Osteopathy Journals and Research by Darren Chandler


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  1. Median nerve (Meyer et al 2018)

    Anatomy of the median nerve

    Nerve roots and cords

    C6-C7: lateral cord. C8-T1: medial cord.

    Fibers in the lateral cord (from the lateral roots) convey most of the sympathetic fibers to the median distribution of the hand (Standring 2017).


    After originating from the brachial plexus in the axilla, the median nerve lies laterally to the brachial artery and then crosses it anteriorly to medially.

    The lower head of the coracobrachialis which is usually suppressed in human beings is sometimes present as the ligament of Struthers. The median nerve and brachial artery passes deep to this ligament.

    After entering the cubital fossa the nerve passes in relation to:

    • Bicipital aponeurosis (aka lacertus fibrosus): the nerve passes beneath the bicipital aponeurosis.

    • Brachialis: passes over the brachialis.

    • Pronator teres: passes between the two heads of the pronator teres.

    In the anterior antebrachial compartment the nerve passes in relation to:

    • Flexor digitorium superficialis: runs under the aponeurotic arch of the flexor digitorum superficialis. Just proximal to the aponeurotic arch of the flexor digitorium superficialis the median nerve gives off the anterior interosseous nerve which innervates the deep flexors in the forearm.

    • Flexor digitorum superficialis and profundus: courses between the flexor digitorum superficialis and profundus muscles.

    In the distal forearm, 3cm proximal to the wrist crease, the median nerve gives rise to the palmar cutaneous branch.This nerve provides sensory innervation to the skin on the proximal side of the palm.

    In the wrist the median nerve passes under the flexor retinaculum into the carpal tunnel.

    Distal to the carpal tunnel the median nerve subdivides into five branches: the recurrent motor branch to the muscles of the thenar compartment and four digital sensory branches.

    The median nerve is palpable:

    • After emerging from the coracobrachialis.
    • Deep to the bicipital aponeurosis.
    • At the wrist where it emerges from behind the superficial flexor tendons just lateral to the palmaris longus.


    Motor function to the forearm.

    Motor and sensory function to the wrist and hand.

    Cutaneous innervation: thenar eminence, lateral side of the palm, palmar side of the 1-3 fingers and lateral 4.

    Anatomy of the carpal tunnel

    The boundaries of the carpal tunnel are:

    • Posteriorly: carpal bones.
    • Laterally: tubercle of scaphoid and trapezium.
    • Medially: pisiform and hook of the hamate.
    • Anterior: the roof of the tunnel is the transverse carpal ligament or flexor retinaculum. The flexor retinaculum is divided into two layers (1) superficial. Formed by the palmaris brevis tendon (2) deep. Made up of transversal fibers.

    The carpal tunnel contains:

    • Tendons: flexor pollicis longus, the four flexor digitorum superficialis tendons and the four flexor digitorum profundus tendons.
    • Neurological: median nerve. Travels between the flexor retinaculum and the flexor tendons of 2 and 3 fingers.

    Entrapment sites of the median nerve

    Entrapement sites of the median nerve are:

    • Carpal tunnel: 90-93% of median nerve entrapments.

    • Supracondylar process continued by the ligament of Struthers: the ligament of Struthers extends from supracondylar process --> medial epicondyle. It encases neurovascular structures including the median nerve, brachial artery, ulnar nerve, ulnar artery and a branch of the musculocutaneous nerve.

    • The bicipital aponeurosis (lacertus fibrosus): extends from the myotendinous junction of the distal bicep to the medial deep fascia of the forearm close to the epicondylar muscles. Covers the median nerve and the brachial artery.

    • Pronator teres: the median nerve runs between the humeral and ulnar heads of the pronator teres.

    • Fibrous arch of the origin of the flexor digitorum superficialis.

    Anatomical variations in the forearm causing entrapment of the median nerve.

    • Accessory head of the flexor pollicis longus.

    • Accessory head of the flexor digitorum profundus.

    • Bicipital bursa.

    Anatomical variations in the carpal tunnel causing entrapment of the median nerve:

    • Accessory palmaris longus.

    • Accessory palmaris profundus.

    • Accessory flexor digitorum muscle.

    • Accessory lumbricals.

    Ulnar nerve (Choi et al (2018)

    Anatomy of the ulnar nerve

    Nerve root and cords

    (C7: lateral cord). C8-T1: medial cord


    Travels medial to the brachial arttery up until the insertion of the coracobrachialis. It then pierces the medial intermuscular spetum, at the arcade of Struthers, 10cm proximal to the medial epicondyle, to enter the posterior compartment of the arm.

    The arcade of Struthers is a fibrous canal on the medial aspect of the lower third of the arm. It consists of the medial head of the triceps (and its fascial sheath) and its aponeurotic expansion which extends into the medial intermuscular septum and internal brachial ligament* (Caetano et al 2017). Because the arcade of Struthers is just a passage way through the medial intermuscular septum for the ulnar nerve to pass into the posterior compartment of the arm Caetano et al (2017) described it as an 'unfolding' of the medial intermuscular septum.

    *: Internal brachial ligament: medial intermuscular septum proximally --> medial intermuscular septum distally (near medial epicondyle).

    It then continues posterior to the medial epicondyle in the cubital tunnel.

    After leaving the cubital tunnel the ulnar nerve crosses the medial collateral ligament of the elbow before entering the forearm.

    Ulnar nerve entered the forearm between the humeral and ulnar origin of the flexor carpi ulnaris.

    The nerve then traveled into a deep fascia septum between the anterior surface of the flexor carpi ulnaris and the posterior surface of the flexor digitorum superficialis. The deep fascia is an anatomically tough structure that lies immediately against the course of the ulnar nerve.

    The ulnar branches to the flexor carpi ulnaris arise proximal to the septum between the flexor carpi ulnaris and flexor digitorum superficialis.

    More distally branches to the flexor digitorum profundus pierced this fascial septum while en route to the posterior surface of this muscle’s ulnar one half.

    The dorsal cutaneous nerve arises from the ulnar nerve 6cm proximal to the ulnar styloid process.

    At the wrist the ulnar nerve divides into superficial (sensory) and deep (motor) components both of which pass through Guyon's canal.

    The ulnar nerve is palpable at:

    • Posterior to the medial epicondyle.
    • At the wrist as it emerges from under the flexor carpi ulnaris.

    Anatomy of the cubital tunnel

    Machhi et al (2014) identified the cubital tunnel as being bordered by:

    • Medially: humeral and ulna heads of the flexor carpi ulnaris.
    • Anteriorly: medial epicondyle.
    • Roof*: arcuate ligament of Osborne. This 'ligament' is a fusion of the deep fascia of the flexor carpi ulnaris and antebrachial fascia spanning from the medial epicondyle --> olecranon process.

    *: Traditionally the roof of the cubital tunnel has been defined by the presence of the arcuate ligament of Osbrone. However Macchi et al (2014) found the roof of the cubital tunnel to be formed from a myofascial trilaminar retinaculum: 

    • Layer one: a layer of loose connective tissues corresponding to the deep fascia. 

    The ulna nerve is covered in a fibrous thickening of brachial fascia. This fascia is at the border between the muscle and the tendon 5 cm from the joint line of the elbow. 

    This thickening of the brachial fascia is formed by two laminae of fibres:

    Lamina one: arises from the triceps fascia. It bridges the elbow attaching from the medial epicondyle to the olecranon process to then spread into the antebrachial fascia.

    Lamina two: appears between the medial intermuscular septum and the triceps.

    • Layer two: a layer of connective tissue corresponding to a tendineous structure.
    • Layer three a bundle of muscle.

    Layer two and three (the tendineous and muscular components) correspond to the triceps proximally and flexor carpi ulnaris distally.

    Anatomy of the Guyons's canal

    Guyon's canal is a fibrosseous tunnel. It's formed by the transverse carpal ligament at the proximal aspect of the pisiform --> origin of the hypothenar eminence at the hook of the hamate.

    Sites of entrapment

    • Arcade of Struthers: it is controversial whether this site is a potential cause for ulnar nerve entrapment. However could it be a potential point of tethering effecting the gliding movement of the nerve?. 
    • Cubital tunnel. Macchi et al (2014) found pathological fusion of the trilaminar roof of the cubital tunnel reduces gliding of the ulnar nerve during movements of the elbow joint.

    • Flexor/pronator muscle origin: formation of “tendinous bands” at the humeral and ulnar head of the flexor carpi ulanris/pronator muscle origin.

    • Macchi et al (2014) found fascial structures (fibrous bands) over the ulnar nerve in the proximal forearm.
    • Medial intermuscular septum: the medial intermuscular septum runs between the flexor carpi ulnaris and flexor digitorum profundus muscles. The ulnar nerve can suffer proximal and distal compression by the medial intermuscular septum.

    • Intermuscular aponeurosis: the intermuscular aponeurosis runs between the flexor digitorum superficialis and flexor carpi ulnaris.

    • Deep fascia septum between the anterior surface of the flexor carpi ulnaris and the posterior surface of the flexor digitorum superficialis: whilst Choi et al (2018) found no ulnar nerve compression by this fascial septum with elbow extension some angulation of the proximal ulnar nerve was noted due to its intimate connection to the deep fascia.

    • Fibrous aponeurosis between the flexor digitorum superficialis and the humeral head of the flexor carpi ulnaris. 

    • Anconeus epitrochlearis muscle. Macchi et al 2014 found this muscle to not always be present.

    Because of the medial head of triceps relation to the arcade of Struthers and the roof of the cubital tunnel (myofascial trilaminar retinaculum) could this explain the similarities in ulnar nerve symptoms and myofascial symptoms of the medial head of triceps.


    The Median Nerve at the Carpal Tunnel … and Elsewhere (2018). Philippe MeyerPierre-Francois LintingreLionel PesquerNicolas PoussangeAlain Silvestre, and Benjamin Dallaudière.

    The Deep Fascia of the Forearm and the Ulnar Nerve: An Anatomical Study (2018). Paul J ChoiChidinma NwaogbeJoe IwanagaGeorgi P GeorgievRod J Oskouian, and R. Shane Tubbs.

    The cubital tunnel: a radiologic and histotopographic study (2014). Veronica MacchiCesare TiengoAndrea PorzionatoCarla SteccoGloria SarasinShane TubbsNicola Maffulli, and Raffaele De Caro

  2. The following is based on the work: Complex regional pain syndrome: a recent update (2017). En Lin Goh, Swathikan Chidambaram, and Daqing Ma


    CRPS types I and II that are characterised by the absence or presence of identifiable nerve injury.

    • CRPS type I: usually develops after an initiating noxious event. Is not limited to the distribution of a single peripheral nerve, and is disproportionate to the inciting event. Associated with oedema, changes in skin blood flow, abnormal sudomotor activity in the region of the pain, allodynia and hyperalgesia and commonly involves the distal aspect of the affected extremity or with a distal to proximal gradient.
    • CRPS type II: defined as a burning pain, allodynia and hyperpathia occurring in a region of the limb after partial injury of a nerve or one of its major branches innervating that region


    CRPS occurs most frequently in: 

    • 61 to 70 yoa.
    • < female (3x more females than males).
    • Increased preponderance for the upper limbs with a ratio of 3:2 compared to the lower limbs.
    • Risk factors: menopause, history of migraine, osteoporosis, asthma and angiotensin-converting enzyme (ACE) inhibitor therapy and elevated intracast pressure due to a tight case or extreme positions.
    • Prognosis poorer in smokers. 



    Acute phase of CRPS supports the hypothesis that the development of this condition is due to an exaggerated inflammatory response to trauma.

    Clinical findings reveal the five cardinal signs of inflammation:  pain, oedema, erythema, increased temperature and impaired function.

    Tissue trauma triggers the release of pro-inflammatory cytokines such as interleukin(IL)-1β, IL-2, IL-6 and tumour necrosis factor-α (TNF-α) along with neuropeptides including calcitonin gene-related peptide, bradykinin and substance P. These substances increase plasma extravasation and vasodilation, producing the characteristic features of acute CRPS

    Altered cutaneous innervation

    Initial neuronal injury, however imperceptible has been implicated as an important trigger in the development of both CRPS types I and II.

    This has been supported by studies demonstrating a reduction in C-type and Aδ-type cutaneous afferent neuron fibre density in the CRPS-affected limb compared to the unaffected limb, with these changes primarily affecting nociceptive fibres.

    The decrease in C-type and Aδ-type fibres was associated with an increase in aberrant fibres of unknown origin, and it has been postulated that the exaggerated pain sensation may be due to altered function of these fibres

    Central and peripheral sensitisation

    Following tissue damage and/or neuronal injury, alterations in the central and peripheral nervous systems lead to increased inflammation, and an enhanced responsiveness to pain. These adaptations act as protective mechanisms to promote avoidance of activities that cause further injury.

    Within the central nervous system (CNS), persistent and intense noxious stimulation of peripheral nociceptive neurons results in central sensitisation.

    Accordingly, there is alteration in nociceptive processing in the CNS and increased excitability of secondary central nociceptive neurons in the spinal cord.

    This is mediated by the release of neuropeptides such as substance P, bradykinin and glutamate by peripheral nerves, which sensitise and increase the activity of local peripheral and secondary central nociceptive neurons resulting in increased pain from noxious stimuli (hyperalgesia) and pain in response to non-noxious stimuli (allodynia).

    Research has shown that CRPS patients have a significantly greater windup to repeated stimulation of the affected limb compared to the contralateral limb or other limbs.

    Altered sympathetic nervous system function

    In the chronic (cold) phase of the clinical course of CRPS, the CRPS-affected limb is cyanosed and clammy as a result of vasoconstriction and sweating. This suggests that excessive sympathetic nervous system outflow is a driving factor in progression of the condition and maintenance of the pain.

    Expression of adrenergic receptors on nociceptive fibres following injury may contribute to sympatho-afferent coupling increasing the pain intensity

    Circulating catecholamines

    Variation in the clinical features of CRPS as the condition progresses from the acute (warm) phase to the chronic phase may be attributed to alterations in catecholaminergic mechanisms.

    During the acute phase, the CRPS-affected limb demonstrates a reduction in the levels of circulating plasma norepinephrine compared to the unaffected limb.

    As a result, there is compensatory upregulation of peripheral adrenergic receptors causing supersensitivity to circulating catecholamines. Consequently, excessive vasoconstriction and sweating occurs following exposure to catecholamines, giving rise to the characteristic cold and blue extremity seen during the chronic phase.


    The presence of immunoglobulin G (IgG) autoantibodies against surface antigens on autonomic neurons in the serum of patients with CRPS suggests that autoimmunity may play a role in the development of this condition.

    This is supported by the results of a small pilot trial where patients with CRPS who were given intravenous immunoglobulin treatment demonstrated a significant reduction in pain symptoms when compared with those given a placebo.

    Brain plasticity

    Neuroimaging studies of patients with CRPS have demonstrated a decrease in area representing the CRPS-affected limb in the somatosensory cortex compared to the unaffected limb.

    The sensory representation of the affected limb, as part of the Penfield homunculus is distorted, with shrinkage and shifting of the area.

    The extent of reorganisation bears significant correlation with the pain intensity and degree of hyperalgesia experienced by the patient, and these alterations return to normal following successful CRPS treatment.

    Genetic factors

    Although there is a lack of consensus regarding the influence of genetic factors in CRPS, family studies have suggested a genetic preponderance towards developing this condition.

    Psychological factors

    Due to the prevalence of anxiety and depression in patients with CRPS and the unusual nature of symptoms, psychological factors have been hypothesised to play a role in the development or propagation of CRPS.


    Physical and occupational therapy

    Physical and occupational therapy is a key component of the rehabilitation process in patients with CRPS and is recommended as the first-line treatment. Patients can develop kinesophobia and the aim of therapy is to overcome this fear of pain and enable the patient to gain the best functional use of the limb. 

    Psychological therapy

    Chronic pain affects the health-related quality of life and places a huge emotional and psychological burden on patients. Thus, it is essential for newly diagnosed patients with CRPS to have a discussion with a psychological care provider regarding their condition and its progression as well as the need for active self-management and participation in a care plan

    Medical management

    • Corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDs) reduce inflammation and have been used in the treatment of CRPS.
    • Anti-oxidants in the treatment of CRPS has been based on the perception that oxygen free radicals generated by the inflammatory process may be a key component of the propagation of the disease process.
    • Anti-convulsant drugs such as gabapentin
    • NMDA (ketamine): the central sensitisation and alteration of brain plasticity that occurs could potentially be reversed with the use of the NMDA receptor antagonist ketamine.
    • Placebo-controlled studies have shown both topical and intravenous administration of ketamine to be effective at alleviating pain and inducing complete remission in treatment resistant patients, thereby highlighting the potential of this approach
    • Phenoxybenzamin: sympathetically mediated pain in CRPS has led to the studies investigating the role adrenergic receptor antagonists or alpha-2 adrenergic agonists in treating this condition.
    • Nifedipine: calcium-channel blockade with nifedipine has been reported to be effective in managing the vasoconstriction occurring in this phase of CRPS 
    • Calcitonin preserves bone mass, has effects on microvasculature and has anti-nociceptive effects, which have been found to be effective in treating acute and chronic pain. Bisphosphonates inhibit osteoclasts, slowing down bone resorption and increasing bone mineral density and are well-established to be effective at providing pain relief. 
    • Opiods: there are contrasting views regarding the use of opioid therapy in the treatment of CRPS. 
    • Intravenous immunoglobulin (IVIG): The discovery of autoantibodies against adrenergic receptors suggesting that CRPS has an autoimmune component provides the basis for the use of intravenous immunoglobulin (IVIG), which is a potent anti-inflammatory and immune-modulator

    Anaesthesia therapy

    An alternative approach studied involves the use of sympathetic blockade, which has diagnostic and therapeutic benefits.

    Surgical management

    • Neuromodulation (spinal cord stimulation): may play a role in treating CRPS, especially in patients in unresponsive to sympathetic blockade.
    • Sympathectomy (including radiofrequency sympathectomy).

    Emerging treatments

    • Immunomodulation (anticancer drugs)

    Chronic regional and neurogenic inflammation are thought to play a key role in the initiation and propagation of CRPS.

    Patients suffering from this condition display systemic elevation of pro-inflammatory cytokines and a corresponding reduction in the anti-inflammatory cytokine IL-10.

    Anti-cancer drugs such as lenalidomide and thalidomide possess anti-inflammatory and immunomodulatory effects and have shown promise in alleviating this condition.

    • Hyperbaric oxygen therapy

    The anti-nociceptive effect of hyperbaric oxygen therapy (HBOT) has been well-documented in animal models. 

    • Botulinum toxin-A (BTX-A)

    BTX-A has been shown to confer pain relief in neuropathic pain, which complicates disorders of the central and peripheral nervous system and may therefore demonstrate efficacy in managing CRPS. 

    • Plasma exchange

    Recent developments in the understanding of the autoimmune aetiology of CRPS have highlighted the potential use of plasma exchange therapy, which has demonstrated benefit in other autoimmune disorders.