ESSOMM European core curriculum and principles of manual medicine

30 h (Table 3).

70 h (Table 4).

40 h (Table 5).

Table 8.

Table 9.

Table 10.

Table 11.

Table 12.

Table 13.

Table 14.

Table 15.

Table 16.

Table 17.

Table 18.

Table 19.

Table 20.

Table 21.

Table 22.

Table 23.

Table 24.

Rib

Rib

Lumbar spine

All movements of SIJ components are defined by the anatomic form of the joint surfaces of the ilium and the sacrum and are physiologically possible only in a minimal range of a few degrees (2–4°). In contrast to all other joints according to the definition of true diarthrosis, actively intentioned movements within the SIJ in a functional direction are not possible. Therefore, movements of the SIJ are not comparable with the functional pattern of other joints.

Sacroiliac joint and pelvic girdle

Sacroiliac joint and pelvic girdle

Therapeutic procedures:

Saddle join: convex–concave in one plane, concave–convex in another plane.

Therapeutic procedures:

The shoulder has five different areas of mobility, which all have to function correctly. All areas and related muscles must be tested.

Table 25.

Tibiofibular, femorotibial, patellofemoral joint.

It is well established that direct or indirect injuries, as well as functional limitations (i.e., without structural damage) can be characterised by inflammatory responses in the affected tissues [17]. In musculoskeletal SD, the pain generators include muscle, tendon, ligament, fascia, intervertebral disc, articular cartilage, joint capsule, bone (periosteum) and vascular stroma [18]. The activation of nociceptor free endings within the connective tissue of visceral, dermal or musculoskeletal structures will cause the local release of peptide transmitters, such as somatostatin and substance P, as well as other inflammatory mediators such as histamine, serotonin and immune complements [15]. This leads to local tissue vasodilation, immune cell activation (e.g., macrophages and lymphocytes) and oedema due to increased leaky capillaries. The modulation of the nociceptive neuron ensures this response spreads from the site of the original nociceptive stimulus to the surrounding area, recruiting other nociceptors and lowering their threshold to respond to further stimulus, creating a cascade response that further assists other branches of the nervous system, such as autonomic response and nociceptive reflex.

The activation of nociceptors has a modulatory effect, via their cell bodies in the dorsal root ganglia, at the corresponding segmental spinal level, where they synapse directly, or indirectly via interneurons, in the dorsal horn. Through a series of interneuronal connections within the spinal laminae, a signal is transmitted to the segmental motor neurones in the anterior horn, which in turn exerts a musculoskeletal reflex in the muscle fibres affected by the nociceptive stimulus, leading to muscle spasm or hypertonicity. However, the web of interneurons amplifies the nociceptive signal beyond the affected segment, thus orchestrating a variety of coordinated sensory, musculoskeletal (somatic) and autonomic (visceral) responses, which affect the functioning of multilevel dermatomes, myotomes and viscerotomes [15]. It is therefore possible to infer that a nociceptive reflex can cause a combination of somatosomatic, somatovisceral, viscerosomatic and viscerovisceral responses.

Theories that the autonomic nervous system modulates peripheral and visceral responses following a peripheral painful or nonpainful stimulus have been proposed since the 1950s [19]. Furthermore, Korr demonstrated that sympathetic pathways at segmental levels correlating to the SD showed increased activity [20], which is thought to explain why pain can persist once the nociceptive stimulus appears to have been removed, with sympathetic activation facilitating the sensitisation of local nociceptors, giving way to clinical signs such as hyperalgesia and allodynia [21]. From a neurophysiological viewpoint, the precursor of the recruitment of the sympathetic system in the development of SD is thought to be the nociceptive reflex, where segmental activation of the sympathetic root ganglia by nociceptors or interneurons causes a nociautonomic reflex commensurate to the autonomic function of the segmental level affected, e.g., increased heart rate, vasoconstriction in viscera and skin, vasodilation in muscles, raised blood pressure, increased gastrointestinal stasis or bronchodilatation [15]. These are the basic mechanisms supposed to be responsible for development of CRPS 1 and 2. Furthermore, an immune component with autonomic modulation cannot be excluded, as the thymus, spleen and lymph nodes receive sympathetic innervations that could modulate T and B cell function [15]. Overall, autonomically driven changes can explain the changes observed in the tissues affected by SD, such as the tissue fullness and movement restriction due to muscular oedema and swelling.

The characteristics noted in an SD, such as tissue changes and tenderness, are thought not to merely limit musculoskeletal movement range and function, but also its spatial sense of position, otherwise known as proprioception [22, 23]. In fact, the changes exerted onto an area of SD via somatic and autonomic pathways affect the position in which a body part is held [15]. For example, the muscle contracture due to a somatic nociceptive reflex or the muscle engorgement due to a sympathetic nociautonomic reflex moves the joint correspondent to the area of SD, away from its neutral position. Not only would this affect the available range of motion of that joint, but recalibrate the afferent sensory input, thus changing its neutral position and proprioceptive balance. Furthermore, the apparent inhibition of deep segmental muscles and increased activation of superficial musculature caused by nociceptive drive may also impair proprioception, further exposing an area of SD to further injury due to poorer motor control [24].

Pain is not merely a passive relay of neuronal action potentials dependent on the location and intensity of the peripheral noxious stimulus, but rather, as Melzak & Wall showed in 1965, pain perception depends on a complex endogenous pain modulation and inhibition system within the CNS [25]. It has become well established that the majority of chronic musculoskeletal pain and SD are characterised by dysfunction of CNS processing, where the balance between descending anti-nociceptive (inhibitory) mechanisms and ascending nociceptive facilitation is disrupted, causing an amplification of pain transmission [16]. The increased sensitisation and excitability of neurons in the central nociceptive pathways, such as dorsal column and laminar interneurons, represents an increase in presynaptic signal strength or postsynaptic response, as well as a reduction in descending inhibition [25]. It therefore gives a neurobiological basis to explain phenomena such as hyperalgesia, where there is an increased and prolonged response to a noxious stimulus, and allodynia, where the pain threshold is reduced [24]. The pain hypersensitivity observed in central sensitisation thus represents an amplification of central nervous signalling [25].

Recently, the role of the fascia has been revisited to give a different dimension to the nociceptive and central sensitisation models used to describe SD. The mechanical importance of the fascia stems from the recognition that normal musculoskeletal movement does not rely solely on each individual structure (tendon, ligament, muscle, fascia, fat pad and bursae), but on their interrelation as a “supertendon”, where the function of the whole is greater than that of its individual parts [26]. Therefore, the idea of fascia as an encompassing organ supporting muscles and viscera organ developed. In this context, a specific insult to the fascia, such as a strain, mechanical overload or painful stimulus, triggers the sensory system and activates a chain reaction that leads to the formation of an SD.

During the clinical examination, the most common sensory changes noted in SD include tenderness, paraesthesia and numbness, as well as alterations in temperature perception and proprioception. Tenderness can arise directly from a physical structure, such as joint capsule or trigger point, thus indicating a specific source of SD, or as formulated in the central sensitisation model, it can manifest as hyperalgesia or allodynia within any tissue or segmental region of the neuromusculoskeletal system. Therefore, pain history and other sensory changes are an important part of the differential diagnostic process, as they provide an insight into the particular anatomical distribution of a SD. In fact, in a cross-sectional study, 455 patients with chronic low back pain were reviewed and a good correlation was found between pain measured using a 0–10 visual analogue scale (VAS) and the location of the tender somatic dysfunction, with the lumbosacral region as the most common site of the SD [28, 29]. Similar findings were noted in an earlier study of 216 patients with chronic musculoskeletal pain, where a good statistically significant link was found between SD and pain distribution [30]. Although the pathophysiology of neuromusculoskeletal pain shows that its location does not always correlate with the underlying aetiological site, these studies lend support to using tenderness and sensory changes as a guide to locate primary or secondary SDs and start “mapping” a diagnostic formulation.

Alongside the sensory dysfunctions noticeable with an SD, changes to the palpatory qualities of a tissue are another integral component of the clinical diagnostic process. In line with the pathophysiological changes expected with SD, changes to tissue texture can be driven by local inflammation, fascial disturbances, and nociautonomic and nociceptive reflexes [15, 21, 25, 31, 32], which in turn can lead to physical tissue changes such as increased skin drag, tissue oedema, temperature changes, increased perspiration, muscle spasm and fascia contracture [14]. These tissue features are the somatosomatic and viscerosomatic representation of SD and can be traced back to a specific structure (e.g., muscle, ligament, tendon, articular joint), as well as a single spinal segment or a group of them [33], thus facilitating the location of the primary and secondary SDs. Overall, despite the variability introduced by the subjective palpatory skills of clinicians, the tissue changes observed define the clinical picture that helps to determine possible differential diagnoses.

In addition to sensory and tissue changes, other clinical features associated with SD include anatomical asymmetry [27], especially affecting the vertebral column and pelvis, although any musculoskeletal structure can show visible anatomical differences with its corresponding opposite. Recognition of anatomical asymmetry rests on the clinical skills of the clinicians, from observation (e.g., for scoliosis, posture or scapular protraction) to palpation, where a sacral torsion or anterior/posterior innominate is confirmed after tactile assessment.

Another important clinical feature that defines SD clinically is motion restriction of an articular joint, typically affecting a zygapophyseal joint of a spinal segment, although any articulation of the musculoskeletal system can be involved [14]. Pathophysiological factors such as joint inflammation or proprioceptive deficits may theoretically create a motion restriction in isolation with no tissue, sensory or visible anatomical changes. However, in reality, motion restriction is a functional impediment due to a combination of elements, from muscle spasm and tissue oedema to pain-induced muscular inhibition and postural adaptations [14, 27]. In fact, it is a recognised practice among manual medicine clinicians to monitor tissue tension and changes to better understand the motion restriction at a specific joint or spinal level [33], thus highlighting the importance of monitoring the overall behaviour of an area to the changes imposed by palpation and motion.

The localised tissue changes driven by inflammation, autonomic and somatic responses can be improved and reversed by soft tissue techniques. The manual mobilisation of tissues facilitates motion, pliability and muscle relaxation [27], probably due to a combination of local effects, for instance mobilisation of oedema by effleurage [34] and segmental feedback via spinal cord autonomic and visceral reflexes. Specific soft tissue and fascial release techniques have been shown to reduce pain, possibly due to modulation of connective tissue viscoelasticity, piezoelectric properties and hydration [36], as well as reduced proinflammatory mediators and fibroblast proliferation [37]. The application of mechanical load appears to be the main modulator of soft tissue responses [31, 32], although this seems to relate to the type, duration and frequency of the kinetic load.

In order to restore normal active and passive articular motion, the application of repetitive and oscillatory movements to engage with the restricted barrier can be effective and is termed joint mobilisation. The normal range of movement needs to be assessed and tested in all its planes, flexion/extension, rotation and side bending, but also in its accessory movements, from anteroposterior to mediolateral and cephalocaudal translation [33]. The joint mobilisation can be delivered passively by the clinician, or it can be facilitated by muscle energy techniques (MET) that relax the hypertonic muscle maintaining the movement restriction by using an isometric contraction to cause motoneuron inhibition via its corresponding somatosomatic reflex mediated by Golgi tendon organ and dorsal column interneurons [38, 39].

HLVA thrusts are frequently considered the defining treatment of manual medicine, and significant research has focused on elucidating the therapeutic properties of these manipulations, although no current mechanistic model is able to fully explain their effect. However, there is supporting evidence showing that manipulations exert improvements in the parameters that define SD and restore homeostasis.

Chronic musculoskeletal pain and its associated SD are often characterised by features of central sensitisation, where addressing the biopsychosocial context is an essential part of the therapeutic approach [16, 25]. In fact, all the manual therapy techniques available are insufficient on their own to treat and benefit patients, as we now know that levels of vigilance, stress and anxiety modulate descending inhibitory nociceptive mechanisms and contribute to aggravate central sensitisation, where patients experience pain as more threatening and catastrophic, developing lower pain tolerance and poorer coping strategies. A promising therapeutic strategy comes not from new pharmacological agents, but from patient education. In fact, pain (neuro)physiology education to reduce the gap between the perception of the patient and their therapist about pain and its treatment was shown to increase patient motivation for rehabilitation [16]. The long-term effectiveness of this approach is currently awaiting validation, but it should already encourage its use in managing SD with patients affected by chronic pain.

As there is growing appreciation of the importance of addressing perpetuating factors behind SD [34], it would appear logical to strengthen traditional therapeutic strategies based on manual therapies with functional treatment or rehabilitation. This recognises the interdependence of neuromusculoskeletal structures with their collective function and use, thus allowing clinicians to add an active, engaged and holistic treatment component where patients are not merely passive recipients of treatment. Therefore, alongside manual medicine and patient education, functional treatments such as prescription of physical activity; respiration, core stability and postural exercises; mindfulness training; and sleep and nutritional advice should form part of a patient-oriented approach to individualise and optimise care [31, 32, 34, 40]. This adds a new and complex dimension to our understanding of SD, but also provides a promising new paradigm.

The degree of serious risks associated with manipulation of the cervical spine is uncertain, with widely differing results being published [197].

In 2002, Haldeman and collaborators reported in an extensive paper on vertebrobasilar accidents in relation to cervical spine manual therapy [11, 218]. According to these authors, stroke represents an infrequent adverse reaction associated with cervical spine manual therapy. Attempts to identify the patients at risk and the type of manual technique most likely to result in these complications of manual therapy have not been successful. A retrospective review of 64 medical legal cases of stroke temporally associated with cervical manual therapy of the spine was performed to evaluate characteristics of the treatment rendered and the presenting complaints in patients reporting these complications. These files included records from the practitioner who administered the manual therapy, post-stroke testing and treatment records usually by a neurologist, and depositions of the patient and the practitioner of manual techniques as well as experts and treating physicians. A retrospective review of the files was carried out by three (2 in 11 cases) researchers, using the same data abstraction instrument, to independently assess each case. These independent reviews were followed by a consensus review, in which all reviewers reached agreement on file content. Whereas 92% of cases presented with a history of head and/or neck pain, 16 (25%) cases presented with sudden onset of new and unusual headache and neck pain often associated with other neurological symptoms that may represent a dissection in progress. The strokes occurred at any point during the course of treatment. Certain patients reported onset of symptoms immediately after the first treatment, while in others the dissection occurred after multiple manual treatments. There was no apparent dose–response relationship to these complications. These strokes were noted following any form of standard cervical manipulation technique including rotation, extension, lateral flexion and non-force and manual techniques in neutral position. The results of this study suggest that stroke, particularly vertebrobasilar dissection, should be considered a random and unpredictable complication of any neck movement including cervical manipulation. They may occur at any point in the course of treatment with virtually any method of cervical manual technique. The sudden onset of acute and unusual neck and/or head pain may represent a dissection in progress and be the reason a patient seeks manual therapy that then serves as the final insult to the vessel leading to ischemia.