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‘Pain is not the only problem’: Explaining Pain

Is it possible to explain ‘pain’ in a way that meets all of the demands of the clinician and the patient? Throughout these articles we have been exploring the definition of pain, and have learned that pain is a sensory experience of the patient, and that the sensory experience can be real or imagined. We also learned that the pain might have a traceable origin to the site of the injury, or not to the injury, or from no source at all. We also learned that the sense-signal (‘pain’) that the patient experiences is not felt at the site of the injury, but rather felt in central processing as an ‘interpretation of pain’, with a cognitive assignment of pain to the injury site; a seemingly sensible and useful process. Should the clinician explain this phenomenon to the patient? I do, but it’s up to you. And, I explain that their course of care will certainly deal with their symptoms.

Diagnosis is largely an act of medical discrimination because it is commonly reductionist, is non-inclusive, and does not explain the ‘entire patient’. Medical discrimination describes the overly common practice of diagnosing with a very small scope of codes, codes that are familiar to the clinician’s scope of practice, and does not require a great deal of effort. These ‘easy codes’ such as S39.92XA unspecified injury of the back, M62.830 back pain, M46.06 enthesopathy, M51.86 lumbar disc disorder, M79.2 neuralgia explain nothing about the patient’s problem. The problem is not the pain or other symptoms. The clinician should be diagnosing the problem, and informing the patient of something that they do not already know. A diagnosis of pain, numbness, tingling, radiation, weakness, acute inflammation are descriptions of patient presentation for the chart (SOAP) notes, not for the diagnosis.

Medical discrimination describes a reductionist and non-inclusive approach, since the diagnosis only explains a few injury-directed codes, it does not explain: R26.89 gait abnormalities, Y93.01 impact on walking-hiking-running ADLs, M99.86 biomechanical lesion, M25.66 knee stiffness, M25.37 ankle instability, Z72.3 lack of exercise, and R29.3 malposture, for example. The clinician’s role is to explain a complete picture of the patient at the moment of reporting the LBP injury/complaint on the first visit without delays of ‘pending’ diagnosis waiting for endless imaging and referrals. Since 90% of the diagnosis is embedded in the history, the physician simply asks the best, most useful questions, and provides a complete diagnosis that represents and explains the LBP injury. A diagnosis of back pain does not explain the injury.

When the physician focuses only on ‘pain’ and its direct relationship to an ‘injury’ the problems begin to arise. Traumatic LBP is easier to explain than non-traumatic in the clinical setting, many times attributed to an event such as a fall or MVA, and may include tissue damage like buns or fractures. However, traumatic LBP may involve: S06.2X traumatic brain injury, S06.0X0 concussion, G44.3 headache, F32.0 depression, H81.1 vertigo, etc. that is not clinical, and should not be oversighted since it explains the ‘entire patient.’ Other diagnosis should be included when diagnosing a LBP patient, not just a diagnosis related to LBP.

LBP may be attributed to clinical pathogenesis such as arthritis and inflammation of the hip M13.859 or knee M13.869. Non-clinical LBP may involve systemic ‘bone pain’, or tissue injury as ‘muscle pain’ however these are sense-signals and not a diagnosis that explain the problem.

Neither event-based LBP trauma nor LBP pathogenesis can explain emotional pain, like that of grieving; pain that feels ‘loud’, amplified, and crushing. Neither can they explain mis-matched pain, intermittent pain, and pain with no historical or clinical basis. Nor can they explain pain that persists beyond healing, or when there is no stimulus such as in phantom pain. How can the clinician insist that a disc herniation is the causative factor for LBP while having no explanation for phantom pain? Worst, is pain brought on by surgical failure since it can be difficult to explain and discuss with the patient.

Can an afferent signal arrive at the brain that is dedicated to describe pain only? No.
Is there a part of the brain that detects and processes pain? No.
Are there neurons in the brain that are pain specific or pain selective? No.

Can you think of any other areas of the brain that might light up along with ‘pain’? Consider these: paying attention to the pain, behavior association & modification due to pain, facial & vocal displays of unpleasantness, pupillary changes, agitation-irritation-shortness-brashness, defensive motor mapping (antalgias), changes in self-care management, social changes, co-related frustrations-worry-loss.

Clearly the physician must explore all of the clinical and non-clinical diagnosis related to LBP, and pay close attention to the non-clinical contributors to LBP, while explaining this ‘thing called pain’ to the ‘entire patient,’ since ‘pain is not the only problem.’

LBP Blog General information

Series Description

These articles intend to (1) re-evaluate the prevailing clinical practices thought to manage low back ‘pain’, (2) submit and debate novel low back ‘pain’ contributors and mechanisms, (3) meet patient expectations & satisfaction and clinically meaningful results, (4) recommend a conservative non-surgical course of care to over-ride ‘pain’ instantly, and (5) restore ADLs and patient confidence on the first visit at low cost. This article has a companion podcast.

Dr. Dean Bio

Forester Dean is a chiropractic and physiotherapy sports medicine doctor practicing in Los Angeles, California. Dr. Dean is a lifetime athlete, and currently teaches tennis, track, boxing, yoga. The Core X System™ Campus flagship location was opened by Dr. Dean in 2020.

© Copyright 2021 SpineSync, Forester Dean, DC
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