The generation of hypotheses is an iterative process that begins when the clinician first meets the patient and evolves during the examination process. The evolution occurs as data are progressively gathered, organized, and prioritized using Bayesian reasoning. Bayesian reasoning involves the application of probability theory to abductive and inductive reasoning.27 As data are progressively collected, it shifts the probability that something is true. There is a growing body of literature to support that theoretical instruction in Bayesian concepts improves the estimation of post-test probabilities during the reasoning process.28–30 Bayesian reasoning includes the reasoning related to musculoskeletal pain irritability.31 Musculoskeletal pain irritability is pain that continues after the symptom provoking activities that produced a patient's symptoms have stopped.32 This concept may be an essential consideration as the clinician plans how to perform the physical exam following the medical history. Given that most testing is provocative, the clinician must do the least amount of testing to attain the greatest amount of information. If the patient has high symptom irritability, symptom alleviation may be the most powerful tool to use at that time and defer a more comprehensive physical exam to a later date, while still offering meaningful information regarding symptom behavior. This hypothesis testing strategy may include using a comparable sign related to the patient's primary symptoms as a benchmark for the hypothesis testing strategy to determine if the hypothesis is probabilistically accurate.31 This involves symptom modification that tests a hypothesis by determining if an examination procedure or intervention changes (increases, decreases, or stays the same) the patient's primary symptoms.26 Rationally, the thought that any procedure or intervention “cause” the modification in symptoms can never be assumed to be completely accurate without the risk of creating cognitive biases and logical fallacies. The principles of any treatment system for LBP may be used to generate and modify hypotheses at any given time during the examination process. The hypotheses, however, must be tested and verified probabilistically within the context of the patient.

Smart et al.33 established the discriminative validity of three classification systems for individuals that suffer from LBP that were derived through a Delphi consensus of clinical indicators. They then used statistical modeling based on patient symptoms to identify predominant sources of a patient’s symptoms who have LBP. Through this approach, they identified a mechanisms-based classification for musculoskeletal pain that included: 1) central sensitization;34 2) peripheral neuropathic (radicular or referred), 35 and 3) nociceptive.36 The ability to identify the predominant mechanism-based classification is reliable in patients with nonspecific cervical pain (kappa=.84 (95% CI: .65, 1.00), p < .001).37 Chimenti et al.38 have modified the work of Smart et al.33; by changing the name of the central sensitization classification to nociplastic, placed each mechanism in an overlapping Venn diagram to illustrate that all three sources of symptoms may occur at the same time, and have put the interaction of these classifications in the context of the movement system and psycho-social factors.38 They have also linked these mechanisms to physical therapy interventions that may be most appropriate to address the patient's symptoms.38 The validity of this classification has not been established in a clinical setting.39 This classification system may, however, be a valuable tool for generating a hypothesis related to the patient's dominant mechanism-based symptoms at any given time. Attempting to modify a patient's symptoms, testing the hypothesis with an exam strategy or intervention that should change their symptoms if the hypothesis is correct, may provide a robust and reasoned approach when applied iteratively within and between treatment sessions.

The lumbar spine, SIJ, and hip are three potential anatomic sources of symptoms with the highest probability of pain generation that should be considered during the examination process in patients who have LBP. The lumbar spine is known to be the most likely primary anatomic source of the patient's symptoms, observed approximately 2/3 of the time.7,8 This should be the starting point in hypothesis testing in the context of symptom modification testing and/or interventions directed to this region. Symptom modification in the lumbar spine, in any portion of the active, passive, or passive accessory motion examination, indicates treatment as identified by symptom behavior but does not rule out distal influences from the hip or SIJ.

In the absence of lumbar symptom modification, the progression of assessment from proximal to distal allows for the most apparent differentiation of the pain generating structure, mainly if there is somatic referred pain. The lumbar spine should not reproduce symptoms before progressing distally, as SIJ dysfunction is generally identified through a process of exclusion.47 Symptom provocation tests have been well researched in this area, and the cluster described by Laslett et al.48 has been shown to have utility in both ruling out and ruling in the SIJ as the anatomic source of the pathology. Once determined as an anatomic source of pain or dysfunction, it should then be determined if the SIJ has issues of hyper or hypomobility. Modifiable symptoms of SIJ hypermobility may be determined through a positive active straight leg raise test49 or if function can be significantly improved by generating internal force closure via muscular contraction50 or externally with an SIJ belt.51 Modifiable symptoms of SIJ hypomobility may be determined via symptom provocation during compressive tests such as the SIJ compression test48 and the FABER test.52

Hip pathology, particularly hypomobility, is a commonly identified potential anatomic source or contributing factor in patients with LBP.53–56 Generating a hypothesis based on the presence of hip hypomobility and testing the hypothesis by providing an intervention that should improve hip hypomobility and then reassessing the impact of the improved mobility on the patient's primary symptomatic complaint may provide an easy access point to understand the role of hip hypomobility as a primary or secondary driver of the patient's symptomatic complaint.57

In the context of determining where the above examples are meant to illustrate one possibility of how the patient's story may unfold. In the context of identifying where, working proximally to distally while first ruling out symptom provocation from the lumbar spine, followed by the SIJ and hip, may provide the most pragmatic way to funnel the primary location that needs the most attention at any given time. In the context of the test-treat-retest model of assessing within and between-session change, it has been our clinical experience that it is easier to get something moving than it is to make something more stable or stronger. With hypermobile presentations, ensuring that distal hypomobility is not contributing to proximal hypermobility before initiating interventions to improve stability may be the most pragmatic approach.

In this context, we are defining the how as the primary mechanical input that significantly changes the patient's primary complaint at any given time if we are addressing nociceptive and/or peripheral neuropathic mechanisms as the why. Independent of the cause of the symptomatic output, the ability to change the patient's primary symptoms through mechanical input suggests that the patient's primary complaint at that time is not primarily nociplastically mediated. In this context, the patient should respond favorably to modifications in load, position, and/or tension. Each mechanism should be considered as an aspect of an overlapping Venn diagram, as all three sources of symptoms may occur at the same time, and the interaction of these factors can all be considered in the context of the movement system.

The influence of load may first be considered mechanically. Load increases through compression or decreases through distraction. Load also may be regarded as relative to changes to the patient's position (standing versus sitting versus laying down), relative to the presence and absence of muscular contractions, or relative to the compressive forces generated by tissues on a stretch. The influence of load is considered in the context of the “wher” as it relates to known effects on anatomic structures.

The impact of the position may be explored by identifying how the patient responds to modifications in end-range positions, posture, mid-range, and end range motion, and mid-range and end range repetitive motion. Exploring these variables and determining their impact on the patient's primary symptomatic complaint should help the clinician identify how to modify and change mechanical interventions to improve the patient's primary symptomatic complaint at any given time. Inherent in this model is the understanding that changes in position cause changes in load and tension around the articular structure in question.

Tension refers to the stretch of tissues, including muscles, ligaments, capsules, and nerves. Modifications in tension frequently overlap with changes in position. This may be explored by muscle length testing, neurodynamic testing, and ligamentous stress tests. For example, if a patient experiences leg symptoms in a slump test position, which is alleviated by returning the lumbar spine to extension, it may indicate tension sensitivity of the nerve, or it may indicate a positional sensitivity to lumbar flexion. Conversely, a patient with leg symptoms in a slump, whose symptoms worsen in lumbar extension, is likely to have a positional sensitivity due to a neuroforaminal interface issue rather than adverse neural tension. Thoughtful use of change in position or tension will allow the sensitivity to be discerned during testing.

If the patient responds to load, tension, and position, then their primary symptoms are probabilistically dominated by nociceptive or peripheral neuropathic mechanisms. If the patient's primary symptoms do not respond to load, tension, or position, or stop responding to modification of these variables, their primary symptoms are probabilistically being driven by a nociplastic mechanism. If this is true, they should respond more favorably to interventions meant to address more centrally mediated changes if the patient does not have red flag findings.

Putting it all together

The performance of the physical exam to rule out serious pathology and contributing factors by region is based on the patient's primary complaint at any given time. This complaint may be related to alterations in body structures and function, activity limitations, and participation restrictions while considering the environment and personal factors that are attained while taking the patient's history. The application of this hypothesis testing strategy may not be possible in patients who have centrally mediated symptoms.26 Focusing on symptoms in this subgroup of patients may erode the therapeutic alliance by creating unrealistic patient expectations regarding physical therapy interventions and/or result in the creation of hypervigilant behaviors. Dominant centrally mediated pain must be identified early in the process of hypothesis generation.

The pain diagram may be useful in hypothesis generation by allowing the patient to provide a visual representation of symptoms: local, proximal to distal, or global, including symptoms that may represent a centrally mediated source of symptoms or red flags that need to be ruled out. Chronic widespread pain, defined as ≥ 20% of coverage of the surface area of a pain diagram, has been shown to be correlated to higher anxiety scores, psycho-social stressors, significant life events, and the use of a greater number of pain management strategies.58 Very early in the exam process, this tool may be valuable in helping the clinician decide to evaluate and treat, evaluate and refer, or refer the patient to a more appropriate practitioner to rule out conditions indicated by findings that may represent red flags.

To apply this model, the clinician must first understand the potential dominant mechanisms of why the patient has symptoms at any given time (nociceptive versus peripheral neuropathic versus nociplastic), where the primary symptoms or primary contributing factor is located (lumbar spine versus SIJ versus hip), and how the patient's primary complaint may be modifiable through changes in load, tension, and position (Fig. 1). The clinician must also understand that if the mechanism (why) of the primary generator of symptoms is related to nociceptive and/or peripheral neuropathic mechanisms, a symptom modification approach is appropriate. Additionally, the clinician must understand that a different approach is required that does not focus on the patient's primary complaint if the why is nociplastically mediated. Once the clinician understands the why, where, and how they should be able to first apply these concepts in series by reflecting on action but eventually realize that these three concepts occur simultaneously with the ability to reflect in action. This is an iterative process that flows and changes based on these variables within and between treatment sessions, guided by a test-treat-retest model of care. Continuous hypothesis testing and re-assessment of the patient's response are used probabilistically to determine the most important variables to consider at any given time.

Figure 1.

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

(0.42MB).

As a theoretical approach, the above theory stands on the same ground as other untested and unproven clinical reasoning approaches and tools.59–62 Although the current method has sought to include the concepts of reasoning and probability to eliminate some of the challenges related to the use of several current paradigms, it is not meant to imply that this approach is the only approach to the problem. While we feel that the utilization of this theoretical model should improve academic performance, clinical performance, and patient outcomes, future clinical research is needed to support these claims.

The theoretical model that we are proposing may help to conceptually integrate the many concepts and challenges related to the teaching and clinical application of clinical reasoning in patients with LBP. A better understanding of what these concepts are and how they are related through the proposed model may help to improve the clinical conversation, academic application of clinical reasoning, and clinical outcomes.

The authors report that they have no conflicts of interest.