Overview

The purpose of this chapter is twofold. The first purpose is to develop the concept that the entire nervous system forms a continuous tissue tract. This concept is central to the idea that movements of the trunk and/or limbs can have a profound biomechanical and physiological impact on the peripheral nervous system (PNS) and central nervous system (CNS). Mobility of the nervous system and some of the responses of the system to movement in normal and sensitized states are discussed.

The second purpose is to develop in the reader an understanding of the neurovascular entrapment syndrome. This is an underrecognized impairment present in some patients with a wide variety of diagnoses; for example, nonspecific arm pain, repetitive strain injury, carpal tunnel syndrome (CTS), and thoracic outlet syndrome (TOS). Standard medical care frequently fails with these patients. A theoretical model for the development and perpetuation of neurovascular entrapment syndrome is presented. Background information regarding the syndrome is provided, and the appropriate screening tools for assessment of the impairment are discussed. Treatment suggestions and a case study are presented at the end of the chapter.

Peripheral neuroanatomy

The PNS is generally regarded as the portion of the nervous system that lies outside the CNS (i.e., the brain and spinal cord). ^, The major components of the PNS include motor, sensory, and autonomic neurons found in spinal, peripheral, and cranial nerves. Although this partitioning is valid from an anatomical perspective, it often leads to a lack of appreciation as to the truly continuous nature and integrative function of the nervous system as a whole. The concept that the entire nervous system is a continuous tissue tract reinforces the idea that limb and trunk movements can have physiological and mechanical effects on the PNS and the CNS, which are local and global.

The nervous system is composed of two functional tissue types. One type of tissue is concerned with impulse conduction. This functional category includes nerve cells and Schwann cells. The second type provides support and protection of the conduction tissues—that is, the connective tissues.

Three levels in the organization of a peripheral nerve have been described ( Fig. 16.1 ). ^, At the innermost level the nerve fiber is the conducting component of a neuron (nerve cell). A connective tissue layer called the endoneurium surrounds each nerve fiber. The endoneurium surrounds the basement membrane of the neuron and plays an important role in maintaining fluid pressure within the endoneurial space. There are no lymphatic channels within the endoneurial space, and the pressure within this space increases with compression of the neuron.

Three Levels of Organization of a Peripheral Nerve or Nerve Trunk.

(A) Nerve trunk and components. (B) Microscopic structure of nerve fiber.

The second level of organization consists of a collection of many nerve fibers (a fascicle) surrounded by a layer of connective tissue called the perineurium. ^, The perineurium acts as a selective barrier to diffusion and as such exerts significant control over the local movement of fluid and ions. This connective tissue layer acts like a pressurized container; that is, extrusion of the contents occurs if the membrane is cut. The compartment enclosed by the perineurium does not contain lymphatic channels. This may be a problem during inflammatory states when edema is present deep to the perineurium. The perineurium is the last connective tissue layer to rupture in tensile testing of peripheral nerves. The outermost connective tissue layer of a peripheral nerve is called the epineurium. The epineurium surrounds, protects, and enhances gliding between the faniculi. Lymphatic channels are found within the epineurial compartment.

All three connective tissue layers are interconnected—they are not separate and distinct, but are continuous tissue layers. ^, Each of the connective tissue layers contains free nerve endings from the nervi nervorum. As a result, all three connective tissue layers are a potential source of pain. In addition, all three layers are continuous with the homologous connective tissue layers of the CNS—that is, the dura mater and the epineurium.

The vascular supply for peripheral nerves is designed to provide uninterrupted blood flow regardless of the position of the trunk and limbs. Extrinsic vessels provide blood flow to segmental vessels that, in turn, supply an extensive intrinsic (intraneural) vasculature within the PNS. These segmental vessels branch off of the extrinsic vessels and enter peripheral nerves in areas of low nerve mobility relative to the surrounding tissue. The intrinsic vasculature supplies all three connective tissue layers within the PNS. Arterioles and venules are found in the epineurial and perineurial spaces, but only capillaries are found in the endoneurial compartment.

Peripheral nerves are regularly subjected to compression and elongation (stretching), which have been shown to raise intraneural pressure. Compression and elongation decrease the diameter of the intrinsic blood vessels, increase the intraneural pressure, and result in a reduction in blood flow within the nerve. Compressive forces of 20 to 30 mm Hg have been shown to adversely affect intraneural blood flow, while compressive forces of 50 to 70 mm Hg have been shown to result in complete arrest of blood flow, which results in damage to myelin and axons. A strain (elongation) of 6% to 8% has been shown to decrease intraneural blood flow by 50% to 70% in the sciatic nerve of rats. ^{, ,} A strain of 15% in the sciatic nerve of a rabbit has been shown to result in complete arrest of blood flow, and the same strain produces an 80% reduction in blood flow in the rat sciatic nerve. Strains of 11% or greater are produced by some of the positions used in neurodynamic tests of the upper limb. Significant increases in intraneural pressure and concomitant decreases in intraneural blood flow have been shown to adversely affect neuronal conduction. ^{, ,} Intraneural blood flow in the median nerve at the wrist can be assessed with Doppler sonography and used in the diagnosis of CTS.

The cytoplasm in cells moves and has thixotropic properties; that is, the viscosity of cytoplasm is lower when it is continuously moving. In neurons, the movement of the cytoplasm from the cell body through the axons (anterograde movement) occurs at two speeds. Fast axoplasmic flow occurs at a rate of about 100 to 400 mm/day and is used to carry ion channels and neurotransmitters (i.e., materials required for normal impulse conduction) to the nerve terminals. Slow axoplasmic flow occurs at a rate of about 6 mm/day and is used to transport cytoskeleton proteins, neurofilaments, and other materials used to maintain the physical health of the cell. A third flow occurs in the opposite direction (retrograde) at a rate of about 200 mm/day. Retrograde transport carries unused substances and exogenous materials taken up at the terminus (e.g., neurotrophic factors). The material carried back to the cell body by retrograde transport has been shown to influence activity in the cell nucleus.

Compression raises intraneural pressure, which has a negative impact on the flow of cytoplasm. Anterograde and retrograde flow of axoplasm is impaired with 30 mm Hg compression on the nerve, hypoxia, or a strain of 11% or greater. Prolonged or intense exposure to compression can result in conduction abnormalities, endoneurial edema, fibrin deposition, demyelination, and axonal sprouting. Each of these events increases the likelihood of developing adhesions and abnormal impulse-generating sites (AIGSs). (The negative impact of AIGSs is discussed in the section on adaptive responses to pain.)

Mobility of the peripheral nervous system

Several types of tissues (e.g., bone, fascia, and muscle) surround peripheral nerves as they “travel” to target tissues. Peripheral nerves can be thought of as passing through a series of tissue tunnels composed of various biological materials. The composition of the tissue tunnel changes with the passage of the nerve from the vertebral column (an osseous tunnel) to the target tissue (e.g., from an osseous tunnel to a soft tissue and/or fibro-osseous tunnel). A “mechanical interface” exists at the junction between the nerve and the material adjacent to the nerve that forms the tissue tunnel. Movement of the trunk and/or limbs can cause three types of movement to occur in the peripheral nerves: unfolding, sliding, and elongation .

When there is little or no tension in a peripheral nerve, the axon typically contains undulations (folds). As tension is applied the axon will unfold so that the undulations disappear. Sliding can be defined as movement between the nerve and the surrounding tissues at the mechanical interface (extraneural movement). Sliding by itself does not cause significant elongation or tension to develop within the nerve, so intraneural pressure remains relatively unchanged. Ultrasound studies have shown that the median, ulnar, sciatic, and tibial nerves undergo extraneural movement (sliding) with movement of the upper and lower limbs, respectively.

Elongation of the nerve occurs when tension is applied to a nerve, and there is little or no unfolding and sliding at the mechanical interface. Elongation causes movement to occur between the neural elements and connective tissue layers (intraneural movement). Elongation decreases the diameter of the nerve, resulting in an increase in the intraneural tension and pressure. An increase in intraneural pressure has been shown to decrease the flow of blood and axoplasm, resulting in altered neural function (see previous section). Elongation within the median and ulnar nerves has been shown to occur with movements of the upper limb.

Both extraneural and intraneural movements may occur simultaneously within a nerve, but they may not be uniformly distributed. When a body moves, some parts of the PNS will undergo primarily extraneural movement (sliding) with little or no development of tension, while other areas will undergo intraneural movement (elongation), which results in an increase in intraneural tension and pressure. As a consequence, some areas within a nerve slide, developing little or no tension, whereas other areas of the same nerve elongate significantly, increasing the amount of intraneural tension. In areas repeatedly exposed to high amounts of tension (e.g., the median nerve at the wrist) the nerves are found to contain a higher-than-average amount of connective tissue.

If one considers the entire nervous system as a continuous tissue tract, then the idea that movement and/or tension developed in one region of the nervous system can be distributed and dissipated throughout the entire nervous system becomes apparent. ^, The inability of a component within the nervous system to dissipate and/or distribute movement and tension can lead to abnormal force development and lesions elsewhere in the continuous tissue tract.

Peripheral nerve entrapment

Seddon’s classification of nerve injury is based upon mechanical trauma. Schaumberg modified this paradigm into an anatomically based scheme containing three classes of injury ( Table 16.1 ). Injuries in class II and III are caused by macrotrauma, which results in some disruption to the integrity of the nerve fiber. The following discussion of entrapment is focused on microtrauma in which there is no breach in the anatomical integrity of the nerve fiber (class I). Mechanical microtrauma resulting in nerve entrapment can occur with excessive or abnormal friction, compression, and/or tension (elongation).

Tissue tunnels, peripheral nerves, and the mechanical interfaces between them are all vulnerable to mechanical microtrauma—that is, abnormal friction, compression, and/or tension. ^, Some peripheral nerves are exposed to bony hard interfaces (e.g., the lower cords of the brachial plexus at the first rib), which are potential sources of abnormal friction. Inflammation and swelling within a tissue tunnel can produce compression of a nerve, for example, the median nerve within the carpal tunnel. The point at which a nerve branches limits the amount of gliding (extraneural movement) available at that location, and increases the amount of local intraneural tension developed with movement (e.g., the tibial nerve in the popliteal fossa). ^,

Microtrauma can produce an intraneural lesion that causes a decrease in intraneural flow of blood and axoplasm, demyelination, and/or conduction defects. ^, If the lesion occurs in the connective tissues of the nerve, there may be pain, inflammation, proliferation of fibroblasts, and scar formation (fibrosis). Ultrasound studies have shown that the median nerve in patients with CTS is enlarged by approximately 30%. An intraneural scar decreases the compliance of the nerve and increases the amount of intraneural pressure and tension generated with elongation. Intraneural lesions can impair or completely block the ability of the nerve to conduct action potentials. ^, Partial or complete conduction blocks can result in abnormal sensation, loss of motor function, autonomic dysfunction, and atrophy of target tissue (e.g., muscle and/or skin). However, several forms of physical activity/exercise, including swimming and treadmill training, have been shown to improve recovery from peripheral nerve injury in animal models (crushed sciatic nerve) using a variety of outcome measures. There is no consensus about the best time to start any form of exercise following peripheral nerve injury although one study suggested earlier intervention was beneficial.

Microtrauma can produce an extraneural lesion. ^{, ,} The damage in an extraneural lesion occurs in the tissue surrounding the nerve—that is, at the mechanical interface. Swelling within the tissue tunnel can produce compression of the nerve. Fibrosis can produce adhesions at the mechanical interface leading to a decrease in sliding of the nerve. A decrease in the ability of a nerve to slide within a tissue tunnel will result in an abnormal increase in intraneural tension and pressure as movement is imposed on the nerve. The increase in local intraneural tension can produce abnormal changes in the conduction of action potentials, and the tension will be distributed in an aberrant pattern throughout the continuous tract of the nervous system. The resultant abnormal distribution of tension predisposes the nervous system to the development of lesions at other sites.

Friction, compression, and tension can produce microtrauma, which results in intraneural and extraneural pathology. ^, For example, fibrosis can produce a combined pathological state that results in a substantial reduction in the ability of a nerve to slide within the tissue tunnel and a substantial increase in intraneural tension during nerve elongation as the compliance of the nerve is decreased. Movement of the median nerve at the carpal tunnel has been shown to occur with movements of the upper limb. Longitudinal and transverse movements of the median nerve at the carpal tunnel have been shown to be reduced in the presence of microtrauma (i.e., CTS, ^, nonspecific arm pain, ^, and whiplash injury).

Intraneural and extraneural lesions result in an abnormal distribution of sliding and tension throughout the nervous system with movement of the trunk and/or limbs. The abnormal distribution of tension within a nerve increases the probability of a second lesion or abnormality developing within the nerve. This situation led Upton and McComas in 1973 to first use the term “double crush injury.” (This term should be considered a misnomer because a “crush” does not necessarily occur.) For example, entrapment of the median nerve at the carpal tunnel can cause the development of abnormal tension in cervical spinal nerves, resulting in a lesion at that site. Upton and McComas have shown that a lesion at the carpal tunnel increases the risk of having a second neural lesion in the cervical region.

Pathogenesis of neurovascular entrapment

Neurovascular entrapment can occur at any point along the continuous tract of the nervous system. The carpal tunnel, a common site of entrapment, has been studied and provides a framework of information regarding the pathogenesis of neurovascular entrapments. Sunderland has reasoned that a change in the normal pressure gradients within the carpal tunnel can lead to compression of the median nerve. In order to maintain homeostasis in the carpal tunnel and the median nerve, blood must flow into the tunnel, then into the nerve and back out of the tunnel. For blood flow to occur in the median nerve the blood pressure must be highest within the epineurial arterioles, and becomes progressively lower in the capillaries and epineurial venules and lowest within the extraneural space of the carpal tunnel. Any increase in the pressure of a single compartment has the potential to disrupt the normal pressure gradients and impair the flow of blood within the compartments of the carpal tunnel and the median nerve. Impaired intraneural blood flow can lead to localized hypoxia, edema, inflammation, and fibrosis.

An increase in pressure within the carpal tunnel can occur for a variety of reasons—for example, synovial hyperplasia, thickening of tendons, venous congestion, inflammation, and/or edema. Venous blood flow within a nerve will be impaired, and venous stasis will develop if pressure within the extraneural space of the carpal tunnel becomes greater than the pressure within the epineurial venules. Because blood pressure within venules is relatively low, partial occlusion of blood flow can begin to occur in the carpal tunnel with pressures as low as 20 to 30 mm Hg. ^, Intraneural blood flow in the median nerve at the wrist can be detected with Doppler sonography.

The pressure within the extraneural space of the carpal tunnel is normally about 3 mm Hg (range of 2 to 10 mm Hg) with the wrist in a neutral position. ^, The pressure can rise to over 20 mm Hg with the wrist in full flexion, and pressure can rise to over 30 mm Hg when the wrist is placed in 90 degrees of extension or with the functional task of using a computer mouse to drag or point at an object. Studies have shown that the pressure within the carpal tunnel in someone with CTS can be 30 mm Hg or more with the wrist in neutral, and can increase to about 100 mm Hg when the wrist is in 90 degrees of flexion ^{, ,} or extension. ^, Compressive forces of 20 to 30 mm Hg have been shown to adversely impact intraneural blood flow, whereas compressive forces of 50 to 70 mm Hg have been shown to result in complete arrest of blood flow and cause demonstrable damage to myelin and axons. Motor and sensory abnormalities begin to manifest at about 40 mm Hg, and complete blockade of the median nerve has been shown to occur at 50 mm Hg. The pressure found in the carpal tunnel of people with CTS is clearly adequate to disrupt the normal flow of blood, axoplasm, and action potentials within the median nerve, causing severe impairment to normal nerve functions.

Sunderland proposed that venous congestion or stasis within the carpal tunnel will lead to localized hypoxia, edema, and fibrosis. Hypoxia causes capillary endothelial cells to deteriorate and local C fibers to secrete substance P and calcitonin gene–related peptide, which in turn causes mast cells to release histamine and serotonin. ^, Together these chemical mediators augment the inflammatory state and cause the endothelial cells of capillaries to further deteriorate by becoming flatter, larger, and leakier, enhancing exudation and edema.

Deterioration of the capillary endothelium results in exudation and the formation of a protein-rich edema in the interstitial space. Protein-rich edema stimulates proliferation of fibroblasts, resulting in fibrosis. This intensifies the abnormal pressure gradients, resulting in more tissue hypoxia; that is, a positive feedback or self-perpetuating cycle of pathology is initiated. Intraneural fibrosis decreases compliance of the nerve, and extraneural fibrosis results in the formation of adhesions at the mechanical interface between the nerve and the tissue tunnel. Fibrosis causes a nerve to become stiffer and less mobile, resulting in an abnormal increase in tension when movement is imposed on the nerve.

This set of circumstances (described above) may be referred to as a neurovascular entrapment syndrome, and it has the potential to cause the development of problems elsewhere in the system—that is, a double crush injury (see previous section). Upton and McComas studied 115 subjects with CTS or ulnar impingement at the elbow. They found that 81 of the 115 subjects also had evidence of a neural lesion at the neck. Because all nerves essentially travel within tissue tunnels, the potential exists for this scenario to occur elsewhere in the continuous tissue tract of the nervous system (e.g., the thoracic outlet). ^{, ,}

Adaptive responses to pain

A thorough discussion of the pain associated with neurovascular entrapment is beyond the scope and intent of this chapter. The topic of pain management is discussed in Chapter 30 of this book. However, we would like to describe the development of hyperexcitable states and AIGSs in neurons as well as their role in the development of pain associated with neurovascular entrapment.

“Normal” or physiological pain occurs when peripheral nociceptors are subjected to a stimulus that is at or above the threshold for firing. “Abnormal” or pathological pain can occur when there is a change in the sensitivity (threshold) of the somatosensory system. Devor wrote that “the crucial pathophysiological process triggered by nerve injury is an increase in neuronal excitability.”

Neurons that become inflamed, hypoxic, and/or demyelinated can enter a hyperexcitable state. ^, A neuron in a hyperexcitable state can begin to discharge spontaneously and/or develop a sustained rhythmic discharge after stimulation. In addition, hyperexcitable neurons can develop mechanosensitivity, chemosensitivity, and/or thermal sensitivity, all of which can result in the production of allodynia, a form of pathological pain. ^{, , , , ,} These changes in the behavior of a nerve can occur in the absence of detectable degeneration. The changes in impulse generation and neuronal sensitivity are characteristics of an AIGS. A hyperexcitable state and an AIGS can develop with the mechanical microtrauma and inflammation often associated with peripheral nerve pathology that result from compression, tension, and friction. ^{, , ,} A variety of chemical mediators have been implicated in the development of a hyperexcitable state in a neuron; for example, neurotrophins, ^, histamine, and other inflammatory mediators. These chemical mediators are thought to act through changes in gene expression, ^{, ,} changes in voltage-gated sodium channel expression, and a reduction in anterograde axoplasmic transport. ^,

The dorsal root ganglion appears to play a significant role in the pain associated with peripheral nerve pathology. ^, Mechanical microtrauma and inflammation of peripheral nerves can cause the dorsal root ganglion to become hyperexcitable (sensitized). The change in sensitivity allows what were weak, subthreshold stimuli to evoke pain and suprathreshold stimuli to evoke exaggerated pain (hyperalgesia). In addition, the dorsal root ganglion can develop mechanosensitivity, chemosensitivity, and thermal sensitivity, resulting in allodynia. This change in sensitivity reflects a change in the physiology of the nerve and may be a component in the development of enhanced central sensitivity to pain and the development of a chronic pain state.

As noted previously, the PNS and CNS represent a continuous tissue tract. The pain and symptoms associated with musculoskeletal injury and/or peripheral nerve pathology can include changes that are the result of an alteration in the autonomic nervous system, which is considered part of the continuous tissue tract of the nervous system. ^, For example, catecholamines do not normally elicit pain. However, if a nerve is injured or if there is local inflammation, the catecholamines can induce pain (chemosensitivity) and maintain or enhance pain in inflamed tissues.

Some patients who are treated for musculoskeletal injuries have signs that may be related to autonomic dysreflexia. Wyke demonstrated that stimulation of nociceptors in spinal joints resulted in reflex changes in the cardiovascular, respiratory, and endocrine systems. Dysregulated breathing has been documented in patients with chronic pain. Patients with nonspecific arm pain have a reduced sympathetic vasoconstrictor response in the hand of the affected limb. Thermal asymmetry has been documented in the hands of patients with neurogenic TOS. Feinstein and colleagues showed that injecting saline solution into the thoracic paraspinal muscles caused pallor, diaphoresis, bradycardia, and a drop in the blood pressure. These cardiovascular and respiratory changes are often associated with an alteration in the output from the autonomic nervous system. ^{, ,}

In patients with cumulative trauma disorder (CTD), signs of abnormal autonomic nervous system output can include (1) vasomotor reflexes leading to cool, pale skin, (2) changes in the pattern of sweating (hypohidrosis and/or hyperhidrosis), (3) trophic changes in the skin, (4) hyperactive flexor withdrawal reflexes, and/or (5) paradoxical breathing patterns. Edgelow has described paradoxical breathing as the predominant use of the scalene muscles for ventilation during quiet breathing versus normal ventilation, which is predominantly a function of the diaphragm. Edgelow found that paradoxical breathing is present in most patients with CTD of the upper extremity. A better appreciation of the contribution of the autonomic nervous system to the pathology and symptoms present in some patients with neurovascular entrapment may enhance the effectiveness of their treatment.

Clinical examination and treatment of neurovascular entrapment

For an effective evaluation of a patient with a neurovascular entrapment problem, the whole person must be addressed and involved in the evaluation and treatment processes. This approach requires the therapist to consider a biopsychosocial approach versus a biomedical approach. In this case, the therapist becomes the evaluator, teacher, and guide for the patient. Traditionally, a biomedical approach has been taken with disorders such as neurovascular entrapment. In a biomedical model, the patient’s disability and impairments are seen as a direct correlation to the tissue pathology. The biopsychosocial model addresses the whole patient and provides a means for the therapist to consider the biomedical factors (underlying tissue) and psychosocial factors influencing a patient’s symptoms. Utilization of this approach has become more accepted in physical therapy practice, along with the understanding that pain is often influenced by a patient’s emotional well-being, thoughts about their condition, cultural beliefs, and environmental influences. Given the impact that neurovascular entrapment symptoms can have on a patient, it is imperative that a clinician understand the interplay between the biomechanical impairments and any underlying psychosocial issues. Neurovascular entrapment can occur in both the upper extremity and lower extremity; however, the most common examples seen by therapists are TOS and CTS. The clinical examination discussed will highlight the specifics regarding neurovascular entrapment of the upper extremity.

Patients with neurovascular entrapment often present with severe and irritable symptoms; therefore a detailed subjective examination is necessary to understand the behavior of the symptoms and the impact the symptoms are having on the patient’s life. Initial goals of the subjective exam include determining if the patient is appropriate for physical therapy, developing a hypothesis list regarding potential sources of the patient’s symptoms, and determining the extent and vigor of the objective examination. The subjective exam should begin with the patient completing a detailed body chart that outlines the specific area of symptoms and the patient’s description of the symptoms. A body chart provides the clinician a thorough picture of symptom location and the potential relationship between areas of symptoms. The patient’s description of the symptoms may provide the clinician with potential hypotheses regarding pain mechanisms and potential neurovascular involvement. The patient with primarily neurological symptoms may have pain that is described as sharp or burning with numbness or paresthesia, and spasms or weakness in the extremity. ^, Vascular symptoms may be due to either arterial or venous compression. Arterial symptoms may include pain in the distal portion of the extremity (vs. pain proximally at the shoulders or neck), swelling, complaints of stiffness or heaviness of the extremity, coldness of the distal extremity, pallor, and paresthesia (likely due to ischemia). Symptoms that originate from venous compression are likely to be described as feelings of stiffness or heaviness of the extremity, asymmetrical extremity edema, paresthesia, and limb discomfort/pain.

Understanding pain mechanisms and the overlap between these mechanisms can be helpful for both the clinician and patient. It is beyond the scope of this chapter to discuss in detail each of these mechanisms and the body of evidence supporting them. However, a brief explanation is appropriate when treating patients with painful conditions. Pain mechanisms have been classified based on the dominant neurophysiological mechanism. Classification of pain mechanisms is a useful way for clinicians to identify the likely neurophysiological source of symptoms. The three main pain classifications are nociceptive, peripheral neuropathic, and central sensitization . Smart and colleagues have identified common signs and symptoms to assist clinicians in classifying pain mechanisms in patients with low back pain with and without leg symptoms. Nociceptive pain is classified by distinct symptoms and signs: pain localized to the area of injury/dysfunction, clear and proportionate mechanical/anatomical aggravating and easing factors. Symptoms are usually intermittent with movement or mechanical provocation; no dysesthesias are present, and there is no night pain, and no description of burning or shooting symptoms. If the patient assumes antalgic postures to relieve pain, the odds of pain being nociceptive are reduced. The strongest predictor of nociceptive pain is pain localized to the area of injury/dysfunction with an odds ratio (OR) of 69. Peripheral neuropathic pain consists of three signs and symptoms: pain referred in a dermatome or cutaneous nerve distribution, a history of nerve injury (pathology or mechanical compromise), and pain or symptoms are provoked with mechanical tests such as neurodynamic testing (e.g., straight leg raise). Symptoms that are in a dermatomal or cutaneous distribution have an OR of 24, suggesting that if symptoms are in a dermatomal or cutaneous nerve distribution the patient is 24 times more likely to have neuropathic pain. Central sensitization is pain that is typically present outside of tissue pathology and is associated with an increase in sensitivity of the CNS. Four signs and symptoms have been associated with central sensitization: pain that is disproportionate and nonmechanical, and is unpredictable in terms of aggravating and easing factors; pain that is disproportionate to the extent of injury or pathology; the presence of maladaptive psychosocial factors; and diffuse nonanatomical areas of pain or tenderness to palpation. The OR for disproportionate pain with nonmechanical/unpredictable aggravating factors is 30.69. It is important for clinicians to understand that patients are likely to present with varying amounts of each of these pain mechanisms regardless of acuity of the injury. For example, a patient may present with a 2-week onset of symptoms that appears to be CTS and have symptoms that are 70% peripheral neuropathic, 20% nociceptive, and 10% central sensitization. Understanding and classifying pain allows the clinician the ability to better plan the objective examination and treatment plan. Establishing symptom behavior by obtaining aggravating and easing factors and the 24-hour behavior of the symptoms provides further insight into the patient’s presentation and the clinician’s potential hypotheses. A discussion of which activities, postures, and positions/movements produce the patient’s symptoms—including the amount of time to onset and location/intensity of symptoms, followed by positions, movements, or activities to settle the symptoms—can aide in determining whether the neural or vascular system is a potential source of the problem and determining the level of tissue irritability. When an extended period of time is required for symptoms to ease after very little activity provokes the symptoms, then irritability may be deemed high. Motor changes of relevance to the potential problem of neurovascular entrapment include complaints of dropping things, weakness, or an inability to perform motor tasks that were done previously without difficulty. Key components that should be discussed with the patient include history of trauma, repetitive activities, sustained static or tension postures (e.g., computer keyboard work), or physical activities performed with a high level of cognitive demand, as seen in a pianist. In addition, the progression of the symptoms or complaints should be determined. The history should include a discussion of general health and screening questions for relevant medical conditions such as asthma, diabetes, and hypothyroidism. Chapter 6 of this text provides more detail regarding medical screening and a differential diagnosis to ensure patients are appropriate for evaluation and intervention.

Health-related quality of life or patient-reported outcome measures are useful in patient management to assess multiple domains such as physical ability, psychological, emotional, and social well-being. Condition specific measures can be utilized for neurovascular entrapments, such as The Michigan Hand Outcomes Questionnaire for patients with CTS. For conditions such as TOS, condition-specific measures do not currently exist; therefore clinicians may choose more generic measures such as the Neck Disability Index or the Disabilities of the Arm, Shoulder, and Hand (DASH). The Fear Avoidance Beliefs Questionnaire was developed to measure fear and avoidance of activity in patients with low back pain; however, it has now gained acceptance for usage in conditions outside of low back pain, to screen for depression risk factors. The depression screening questions consist of a cluster of three questions that have established likelihood ratios (LR), +LR of 9.1 and −LR 0.05. Use of these tools in daily practice provide the clinician with a broader view of the patient’s self-rated function and insight into potential psychosocial barriers to treatment. Health-related quality of life measures provide reliable, valid, and responsive tools to measure the outcome of interventions.

Objective examination

The objective examination in patients with neurovascular entrapment can be complex, and the clinician needs to utilize tests and measures that help rule out potential competing diagnoses. The differential diagnosis for a suspected neurovascular entrapment of the upper extremity includes cervical spine referral/radiculopathy, brachial plexus injury, rotator cuff pathology, glenohumeral joint dysfunction, lateral epicondylalgia, medial epicondylalgia, complex regional pain syndrome (CRPS I or II), systemic disorders, and upper extremity deep vein thrombosis.

Given the extensive differential diagnosis list, both the subjective and objective exams will be comprehensive. The clinician must gauge the patient’s level of irritability during the subjective exam to determine the vigor of the objective exam, thereby avoiding excessive or unintentional provocation of the patient’s symptoms. Table 16.2 provides the suggested modifications to a standard biomechanical examination of the upper quarter necessary to rule in/out potential neurovascular entrapment. The clinician must adjust the examination based on the patient’s unique presentation and the irritability of the condition. Generally, it is recommended that the examination proceed from active movement produced by the patient to passive assessment. When possible, testing maneuvers should be performed by the patient so that he or she can learn to self-assess his or her status before and after treatment procedures. This self-assessment gives the patient control, thus decreasing the fear of movement or reinjury. The concept of the patient gaining control of the problem(s) is fundamental and must be integrated into the initial patient contact for development of an effective self-management approach. Without an effective self-management strategy, the patient is at risk for recurrent problems and the development of a chronic condition. The objective examination scheme presented here is considering neurovascular entrapment of the upper extremity. Emphasis will be placed on CTS and TOS; however, the sequence of the examination can remain the same for the lower extremity by replacing the regions examined and the special tests utilized.

TABLE 16.2

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