Osteopathy Journals and Research by Darren Chandler


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  1. 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.




  2. Diaphragm

    Surface anatomy of diaphragm

    Standring (2015) found the surface anatomy of the diaphragm to be at end tidal inspiration to extend down to the right 5th intercostal space and left r6 both in the midlclavicular line. It can range from the 4th intercostal space to below the costal margin.

    Anatomy of the thorax and diaphragmatic rib attachments

    5th intercostal space attaches onto the lower part of the manubrium. It is formed between r5 and r6.

    r7 costal cartilage forms the upper and lateral part of the epigastrium.

    Diaphragmatic attachment to the ribs are r6-12.

    Stomach (gastro-oesophageal margin) (Standring 2015)

    Left of the midline posterior to the left r7 costal cartilage (upper and lateral part of the epigastrium). This is at the level of T11 (range T10-L1/2). Lower in females and higher in the obese.

    Duodenum (Standring 2015)

    The transpyloric plane (half way between xiphisternum --> umbilicus) lies at L1. This is the landmark that is palpated around to locate the duodenum:

    • D1: sometimes ascends above the transpyloric plane (L1).
    • D2: just to right of the midline L2-3.
    • D3: crosses the midline at L3.
    • D4: ascends to the left side of L2 reaching the transpyloric plane (L1).
    • D/J flexure: left side of L1 (T11-L3). 

      Suspensory ligament of the duodenum (ligament of Trietz): right crus of the diaphragm --> connective tissue around the superior mesenteric artery & coeliac artery --> D/J flexure. Suspends the D/J flexure. The surface anatomy of this ligament as well as its relations with the root of the small intestine mesentery, transverse mesocolon and renal fascia is discussed in 'superior mesenteric artery'.

    Small intestine mesentery

    Anatomy of the small intestine mesentery

    Coffey and O’Leary (2017) found the mesentery to be suspended by the superior mesenteric artery alone, with a resultant tendency to twist around it. This suspension from the artery holds the mesentery up preventing it from collapsing down into the pelvis.

    From this location, the mesentery fans out to span the entire gastrointestinal tract from the D/J junction to its termination at the distal mesorectum. Interestingly the attachments these authors describe parallel the work of Leonardo da Vinci.

    The mesentery of the small and large intestine is thus likened to a Chinese fan.

    The handle of the fan is the mesenteric root twisted around the superior mesenteric artery.

    The leaves of the fan, the small intestine mesentery, flatten against the posterior abdominal wall, attached to it by a peritoneal reflection. This attachment is a line running from just to the left of L1 between T11-L3 (paralleling the D/J flexure on the posterior abdominal wall) and extends obliquely down to the right anterior sacroiliac region (paralleling the I/C junction on the posterior abdominal wall) and then onto the small intestine.

    These leaves of the small intestine mesentery continue laterally forming the large intestine mesentery the mesocolon. 

    Okino et al (2001) found the root of the mesentery contiguous with:

    • Superiorly: hepatoduodenal ligament around the superior mesenteric vein and portal vein*.
    • Anteriorly: transverse mesocolon around the gastrocolic trunk and uncinate process of the pancreas. The gastrocolic trunk represents the convergence of the transverse mesocolon, greater omentum, and mesenteric root (Aldouri 2017).
    • Posterolaterally: ascending and descending mesocolons (anterior pararenal space).
    • Superior mesenteric artery and vein and the gastrocolic trunk pass through the root of the mesentery (Aldouri 2017)

    *: the portal vein is formed at the confluence of the splenic vein and superior mesenteric vein. It passes into the liver via the hepatoduodenal ligament at the liver hilum.

    The attachments of the root of the small intestine mesentery, transverse mesocolon, suspensory ligament of the duodenum (ligament of treitz) and anterior kidney fascia to the superior mesenteric artery is discussed under 'superior mesenteric artery'.

    Surface anatomy of the root of the small intestine mesentery

    The surface anatomy of the root of the small intestine mesentery is:

    • Root of the small intestine mesentery at the superior mesenteric artery: transpyloric plane close to the left midclavicular-umbilical line (left side of L1).
    • Follows an oblique line to attaching to the posterior abdominal wall by peritoneal reflections to ....
    • Termination of the small intestine mesentery at the right iliac fossa (anterior to the right sacroiliac joint): I/C junction

    Large Intestine 

    Anatomy of the mesocolon

    The mesocolon attaches the large intestine to the posterior abdominal wall and superior mesenteric artery.

    Coffey et al (2015) found the ascending and descending mesocolon attaches the ascending and descending colon to the posterior abdominal wall via Toldt's fascia and the transverse mesocolon attaches the transverse mesocolon to the superior mesenteric artery.

    The attachments of the ascending and descending mesocolon to Toldt's fascia is by its flattening against this tissue rather than by strong fibrous bonds.

    The descending mesocolon is continuous at its superior end with the transverse mesocolon and at its inferior end with the mesosigmoid and mesorectum (+ Chang et al 2019).

    The mesorectum is the fat surrounding the rectum. It blends superiorly with the sigmoid mesentery and extends down to the levator ani. It is enclosed by the mesorectal fascia.  

    The attachments of the transverse mesocolon, root of the small intestine, suspensory ligament of the duodenum (ligament of treitz) and anterior renal fascia is discussed under 'superior mesenteric artery'.

    Surface anatomy of the large intestine

    The surface anatomy of the large intestine corresponds to the midclavicular line (lateral border of rectus abdominis) and the transpyloric plane:

    • Ascending colon: on and just to the right of the midclavicular line.
    • Transverse colon: middle section goes through the transpyloric plane*.
    • Descending colon: on and just to the left of the midclavicular line.

    Appendix: right lower quadrant abdomen. Highly variable. Rarely McBurney’s point.

    *The middle section of the transverse colon going through the transpyloric plane corresponds to the transverse mesocolon attachments to the superior mesenteric artery (transpyloric plane close to the left midclavicular-umbilical line, refer 'superior mesenteric artery').

    Liver (Standring 2015)

    Inferior border

    End tidal inspiration: right r10 costal cartilage in the midaxillary line  --> left 5th costal interspace/r6 in the midclavicular line.

    Superior border

    Right r5 or intercostal space in the midclavicular line --> left 5th intercostal space/r6 in the midclavicular line

    Gall Bladder (Standring 2015)

    Fundus: tip of right 9th costal cartilage in or just below the transpyloric plane. 

    Spleen (Standring 2015) 

    Normal size spleen equates to that of a clenched fist.

    It is located at the left r9 to 12 in anterior midaxillary line.

    Medial border: 5cm to the left of T11 SP (PSIS to a line perpendicular to T11)  --> lateral border: 3cm anterior to the midaxillary line.

    Pancreas (Standring 2015)

    The pancreas is located at the right side of L2 (in duodenal curve)

    Neck: transpyloric plane (L1-2 IVD)

    Body: slightly above transpyloric plane. 

    Kidney (Standring 2015)

    Left kidney

    The left kidney is located between r12(11) T12 --> L3/4

    Renal hilum: L1/2 or L2.

    Right kidney

    The right kidney is located between r12(11) L1 --> L4 (T11-L5)

    Renal hilum: slightly lower than L2.

    The relations of the anterior renal fascia with the suspensory ligament of the duodenum (ligament of Treitz), root of the small intestine mesentery and transverse mesocolon is discussed under 'superior mesenteric artery'.

    Ureter (Standring 2015)

    The ureter is located in the transpyloric plane, (slightly lower on the right) 5cm from the midline (just medial to the tips of L1-5 TP’s). In pelvic cavity curves medial to the midline to enter the bladder.

    Superior mesnteric artery

    Anatomy of superior mesenteric artery

    The origin of the superior mesenteric artery from the abdominal aorta is at L1 which corresponds to the transpyloric plane (half way between the xiphoid --> umbilicus) close to the left midclavicular-umbilical line. This is slightly to the right of the D/J junction.

    The artery then descends to the right iliac fossa supplying along its course the pancreas and intestine (lower part of the duodenum --> appendix, ascending and transverse colon).

    Connective tissue anatomy of the superior mesenteric artery

    The superior mesenteric artery is an important landmark for the:

    • Anterior renal fascia.
    • Root of the small intestine mesentery and transverse mesocolon.
    • Suspensory ligament of the duodenum (ligament of Treitz).

    Martin (1942) found below the superior mesenteric artery the anterior renal fascia crosses the midline to join the contralateral anterior renal fascia. Superior to the artery it covers the mass of connective tissue surrounding the origins of the coeliac axis (artery) and superior mesentery artery (in which lies the coeliac and superior mesenteric autonomic plexus). 

    Coffey et al (2015) found the root of the mesentery for the small and large intestine to start from where the superior mesenteric artery originates from the pancreatic bed (retroperitoneal space the pancreas and D1 shares).

    Suspensory ligament of the duodenum (ligament of Trietz): double fold of peritoneum. It comprises two parts:

    • Part one: right crus of diaphragm --> connective tissue around coeliac and superior mesenteric artery. 
    • Part two: muscular part which suspends D/J junction. Connective tissue around coeliac artery --> duodenum: between pancreas and left renal vein.

    The suspensory ligament of the duodenum (ligament of Trietz) as well as suspending the D/J junction from the retroperitoneum surrounds and protects the superior mesenteric artery and coeliac trunk.

    Surface anatomy

    The superior mesenteric artery branches from the abdominal aorta in the transpyloric plane (L1) close to the left midclavicular-umbilical line.


    Standring S. Gray’s Anatomy 41st edition. Anatomy. The anatomical basis of clinical practice


    Mesenteric-Based Surgery Exploits Gastrointestinal, Peritoneal, Mesenteric and Fascial Continuity from Duodenojejunal Flexure to the Anorectal Junction. A Review (2015). J. Calvin Coffey, Mary E. Dillon, Rishabh Sehgal, Peter Dockery, Fabio Quondamatteo, Dara Walsh, Leon Walsh

    Respiration-Induced Deformations of the Superior Mesenteric and Renal Arteries in Patients with Abdominal Aortic Aneurysms (2013). Ga-Young Suh, Gilwoo Choi, Robert J. Herfkens, Ronald L. Dalman and Christopher P. Cheng

    Navigating the Root of the Mesentery: A Guided Approach to an Artery-First Pancreatoduodenectomy (2017). Amer Aldouri, M

    Root of the Small-Bowel Mesentery: Correlative Anatomy and CT Features of Pathologic Conditions (2001). Yuriko Okino, Hiro Kiyosue, Hiromu Mori, Eiji Komatsu, Shunro Matsumoto, Yasunari Yamada, Koji Suzuki, Kenichiro Tomonari

    Anatomical relationship between fascia propria of the rectum and visceral pelvic fascia in the view of continuity of fasciae (2019). Chang Y, Liu HL, Jiang HH, Li AJ, Wang WC, Peng J, Lyu L, Pan ZH, Zhang Y, Xiao YH, Lin MB