1. 1. Can you outline the range of hypotheses you had at this stage regarding the possible sources of symptoms? Did you recognize a pattern emerging following the subjective examination?

For a patient such as Dave with acute back pain, the first hypotheses to consider and rule out are more sinister or serious causes of back pain. Recent research has questioned the validity of the so-called ‘low-back-pain red flags’ as being indicative of serious pathology such as cancer or fractures (Downie et al., 2013). As clinicians, informed by the research, we recommend and use a health history screening questionnaire with follow-up questioning to probe for the potential presence of serious pathology. Based on the totality of the information and clinical judgement, we determine the probability of serious pathology. In Dave’s case, there was no indication of any potential serious pathology based on the following: (1) He was younger than 50. (2) He did not report significant personal or family health history making him more likely to have serious pathology as the cause of his back pain. (3) He denied symptoms that could indicate serious pathology, such as constant pain that does not change with position, prolonged morning stiffness, night pain, weight loss or changes to bowel or bladder function. Even though the possibility of serious pathology after the history/interview seemed remote, we would still be mindful to consider it throughout the physical examination and subsequent treatment. For example, if Dave’s examination did not match up with what we might typically expect, if he did not respond to treatment as expected or if his status changed over the course of time, we would reconsider the possibility of more serious pathology. Once we have considered serious pathology, the next condition to consider is to assess for lumbar nerve root pathology. He denied any lower extremity symptoms at the time. It did not appear that he had a lumbar radiculopathy, but there was a chance that a radiculopathy could subsequently develop or be present without him overtly sensing or reporting typical radicular symptoms. Therefore, part of our physical examination for Dave consisted of a lower-quarter neurological examination and passive straight leg raise test to assess for the presence of a radiculopathy. Once serious pathology and specific nerve root disorders have been considered, the remaining back disorders have been described as non-specific, indicating there is no readily identifiable pathology for the patient’s back pain. There are a variety of methods to sub-classify this group of patients, and as clinicians, we would consider the treatment-based classification (TBC) (Alrwaily et al., 2016) (Table 8.1) scheme for a patient such as Dave with acute back pain. Using the TBC, Dave would likely fit into the manipulation group given his recent onset of back pain (<16 days) and his denial of symptoms radiating below the knee. He could also fit into the specific exercise category if he demonstrated a directional preference. Other possibilities of sources of symptoms from outside the low back include the hip joint and related soft tissues and the pelvic girdle. The sudden onset of his symptoms, the pattern and location of his symptoms and the aggravating and easing factors did not seem to implicate the hip as a source of symptoms. However, as part of the examination, we would examine Dave’s hips to determine if symptoms arise with provocation of the hip joint or if there are relevant movement impairments, such as mobility, muscle length, strength or motor control impairments. Given his age and gender, pelvic girdle pain seemed a remote possibility for Dave. However, if assessment of the lumbar did not reproduce his symptoms, we would next consider pelvic girdle pain provocation tests to explore that region as a potential source of symptoms.

1. 2. What was your hypothesis regarding the ‘pain type’ (nociceptive, neuropathic, nociplastic)? Did the scores Dave achieved on the questionnaires influence your hypothesis?

Dave seemed to present with a dominant peripheral nociceptive pain mechanism (Smart et al., 2011). He had acute, relatively localized pain, and the behavior of his symptoms, including the aggravating and easing factors, indicated a mechanical pattern. As described previously, there was a possibility of a potential lumbar radiculopathy developing, which in that case, the dominant mechanism would be peripheral neuropathic. A dominant nociplastic pain type was not present. His symptoms were not widespread, they followed a mechanical pattern and he did not report additional symptoms (sensitivity to pressure, temperature, light) or comorbid conditions (additional regions of pain, gastro-intestinal [GI] distress, headaches) that are suggestive of a dominant central pain pattern. His ODI score of 42 is typical of a patient with acute low back pain (LBP); a much higher score might have indicated significant psychosocial distress and/or a more dominant central pain mechanism. His FAB-Q scores indicated low fear avoidance for work and physical activities, supporting a more peripheral nociceptive pain pattern and suggesting that maladaptive beliefs are minimal.

1. 3. How did the previous lack of contact with a physical therapist, Dave’s beliefs about his injury and his reference to friends who have developed chronic pain influence your clinical reasoning at this stage?

Clinical reasoning regarding ‘sources of symptoms’ follows a triage approach that initially considers sinister sources informed through a combination of broad health screening and follow-up questioning in the patient interview. As discussed in Chapter 1, screening for other symptoms, health comorbidities and other potential aggravating and easing factors is an important strategy to minimize the chance of missing relevant information the patient may not spontaneously provide. Although sinister pathology was not supported at this stage of the assessment, consistent with the hypothesis-oriented reasoning framework, this would be ‘tested’ further through an analysis of the physical examination findings and response to treatments. Similarly, a lumbar nerve root source for Dave’s symptoms was not supported by the presenting features but would be tested further in the physical examination. Lastly, somatic low back, hip and pelvic girdle sources would be considered, with the clinical pattern thus far supporting a non-specific low lumbar source. The TBC scheme promotes classification of impairments as identified through the examination. This is consistent with the reasoning framework proposed in Chapter 1 that argues for a balance in pathology- and impairment-based reasoning. Although classification systems assist structured assessments and reasoning, patients do not always fit the designated boxes, and initial classification hypotheses may need to be revised, highlighting the importance of continued reappraisal (i.e. reasoning) over time.

A clinical pattern of a nociceptive dominant pain type was recognized. Although fear avoidance screened via the FAB-Q was judged as low, and Dave’s beliefs are not considered maladaptive, the Answer to Reasoning Question 3 illustrates the importance of analyzing patients’ beliefs (component of ‘patient perspectives’ hypothesis category discussed in Chapter 1) within the broader context of their personal circumstances. That is, beliefs such as understanding of the problem and concerns regarding the future cannot be judged normatively (like range of movement or strength) on their own as adaptive versus maladaptive and need to be explored further, for example, with respect to their relationship to symptom behavior and patient behavior (e.g. coping strategies). As seen here, even when beliefs are judged as reasonable (i.e. not maladaptive), it is still important to address them through education and reassurance within management.