Episodic Low Back Pain

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Most of the low back pain literature divides patients temporally into acute (under 3 months) and chronic (over 3 months). However there is a third group - the episodic low back pain patient, also called recurrent low back pain, and is almost exclusively caused by internal disc disruption.

Epidemiology and Risk Factors.

Recurrence of back pain is common, but rates vary widely in the literature (see Prognosis of Low Back Pain). For example in one study of 250 patients who had recovered from acute low back pain, 70% had a recurrence within one year, with a median time of 139 days.[1] The same study identified the following statistically significant risk factors: frequent exposure to awkward postures, longer time sitting (> 5 hours per day), and more than two previous episodes.

Aetiology and Pathophysiology

The episodic pattern of pain has a LR of 4.7 for a discogenic source (i.e. internal disc disruption)[2], but not a vertebrogenic source (i.e. not Modic change).[3] Modic change still occurs, it is just that the episodic pattern is not specific for it.

The pain mechanism in IDD is twofold, involving both mechanical and chemical nociception.

  • Chemical nociception: The healthy adult disc is largely aneural, with nociceptive fibers confined to the outer one-third of the anulus fibrosus. In IDD, the radial fissures act as conduits, allowing degraded, inflammatory material from the nucleus pulposus to come into contact with these nerve endings. This triggers a potent inflammatory response, mediated by cytokines such as tumor necrosis factor-alpha (TNFāˆ’Ī±) and interleukin-1 beta (ILāˆ’1β), leading to chemical nociception.
  • Mechanical nociception: Concurrently, the structural failure of the anulus leads to altered load distribution and stress concentration on the remaining intact fibers, causing mechanical nociception.

During periods of remission, the disc exists in a fragile, sub-clinical state, mechanically compromised but not actively inflamed. It is primed for a flare, awaiting a trigger that exceeds its diminished capacity to manage mechanical stress.

Episodic back pain can therefore be conceptualised as a two-hit process. The first hit is a biomechanical trigger that acts upon a pre-existing, mechanically insufficient disc with IDD. This insult causes further micro-damage and forces inflammatory nuclear material into the innervated outer anulus. The second hit is the subsequent biochemical cascade of inflammation and chemical nociception, which dramatically amplifies and sustains the painful episode.

This model gives rise to the clinically useful concept of a "flare threshold." This is a patient-specific biomechanical limit, determined by the severity of their underlying IDD and the capacity of their surrounding neuromuscular system to protect the vulnerable segment. During periods of remission, the patient's daily activities remain below this threshold. A flare occurs when a specific activity or cumulative loading exceeds it, initiating the cascade.

The flare threshold can be explained to the patient using the metaphor of a "stress bucket." The bucket is filled by various mechanical stresses throughout the day (sitting, bending, lifting). A flare occurs when the bucket overflows. The goal of prevention is twofold: 1) make the bucket bigger (through strengthening and conditioning exercises), and 2) learn to recognize when the bucket is getting full and avoid activities that will make it overflow (ergonomics and pacing).

Clinical Features

The hallmark of this condition is the occurrence of discrete, severe, and often disabling episodes of axial LBP, commonly referred to as flares. These flares are followed by periods of complete or near-complete remission, during which the patient may experience little to no pain and a full return to function. The transition from a state of relative wellness to acute disability can be abrupt and is often precipitated by seemingly innocuous physical triggers.

Prevention of Flares

The single most consistent predictor of a future episode is a previous history of low back pain. This is obviously not modifiable. Prevention is focused on modifiable factors. However it is not possible to convert a disc with IDD and impaired biomechanical properties into one with normal biomechanical properites. Hence it is very unlikely that complete prevention is routinely possible.

Modfiable risk factors are as follows[4][1][5]

  • Biomechanical Factors: Difficult working positions (optimise workstation setup), prolonged sitting (target postural variation, utilise a lumbar roll), frequent bending, and carrying heavy loads.
  • Lifestyle Factors: Obesity increases the static and dynamic load on the lumbar spine. Smoking is also a significant risk factor, believed to impair disc nutrition and accelerate degeneration. Addressing both of these factors should be prioritised, as without addressing them it is usually a losing battle.
  • Psychosocial Factors: Depression, general anxiety, maladaptive coping strategies, and fear-avoidance beliefs (the belief that movement will cause further injury) are predictors of poor outcomes and the transition to chronic, disabling pain.

A large 2016 systematic review and meta-analysis published in JAMA Internal Medicine, which included 21 randomized clinical trials and over 30,000 participants, provides a clear directive for clinical practice. The review found:[6]

  • Exercise combined with education is the most effective strategy, reducing the risk of a new episode of LBP by 45% (Relative Risk 0.55; 95% CI 0.41-0.74) based on moderate-quality evidence.  
  • Exercise alone is also effective, reducing the risk of an LBP episode by 35% (RR 0.65; 95% CI 0.50-0.86) based on low- to very low-quality evidence.  
  • Education alone, back belts, and shoe insoles were found to be ineffective in preventing LBP episodes.  

Flare Treatment

Patients may benefit from a flare treatment plan, i.e. expecting and planning for flares in order to hopefully reduce their intensity and duration, as well as early recognition. This may include various modalities such as activity modification, NSAIDs, heat or cold therapy, McKenzie based exercises (e.g. for extension-preference patients, they should do back bends every 1-2 hours), and self massage (e.g. with a massage cane).

Resources

References

  1. ↑ 1.0 1.1 da Silva, Tatiane; Mills, Kathryn; Brown, Benjamin T; Pocovi, Natasha; de Campos, Tarcisio; Maher, Christopher; Hancock, Mark J (2019-07). "Recurrence of low back pain is common: a prospective inception cohort study". Journal of Physiotherapy (in English). 65 (3): 159–165. doi:10.1016/j.jphys.2019.04.010. Check date values in: |date= (help)
  2. ↑ Levi, David; Carnahan, Diana; Horn, Scott; Levin, Josh (2018-07-01). "Is a History of Severe Episodic Low Back Pain an Indicator of a Discogenic Etiology?". Pain Medicine (in English). 19 (7): 1334–1339. doi:10.1093/pm/pnx147. ISSN 1526-2375.
  3. ↑ Levin, Josh; Schirmer, Derek; Garcia, Roxana; Levi, David (2023-03). "Is a history of episodic low back pain an indicator of Modic changes?". Interventional Pain Medicine. 2 (1): 100239. doi:10.1016/j.inpm.2023.100239. ISSN 2772-5944. PMC 11372870. Check date values in: |date= (help)CS1 maint: PMC format (link)
  4. ↑ Nieminen, Linda Karoliina; Pyysalo, Liisa Maria; KankaanpƤƤ, Markku Juhani (2021-01). "Prognostic factors for pain chronicity in low back pain: a systematic review". PAIN Reports (in English). 6 (1): e919. doi:10.1097/PR9.0000000000000919. ISSN 2471-2531. Check date values in: |date= (help)
  5. ↑ Krishnamurthy, Ilanchezhiyan; Othman, Rani; Baxter, George David; Mani, Ramakrishnan (2018-05-04). "Risk factors for the development of low back pain: an overview of systematic reviews of longitudinal studies". Physical Therapy Reviews (in English). 23 (3): 162–177. doi:10.1080/10833196.2018.1468965. ISSN 1083-3196.
  6. ↑ Steffens, Daniel; Maher, Chris G.; Pereira, Leani S. M.; Stevens, Matthew L; Oliveira, Vinicius C.; Chapple, Meredith; Teixeira-Salmela, Luci F.; Hancock, Mark J. (2016-02-01). "Prevention of Low Back Pain: A Systematic Review and Meta-analysis". JAMA Internal Medicine (in English). 176 (2): 199. doi:10.1001/jamainternmed.2015.7431. ISSN 2168-6106.