https://www.facebook.com/2065987960387192/

The Musculoskeletal Wrangler

Home
Australia
Wonthaggi, VIC
The Musculoskeletal Wrangler

I am an APA Musculoskeletal Physiotherapist and an emerging APA "Pain" Physio passionate about evidence based practice (EBP).

This page keeps me accountable with EBP, and can hopefully serve as a useful resource for health professionals and consumers.

14/03/2026

Patient satisfaction:
Validated instruments
BACKGROUND:
🔎Patient satisfaction is widely recognised as an important indicator of healthcare quality and service effectiveness. Measuring satisfaction reliably requires validated instruments with strong psychometric properties.
📍A systematic review by Gutierrez-Sanchez et al. (2020) evaluated 9 validated instruments designed to measure satisfaction with physical therapy care and assessed the quality of evidence supporting them.
INSTRUMENTS & UTILITY (pictured):
INSTRUMENT DIMENSIONS:
🔆Therapist-patient interaction and communication
🔆Professional competence
🔆Treatment effectiveness
🔆Organisation of services and clinical environment
SUMMARY:
📖Although the MedRisk instrument appears to have the most robust supporting evidence, no tool demonstrates comprehensive psychometric validation across all domains. Continued methodological research is required to develop and validate more reliable instruments for assessing patient satisfaction in physical therapy
MW
Reference:
Gutiérrez-Sánchez D, Pérez-Cruzado D, Cuesta-Vargas AI. Instruments for measuring satisfaction with physical therapy care: a systematic review. Phys Ther. 2020;100(9):1690–1705.

09/03/2026

Neuroplasticity:
Part 2: non-invasive neuromodulatory interventions
BACKGROUND:
🔎Conventional treatments—including pharmacological therapies and invasive procedures—often have limited efficacy and may produce adverse effects, prompting interest in alternative approaches that directly target neural plasticity.
📍A recent and comprehensive narrative review by Jayathilake et al. (2025) examines the biological mechanisms underlying neuroplastic changes in chronic pain and evaluates the therapeutic potential of non-invasive neuromodulation techniques. They focus on how neuromodulation can modify neural circuits involved in pain processing and potentially reverse maladaptive plasticity across peripheral, spinal, and cortical levels of the nervous system
REPETITIVE TRANSCRANIAL MAGNETIC STIMULATION (rTMS):
🔆Modulates cortical excitability and neurotransmitter systems, particularly when applied to the motor cortex, producing analgesic effects through top-down modulation of pain networks.
TRANSCRANIAL DIRECT CURRENT STIMULATION (tDCS);
🔆Alters neuronal membrane potentials and influences receptor expression (e.g., NMDA receptors), contributing to modulation of pain processing pathways.
TRANSCRANIAL RANDOM NOISE STIMULATION (tRNS):
🔆Enhances cortical excitability by influencing ion channel dynamics and neuronal firing patterns.
TRANSCRANIAL ULTRASOUND STIMULATION (tUS):
🔆Emerging modality capable of modulating deep brain regions and altering neurotransmitter levels and connectivity within pain networks.
SUMMARY:
📖Non-invasive neuromodulation represents a promising therapeutic strategy for chronic pain by targeting maladaptive neuroplasticity in pain pathways. However, further research is needed to clarify mechanisms, optimise stimulation parameters, determine long-term efficacy, and integrate neuromodulation with other treatments such as behavioural therapies.
MW
Reference:
Jayathilake NJ, Phan TT, Kim J, Lee KP, Park JM. Modulating neuroplasticity for chronic pain relief: noninvasive neuromodulation as a promising approach. Exp Mol Med. 2025;57(3):501-514.

09/03/2026

Neuroplasticity:
Part 1: maladaptive mechanisms
BACKGROUND:
🔎Chronic neuropathic pain is increasingly understood as a disorder of maladaptive neuroplasticity, where persistent changes in neural structure and function lead to abnormal pain processing and central sensitisation.
📍A recent and comprehensive narrative review by Jayathilake et al. (2025) examines the biological mechanisms underlying neuroplastic changes in chronic pain and evaluates the therapeutic potential of non-invasive neuromodulation techniques. They focus on how neuromodulation can modify neural circuits involved in pain processing and potentially reverse maladaptive plasticity across peripheral, spinal, and cortical levels of the nervous system
PERIPHERAL SENSITISATION:
📝Neuroplastic changes occur in primary nociceptors following tissue injury or inflammation, which amplify nociceptive input to the spinal cord and contribute to ongoing pain signalling:
🔆increased expression and sensitivity of ion channels (e.g., sodium and TRP channels)
🔆enhanced release of inflammatory mediators, and lowered activation thresholds of nociceptors.
CENTRAL SENSITISATION:
📝Within the dorsal horn of the spinal cord, persistent nociceptive input induces long-term plastic changes characterised by:
enhanced excitatory neurotransmission and reduced inhibitory signalling
🔆increased glutamatergic transmission
activation of NMDA receptors
🔆reduced activity of inhibitory interneurons that utilise GABA and glycine
🔆glial cell activation (microglia and astrocytes)
🔆pro-inflammatory cytokine and neuromodulator release
🔆increase neuronal excitability and maintain sensitisation.
SYNAPTIC PLASTICITY:
📝Long-term potentiation (LTP)-like mechanisms within nociceptive pathway that strengthen synaptic connections transmitting pain
SUPRASPINAL/CORTICAL REORGANISATION:
📝Functional and structural reorganisation of brain regions involved in pain processing leading to altered pain perception, and amplified emotional responses to, and cognitive processing of nociceptive input.
NEUROIMMUNE & EPIGENETICS:
📝Activated glial cells release cytokines and chemokines that sustain neuronal sensitisation.
Epigenetic modifications (eg: changes in DNA methylation and histone acetylation) can alter gene expression related to neurotransmission, inflammation, and neuronal excitability, contributing to the persistence of chronic pain states.
SUMMARY:
📖These maladaptive neuroplastic changes collectively produce heightened excitability of pain pathways and impaired inhibitory modulation, which sustain chronic pain even after the initial tissue injury has resolved.
MW
Reference:
Jayathilake NJ, Phan TT, Kim J, Lee KP, Park JM. Modulating neuroplasticity for chronic pain relief: noninvasive neuromodulation as a promising approach. Exp Mol Med. 2025;57(3):501-514.

08/03/2026

Neuroplasticity vs. diet?
BACKGROUND:
🔎Chronic pain is associated with structural and functional changes to the nervous system (i.e.: neuroplasticity), which can reinforce maladaptive pain processing. Can metabolic interventions enhance neuroplasticity and thereby improve outcomes of chronic pain treatments?
📍A narrative review by Sibille et al. (2016) synthesized the available evidence from neuroscience, nutrition, and pain research. They propose that pairing conventional pain treatments (e.g., psychological, pharmacological, or physical therapies) with interventions that increase neuroplasticity could amplify treatment effects.
DIETARY FACTORS:
💡Intermittent fasting and acute glucose administration have been proposed to potentially enhance learning, memory, and synaptic plasticity—processes that are critical for successful pain rehabilitation and behavioural interventions
INTERMITTENT FASTING (e.g., 16–24 h) can trigger metabolic and cellular changes that support neural adaptation through proposed mechanisms:
🔆Increased brain-derived neurotrophic factor (BDNF) and synaptic plasticity
🔆Reduced inflammation and oxidative stress
🔆Enhanced neurogenesis and cellular metabolism
ACUTE GLUCOSE ADMINISTRATION (typically ~25–50 g) has been shown to improve memory and cognitive performance in many studies, through proposed mechanisms:
🔆Increased hippocampal activity and connectivity
🔆Enhanced acetylcholine synthesis
🔆Modulation of ATP-sensitive potassium channels affecting neuronal excitability
IMPLICATIONS:
📝The two dietary interventions are non-invasive, inexpensive, and widely accessible compared with neuromodulation techniques such as transcranial stimulation.
LIMITATIONS:
⚠️The evidence remains largely theoretical and based on indirect research, highlighting the need for clinical trials testing these strategies alongside pain interventions. Further research is needed to determine optimal dosing, timing, and safety in chronic pain populations.
MW
Reference:
Sibille KT, Bartsch F, Reddy D, Fillingim RB, Keil A. Increasing neuroplasticity to bolster chronic pain treatment: a role for intermittent fasting and glucose administration? J Pain. 2016;17(3):275-281.

08/03/2026

Chronic musculoskeletal pain (CMP):
A new concept
BACKGROUND:
🔎CMP reflects pain that persists beyond three months and cannot be attributed solely to identifiable tissue pathology. It is mechanistically described as a pain arising from altered pain processing in the nervous system rather than direct tissue injury (i.e.: nociplastic pain)
📍A perspective paper by Fitzcharles et al. (2022) outlined a proposed clinical criteria for identifying this pain type, emphasize its distinction from secondary and nociceptive musculoskeletal pain, and discuss the implications of adopting this framework in clinical practice.
CHARACTERISTICS (see image):
CHALLENGES:
⚠️The new concept overlaps with and may subsume previous constructs like myofascial pain, which lacked consistent evidence of specific tissue pathology and had subjective diagnostic signs.
⚠️Differentiating chronic primary musculoskeletal pain from other regional pain syndromes is complex, and widespread acceptance and validation of diagnostic criteria are still lacking
SUMMARY:
📖The classification of CMP, with a predominant nociplastic mechanism, may be easiest understood as “regional fibromyalgia,” a novel concept that will require acceptance by mainstream medicine. Further research and consensus on diagnostic criteria and effective therapies are needed for widespread clinical adoption.
MW
Reference:
Fitzcharles MA, Cohen SP, Clauw DJ, Littlejohn G, Usui C, Häuser W. Chronic primary musculoskeletal pain: a new concept of nonstructural regional pain. Pain Rep. 2022;7(5):e1024

07/03/2026

Immune control of pain
Part 2: treatment considerations
📍A very recent and publicised article by Paolini et al. (2026) describes how immune cells, including macrophages, neutrophils, mast cells, B&T cells, and glial cells, interact with peripheral nociceptors and central pain pathways.
🔆CYTOKINE-TARGETED THERAPIES are currently central to treatment. Biologic agents that inhibit pro-inflammatory cytokines—such as TNF, IL-1, IL-6, and IL-17—can significantly reduce pain in rheumatic conditions
🔆IMMUNE CELL MODULATIONS also represents a promising strategy. Regulatory T cells (Tregs) and M2-like macrophages play key roles in resolving inflammation and may contribute to neuropathic pain resolution. Approaches such as low-dose IL-2 therapy to expand Tregs or adoptive transfer of expanded autologous Tregs are being investigated as potential therapies.
🔆JANUS KINASE (JAK) INHIBITORS including Baricitinib, are established treatments for rheumatoid arthritis and may provide faster and greater pain reduction than some anti-TNF therapies such as Adalimumab. These drugs influence inflammatory signaling pathways (e.g., IL-6/JAK/STAT3) and may reduce both inflammatory and neuropathic pain through actions on dorsal root ganglia.
🔆NEUROMODULATION via vagus nerve stimulation can activate the cholinergic anti-inflammatory pathway, reducing systemic TNF production via α7 nicotinic acetylcholine receptors. Early clinical studies suggest anti-inflammatory and analgesic benefits in conditions such as RhA and Crohn’s Disease.
🔆GUT-BRAIN AXIS and gut microbiota influences inflammatory and neuropathic pain through immune, metabolic, and neurotransmitter signaling. Interventions such as dietary modification, probiotics, and f***l microbiota transplantation may therefore offer future pain management strategies.
🔆PRO-RESOLVING MEDIATORS (SPMs) including resolvins, protectins, and maresins, are endogenous lipid mediators involved in resolving inflammation. Experimental studies demonstrate potent analgesic effects in models of inflammatory, neuropathic, and cancer-related pain, suggesting potential for future pharmacological development.
MW
Reference:
Paolini L, Sigaux J, Boissier MC, Rivière E. Immune control of pain. Joint Bone Spine. 2022;89(3):105303.

03/03/2026

Immune control of pain
Part 1: mechanisms
BACKGROUND:
🔎Pain is not solely a neuronal phenomenon; it is closely regulated by the immune system. Interactions between immune cells and the nervous system play a critical role in the initiation, amplification, and persistence of pain, particularly in inflammatory and chronic pain conditions.
📍A very recent and publicised article by Paolini et al. (2026) describes how immune cells, including macrophages, neutrophils, mast cells, B&T cells, and glial cells, interact with peripheral nociceptors and central pain pathways. These cells release cytokines, chemokines, growth factors, and lipid mediators that can either sensitise or suppress nociceptive signalling. Thus, immune activity can both promote and resolve pain.
PERIPHERAL:
How immune cells trigger and amplify pain at the site of injury:
🔆Innate immune cells (eg: macrophages, neutrophils, mast cells)
🔆Pro-inflammatory mediators (TNF-a, IL-1B, IL-6, prostaglandins)
🔆Peripheral sensitisation of nociceptors
CENTRAL:
How immune process contribute to central sensitisation and chronic pain:
🔆Microglia and astrocyte activation in spinal cord
🔆Cytokine-mediated enhancement of excitatory transmission
🔆Reduction of descending inhibitory modulation
🔆Neuroimmune ‘cross-talk’ ~ the bidirectional communication between nervous and immune system
SUMMARY:
📖Persistent immune activation or dysregulation can sustain sensitisation even after tissue healing, contributing to chronic inflammatory, neuropathic, and nociplastic pain states. Neuroimmune interactions therefore represent a key mechanism in pain chronification.
📖Pain is tightly regulated by bidirectional neuroimmune interactions. Immune cells and their mediators can initiate and amplify nociceptive signalling, but they also play a crucial role in active pain resolution. Dysregulation of these processes contributes to chronic pain, making immune pathways important therapeutic targets.
MW
Reference:
Paolini L, Sigaux J, Boissier MC, Rivière E. Immune control of pain. Joint Bone Spine. 2026;93:105999.

02/03/2026

The ICF framework
BACKGROUND:
🔎The International Classification of Functioning, Disability and Health (ICF) was endorsed by the World Health Organization (WHO) in 2001 as a biopsychosocial framework for describing health and disability.
📍An original paper of its time by Stucki et al. (2002) provided a comprehensive overview of the structure of the ICF, while highlighting its value and application in rehabilitation medicine.
BODY STRUCTURE & FUNCTION:
💪 Physiological functions of body systems (including psychological functions) and the anatomical parts of the body (organs, limbs, structures). Impairments refer to problems such as loss, deviation, or dysfunction in these areas.
ACTIVITIES & PARTICIPATION :
🏀 Activities are the ex*****on of tasks or actions by an individual (e.g., walking, dressing), while participation refers to involvement in life situations (e.g., employment, social roles). Limitations or restrictions reflect difficulties in performing tasks or engaging in society.
ENVIRONMENTAL & PERSONAL FACTORS:
🌳 Environmental factors are the physical, social, and attitudinal surroundings that influence functioning (e.g., accessibility, support, policies). Personal factors are individual characteristics such as age, coping style, education, and life experience that shape how a person experiences health and disability.
VALUE:
🔆A universal language for interdisciplinary communication in rehabilitation.
🔆A standardised framework for describing patient functioning beyond diagnosis.
🔆A biopsychosocial model that bridges medical and social perspectives on disability.
🔆A basis for outcome measurement, goal setting, and evaluation in clinical and research contexts.
APPLICATION:
📝 Structure comprehensive patient assessments.
📝Guide interdisciplinary team communication.
📝Inform goal setting focused on participation and real-world functioning.
📝Support outcome measurement and documentation.
📝Frame research and health reporting.
SUMMARY:
📖The ICF is positioned as a foundational framework for rehabilitation medicine, providing a shared conceptual model and common language that integrates biological, individual, and social dimensions of health. Its strength lies in supporting holistic assessment, enhancing interdisciplinary communication, and prioritising function- and participation-focused outcomes, making it highly applicable to both rehabilitation practice and research.
MW
Reference:
Stucki G, Ewert T, Cieza A. Value and application of the ICF in rehabilitation medicine. Disabil Rehabil. 2002;24(17):932–938.

01/03/2026

Descending modulation of pain
BACKGROUND:
🔎Pain perception is not solely determined by ascending nociceptive input but is dynamically regulated by descending pathways from the brain to the spinal cord. These systems are typically inhibitory, suppressing nociceptive transmission; however, in chronic pain states they may become facilitatory, enhancing spinal nociceptive signalling and contributing to increased pain intensity and persistence.
📍An overview paper by Kirsty Bannister et al. (2020) describes descending pain modulation as a network of brain regions, including the periaqueductal grey (PAG), rostroventromedial medulla (RVM), and the dorsal horn of the spinal cord, which together regulate nociceptive signalling.
CONTEXT:
🧠 Chronic pain is associated with dysfunction in descending modulation, typically involving reduced inhibitory control and increased facilitatory activity. This imbalance contributes to central sensitisation and the persistence of pain even in the absence of ongoing tissue damage. Altered descending modulation is a key feature of nociplastic pain and other chronic pain conditions.
IMPLICATIONS:
👨‍⚕️ Understanding descending modulation helps explain why pain is influenced by psychological, emotional, and contextual factors. It also underpins treatments targeting central mechanisms, which can enhance endogenous inhibitory pathways and restore modulation balance.
SUMMARY:
📖Descending pain modulation is a dynamic brain–spinal cord system that regulates nociceptive transmission through inhibitory and facilitatory mechanisms. Dysfunction in these pathways contributes to chronic pain by amplifying nociceptive signalling and reducing endogenous pain inhibition, highlighting their importance as targets for mechanism-based pain management.
MW
Reference:
Bannister K, Patel R, Hughes S. The descending modulation of pain. Br J Pharmacol. 2020;177(5):1006–1016.

28/02/2026

Nociplastic pain
Part 3: management principles
📍A recent position paper by Hauser & Kosek (2025) provides an overview of the principles of management of chronic pain conditions with predominant nociplastic pain mechanisms.
MANAGEMENT PRINCIPLES (see image):
SUMMARY:
👨‍⚕️ Management of nociplastic pain should prioritse non-pharmacological treatments, including patient education, promotion of self-efficacy, maintenance of normal life activities, and healthy lifestyle habits.
💪 Physical therapy, psychological therapies, and meditative movement approaches are key interventions, with interdisciplinary care recommended for more severe cases.
💊 Pharmacological treatments, such as centrally acting neuromodulators, may be used as adjuncts, while opioids and simple analgesics are generally ineffective and discouraged.
🧠 Management should also address sleep disturbances and comorbid psychological conditions to optimise overall outcomes.
MW
Reference:
Häuser W, Kosek E. Nociplastic pain: facts, controversies and future tasks. J Clin Med. 2021;10(24):1–14.

28/02/2026

Nociplastic pain
Part 2: terminology and algorithm for clinical criteria
TERMINOLOGY:
📝 “Nociplastic pain” is a mechanistic descriptor referring to altered nociceptive processing without clear tissue or nerve damage.
📝 “Chronic primary pain” is a diagnostic classification describing chronic pain as a disease in its own right, often involving nociplastic mechanisms but defined by clinical impact rather than mechanism alone.
📝 “Central sensitisation” is a specific neurophysiological mechanism involving increased CNS responsiveness that may contribute to, but does not fully define, nociplastic pain.
📍A recent position paper by Hauser & Kosek (2025) provides a stepwise approach to classify pain as possible or probable nociplastic pain, based on clinical features rather than definitive biomarkers.
CLINICAL CRITERIA (see image):
APPLICATION:
🔆The criteria form a clinical classification tool, NOT a definitive diagnostic test.
🔆Nociplastic pain may coexist with nociceptive and neuropathic pain (mixed pain states).
🔆The algorithm helps guide mechanism-informed management, emphasising central nervous system–focused treatments such as education, exercise, and psychological approaches
MW
Reference:
Häuser W, Kosek E. Nociplastic pain: facts, controversies and future tasks. J Clin Med. 2021;10(24):1–14.

28/02/2026

Nociplastic pain
Part 1: Facts, controversies and future tasks
DEFINITION:
📝 Nociplastic pain is defined as pain arising from altered nociception without clear evidence of tissue damage or somatosensory system disease (i.e.: not fully explained by nociceptive or neuropathic pain mechanisms).
📍A recent position paper by Hauser & Kosek (2025) provides a summary of the facts, controversies and future directions for the classification and application of nociplastic pain.
FACTS:
🔆Nociplastic pain is characterised by clinical features such as widespread pain, hypersensitivity (hyperalgesia and allodynia), fatigue, sleep disturbance, and cognitive symptoms.
🔆Neurobiological mechanisms include central sensitisation, altered brain connectivity, and dysregulation of descending inhibitory pathways.
🔆Diagnosis is clinical, based on history, symptom patterns, and exclusion of dominant nociceptive or neuropathic mechanisms.
🔆Recognition of nociplastic pain supports multimodal management, including education, exercise, and psychological therapies, rather than tissue-focused interventions alone.
CONTROVERSIES:
⚠️There is ongoing debate regarding the validity, specificity, and clinical utility of the nociplastic pain construct. Critics argue that its mechanisms are incompletely understood and lack definitive biomarkers, raising concerns about diagnostic uncertainty and overlap with nociceptive and neuropathic pain.
⚠️Some question whether nociplastic pain represents a distinct mechanistic category or a descriptive label for unexplained chronic pain, while others caution against overuse or misapplication in clinical settings.
FUTURE TASKS:
👨‍🔬 Future priorities include improving diagnostic criteria, identifying objective biomarkers, and clarifying underlying mechanisms through neurophysiological and imaging research.
👨‍⚕️ There is also a need to develop targeted treatments, refine patient stratification, and improve clinician education to support appropriate recognition and management of nociplastic pain.
MW
Reference:
Häuser W, Kosek E. Nociplastic pain: facts, controversies and future tasks. J Clin Med. 2021;10(24):1–14.

Address

Wonthaggi, VIC
3995

Telephone

+61356725866

Website

facebook.com

Alerts

Be the first to know and let us send you an email when The Musculoskeletal Wrangler posts news and promotions. Your email address will not be used for any other purpose, and you can unsubscribe at any time.

Shortcuts

Want your practice to be the top-listed Clinic in Wonthaggi?

The Story

‘Evidence-based practice’ is a cornerstone of good quality physiotherapy practice.

Whilst completing my post-graduate training in musculoskeletal physiotherapy, I had developed a hunger for keeping up to date with good quality contemporary research.

This page is aimed at providing high quality research reviews and summaries on contemporary topics within the field of musculoskeletal physiotherapy.

Posts within this page are structured to provide ‘easy-to-understand’ information for health professionals and health consumers, and will also endeavour to provide the relevant reference(s) for each discussion.

The Musculoskeletal Wrangler

14/03/2026

09/03/2026

09/03/2026

08/03/2026

08/03/2026

07/03/2026

03/03/2026

02/03/2026

01/03/2026

28/02/2026

28/02/2026

28/02/2026

Address

Telephone

Website

Alerts

Shortcuts

Share

Category

The Story