The Musculoskeletal Wrangler

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.

Analgesic pharmacology seriesPart 6: routes of administrationORAL:🟢Pros: convenient, suitable for long-term use, allows ...
29/09/2025

Analgesic pharmacology series
Part 6: routes of administration
ORAL:
🟢Pros: convenient, suitable for long-term use, allows self-administration
🔴Cons: variable absorption, first-pass metabolism
📝Examples: paracetamol, ibuprofen, oral morphine.
INTRAVENOUS (IV):
🟢Pros: rapid onset, precise plasma control, no first-pass metabolism (ie: 100% bioavailability)
🔴Cons: need for trained personnel, infection risk, less suitable outpatient
📝Examples: IV morphine, fentanyl, ketorolac.
INTRAMUSCULAR (IM):
🟢Pros: moderately rapid absorption, avoids first-pass metabolism
🔴Cons: pain, tissue irritation, variable absorption
📝Examples: IM morphine, certain NSAIDs.
SUBCUTANEOUS:
🟢Pros: slower, sustained absorption, fewer systemic side effects
🔴Cons: limited volume, injection site reactions
📝Examples: subcutaneous morphine, opioids in palliative care.
TRANSDERMAL (eg: pain patches):
🟢Pros: continuous controlled release, convenient
🔴Cons: slow onset, skin irritation, unsuitable for acute pain
📝Examples: fentanyl patch, buprenorphine patch.
RE**AL:
🟢Pros: useful when oral intake is not possible, relatively rapid absorption
🔴Cons: discomfort, variable absorption, social inconvenience
📝Examples: paracetamol, morphine suppositories.
SUBLINGUAL/BUCCAL:
🟢Pros: rapid absorption, bypasses first-pass metabolism
🔴Cons: limited dosing, affected by saliva/oral conditions
📝Examples: sublingual fentanyl, buprenorphine.
INHALATIONAL (eg: puffers)
🟢Pros: very rapid onset, useful for acute/procedural pain
🔴Cons: need for cooperation, specialized equipment, respiratory irritation
📝Examples: nitrous oxide, inhaled opioids.
INTRATHECAL & EPIDURAL:
🟢Pros: potent analgesia with low systemic exposure
🔴Cons: invasiveness, infection & complication risk, specialized monitoring required
📝Examples: intrathecal morphine, fentanyl, bupivacaine.
SUMMARY:
✅Analgesics can be delivered through several routes, each with pros and cons. Choice of route depends on speed, duration, patient condition, and practicality etc.
MW
Reference:
Kim J, Coskun M, Debreli J. Route of administration, distribution, and tissue-specific challenges. In: Organelle and Molecular Targeting. 1st ed. CRC Press; 2021. p. 20.

Analgesic pharmacology seriesPart 5: brain-acting analgesics (overview)SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS (SNR...
29/09/2025

Analgesic pharmacology series
Part 5: brain-acting analgesics (overview)
SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIs):
🔎Mechanism: Increase levels of serotonin and norepinephrine in central descending inhibitory pathways, enhancing pain inhibition.
📝Examples: Duloxetine, Venlafaxine
TRICYCLIC ANTIDEPRESSANTS (TCAs)
🔎Mechanism: Inhibit reuptake of serotonin and norepinephrine, enhancing descending inhibitory pathways. Some TCAs also block sodium channels and NMDA receptors, contributing to analgesia.
📝Examples: Amitriptyline, Nortriptyline
CANNABINOIDS:
🔎Mechanism: Cannabinoids act primarily in the brain and central nervous system by binding to cannabinoid type 1 and type 2 receptors. Type 1 receptors are abundant in areas involved in pain processing, including the periaqueductal gray, thalamus, and dorsal horn of the spinal cord, where they inhibit neurotransmitter release, such as glutamate and substance P, and modulate descending pain inhibitory pathways. Type 2 receptors are mostly peripheral but can influence central inflammation and nociceptive signaling. Cannabinoids also affect the emotional and affective components of pain through pathways in the limbic system.
📝Examples: Tetrahydrocannabinol, cannabidiol, Nabiximols (combination of tetrahydrocannabinol and cannabidiol)
TRIPTANS
🔎Mechanism: Selective serotonin (5-HT1B/1D) receptor agonists that act centrally to induce vasoconstriction of cranial blood vessels and inhibit trigeminal nociceptive neurotransmission, reducing migraine pain.
📝Examples: Sumatriptan, Rizatriptan, Zolmitriptan
OTHERS (dual effects across various aspects of the CNS- see previous posts):
🔆Opioids
🔆NMDA receptor antagonists
🔆Gabapentinoids
🔆Paracetamol
SUMMARY:
✅Analgesics that act on the brain primarily modulate pain perception, affective components of pain, and descending inhibitory pathways, rather than blocking peripheral nociception. Classic examples include opioids, paracetamol, NMDA antagonists, gabapentinoids, SNRIs, and centrally acting adjuvants like tramadol and cannabinoids.
MW
Reference:
Sawynok J, Liu J. Contributions of peripheral, spinal, and supraspinal actions to analgesia. Eur J Pharmacol. 2014;724(1–3):1–10.

Analgesic pharmacology seriesPart 4: agents targeting the spinal cord (overview)OPIOIDS🔎Mechanism: Bind mu-opioid recept...
29/09/2025

Analgesic pharmacology series
Part 4: agents targeting the spinal cord (overview)
OPIOIDS
🔎Mechanism: Bind mu-opioid receptors in the dorsal horn of the spinal cord, inhibiting neurotransmitter release (e.g., substance P, glutamate) from primary afferent neurons and hyperpolarizing postsynaptic neurons, reducing pain transmission.
📝Examples: Morphine, Hydromorphone, Fentanyl, Oxycodone
GABAPENTINOIDS
🔎Mechanism: Bind alpha2-delta subunit of voltage-gated calcium channels in the dorsal horn, reducing excitatory neurotransmitter release and hyperexcitability of spinal neurons.
📝Examples: Gabapentin, Pregabalin
ALPHA2- ADRENERGIC AGONISTS
🔎Mechanism: Activate alpha2-adrenoceptors in the dorsal horn, inhibiting release of nociceptive neurotransmitters and enhancing inhibitory interneuron activity.
📝Examples: Clonidine, Dexmedetomidine
NMDA RECEPTOR ANTAGONISTS
🔎Mechanism: Block N-methyl-D-aspartate (NMDA) receptors in the spinal cord, reducing excitatory neurotransmission and preventing central sensitization associated with chronic pain.
📝Examples: Ketamine
SUMMARY:
✅Spinal analgesics reduce pain by modulating neurotransmission in the dorsal horn, inhibiting excitatory signalling, and enhancing inhibitory pathways. Classic examples include opioids, α2-adrenergic agonists, NMDA antagonists, local anaesthetics, gabapentinoids, and spinal corticosteroids.
MW
Reference:
Carinci AJ, Kamdar MM, Manion SC, Mao J. Mechanisms of Spinal Analgesia. In: Neuroscientific Foundations of Anesthesiology. Oxford University Press; 2011. p. 120–130.

Analgesic pharmacology seriesPart 3: peripherally-acting agents (overview)Paracetamol🔎Mechanism: Inhibits prostaglandin ...
29/09/2025

Analgesic pharmacology series
Part 3: peripherally-acting agents (overview)
Paracetamol
🔎Mechanism: Inhibits prostaglandin synthesis in peripheral tissues under conditions of low peroxides, reducing pain and fever. It has minimal anti-inflammatory activity and also exerts some central effects in the brain and spinal cord.
📝Examples: Paracetamol (acetaminophen)
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
🔆COX-1 inhibitors
🔎Mechanism: Inhibit cyclooxygenase (COX) enzymes, which reduces prostaglandin synthesis and decreases inflammation and peripheral sensitization.
📝Examples: Ibuprofen, Naproxen, Diclofenac, Indomethacin, Ketorolac
🔆COX-2 Selective Inhibitors
🔎Mechanism: Selectively inhibit COX-2 enzymes with less gastric toxicity (and associated adverse events), still reduce peripheral prostaglandins.
📝Examples: Celecoxib, Etoricoxib, Parecoxib
TOPICAL AGENTS:
🔎Mechanism: Act locally to reduce nociceptor activation or inflammation.
📝Examples: Capsaicin (depletes substance P in nociceptors), Lidocaine patches/cream, NSAID gels (diclofenac gel, ibuprofen gel)

LOCAL ANAESTHETICS (LAs):
🔎Mechanism: Block voltage-gated sodium channels to prevent peripheral nociceptor depolarization and thereby inhibit pain signal initiation.
📝Examples: Lidocaine, Bupivacaine, Ropivacaine
SUMMARY:
✅Peripheral analgesics mainly reduce inflammation, block nociceptor activation, or act locally at the injury site. Classic examples include NSAIDs, COX-2 inhibitors, local anaesthetics, topical agents, and peripherally restricted opioids (uncommon).
MW
Reference:
Sawynok J. Topical and peripherally acting analgesics. Pharmacol Rev. 2003;55(1):1–20.

Analgesic pharmacology seriesPart 2: basic neuroanatomy of the 'pain pathway'🔎Before exploring the full range of pharmac...
22/09/2025

Analgesic pharmacology series
Part 2: basic neuroanatomy of the 'pain pathway'
🔎Before exploring the full range of pharmacological analgesic interventions and their sites of action within the nervous system, let’s first review the basic neuroanatomy of the pain pathway (see image)
📍“Explain pain” by Moseley and Butler provides an excellent, evidence-based resource for patients and clinicians alike for assisting in understanding a model of the ‘pain pathway’
It begins in the PNS, with:
TRANSDUCTION, TRANSMISSION & NOXIOUS DETECTION:
🔆Nociceptors in peripheral tissues detect potentially harmful stimuli (mechanical, thermal, or chemical) and send signals via A-delta and C fibers to the spinal cord.
SPINAL RELAY & MODULATION:
🔆Incoming signals are processed in the dorsal horn, where excitatory and inhibitory interneurons integrate peripheral input with descending signals from the brain. This modulation can amplify or dampen nociceptive transmission.
ASCENDING PATHWAYS:
🔆Signals travel to the brain through multiple tracts (e.g., spinothalamic, spinoreticular), reaching areas such as the thalamus, somatosensory cortex, insula, anterior cingulate cortex, and amygdala.
BRAIN INTEGRATION (NEUROMATRIX):
🔆The brain integrates sensory input with contextual information, such as prior experience, attention, emotion, and expectation in order to generate the subjective experience of pain as a conscious output of the brain. Essentially, the brain decides whether to produce a pain experience.
DESCENDING MODULATION:
🔆The brain can either suppress (inhibitory) or facilitate (excitatory) nociceptive signals via descending pathways, explaining why the same injury can be perceived differently depending on context, stress, or attention.
👉🏻Throughout this series, we will examine how different analgesic medications act on specific components of the ‘pain pathway’
MW
Reference:
Butler DS, Moseley GL. Explain Pain [eBook]. 2nd ed. Adelaide: Noigroup Publications; 2013.

Analgesic pharmacology seriesPart 1: drug administration routes📍Pharmacology mentor provides a useful overview of the ad...
20/09/2025

Analgesic pharmacology series
Part 1: drug administration routes
📍Pharmacology mentor provides a useful overview of the administration routes of drugs, which is an essential aspect of medical practice.
LOCAL vs. SYSTEMIC
📝While local administration delivers drugs directly to target tissues, systemic administration introduces the drug into the bloodstream, allowing it to circulate throughout the body and act on multiple sites.
📝Local delivery minimizes systemic exposure and side effects, whereas systemic administration relies on absorption, distribution, metabolism, and excretion to achieve effective plasma concentrations.
FACTORS:
🔆Physical and chemical properties of the drug, incl. solubility, stability, pH, irritancy etc.
🔆Site of desired action and effect: localised vs systemic
🔆Rate, speed and extent of absorption
🔆First-pass metabolism considerations (eg: oral)
🔆Patient condition (ie: conscious vs. unconscious etc)
👉🏻Next we will explore each of the major classifications of analgesics, their mechanisms of effect, alongside any special considerations.
MW
Reference:
https://pharmacologymentor.com/understanding-drug-administration-routes-and-factors-influencing-their-choice/?utm_source=chatgpt.comaol

Self-management for low back pain (LBP)Part 2: 📍A recent masterclass paper by Kongsted et al. (2021) explored the action...
18/09/2025

Self-management for low back pain (LBP)
Part 2:
📍A recent masterclass paper by Kongsted et al. (2021) explored the action steps clinicians can take in order to facilitate and enable self-management in clinical practice.
PLAN:
🔆Let patient value-based goals guide management
🔆Enable shared decision-making
🔆Define readiness for change, identify and mitigate barriers and challenges
DELIVER:
🔆Help patients make sense of their symptoms, reduce fear and address misconceptions
🔆Teach skills to address everyday problems, incl. exercises and self-mgmt strategies
🔆Set patients up for success, explore new and feared activities
EVALUATE:
🔆Reflect on goals and adjust accordingly
🔆Explore patient understanding and experiences
🔆Assist in action planning, such as, flare up plans and broader integration with ADLs, goals and social connection etc.
MW
Reference:
Kongsted A, Ris I, Kjaer P, Hartvigsen J. Self-management at the core of back pain care: 10 key points for clinicians. Brazilian Journal of Physical Therapy,2021;25:396-406.

Self-management for low back pain (LBP)Part 1: BACKGROUND:📝There has been a significant paradigm shift from clinician-le...
16/09/2025

Self-management for low back pain (LBP)
Part 1:
BACKGROUND:
📝There has been a significant paradigm shift from clinician-led management to self-management for individuals with chronic conditions. However, there is currently no clear evidence indicating how self-management of low back pain (LBP) can be most effectively supported in clinical practice.
📍A recent masterclass paper by Kongsted et al. (2021) explored the inherent principles that should underpin self-management in clinical practice.
PRINCIPLES:
🔆Patients should self-manage most of the time!
🔆Its not all about back pain! Consider general health, function, participation and quality of life.
Clinicians should…
🔆Support patient autonomy
🔆Help develop patient self-efficacy
🔆Foster an environment conducive to self-management
ACTIONS:
Clinicians should…
🔆Be patient-centred: letting patient values and goals guide-management
🔆Help patients make sense of their problem (incl. symptoms)
🔆Teach skills and provide tools for pain-management
👉🏻Next, we’ll explore the steps a clinician can take to foster effective self-management support.
MW
Reference:
Kongsted A, Ris I, Kjaer P, Hartvigsen J. Self-management at the core of back pain care: 10 key points for clinicians. Brazilian Journal of Physical Therapy,2021;25:396-406.

Cellular mechanisms of painPart 1: Sensory neurons and nociceptors📍A detailed paper by Basbaum et al. (2009) provides a ...
31/08/2025

Cellular mechanisms of pain
Part 1: Sensory neurons and nociceptors
📍A detailed paper by Basbaum et al. (2009) provides a comprehensive overview of the cellular and molecular mechanisms of pain. This includes an important update on basic principles and processes that underpin the neurophysiology of pain.
NOCICEPTORS:
Two major classes:
🔆A-delta (medium diameter) myelinated afferents that mediate acute, well-localised “first”, or fast pain
🔆C-fibers (small diameter) unmyelinated afferents that convey poorly localised “second”, or slow pain
Other sensory neurons:
🔆A-beta fibers (large diameter) myelinated afferents that convey innocuous mechanical stimuli (eg: light touch) – can be recruited in pain processing!
NOCICEPTOR DIVERSITY (figure 3):
📝Nociceptor subtypes are designed to detect one or more stimuli, eg: sensitivity to:
Heat (TRPV1), cold (TRPM8), acids (ASICs) and chemical irritants (TRPA1).
CONNCETIONS TO SPINAL CORD (figure 1):
📝Very precise laminar organisation of the dorsal horn of the spinal cord where primary afferents converge and transmit incoming impulses (noxious and non-noxious).
ANATOMY OF PAIN PATHWAY (figure 2):
📝Primary afferents convey noxious information to projection neurons within the dorsal horn and through to the somatosensory cortex via ascending pathways and the thalamus.
CONCLUSION:
✅Understanding the anatomical and neurophysiological mechanisms of pain is essential for accurately diagnosing pain disorders and developing targeted, effective treatments that address both peripheral and central contributors to pain.
MW
Reference:
Basbaum AI, Bautista DM, Scherrer G, Julius D. Cellular and molecular mechanisms of pain. Cell,2009;139:267-284.

Chronic regional pain syndrome (CRPS)Part 4: symptom mechanisms & differential diagnosis📍An update article by Birklein &...
23/08/2025

Chronic regional pain syndrome (CRPS)
Part 4: symptom mechanisms & differential diagnosis
📍An update article by Birklein & Schlereth (2015) provides an overview of CRPS, including key considerations for symptomatology and differential diagnosis.
DIAGNOSTIC CRITERIA:
📝Continuing pain, disproportionate to any inciting event (especially trauma)
📝At least 1 sign and 1 symptom:
🔆Sensory: hyperalgesia and/or allodynia
🔆Vasomotor: temperature and/or colour changes
🔆Sudomotor/oedema: sweating and/or oedematous changes
🔆Motor/trophic: altered motor function (eg: ROM, strength, tremor, dystonia) or trophic changes (eg: hair, nails, skin).
SYMPTOM MECHANISMS & DIFFERENTIAL DIAGNOSIS: (see image)
Reference:
Birklein F & Schlereth T. Complex regional pain syndrome–significant progress in understanding. Pain,2015;S94-S103.

Chronic regional pain syndrome (CRPS)Part 3: management📍An update article by Birklein & Schlereth (2015) provides an ove...
23/08/2025

Chronic regional pain syndrome (CRPS)
Part 3: management
📍An update article by Birklein & Schlereth (2015) provides an overview of CRPS, including key considerations for management.
UPDATE:
🔎CRPS is a chronic and complex pain condition that typically affects a limb after injury, surgery, or immobilization, in which the pain is often disproportionate to the original event. Its multifactorial pathophysiology encompasses neuroinflammation, autoimmunity and central sensitisation, along with autonomic and vascular dysregulation.
MANAGEMENT OVERVIEW:
📝Chronic CRPS is most likely to respond to comprehensive, integrated multidisciplinary treatment that includes, medical, psychological, physical and occupational therapy components. Treatment mechanisms should be individually-tailored to target peripheral and/or central mechanisms underpinning the disorder.
PERIPHERAL INFLAMMATION:
🔆High dose bisphosphonates (eg: oral: alendronate, IV: pamidronate, clodronate, ibandronate)
🔆Oral glucocorticoids
🔆IV polyvalent immunoglobulins
🔆Topical dimethyl sulfoxide
🔆Physical and sensory-integrative occupational therapy
CENTRAL NEUROPLASTIC CHANGES:
🔆Physiotherapy and cognitive-behavioural therapies (incl. mirror therapy, graded motor imagery, graded exposure/pain exposure therapies
🔆IV ketamine and/or intrathecal baclofen
🔆Oral antidepressants, anticonvulsants and/or opioids
🔆Spinal cord stimulation
👉🏻More high quality research and clinical practice guidelines are required!
MW
Reference:
Birklein F & Schlereth T. Complex regional pain syndrome–significant progress in understanding. Pain,2015;S94-S103. dcaluird

Chronic regional pain syndrome (CRPS)Part 2: pathophysiological and aetiological factors📍A comprehensive article by Brue...
23/08/2025

Chronic regional pain syndrome (CRPS)
Part 2: pathophysiological and aetiological factors
📍A comprehensive article by Bruehl (2015) provides an in-depth overview of CRPS, including its pathophysiological mechanisms, aetiological factors and key considerations for assessment and management.
CLASSIFICATION:
🔎CRPS type I- no identifiable evidence of nerve injury
🔎CRPS type II- evidence of nerve injury
PATHOPHYSIOLOGY (see image):
📝A largely unknown, multifactorial process involving both peripheral and central mechanisms along with a plethora of other potential mechanisms, including:
🔆Central and peripheral sensitisation
🔆Altered sympathetic NS function and sympatho-afferent coupling
🔆Inflammatory and immune factors
🔆Brain changes: altered somatosensory representation, motor cortex disinhibition, reduced grey matter volume etc.
🔆Genetic factors
🔆Psychological factors: comorbid psychiatric disorders (eg: major depression), anxiety, anger expression, distress
👉🏻Next, we will explore the various treatment options for this complex syndrome.
MW
Reference:
Bruehl S. Complex regional pain syndrome. BMJ,2015;350:h2730.

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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.