2.1 Differential Diagnostics

So as not to “reinvent the wheel,” this textbook follows the differential diagnostic and treatment concepts described by Dr. James Cyriax.

Nonsurgical, orthopedic medicine originated in England in the 1920s where an internist and orthopedic surgeon, Dr. James Cyriax, developed a system of accurately delineating a musculoskeletal diagnosis of soft-tissue musculoskeletal lesions, noting a lack of satisfactory methodology in assessing the radiotranslucent moving tissues. Dr. Cyriax realized that joints become arthritic, muscles/tendons become strained, ligaments become sprained, bursas become inflamed, nerve roots/trunks and dura mater are liable to be compressed, and joints are prone to internal derangements.

The basic principles of orthopedic medicine, according to Dr. Cyriax, are ¹ , ² :

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  Every pain has a source.

  
  
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  Treatment must reach the source.

  
  
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  Treatment must benefit the source to relieve the pain.

Dr. Cyriax utilized a systematic approach that isolated the cause of pain and that lends itself to a specific diagnosis and subsequent effective treatment, based on an interpretation of positive and negative findings as they relate to applied anatomy. Active and resistive motions assess the contractile tissues and willingness to move allowing the clinician to gain an understanding of the integrity of the musculotendinous structures of the region being inspected. Passive movements are utilized during an examination to determine the integrity of noncontractile structures, ligaments, and joint surfaces. Resistance tests, otherwise known as manual muscle tests (MMT), serve a twofold function. The first is to determine the individual’s capacity to initiate a muscle contraction by assessing neurological status, and the second is to determine the integrity of the muscle, tendon, and the tendinous interaction with the periosteum. In doing so, the clinician will find one of the following to be true as it relates to the patient’s ability to form a muscle contraction. The contraction is:

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  Strong and painless; interpretation: normal

  
  
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  Strong and painful; interpretation: tendinopathy/minor breach of the muscle tendon unit

  
  
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  Weak and painful; interpretation: severe musculotendinous lesion or local boney fracture

  
  
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  Weak and painless; interpretation: neurological compromise or severely deconditioned

A capsular pattern is a term that Dr. Cyriax used to describe the presence of joint capsular changes that are associated with the normal aging process and exist in the presence of an inflammatory process. The capsular pattern is associated with a specific pattern of limitation respective to each joint. The presence of a noncapsular pattern implies that the capsule is not involved and that intra- or extraarticular tissue is inflamed or injured and is the likely source of the pain.

A critical component as it relates to the concepts of differential diagnostics revolves around the muscle spasm. Often addressed as the pathology itself, Dr. Cyriax viewed a muscle spasm as a secondary phenomenon to an affliction or injury elsewhere; a symptom, not pathology in and of itself. ¹ , ² Utilizing this perspective allows the treating clinician the opportunity to deduce the cause of the muscle spasm(s), and to provide the patient a tissue-specific treatment that allows the muscle spasm(s) to release, often with pain alleviation.

2.2 Reflexive Arcs

A monosynaptic reflex arc is the activation of a striated or smooth muscle that involves a single spinal cord segment. This occurs when there is an applied afferent stimulation (i.e., deep tendon reflex of the patella). This afferent stimuli synapses with a motor neuron within the ventral gray column, initiating an efferent action that terminates in the same organ in which the stimulus originated. ³ , ⁴ A disynaptic reflex arc is present when an afferent fiber enters the dorsal gray column and synapses with an association neuron that then synapses with a motor neuron within the ventral gray column. There may be modification of the motor neuron due to the input from other neurons; these neurons may be located at other levels of the spinal cord, or on the other side of the spinal cord or centrally (central nervous system [CNS]), which will allow a conscious modification of a spinal reflex. ³ , ⁴

During the course of the evaluation of the patient with pelvic pain, the quadriceps, achilles, and bulbospongiosus reflexes will be performed to determine the neurological status of their respective nerve roots. The accurate use and interpretation of the bulbospongiosus reflex in particular is useful for the clinician in determining the cause of an asymmetrical recruitment of the pelvic floor musculature (PFM).

2.3 Embryological Derivation ¹ , ²

It is through an understanding of embryogenesis that the clinician will have the greatest opportunity to discover the origins, not only the perpetuator, of pain for the patient suffering with either pelvic or visceral pain. Due to the dearth of accurate clinical testing available for medical professionals with regard to patients experiencing pelvic pain, it behooves the clinician to understand the interrelationship that the various pelvic structures have with one another, and how structures from independent systems are intimately related from an embryological perspective. Utilizing this knowledge provides the clinician the opportunity to map out which visceral structures appear to be involved in the patient’s condition, and by cross-testing with special tests and active motions where possible and utilizing the enclosed chart a common spinal segment or segments is often found that unites the two viscera (Table 2.1). In doing so, the clinician will be able to deduce the exact spinal segment that will offer their patients immediate pain resolution, and initiate the healing process.

It is during the third week of gestation that cells of the dorsal midline of the embryo differentiate into the pseudocolumnar neuroepithelium of the neural plate from the surface ectoderm. ³ This neural plate will form the brain and spinal cord, and at the fourth week the neural plate folds dorsally and medially, eventually closing off and forming a hollow neural tube. The neural tube is a precursor to the neural canal that further differentiates into the ventricles of the brain and the central canal of the spinal cord. The lateral borders of the neural plate migrate and form the neural crest, which then further differentiates into neurons and neuroglia within the peripheral ganglia of the peripheral nervous system. The epidermis is formed from the closure of the ectoderm over the neural tube (Fig. 2.1) .

The caudal eminence is composed of the most caudal segment of the spinal cord that develops from specialized mesodermal structures. Secondary neurulation is the process in which the most caudal segments of the spinal cord arise from the caudal eminence, S2 to the coccygeal region. The caudal eminence further gives rise to the filum terminale, which is the anchoring attachment of the caudal end of the spinal cord.

With the closure of the neural tube, there is an elongation of the neural canal as the neuroepithelial cells elongate and retract in rhythmical fashion, which allows for the formation of the neuroblasts of the mantle layer, the precursor of the gray matter of the spinal cord, or they continue to divide as stem cells within the ventricular layer. Neuroblast differentiation continues as axon formation occurs within the neurons within the mantle layer. ³ Continued elongation and retraction produce glioblasts and neuroglial cells. Further ventricular divisions form the ependymal cells that line the central canal of the spinal cord. Axons formation occurs as neuroblasts further differentiate into neurons. White matter of the spinal cord is a result of the axonal proliferation and elongation. Synapses are found once the axonal growth cones find their targets in the brain, spinal cord, and peripheral nerve ganglia. The gray matter further differentiates into an H-shaped column as it elongates and extends the spinal cord.

The expansion of the gray matter contains neurons that receive sensory impulses (afferent) from the sensory organs, also known as dorsal, sensory, gray columns of the spinal cord. The ventral arms of the “H” originate the motor impulses (motor) to the muscles, also known as ventral, motor gray columns of the spinal cord. The gray commissure is the area of the gray matter that connects the left and the right side of the spinal cord and is seen as the crossbar of the “H” formation. It allows for right-left and left-right communication.

Autonomic motor neurons originate at T2 to L1 and are noted as projections from either side of the “H” between the dorsal and ventral columns, the lateral gray columns. These constitute the intermediolateral gray columns of the sympathetic division of the autonomic nervous system (ANS). The sympathetic motor neurons of the sympathetic division of the ANS have two sets of components: central motor neurons that are located within the intermediolateral gray columns, and the sympathetic chain ganglia and prevertebral ganglia. The autonomic motor nervous system parasympathetic nervous system lacks the telltale gray columns; however, they can be found at S2–4, and can be classified as central motor neurons of the two motor neuron parasympathetic divisions of the ANS. The parasympathetic nervous system will also be found centrally in the hindbrain and midbrain of the brain stem, and it is due to this fact that the parasympathetic system is commonly referred to the craniosacral system. ³ Research confirms that the utilization of antibiotics, and vaccines have deleterious effects on the function of the ANS and are noted clinically as “leaky gut syndrome” and the like disrupting the function of the enteric nervous system.

The white matter of the spinal cord consists of ventral, dorsal, and lateral funiculi that transmit ascending and descending nerve impulses between different regions of the spinal cord and between the spinal cord and the brain. Blood vessels infiltrate the white matter of the spinal cord and provide the vascularization of the spinal cord. The development of the peripheral nervous system occurs as the paired somites become segmented from the paraxial mesoderm and they then interact with the neural tube, inducing a growth of the motor nerve axons from either side of the tube ventrally, the ventral/motor nerve roots. As this is occurring, the neural crest cells become detached from lateral edges of the neural plate and aggregate adjacent to the dorsolateral region of the neural tube and associate with each pair of ventral roots. These dorsal pairs differentiate into the neurons and glioblasts of the sensory dorsal root ganglia (DRG); this occurs at each level except C1. Nerve fiber projections of the DRG extend into the spinal cord and synapse with neurons in the dorsal (sensory) column. Concurrently, an outward sprouting from the DRG joins with motor fibers of the ventral root to form a spinal nerve. A dorsal root is then formed from the dorsal root ganglion and its outward growing and inward growing projections, a 31-pair spinal nerve: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral ,and 1 coccygeal. This is the theoretical model for referred pain. ¹ , ² , ³ , ⁴ Just beyond where the spinal nerve is formed, there is another splitting; the outcome is the dorsal primary ramus and ventral primary ramus. The aforementioned rami contain the same functional makeup of axons that is present from the spinal nerves from which they originate. The dorsal ramus provides motor innervation to the true back muscles and sensory innervation to the skin over the back. It also contains sympathetic efferent and visceral afferent fibers that innervate blood vessels and glands. The ventral primary ramus provides motor innervation to the anterolateral musculature of the body wall and neck and to the upper/lower extremities. Their sensory fibers provide sensory innervation to the skin overlying these muscles and the parietal pericardium (C3 to C5), parietal pleura (T1 to T11), and parietal peritoneum (T12 to L1) of the body cavities. The ventral primary rami also contain sympathetic efferent and visceral afferent fibers. ³ With this information and understanding, the clinician will better understand the complexity of neural anatomy as it relates to the patient with pelvic pain, and will appreciate the appropriateness of performing an evaluation that is comprehensive and inclusive of the thoracic, lumbar, and sacral spines.

The superior aspect of the vagina, uterus, fallopian tubes, and oviducts are derived from the paramesonephric (müllerian) ducts. These ducts are common in both sexes; however, in male embryos they degenerate under the influence of antimüllerian hormone. With the absence of antimüllerian hormone, the female paramesonephric ducts continue to grow and develop, fusing at the second trimester in a distal to proximal fashion as they form the superior end of the vagina and uterus.

In female embryos, the gubernacula, embryonic structures on either side of the gonads that function to guide the terminal positioning of the gonad, form the labioscrotal folds inferiorly to the ovary superiorly. The gubernacula become attached to each paramesonephric duct and are being drawn medially as they fuse to form the vagina and uterus. This directly pulls the ovaries distally from the superior position within the posterior thoracic wall into the broad ligaments of the uterus (Fig. 2.2) . The two broad ligaments separate the true pelvis of females into an anterior and a posterior compartment containing the bladder and rectum, respectively. The fascia enclosed between the anterior and posterior mesothelium of the broad ligaments contains the arteries, veins, and nerves of the uterus, vagina, and ovarian ducts; the ovaries; the ovarian ligaments; and the superior ends of the round ligaments of the uterus. ³ , ⁴

2.4 Enteric Nervous System

The enteric nervous system (ENS) is located within the wall of the gastrointestinal tract, and it shares a common embryogenesis with the brain, and it also shares common neurotransmitters including serotonin, opiates, and cholecystokinin (CCK). Under normal circumstances, the ENS automatically and independently controls motility, absorption, and secretion. Local inflammation, however, has been shown to create long-lasting and sometimes permanent changes of the ENS structures leading to functional alterations of sensory processing and motility. ³ , ⁴

Research confirms strong interconnections between the stress response and visceral pain, acknowledging the considerable overlap within the central and peripheral nervous systems regarding the regions involved in the processing of visceral sensations and emotional regulation. Referred visceral pain can be due to alterations in the physiology of peripheral sensory neurons innervating the gut, and/or from an abnormal processing or modulation of visceral sensory information at the level of the CNS—the spinal cord, brain, or both. ⁵

2.5 Behavior of Nerves

It is imperative that the clinician appreciate the typical reaction of nerves to irritation and entrapment when evaluating and treating a patient with pelvic pain and dysfunction so as to have a better means of appreciating what the patient is demonstrating and reporting, and how the patient is responding to treatment.

The reduction of radial dimensions of the peripheral nerve as a result of local entrapment will lead to pain, paresthesias, or loss of function of that nerve. Pain is due to the depolarization of free nerve endings within the investments in the target tissue connective tissues, or the dural investments of the nerve root. The degree of pain depends upon the density of nociceptive receptors within the supportive connective tissue, the intensity of compression, and where along the neuroaxis the compression is located.

Pressure upon a cutaneous nerve will present as numbness along the cutaneous region innervated by that nerve where the edges will be well defined and the center often being full of anesthesia. With continued pressure the symptoms will progress and be noted as a paresthesia (“pins-and-needles”), and finally pain. This paresthesia will be provoked by the passive movement or stroking over of the affected skin, whereas active movement does not provoke symptoms. ¹ , ² With continued pressure there will be an alteration along the blood–nerve barrier and this has been noted as the primary cause of nerve root dysfunction. Persistent compression will lead to atrophy of the nerve, and subsequent wallerian degeneration is likely to follow. Local edema and proliferation of connective tissue ingrowths makes recovery unlikely. Pressure on a nerve trunk will demonstrate what is known as a release phenomenon, that is, initial compression of pins-and-needles results in its subsiding to absent, only to re-present itself upon release of compression. This may be experienced as more painful paresthesia than that of the initial compression. Movement of the limb or region will provoke more pins-and-needles. Direct nerve root compression will demonstrate segmental pain if the dural investment is compressed and compromised. Otherwise, the nerve root is insensitive along its length. Persistent pressure will lead to pins-and-needles along its respective dermatome where the edge and aspect are poorly defined, and stroking of the skin may be provocative of pins-and-needles. Movement will not provoke pins-and-needles; however, a nerve root with impeded mobility will often be painful if the joints relative to the nerve root are taken into a motion that further stretches the nerve root. Examples of this are noted with the straight leg raise and the prone knee flexion procedures that are performed during the evaluation. Upon tensioning of the nerve root, the clinician with a well-placed hand may be able to notice local muscle fasciculations under the palpating hand.

Pressure upon the dural sleeve will lead to a dermatomal reference of pain, and with persistent pressure upon the dural sleeve, eventual segmental numbness will occur due to the local necrosis of the dural sleeve. This is common with a posterolateral disk lesion. If the dura mater is compromised and infringed upon, the patient will experience what Dr. Cyriax termed extrasegmental reference of pain. This extrasegmental reference of pain will be experienced as an amorphic pain distribution with palpable nodules within the local musculature. These painful nodules are commonly mistaken as “trigger points,” where the treatment is often directed at the alleviation of the palpable muscle nodule, whereas it should be directed at the mechanical lesion that initiated the irritation of the dura mater at the spine.

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