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Dr Abdelrahman Taha, السويس, Suez (2025)

29/09/2025

Neuropathic pain is pain coming from damaged nerves. It is different from pain messages that are carried along healthy nerves fromdamaged tissue (e.g. a fall or cut, or arthritic knee).

Neuropathic pain is often treated by different medicines (drugs) to those used forpain from damaged tissue, which we often think of as painkillers. Medicines that are sometimes used to treat depression or epilepsy(fits) can be very effective in some people with neuropathic pain. But sometimes paracetamol is used to treat neuropathic pain, eitherby itself or with the opioid painkillers codeine or dihydrocodeine.

Paracetamol has been widely available for over 50 years. There is evidence it works as a painkiller in some short-lived pains, but it doesnot appear to work well for long lasting pains.

👉 "There is insufficient evidence to support or refute the suggestion that paracetamol alone, or in combination with codeine or dihydrocodeine, works in any neuropathic pain condition".

29/09/2025

Peripheral glia (i.e. Schwann cells and satellite glial cells (SGCs) and central glia (i.e. microglia, astrocytes and oligodendrocytes) are activated during neuroinflammation (Ji, et al. 2013). Glial activation can further be detected in patients with chronic low back pain using positron emission tomography (PET) imaging (Loggia, et al. 2015). Thus, targeting excessive neuroinflammation will be a promising approach to alleviate chronic pain and control the progression of neurological and psychiatric diseases (Matsuda et al. 2019).

References:
- Matsuda, M., Huh, Y., & Ji, R. R. (2019). Roles of inflammation, neurogenic inflammation, and neuroinflammation in pain. Journal of anesthesia, 33(1), 131–139.
- Ji, R. R., Berta, T., & Nedergaard, M. (2013). Glia and pain: Is chronic pain a gliopathy? Pain.
- Loggia, M. L., Chonde, D. B., Akeju, O., Arabasz, G., Catana, C., Edwards, R. R., Hill, E., Hsu, S., Izquierdo-Garcia, D., Ji, R. R., Riley, M., Wasan, A. D., Zurcher, N. R., Albrecht, D. S., Vangel, M. G., Rosen, B. R., Napadow, V., & Ho**er, J. M. (2015). Evidence for brain glial activation in chronic pain patients. Brain, 138(3), 604–615.

29/09/2025

What are the "nociceptors" 🤔

"Nociceptors" are a subset of primary afferent neurons, with cell bodies located in the DRG and trigeminal ganglia, that respond to tissue injury, and are made up of both unmyelinated C-fibers and myelinated A delta-fibers innervating skin, muscle, joint, and visceral organs. These tissue-injury sensitive neurons signal through the activation or sensitization of G-protein coupled receptors (GPCRs), ionotropic receptors, and tyrosine kinase receptors located on nerve terminals and cell bodies. These receptors are directly bound and activated by a variety of inflammatory mediators, including but not restricted to, bradykinin, prostaglandins (e.g., PGE2), H+, ATP, nerve growth factor (NGF), as well as proinflammatory cytokines and chemokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and CCL2 (Ji, et al. 2014; Julius & Basbaum. 2001; Gold & Gebhart. 2010; White, et al. 2005; Amaya, et al. 2013).

References:
- Ji, R. R., Xu, Z. Z., & Gao, Y. J. (2014). Emerging targets in neuroinflammation-driven chronic pain. Nature Reviews Drug Discovery, 13(7), 533–548.
- Julius, D., & Basbaum, A. I. (2001). Molecular mechanisms of nociception. Nature, 413(6852), 203–210.
- Gold, M. S., & Gebhart, G. F. (2010). Nociceptor sensitization in pain pathogenesis. Nature Medicine, 16(11), 1248–1257.
- White, F. A., Bhangoo, S. K., & Miller, R. J. (2005). Chemokines: Integrators of pain and inflammation. Nature Reviews Drug Discovery, 4(10), 834–844.
- Amaya, F., Izumi, Y., Matsuda, M., & Sasaki, M. (2013). Tissue injury and related mediators of pain exacerbation. Current Neuropharmacology, 11(6), 592–597.

29/09/2025

Unraveling the 'Neuro' in Pain: A Closer Look at Inflammation 🔥🔥

Pain isn't just a simple signal—it's a complex biological event involving a symphony of systems. While we often think of inflammation as the body's straightforward response to injury, the "neuro" part adds a fascinating layer to chronic pain conditions.

💥 Inflammation vs. Neuroinflammation

- Inflammation is the initial protective response to tissue damage or infection. It involves key players like prostaglandins, cytokines, and chemokines that directly activate nociceptors—the pain-sensing neurons. This is the classic "ow, that hurts" feeling.

- Neurogenic inflammation is a specific type of inflammation triggered by nerve activation. When nerves are stimulated, they release neuropeptides, causing rapid swelling (edema) and contributing to conditions like headaches.

- Neuroinflammation, however, is a localized inflammation within the central nervous system (CNS) and peripheral nervous system (PNS). A key feature is the activation of glial cells—the brain's immune cells—in areas like the spinal cord and brain. This activation leads to a continuous loop of pro-inflammatory cytokine and chemokine production, which drives peripheral and central sensitization. Essentially, the nervous system becomes hypersensitive, amplifying pain signals and making them more persistent.

This distinction is crucial, especially in conditions like neuropathic pain, postoperative pain, and opioid-induced hyperalgesia, where neuroinflammation plays a significant role in making pain chronic and difficult to manage.

Understanding these different pathways is key to developing more effective treatments.

26/09/2025

"Nociceptive, neuropathic, and nociplastic shoulder pain: definitions according to the International Association for the Study of Pain (IASP) and possible shoulder pain examples". Along with "Key features per pain phenotype as evident from the interview, clinical examination, and instrumented assessment".

References:
- Dean BJF, Gwilym SE, Carr AJ. Why does my shoulder hurt? A review of the neuroanatomical and biochemical basis of shoulder pain. Br J Sports Med. 2013;47(17):1095.
- Accessed April https://www.iasp-pain.org/resources/terminology/; 2023. Accessed April.
- Lo CN, van Griensven H, Lewis J. Rotator cuff related shoulder pain: an update of potential pathoaetiological factors. New Zealand Journal of Physiotherapy. 2022.
- BJFDaD Griffin. In: Fernandes-de-las-Penas JLaC, ed. The Shoulder: Theory and Practice. 1 ed. Handspring Publishing; 2022.
- Lo CN, van Griensven H, Lewis J. Rotator cuff related shoulder pain: an update of potential pathoaetiological factors. New Zealand Journal of Physiotherapy. 2022.
- Haik MN, Evans K, Smith A, Bisset L. Investigating the effects of mobilization with
movement and exercise on pain modulation processes in shoulder pain - a single cohort pilot study with short-term follow up. J Man Manip Ther. 2022;30(4): 239–248.
- Struyf F, Geraets J, Noten S, Meeus M, Nijs J. A multivariable prediction model for the chronification of non-traumatic shoulder pain: a systematic review. Pain Physician. 2016;19(2):1–10.
- Delen M, Sendil A, Kaux JF, et al. Self-reported bio-psycho-social factors partially distinguish rotator cuff tendinopathy from other shoulder problems and explain shoulder severity: a case-control study. Musculoskeletal Care. 2023;21(1):175–188.
- Clausen MB, Witten A, Holm K, et al. Glenohumeral and scapulothoracic strength
impairments exists in patients with subacromial impingement, but these are not reflected in the shoulder pain and disability index. BMC Musculoskelet Disord. 2017; 18(1):302.
- Alaia EF, Day MS, Alaia MJ. Entrapment neuropathies of the shoulder. Semin Musculoskelet Radiol. 2022;26(2):114–122.
- Woolf CJ. Central sensitization: implications for the diagnosis and treatment of pain.
Pain. 2011;152.
- Arendt-Nielsen L, Morlion B, Perrot S, et al. Assessment and manifestation of central
sensitisation across different chronic pain conditions. Eur J Pain. 2018;22(2): 216–241.
- Kosek E, Cohen M, Baron R, et al. Do we need a third mechanistic descriptor for chronic pain states? Pain. 2016;157(7):1382–1386.
- Arendt-Nielsen L, Morlion B, Perrot S, et al. Assessment and manifestation of central
sensitisation across different chronic pain conditions. Eur J Pain. 2018;22(2): 216–241.
- Shraim MA, Sluka KA, Sterling M, et al. Features and methods to discriminate between mechanism-based categories of pain experienced in the musculoskeletal system: a Delphi expert consensus study. Pain. 2022;163(9):1812–1828.
- Kosek E, Clauw D, Nijs J, et al. Chronic nociplastic pain affecting the musculoskeletal system: clinical criteria and grading system. Pain. 2021;162(11): 2629–2634.
- Shraim MA, Masse-Alarie H, Hodges PW. Methods to discriminate between mechanism-based categories of pain experienced in the musculoskeletal system: a systematic review. Pain. 2021;162(4):1007–1037.
- Bilika P, Nijs J, Fandridis E, Dimitriadis Z, Strimpakos N, Kapreli E. In the shoulder
or in the brain? Behavioral, psychosocial and cognitive characteristics of unilateral chronic shoulder pain with symptoms of Central sensitization. Healthcare (Basel). 2022;10(9).

26/09/2025

Notes on: The seven-steps clinical decision-making algorithm of the IASP clinical criteria for nociplastic pain

Understanding and Diagnosing Nociplastic Pain
The International Association for the Study of Pain (IASP) has developed a valuable clinical criteria and grading system to help clinicians determine if a patient's pain experience is partly due to nociplastic pain (Kosek, et al. 2021). This provides a structured approach and greater confidence in identifying pain phenotypes.

However, a recent paper by De Baets et al. (2025) highlights an important consideration: while this graded approach is a helpful tool, it has not yet been validated in people with musculoskeletal pain conditions. Therefore, it cannot replace the nuanced judgment and expertise of a trained clinician.

Moving forward, a key area for research is validating these diagnostic criteria to ensure they are clinically applicable and easy for healthcare professionals to use. This will be a crucial step toward more precise and effective management of persistent musculoskeletal pain.

Reference:
- De Baets, L., Kuppens, K., Labie, C., Haik, M. N., Kapreli, E., Bilika, P., Struyf, F., Borms, D., Fernández-de-Las-Peñas, C., Kosek, E., Lluch, E., Testa, M., Lewis, J., Goossens, Z., Schilz, M., Bonneux, I., & Nijs, J. (2025). Shoulder pain phenotyping: A guide for clinicians to determine predominant nociceptive, neuropathic, or nociplastic shoulder pain. Brazilian journal of physical therapy, 29(6), 101240. Advance online publication.
- Kosek E, Clauw D, Nijs J, et al. Chronic nociplastic pain affecting the musculoskeletal system: clinical criteria and grading system. Pain. 2021;162(11):
2629–2634.

26/09/2025

Is Your Exercise Program Right for Your Pain Type? 🤔🤔

When it comes to chronic pain, a one-size-fits-all approach to exercise might not be effective. A fascinating study by Falla and Hodges (2017) explored how a specific neck exercise program affected two groups: people with idiopathic neck pain and those with chronic whiplash-associated disorders.

The results were telling. Individuals with mild to moderate idiopathic neck pain saw a significant 47% reduction in their pain intensity (Falla et al., 2004). However, the response was much different for people with whiplash. Those with mechanical hyperalgesia (increased pain sensitivity) experienced only a 37% reduction, while those with widespread hyperalgesia saw a minimal 16% reduction in pain (Jull et al., 2007).

This research highlights a crucial point: the body's response to exercise is influenced by how the central nervous system processes pain. For individuals with a more sensitive pain system, a conventional exercise program may not be the most effective solution. This suggests that tailoring exercise therapy to the specific pain phenotype could lead to much better outcomes.

References:
- Falla D, Hodges PW. Individualized exercise interventions for spinal pain. Exerc Sport Sci Rev. 2017;45(2):105–115.
- Falla DL, Jull GA, Hodges PW. Patients with neck pain demonstrate reduced electromyographic activity of the deep cervical flexor muscles during performance of the craniocervical flexion test. Spine (Phila Pa 1976). 2004;29(19):2108–2114.
- Jull G, Sterling M, Kenardy J, Beller E. Does the presence of sensory hypersensitivity influence outcomes of physical rehabilitation for chronic whiplash?–A preliminary RCT. Pain. 2007;129(1–2):28–34.

26/09/2025

A New Approach to Persistent Shoulder Pain

Persistent shoulder pain is a common issue, with nearly half of all patients not fully recovering within six months. The reason for this prolonged pain is a mystery, but one potential solution lies in a more targeted approach to treatment.

A recent study suggests that understanding the underlying pain phenotype—whether the pain is nociceptive, neuropathic, or nociplastic—could be the key. The International Association for the Study of Pain (IASP) has developed clinical criteria and a grading system to identify nociplastic pain, which may help clinicians determine the predominant pain type and tailor treatment accordingly.

The paper provides a clinical reasoning framework to help clinicians evaluate pain phenotypes and their underlying mechanisms. By moving toward a more precise, individualized approach, we may finally be able to improve outcomes for those suffering from chronic musculoskeletal pain.

Future research is needed to validate the IASP algorithm and to test the effectiveness of tailored treatments in clinical trials. This is a significant step toward developing more precise care for people with persistent shoulder pain.

24/09/2025

Foot Drop & The Critical Window for Surgery: What Clinicians Need to Know

Foot drop due to a lumbar disc herniation is a serious condition. Our recent analysis of patient data reveals key factors that determine surgical outcomes and highlights a crucial timeframe for intervention.

Key Takeaways for Clinicians:

1) Time is of the essence: The most critical factor is the duration of symptoms. Operating within the first six weeks of foot drop onset dramatically increases the chance of a successful recovery. Delays can lead to irreversible nerve damage.

2) Age and strength matter: Younger patients and those with less severe weakness (higher pre-operative MRC grades) are more likely to achieve greater motor recovery. This should be part of the pre-op discussion with patients.

3) Early recovery is a good sign: If a patient shows any improvement in muscle strength within the first three months after surgery, they are highly likely to continue recovering.

🛑 The Bottom Line:
For patients with unilateral foot drop from a lumbar disc herniation, a diagnosis requires urgent action. The first six weeks are a critical window for surgical decompression to maximize the potential for full functional recovery.

24/09/2025

A key limitation in studies suggesting that running improves disc health is that they often use observational designs, making it difficult to establish a direct causal link. While recreational runners tend to have healthier discs compared to non-exercisers (Owen, et al. 2020; Mitchell, et al. 2020; Belavý, et al. 2017), this correlation may be influenced by other factors, such as shared healthy habits or genetic predispositions. Therefore, the improved disc health seen in runners may not be a direct result of the running itself.

Furthermore, the specific type of load from recreational running—predictable and moderate—is known to be beneficial for discs based on laboratory findings (Shapiro & Risbud, 2014). This raises the question of whether running is a unique case of disc adaptation rather than evidence of a broader anabolic capacity in response to exercise. In contrast, both laboratory research and some studies on runners suggest that higher-magnitude loading may be catabolic for disc tissue (Belavý, et al. 2017; Shapiro & Risbud, 2014).

An important piece of evidence supporting this distinction comes from a randomized controlled trial (RCT) which found no significant change in disc health following a running intervention (Owen, et al. 2020). This finding directly challenges the hypothesis that running causally leads to healthier discs.

References:
- Owen PJ, Hangai M, Kaneoka K, Rantalainen T, Belavy DL. Mechanical loading influences the lumbar intervertebral disc. A cross-sectional study in 308 athletes and 71 controls. J Orthop Res. 2020
- Mitchell UH, Bowden JA, Larson RE, Belavy DL, Owen PJ. Long-term running in middle-aged men and intervertebral disc health, a cross-sectional pilot study. PLOS ONE. 2020 Feb 21;15(2):e0229457.
- Belavý DL, Quittner MJ, Ridgers N, Ling Y, Connell D, Rantalainen T. Running exercise strengthens the intervertebral disc. Sci Rep. 2017 Apr 19;7(1):45975.
- Shapiro IM, Risbud MV, editors. The Intervertebral Disc: Molecular and Structural Studies of the Disc in Health and Disease [Internet]. Vienna: Springer Vienna; 2014.
- Owen PJ, Miller CT, Rantalainen T, Simson KJ, Connell D, Hahne AJ, et al. Exercise for the intervertebral disc: a 6-month randomised controlled trial in chronic low back pain. Eur Spine J. 2020 Aug;29(8):1887–99.

24/09/2025

RCT found that 👉 a running intervention did not make discs healthier (or unhealthier)

Reference:
- Owen, P. J., Miller, C. T., Rantalainen, T., Simson, K. J., Connell, D., Hahne, A. J., et al. (2020). Exercise for the intervertebral disc: a 6-month randomised controlled trial in chronic low back pain. European Spine Journal, 29(8), 1887–1899.

24/09/2025

According to Adams and Roughley (2006), adult intervertebral discs (IVDs) are unable to repair significant damage. Similarly, Belavý et al. (2016) note that a damaged or degenerated IVD won't respond to physical loading in the same way a healthy disc would.

References
Adams, M. A., & Roughley, P. J. (2006). What is Intervertebral Disc Degeneration, and What Causes It? SPINE, 31(18).
Belavý, D. L., Albracht, K., Bruggemann, G. P., Vergroesen, P. P. A., & van Dieën, J. H. (2016). Can Exercise Positively Influence the Intervertebral Disc? Sports Medicine, 46(4), 473-485.

Dr Abdelrahman Taha

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