1999 Annual Meeting
Scientific Program
|
American Academy of Orthopaedic Surgeons
1999 Annual Meeting Scientific Program |
Saturday, February 6, 1999
03:30 PM - 05:30 PM
Location: A1
SYMPOSIUM
Boyd R Buser, DO, Biddeford, ME
John M Jones, III, Pomona, CA
Mitchell Kasovac, Pomona, CA
Michael L Kuchera, DO, Kirksville, MO
Frank H Willard, PhD, Biddeford, ME
Osteopathic medicine is a system of medical care with a philosophy that combines the needs of the patient with the current practice of medicine, surgery and obstetrics an d emphasizes the inner relationship between structure and function and the appreciation of the body's ability to heal itself.
Mitchell Kasovac, DO
Announces a new form of diagnosis and treatment which he calls "osteopathy". (osteon = bone, and pathy = source of diseases). He determines that the malalignment of the skeleton and muscles was the source of the body's vulnerability to illness). He was a Civil War physician and very concerned with the many people dying from Influenza epidemic.
Dr. Still worked for almost 20 years developing his osteopathic manipulative techniques of the spine. He intensely studied the neuro-musculo-skeletal systems to demonstrate his belief in the importance of optimal structural integrity to facilitate optimal body function.
An osteopathic physician evaluating a patient performs all of the standard physical examination, including special tests as indicated. In addition, the osteopathic physician examines visually, by palpation and motion testing for the following criteria of somatic
The osteopathic examination starts with an overall screening examination of the patient as a whole, and progresses through regional examination to segmental examination. Although ideally each of ten regions is examined for the four criteria listed above, time demands may indicate an abbreviated examination limited to the most likely areas related to the complaint on a particular occasion.
Spinal regions are examined both for evidence of unilateral long muscle hypertonicity and shortening, and for short or deep intrinsic muscle and connective tissue restriction. The latter is implicated by asymmetric position and decreased motion of vertebral segments.
Treatment is aimed at restoring symmetrical length and strength to the muscles, decreasing inappropriate connective tissue constriction, improving arterial flow, venous and lymphatic return, and restoring physiologic motion as appropriate.
Somatic dysfunction is a significant finding on Osteopathic structural examination. It presents clinically as a palpable, pathologic alteration in tissue quality. Somatic dysfunction represents underlying pathology in the neuromuscular system and can be indicative of disease processes in visceral organs as well. The four cardinal characteristics of somatic dysfunction are (Denslow, 1975):
An explanation of somatic dysfunction needs to provide a common rationale behind the presentation of each criterion in this list.
Several animal models exist for examining the pathophysiological basis of somatic dysfunction. Typically, these models involve the injection of inflammatory compounds into a joint or surrounding fibromuscular tissue (He et al, 1988; Dubner and Ruda, 1992) or the use of ultraviolet radiation (Urban et al., 1993). Other models have used electrical stimulation of peripheral nerves (Anderson and Winterson, 1995). The results of these studies provide an understanding of the events occurring in peripheral tissue as well as the central nervous system during the development and maintenance of somatic dysfunction.
At the peripheral tissue level, the release of proinflammatory substances, consequent to irritation results in increased permeability of capillaries and extravasation of fluids (Payan, 1992). Biopsy of palpable somatic lesions demonstrated histopathological signs of edmentous infiltration (Denslow, 1975). A reasonable conclusion suggests that these extravastated fluids are responsible for the altered tissue texture.
In zones of tissue inflammation, the altered extracellular chemistry results in sensitization of primary afferent fibers (Woolf and Chong, 1993). Typically, this peripheral sensitization involves altered thresholds for C-fibers and Ao-fibers as well as modification of AB-fiber activity (Neumann et al., 1996). At the level of the spinal cord, activation of wide dynamic range neutrons in the dorsal horm through the opening of N-methy-D-aspartate channels as well as the induction of immediate-early genes are dependent on primary afferent nociceptor activity and precede the development of central sensitization (Coderre et al., 1993) Sensitization of peripheral and central components of the nervous system is thought to be a major contributor to the development of hyperalgesia (Woolf and Chong, 1993), the second characteristic of somatic dysfunction.
Excessive activation of primary afferent nociceptive fibers leads to altered activity of both a- and y-motoneurons in the ventral horn (He et al., 1988). Increased output of a-motoneurons through the ventral roots results in facilitation of muscles, particularly of the flexors muscles (Mense, 1993). This facilitation is experienced clinically as increased tone in the muscles related to the affected spinal cord circuit. Finally, expression of the altered muscle tone, consequent to spinal facilitation, is seen as a change in range or ease of motion about a joint. Thus, all four of the cardinal manifestations of somatic dysfunction can be explained by a common mechanism.
The above model of somatic dysfunction begins with the release of proinflammatory compounds into the local tissue. External factors such as infection and trauma can be sources of proinflammatory substances, however, an internal source of these substances has recently been described (Sluka et al., 1995; Cervero and Laird, 1996). Dorsal root reflexes, involving the antidromic conduction of neural activity along primary afferent fibers, have been demonstrated to initiate the release of proinflammatory peptides from the peripheral terminals into the local tissue (Rees et al., 1994). These reflexes are initiated by activity in primary nociceptive fibers at adjacent spinal segments (Rees et al., 1996). The release of proinflammatory substances by the central activation of primary afferent fibers provides an explanation for the development of idiopathic somatic dysfunction and could therefore be a diagnostic harbinger of dysfunction in other portions of the body.
The pathophysiology of somatic dysfunction, the major diagnostics findings of the Osteopathic palpatory examination, can be explained by a single mechanism. This has become known as the Nociceptive Model of Somatic Dysfunction (Van Buskirk, 1990; Willard et al., 1997). Primary nociceptive activity is initiated by the presence of proinflammatory compounds at the local tissue level. This is followed in sequence by sensitization of peripheral afferent fibers and of dorsal horn neurons contributing to hyperalgesia and underlying spinal facilitation. The segmental level facilitation of the spinal cord results in enhanced outflow from the ventral horn a-motoneurons and concomitant muscle spasm, altering joint range or ease of motion. Tissue injury at one location in the body could, through the activation of dorsal root reflexes, initiate the formation of somatic dysfunction in multiple, desperate sites in the patient. In summary, the experimental models of somatic dysfunction have provided a common explanation of its four cardinal criteria. It is now hoped that these same models can be expanded and used to explore the influence of somatic dysfunction on general body homeostasis (Willard et al., 1997).
Reference List
Anderson MF and Winterson BJ (1995) Properties of peripherally induced persistent hindlimb flexion in rat: Involvement of N-methyl-D-aspartate receptors and capsaicin-sensitive afferents. Brain Res. 678:140-150.
Cervero F and Laird JM (1996) Mechanisms of touch-evoked pain (allodynia): A new model. Pain 68:13-23.
CoderreTJ, Katz J, Vaccarina AL and Melzack R. (1993) Contribution of central neuroplasticity to pathological pain; review of clinical and experimental evidence. Pain 52:259-285.
Denslow JS. (1975) Pathophysiologic evidence for the ospeopathic lesion: the known, unknown, and controversial. J.A.O.A. 74:415-421.
Dubner R and Ruda MA. (1992) Activity-dependent neuronal plasticity following tissue injury and inflammation. Trends Neurosci. 15:96-103.
He X, Proske U, Schaible HG, and Schmidt RF. (1988) Acute inflammation of the knee joint in the cat alters responses of flexor motoncurons to leg movements. J. Neurophysiol. 59:326-340.
Mense S. (1993) Nociception from skeletal muscle in relation to clinical muscle pain. Pain 54:241-289.
Neumann S, Doubell TP, Leslie T, and Woolf CJ. (1996) Inflammatory pain hypersensitivity mediated by phenotypic switch in myelinated primary sensory neurons. Nature 384:360-364.
Payan DG. (1992) The role of neuropeptides in inflammation. In J.I. Gallin, I.M. Goldstein, and R. Snyderman (eds): Inflammation: Basic Principles and Clinical Correlations, New York: Raven Press, pp. 177-192.
Rees H, Sluka KA, Lu Y, Westlund KN, and Willis WD. (1996) Dorsal root reflexes in articular afferents occur bilaterally in a chronic model of arthritis in rats. J. Neurophysiol. 76:4190-4193.
Rees H, Slukav, Westlund KN and Willis WD. (1994) Do dorsal root reflexes agument peripheral inflammation? NeuroReport. 5:821-824.
Sluka KA, Rees H, Westlund KN and Willis WD. (1995) Fiber types contributing to dorsal root reflexes induced by joint inflammation in cats and monkeys. J.Neurophysiol. 74:981-989.
Urban L MN, Campbell Perkins E, and Dray A. (1993) Activity of deep dorsal horn neurons in the annesthetized rat during hyperalgesia of the hindpaw induced by ultraviolet irradiation. Neuroscience 57:167-172.
Van Buskirk RL. (1990) Nociceptive reflexes and the somatic dysfunction: a model. J.A.O.A. 90:792-809.
Willard FH, Mokler DJ, and Morgane PJ. (1997) Neuroendocrine-immune system and homeostasis. In R.C. Ward (ed): Foundations for Osteopathic Medicine. Baltimore: Williams & Wilkins. Pp. 107-135.
Woolf CJ and Chong MS. (1993) Preemptive analgesia - treating postoperative pain by preventing the establishment of central sensitization. Anesthesia and Analgesia 77:362-379.
References
Somatic dysfunction: Impaired or altered function of somatic tissues - skeletal, arthrodial, and myofascial - related neural, vascular, and lymphatic elements.
Introduction
A "distinctive osteopathic approach" extends far beyond a fully-licensed physician who may also apply manual techniques to other recognized treatment modalities. Likewise, the distinctiveness of "osteopathic manipulative treatment (OMT)" implies much more than application of a manipulative technique by an osteopathic physician. Distinctive osteopathic care integrates three philosophic elements - a recognition of the patient's self-healing tendencies: the inter-relationships between structure and function within and between all systems; and the importance of the biopsychosocial model in "disease" and recovery. Combined with the osteopathic education system in which every practitioner - generalist or specialist - is first educated to be a primary care physician, documentation shows that D.O.'s are exceptionally cost effective in managing workman's compensation cases (Tillinghast).1 Regardless of the region of the body involved, D.O.'s were more cost effective than all five other practice groups - including chiropractors, physical therapists, surgical M.D.'s and conservative M.D.'s - in managing these cases in each of the states studied.
OMT was not part of every osteopathic approach in the Tillinghast studies, nor is it uniformly integrated into every patient visit. The decision to incorporate OMT as well as the choice of technique, its extent and its frequency usually depends on the clinician's assessment of the role that somatic dysfunction plays in the patient's condition. This means that somatic dysfunction (identified during the palpatory portion of the physical examination) must be placed in context with the patient's history, physical, and affective signs and symptoms. An osteopathic physician will assess whether the somatic component is relevant, marginally relevant, or not relevant to the condition. Treatment of somatic dysfunction may itself consist of one or more approaches including OMT, physical therapy modalities, patient exercises, medication, orthotics, and/or injections. Thus OMT, when performed, is part of a complete patient encounter. OMT is not synonymous with an osteopathic approach, nor in the strictest sense, with generic manipulation.
OMT For Thoracic And Lumbopelvic Somatic Dysfunction
As previously discussed in this symposium and documented in the literature2 regional somatic dysfunction is commonly denoted by its motion characteristics. Active and passive motion testing in the weight-bearing and non-weight -bearing positions may each provide different motion characteristics for somatic dysfunction in these regions. Likewise, OMT can be performed in many positions - seated, prone, supine, lateral recumbent, and even standing. It can be performed, out of necessity or convenience, in a hospital bed, a wheel chair, or other clinical venue beyond traditional osteopathic treatment tables.
Treatment goals are generally more important to choose than technique - which includes a wide range of methods and activating forces. Nonetheless, a knowledge of the indications and contraindications as well as an appreciation of risk-to-benefit ratios for OMT in general and for specific elements of certain techniques is required for physicians wishing to prescribe or perform manipulation in these regions. For example, manipulation is contraindicated over areas of known metastatic or primary carcinoma, but may only carry a relative contraindication to certain techniques in known lumbar disk herniation. As reported in the world literature, exacerbation of pre-existing disk disease is rare; creating disk rupture in the lumbar or thoracic region has been calculated to occur in 1:2,000,000 to 1:6,000,000 manipulations respectively; and cauda equina syndrome may occur in 1:1,000,000 manipulations.3 If OMT is performed, appropriate choice of technique, careful localization of all motion planes, avoidance of extreme rotatory thrust activation, and preparation of adjacent soft tissues further limit risks. Most clinicians will never see a significant negative sequela of OMT and any minor musculoskeletal flare-up (>24 hours) can be managed by modifying OMT method, activation, or dosage.
A series of examples illustrate that the most prominent characteristic findings of somatic dysfunction - asymmetry, restricted motion, and tissue texture change - affect structure-function relationships in the region and beyond. An asymmetrical sacral base in the standing position, for example, creates a constellation of dysfunction throughout the body including functional scoliosis in the lumbar and/or thoracic spine. "Restricted motion in one area has been shown to create overuse in mymyotatic structures6 and/or compensatory hypermobility in adjacent segments that are, in turn, subjected to increased functional demand.7 When myofascial tissue texture changes with trigger point characteristics are palpated in the thoracic, lumbar, and/or pelvic regions, pain and dysfunction has been documented to result. 'In each instance, removal of the somatic dysfunction and restoring symmetry, motion, and normal tissue characteristics have resulted in improved structure-function relationships paralleling reduction in presenting signs and symptoms.'"
OMT In Spinal Conditions With Recurrent Somatic Dysfunction
Regional structure-function inter-relationships must permit both stability and flexibility. For example, interdisciplinary experts report9,10 the importance of the self-locking function of the sacroiliac joint and the force closure function of lumbopelvic musculature in creating stability while documenting the need for motion, symmetry and normal tissue characteristics in maintaining flexibility. Chronic imbalance in structure-function relationships results in varying combinations of recurrent somatic dysfunction and structural pathophysiology. Lasting outcomes for treatment protocols integrating OMT depend on addressing underlying causes while assisting peripheral and central mechanisms to re-integrate balance. Here, OMT is only part of any osteopathic approach designed to restore structure-function relationships.
Recurrent somatic dysfunction is often the result of underlying postural imbalance or gravitational strain pathophysiology.7 OMT alone in these situations results in immediate but temporary improvement in patient symptomatology and satisfaction scores, but no objective long term benefits. On the other hand, treatment of underlying postural imbalance using appropriate orthotics (including heel lifts8,11, anterior sole lifts5, and/or Levitor® Orthotic Device12,9 for coronal, horizontal and sagittal plane postural disorders resspectively), combined with OMT and patient education, results in long term reduction of somatic dysfunction and pain while increasing patient satisfaction.9 For example, patients with functional "idiopathic" scolioses who also demonstrated radiographic evidence of an unlevel sacral base responded to an osteopathic approach8 which incorporated heel lifts, OMT, and patient self-stretching exercises; failure to incorporate the manipulative component often resulted in at least short term increased pain and decreased patient compliance with the total protocol. Even when the function-structure continuum is seemingly dominated by a structural change such as isthmic L5-S1 spondylolisthesis (grade I-II), a conservative osteopathic approach may focus on improving underlying dysfunctional sagittal plane biomechanical stressors rather than addressing the structural consequence directly.12 Incorporating OMT in conjunction with protocols to modify postural alignment is the standard of care taught in all osteopathic colleges.13
Recurrent spinal somatic dysfunction may also be indicative of underlying visceral dysfunction. Viscerosomatic reflexes have been shown to create segmental facilitation which is capable of maintaining spinal somatic dysfunction. In these cases, tissue texture change often predominates over other palpatory characteristics. Direct method, HVLA manipulations often are unsuccessful and often are perceived as encountering a "rubbery" barrier. Because visceral afferents travel with autonomic efferents, segmentally related findings from primary visceral problems are predictably seen in the thoracic and lumbar region consistent with sympathetic innervation levels and/or in the C2-cranial and sacral regions consistent with parasympathetic innervation levels. The importance of the generalist physician perspective in differentiating somatic problems from viscerosomatic conditions is especially important in this type of recurrent somatic dysfunction.
Specific Points Related To Thoracic & Lumbar Regional Technique
Examples/Demonstrations Of Thoracic, Lumbar & Sacral Omt
References
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