THE CHRONOLOGY OF THE DEVELOPMENT OF A DYSFUNCTION

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1 OSTEOPATHIC PHYSIOPATHOLOGY A dysfunction is an alteration to a movement within the three-dimensional parameters, which may be in hypo- or hypermobility. Bearing in mind that these hypomobilities will cause reactional hypermobilities, treatment should be focussed on the areas of the fixations. These are caused by muscle processes (hypertonias), ligament processes (histopathological changes), intraarticular processes (synovial alterations or changes in the intraarticular pressure), amongst other factors. THE CHRONOLOGY OF THE DEVELOPMENT OF A DYSFUNCTION Primary dysfunction: corresponds to the first incidence of stress that occurs in the organism. The primary dysfunction may be: A trauma: (crashes, falls, etc.) they do not obey any laws. Physiological: in FRS or ERS, affecting a vertebral segment. A nonneutral dysfunction (2nd law of Fryette). Secondary dysfunction: an adaptation resulting from the need to "accommodate" a given situation, for example a primary dysfunction in a vertebral segment or a primary dysfunction in another area of the body (e.g. the talus bone, the iliacus etc). The resulting adaptation may occur close to or far from the primary dysfunction and is entirely reversible- by correcting the primary lesion, the adaptation will disappear. However, if the primary dysfunction persists over time, it will cause structural changes to occur in the secondary dysfunction, meaning that it is no longer an adaptation, but a compensation. Correcting the primary dysfunction will therefore not bring about the immediate disappearance of the secondary dysfunction (compensation). It will not require direct and specific treatment. These dysfunctions comply with the 1 st Law of Fryette. OSTEOPATHIC LESIONS OR SOMATIC DYSFUNCTIONS Somatic dysfunctions are a three-dimensional disparity in the mobility of a joining element. They are characterized by restricted mobility (hypomobility) in one or more of the physiological parameters of movement, which is almost always painful. The dysfunction relates to: Capsuloligamentous sensory receptors. Neuromuscular spindles. The spinal cord. A neurological phenomenon occurs (gamma hyperactivity) which maintains the spasm in the monoarticular muscles, responsible for joint fixation. There are other, associated factors that explain the chronicity of the dysfunction: A local sympathicotonia. A neurovascular dysfunction. Spinal cord facilitation Alterations to metameric elements. Somatic dysfunction can affect: 1

2 Joins and bones. Capsules and ligaments. The dura mater. Fascia. Muscles. Nerves. HYPER- AND HYPOMOBILITY Areas of hypomobility tend to come with (often neighbouring) areas of hypermobility, the latter trying to compensate for the lack of mobility caused by the former. 2

3 Certain movements are limited in hypomobilities that are compensated for by hypermobilities, which puts stress on the tissue in the hypermobile structures. When analysing vertebral somatic dysfunctions in an isolated vertebra, we observe areas of hypomobility and hypermobility in one vertebra but in different joints. There are three possible combinations: A fixation of the facet joint on one side, which causes (reactional) painful hypermobility on the opposite side. A fixation of a facet joint with reactional somatic disc hypermobility. In those cases, the intervertebral disc will degenerate. This may occur before a disc hernia. A fixation of discosomatic space (in the case of discarthrosis), with reactional hypermobility in the posterior part of the vertebra (interapophyseal joints). 3

4 THE OBJECTIVES OF OSTEOPATHIC TREATMENT: There are different objectives depending on whether we are dealing with a hypomobility or hypermobility dysfunction. Remember that hypermobilities are, in most cases, secondary to hypomobilities, so: For hypomobilities, we look to: Restore the limited joint mobility. Restore the ligament and muscle balance. For hypermobilities we look to: Reduce the inflammation caused by tissue hypersolicitation. Reduce the edema. Reduce the pain. Generally, the symptoms that lead the patient to seek medical advice are experienced in hypermobile areas. Hypermobile joints are not manipulated as we want to avoid creating more movement in joints that already have excess mobility. We manipulate the hypomobile joints as these are the ones that have restricted movement. SOME EXAMPLES OF THESE DYSFUNCTIONS Hypomobility of: D1 to D7: causes torticollis or cervicobrachial neuralgia. D11 to L1: acute low back pain in the adjacent area. Sacroiliac joint: causes sciatica, cruralgia or pubalgia (a sports hernia). Sacroiliac joint: to illustrate this point, we will carry out a brief analysis of the walking motion. When a person is walking normally, they make alternating anterior and posterior rotation movements of the iliac muscles while the sacrum, on its oblique axes, completes torsion movements from side to side. These movements are made through the sacroiliac joint. If you start walking with your right leg, the hip flexion is produced by a contraction of the iliopsoas muscle which also posteriorizes the sacroiliac joint on that side. The left gluteus medius muscle contracts to stabilize the pelvis horizontally, while the left erector spinae muscles stabilize the lumbar spine, anteriorizing the sacroiliac joint on that side. Hypomobility of the sacroiliac joint on the right side, for example, would affect the biomechanics of the whole movement. When the anterior step is taking on the right side, it produces an adaptation in the left lumbar scoliosis (left NSR) which the erector spinae muscles on that side will then fix. The sacrum completes a compensatory rotation on the opposite side which causes a reactional hypermobility in the L5-S1 region. 4

5 FRYETTE'S LAWS The Laws of Fryette are known as a set of principles, developed by Harrison H. Fryette D.O. in the second decade of the 20th century, that outline the different patterns of spine movements. The laws of Fryette describe the movements of a vertebral segment or a group of vertebrae performed automatically as part of normal, every day joint activity. The automated movements are different depending on whether the vertebral segment or group of vertebrae are in an easy-flexion (N: neutral), flexion (F) or extension (E) position. Understanding the terms: Easy-flexion (N): the vertebral segments or vertebral group are in a neutral position. The facet joints of the articular processes are neither open nor closed and the body's weight is evenly balanced over the vertebral body. In easy-flexion, the facet joints of the articular processes are parallel, in a balanced position, three degrees of movement away from either flexion, with the resulting opening of the facet joints, or extension, with the resulting closing of the facet joints. This description corresponds to the central or neutral vertebra of a physiological curve (C4, D6, L3). The degrees of movement needed for a vertebral segment to move from the easy-flexion position to flexion or extension will depend on the position of the segment in the physiological curve. Flexion (F): the position of a vertebral segment or group of vertebrae when the facet joints of the articular processes are open and the weight of the body is displaced to the most anterior part of the vertebral body, forcing the nucleus pulposus of the intervertebral disc to be displaced posteriorly. Extension (E): the opposite of flexion, with the facet joints closed. 1ST LAW OF FRYETTE N.S.R. N: neutral. S: side bending R: rotation. Determines the movement of a vertebra from a neutral position. In order for a vertebra or group of vertebrae in easy-flexion (neutral position), to make a rotation (R) to one side, it will first have to complete a sidebending movement (S) to the opposite side. This is a physiological movement and will behave in the same way in all regions of the spine, except the cervical region. THE BIOMECHANICS OF NSR ON THE LEFT 1st step: the vertebra is in the easy flexion (N) position and it completes a side bending movement (S) to the right. 2nd step: this causes the vertebral body to glide to the left, towards the convexity. 3rd step: this triggers a left rotation (R) in the vertebra or vertebral group. 5

6 These three steps are completed simultaneously and automatically, causing the nucleus pulposus to be displaced towards the convexity. 2ND LAW OF FRYETTE ERS/ FRS E/F: extension/flexion. R: rotation. S: side bending. Determines the movement of a vertebra from a flexion or extension position. In order for a vertebra or a group of vertebrae in a hyperflexed or hyperextended position to complete a side-bending movement, it will first have to complete a rotation on the same side. This applies in all regions of the spine. THE BIOMECHANICS OF ERS OR FRS TO THE RIGHT 1st step: the vertebra, in a hyperflexion (F) or hyperextension (E) position, rotates (R) to the right 2nd step: gliding towards the convexity, in this case the left. 3rd step: the vertebra or group of vertebrae side bends (S) to the right. These three steps are completed simultaneously and automatically, causing the nucleus pulposus to be displaced towards the convexity (contralateral to the side bending). We should remember that spine movements are not unrelated to the movements that the body's levers make in the different activities we do on a daily basis. All of these static and dynamic activities require the use of different segments of the spine at the same time. This means that one vertebral group could make an NSR movement while another makes an E or FRS movement. While the laws of Fryette apply to the normal joint physiology of a vertebral segment or a vertebral group, it is also worth noting that dysfunctions also respond to this behaviour but in different ways. THE LOVETT BROTHERS Lovett established a relationship between superior and inferior vertebrae, through the dura mater, putting them in pairs. The biomeochanics of the cervical and upper thoracic spine is synchronized with the biomechanics of the lumbar and lower thoracic spine. This means that if a cervical vertebra dysfunctions, its equivalent vertebra in the lumbar spine will also dysfunction. For example, if C1 has a posteriority dysfunction to the right, L5 will also have a posteriority dysfunction to the right. L5 is the "Lovett Brother" of C1. Treating L5 will help to stabilize C1 and the cranium, modifying the lines of gravity. MARTINDALE LAWS Martindale states that when a non-neutral dysfunction occurs in a vertebral segment, the spine will seek to regain its balance. It will do this through groups of 6

7 vertebrae that make adaptations in NSR. (R. on the opposite side to the primary dysfunction). This adaptation is possible because the multifidus muscles in the cervical and upper thoracic spine are inserted into groups of three vertebrae, while in the lumbar and mid and lower thoracic vertebrae, they are inserted into groups of four vertebrae, making four groups of three vertebrae and three groups of four vertebrae. FRS movements produce an adaptation in the vertebral groups below, with the superior vertebra with a non-neutral dysfunction being the starter vertebra. ERS movements produce an adaptation in the vertebral groups above, with the inferior vertebra with a non-neutral dysfunction being the starter vertebra. The vertebra apex is the vertebra that rotates the most in the adaptive curve. This is generally the most central vertebra. Corrections for these dysfunctions should be carried out as follows: The starter vertebra should be corrected. If the curve (above or below) is adaptive, it will be corrected spontaneously. If the curve does not disappear, it is a compensatory curve. To treat it, the vertebra apex must first be treated. C1-C2-C3 GROUP This group generally results from an adaptation to a cranial dysfunction, especially in C0-C1. It is associated with dysfunctions in the upper limb. It produces symptoms in the cephalic sphere: this is often a reflection of a cerebrovascular problem but could also indicate occular, nasal fossa, bone or sympathetic craniocervical problems such as: Cephalalgia and migraines. Occipital neuralgia (Arnold's neuralgia). Problems with the vision. Problems with the throat. The group will be dysfunctioning if muscles like the levator scapulae, scalene, trapezius or sternocleidomastoid muscle are in spasm. C4-C5-C6 GROUP This group adapts to fixations in the upper cervical spine or the cervicothoracic junction, associated with glenohumeral, acromioclavicular and scapulothoracic pathologies. Arterial hypertension. Pain in the upper limbs. Stomach problems associated with duodenum, liver or gall bladder problems. Respiratory problems (as it is responsible for the nerve supply of the diaphragm). 7

8 C7-D1-D2 GROUP Associated with all scapular problems and problems with the upper limbs involving the hands, such as cervicobrachial neuralgias. A reflection of an ascending dysfunction of the pelvis. Disruptions to the sympathetic thoracic and cervical ganglion system (associated with cardiac pathologies such as hypertension, as well as lung pathologies such as asthma or bronchitis). Lymphatic diseases in the upper limbs. D3-D4-D5 GROUP Cardiac, respiratory and gastric problems. D6-D7-D8-D9 GROUP The greater splanchnic nerve and celiac plexus group (stomach, liver, gall bladder, duodenum). Digestive problems. D10-D11-D12-L1 GROUP Contributes to problems with the diaphragm, this group also controls the lymphatic system of the lower limbs. Also supplies the intestines, together with the abdominal and pelvic splanchnic nerves and the superior mesenteric plexus. Intestinal problems (colitis, constipation). Urinary problems (kidneys, ureters). Gynecologic hemorrhage area. L2-L3-L4-L5 GROUP Supplies the lesser pelvis, alongside dysfunctions of the sacrum and the iliac muscles as well as the psoas muscle, the laterovertebral sympathetic chain ganglia and the pelvic splanchnic nerves, which form an anastomosis with the hypogastric plexus. It is difficult to correct an iliac dysfunction if this group is not balanced: In postflexion (backwards) dysfunctions, we find an anterior iliac dysfunction (starter vertebra L5). In anteflexion (forwards) dysfunctions, we find a posterior iliac dysfunction (starter vertebra L2). Pain in the lower limbs (cruralgia, sciatica). Intestinal problems (sigmoid colon). Gynecological problems (dysmenorrhea). A descending force causes a dysfunction in flexion that produces a descending adaptation. 8

9 An ascending force causes a dysfunction in extension that produces an ascending adaptation. REFERENCE: Ricard F, Sallé JL. Tratado de osteopatía. Medos Editorial.2014 Ricard F. Osteopathic treatment of the low back pain and sciatica caused by disc prolapse. Medos: Madrid