys Ther. 2020, https://doi.org/10.1016/j.bjpt.2020.12.001
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Please cite this article in press as: Riley SP, et al. The why, where, and how clinical reasoning model for the BJPT
evaluation
322 1---8
and treatment of patients with low back pain. Braz J Phys Ther. 2020, https://doi.org/10.1016/j.bjpt.2020.12.001