Defining pain

The primary purpose of pain is to protect the body. It occurs whenever there is tissue damage, and it causes the individual to react to remove the painful stimulus. Pain is also a sensation with more than one dimension. To the individual, pain is both an objective and a subjective experience. The objective dimension is the physiological tissue damage causing the pain. The subjective dimensions include the following⁹:

All of these components taken together constitute the client’s pain experience. Thus all must be addressed for a successful pain management program. When the subjective components of the pain experience are ignored, it is entirely possible that the client’s underlying tissue damage may be corrected without her or his pain perception being cured.

In addition, recognizing that pain is more than simply a physical injury or disease process helps clinicians explain some of the inconsistencies observed in patients with chronic pain. Why is a client’s pain report out of proportion to the magnitude and duration of the injury? Why is pain intolerable to one person and merely uncomfortable to another? And why is pain tolerable in one instance but overwhelming to the same individual when experienced at a different time?

The answers lie in the interconnectedness of the nervous system and the fact that pain transmission involves several higher centers. To select the most appropriate intervention, it is important for clinicians to have at least a general idea of the pain pathways. An overview of pain anatomy and physiology is discussed next.

Pain anatomy

Pain arises from the stimulation of specialized peripheral free nerve endings called nociceptors. Injurious stimulation to the skin, muscle, joint, viscera, or tissue can trigger these peripheral terminals, whose cell bodies are located in the dorsal root ganglia and trigeminal ganglia. The density of nociceptors varies between as well as within these tissues. Nociceptors are extremely heterogeneous, differing in the neurotransmitters they contain, the receptors and ion channels they express, their speed of conduction, their response properties to noxious stimuli, and their capacity to be sensitized during inflammation, injury, and disease.¹⁰

Nociceptors found in interstitial tissues become excited with extreme mechanical, thermal, and chemical stimulation,¹¹ whereas nociceptors found in vessel walls become excited with these stimuli plus marked constriction and dilation of the vessels.¹² These receptors respond directly to some noxious stimuli and indirectly to others by means of one or more chemicals (histamine, potassium, bradykinin) released from cells in the traumatized tissues.¹³

Thermal nociceptors are triggered by intense hot or cold temperatures (>45° C or <5° C). They have fibers that are of small diameter and thinly myelinated with moderately fast conduction signals of 5 to 30 m/s. Mechanical nociceptors are triggered by intense pressures applied to the skin, such as a pinch. They also have thinly myelinated, moderately conducting fibers with speeds of 5 to 30 m/s.

Polymodal nociceptors are triggered by more than one sensory modality (mechanical, chemical, or thermal). These nociceptors have small-diameter, nonmyelinated fibers that conduct more slowly, generally at velocities less than 1.0 m/s. Stimulation of these receptors causes sensations of diffuse burning or aching pain. The difference in the fibers’ size and lamination determines the speed at which impulses will travel to the brain.

These three types of nociceptors are broadly distributed in the skin and tissues and may work together. One example would be hitting one’s shin against a table: a sharp “first pain” is felt immediately, followed later by a more prolonged aching, sometimes burning, “second pain.”¹³ The fast, sharp pain is transmitted by A delta fibers that carry information from thermal and mechanical nociceptors. The slow, dull pain is transmitted by C fibers that are activated by polymodal nociceptors.

Nociceptive input travels on A delta and C fibers into the dorsal horn of the spinal cord, where the gray matter is laminated and organized by cytological features. The first-order A delta and C fibers synapse with second-order neurons in lamina I (marginal layer), II (the substantia gelatinosa [SG]), and V. The second-order neurons do one of three things. A small number synapse with motor neurons, causing reflex movements (e.g., withdrawing the hand from a hot object). Others synapse with autonomic fibers, causing responses such as changes in heart rate and blood pressure and localized vasodilation, piloerection, and sweating. Most, however, travel a multisynaptic route to the higher centers by means of the ascending tracts.^11,14

There are four major classes of neurons¹⁵ responding to pain in the dorsal horn: low-threshold nociceptive-specific neurons designated class I; wide dynamic range (WDR) neurons designated class II; high-threshold nociceptive neurons designated class III; and a fourth, nonresponder group of neurons that develop spontaneous activity with exposure to endogenous inflammatory cytokines, designated class IV. Nociceptive-specific neurons are most abundant in superficial lamina; their receptor fields are discrete and vary from one to several square centimeters.¹⁶ WDR neurons, in contrast, respond to a wide range of stimuli from A delta, A beta, and C fibers in a graded manner (i.e., the rate of firing escalates with increasing intensity of stimulation), can be found in all lamina, and are the most prevalent cells in the dorsal horn.¹⁶ Because of their unique response to innocuous or nociceptive input, as well as their larger receptor field, WDR neurons play an important role in the central sensitization and the plasticity of the spinal cord.¹⁶

Nociceptive input crosses at the cord level to the anterolateral quadrant of the ascending contralateral spinothalamic tract (Figure 32-1). The axons of the anterolateral quadrant are arranged so that the sacral segments are most lateral, with the lumbar segments more medial and the cervical segments most central. This arrangement may be important clinically in that symptoms may be provoked according to dermatomal maps to some degree.¹⁷ Pain dermatomes overlap to several adjacent dorsal roots so boundaries can be less distinct, requiring the clinician to distinguish the pain and dysfunction.

The anterolateral tract is divided into three ascending pathways: the spinothalamic, spinoreticular, and spinomesencephalic. The spinothalamic tract conveys information about painful and thermal stimulation (location and intensity) directly to the ventral posterior lateral nucleus of the thalamus, as well as sending collaterals off at the brain stem to join the spinoreticular tract. Axons within the spinoreticular tract synapse on neurons of the reticular formation of the medulla and pons, which relay information to the intralaminar and posterior nuclei of the thalamus and to other structures in the diencephalon, such as the hypothalamus (emotional response to pain).

Axons in the spinomesencephalic tract relay information to the mesencephalic reticular formation and periaqueductal gray matter by way of the spinoparabrachial tract. It then projects to the limbic system, which is involved with the affective component of pain (central modulation of pain).

The thalamus processes and relays information to several higher centers.¹² Each projection serves a specific purpose. Axons of the spinothalamic tract project information to both the lateral and medial nuclear groups of the thalamus. The lateral nuclear group of the thalamus is where information about the location of an injury is thought to be mediated.¹³ Injury to the spinothalamic tract and the lateral nuclear group of the thalamus causes central neuropathic pain, which is discussed in further detail later.

Projections from the spinoreticular tract to the medial nuclear group of the thalamus are concerned with processing information about nociception, and they also activate nonspecific arousal systems. These pathways project from the thalamus to the basal ganglia and many cortical areas.

Projections to the postcentral gyrus (sensory cortex) are responsible for pain perception. It is from this projection that pain can be localized and characterized. Projections from the thalamus to the frontal lobes and limbic system are concerned with pain interpretation. It is from all these projections that an individual perceives pain as hurting. Projections from the thalamus, as well as from the limbic system and sensory cortical areas, to the temporal lobes are responsible for pain memory; and projections from the thalamus to the hypothalamus are responsible for the autonomic response to pain.

Pain transmission

Ascending transmission of pain impulses is mediated by the action of the chemical excitatory neurotransmitter glutamate (A delta and C fibers) and tachykinins such as substance P (C fibers). Glutamate and neuropeptides have distinct actions on postsynaptic neurons, but they act together to regulate the firing properties postsynaptically.¹³ Tachykinins’ activity is thought to prolong the action of glutamate, as levels are increased in persistent pain conditions.¹⁶ The substrates of nociception that exist at the spinal level are complex in that more than 30 different neurotransmitters acting on more than 50 different receptors have been identified in the spinal cord and associated with some pain-related phenomenon.¹⁸ Modulation of these substrates will assist in the effectiveness of therapeutic interventions and will be discussed next.

Pain modulation

Nociceptive transmission is modulated at several points along the neural pathway by both ascending and descending systems.

The gate control theory

The SG contains an ascending gating mechanism to block nociceptive impulses from leaving the dorsal horn of the spinal cord. The first-order neurons for both nociceptive and nonnociceptive information synapse with second-order neurons in the SG. The second-order neurons for both types of information project to specialized neurons named T cells (transmission cells) in lamina V. For pain transmission to occur, T cells must be stimulated while the SG is inhibited. The input from A delta and C fibers stimulates the T cells and inhibits the SG (Figure 32-2). Therefore A delta and C fiber input opens the gate, allowing pain transmission to the higher centers. On the other hand, when the SG and T cells are both stimulated, the T cells are inhibited and the gate is closed to pain transmission. The input from nonnociceptive A beta fibers carrying information from pressoreceptors and mechanoreceptors stimulates both the T cells and the SG. Therefore A beta fiber input closes the gate, blocking pain transmission.¹⁷

One example that illustrates the gate control theory is the use of transcutaneous electrical nerve stimulation (TENS) in an area that overlaps the injury. It works to reduce pain by activation of large-diameter A beta fibers that “closes the gate,” thereby preventing pain transmission to the higher centers of the brain. This is also why shaking (vibrating) your hand after hitting your thumb with a hammer temporarily relieves pain.

Categorizing pain

Pain is grouped into several categories: acute, chronic, referred, central neuropathic, autonomic, and peripheral.

Acute pain is the normal predicted physiological response and serves as a warning. It alerts the individual that tissues are exposed to damaging or potentially damaging noxious stimuli. Acute pain is localized, occurs in proportion to the intensity of the stimuli, and lasts only as long as the stimuli or the tissue damage exists (1 to 6 months).³² Although acute pain is associated with anxiety and increased autonomic activity (increased muscle tone, heart rate, and blood pressure),³³ it is usually relieved by interventions directed at correcting the injury. The pain experience is usually limited to the individual.³⁴

Chronic pain is usually referred to as intractable pain if it persists for 6 or more months. It is defined as pain that continues after the stimulus has been removed or the tissue damage heals. Physiologically, chronic pain is believed to result from hypersensitization of the pain receptors and enlargement of the receptor field in response to the localized inflammation that follows tissue damage.³⁵ Chronic pain is poorly localized, has an ill-defined time of onset, and is strongly associated with the subjective components outlined previously. It does not respond well to interventions directed solely at correcting the injury. Chronic pain patients frequently report other symptoms, such as depression, difficulty sleeping, poor mental and physical function, and fatigue. The effects of the pain experience extend beyond the individual and affect the family, the workplace, and the social sphere of the individual.³⁴

Referred pain is felt at a point other than its origin. Pain can be referred from an internal organ, a joint, a trigger point, or a peripheral nerve to a remote musculoskeletal structure. Referred pain usually follows a specific pattern. For example, cardiac pain is frequently referred to the left arm or jaw; the referral pattern for trigger points is exact enough to be used as a diagnostic tool and is often used by physicians to diagnose pathology. Referred pain is the result of a convergence of the primary afferent neurons from deep structures and muscles to secondary neurons that also have a cutaneous receptive field.^36,37

Although it is now recognized that all neuropathic pain results in abnormal activity within the CNS,³⁸ pain initiated or caused by a primary lesion or dysfunction of the CNS³⁹ is referred to as central neuropathic pain. The involvement of the nervous system can be at many levels: nerves, nerve roots, and central pain pathways in the spinal cord and brain. In this circumstance, there is permanent damage to the nervous system (usually a peripheral nerve) and likely anatomical reorganization of spinal terminations of surviving axons or ectopic activity from a neuroma that contributes paroxysmal, persistent input to the spinal cord.⁴⁰ In addition to anatomical reorganization in the spinal cord, there could be some reorganization in the rostroventral medulla (RVM) as well, but more likely there is prolonged input to the RVM that sustains facilitatory influences that descend to the spinal cord. Less appreciated, descending facilitatory influences on spinal sensory processing could also be important to maintenance of chronic pain conditions, particularly those that persist in the absence of obvious tissue pathology.⁴⁰

Central neuropathic pain is medically diagnosed by its defining neurological signs and symptoms; it is verified with neuroimaging tests that identify a CNS lesion and rule out other causes. It is important that the therapist be able to localize the level and differentiate between central and peripheral pain. Central neuropathic pain can be caused by vascular insult; traumatic, neoplastic, and demyelinating diseases; and surgery (including vascular compromise during surgery). Central neuropathic pain is distinct from nociceptive pain (nonneuronal tissue damage).

The onset of central neuropathic pain is usually delayed after the occurrence of the initial episode that results in damage to the CNS; onset of pain may occur during the phase of recovery from neurological deficits.⁴¹ Pain originating from a cerebrovascular incident and spinal cord injury usually begins weeks or months after the insult, whereas pain originating from tumors may take years to begin.³⁸

Individuals with central neuropathic pain may have difficulty describing their pain and report burning, aching, pricking, squeezing, or cutting pain after cutaneous stimulation, movement, heat, cold, or vibration. A normally nonnoxious stimulus, such as moving clothing across skin, becomes agonizing. In some cases the pain begins spontaneously.⁴² Pain intensity varies, but it does seem to be associated to some degree with the location of the lesion.³⁸ Allodynia (pain from normally nonnoxious stimuli) and dysesthesia are common, and one of the characteristic features of central neuropathic pain is that the clinical symptoms persist long after the stimulus has been removed.

Central neuropathic pain is topographical. The site of the lesion determines the location of the symptoms. The pain may involve half the body, an entire extremity, or a small portion of one extremity.³⁸ It is frequently migratory. Thalamic pain is the classic example of central neuropathic pain.

Central neuropathic pain is difficult to treat. Surgery is not helpful for most individuals with central neuropathic pain, and medications have not been effective in permanently relieving the symptoms.¹¹ Therefore the treatment of clients with central neuropathic pain stresses coping strategies and prevention of loss of activity and participation. The ideal management of a chronic pain patient is by a multidisciplinary approach, including disciplines such as internal medicine, neurology, anesthesia, nursing, psychology, pharmacy, rehabilitation medicine, physical therapy, occupational therapy, and others. The limitation of this approach is that access to such a wide range of specialists is often available only at large medical centers and special pain clinics, which restricts access to a limited number of patients.

Under normal conditions there is a fine balance between the parasympathetic and sympathetic branches of the autonomic nervous system (ANS). Parasympathetic activity maintains homeostasis, whereas sympathetic activity functions to make “fight-or-flight” changes in response to stress. Stimulation of the autonomic efferent fibers is not normally painful. However, the balance between afferent input and the descending sympathetic nervous system (SNS) is disrupted when there is injury, resulting in exaggerated and prolonged sympathetic activity, allodynia, and hyperalgesia (increased response to normally painful stimuli)—hence, autonomic pain.

Allodynia is a product of the phenomenon of central sensitization.⁴³ After injury, new axons sprout from the sympathetic efferent neurons. These fire spontaneously and, because they synapse on the cell bodies of the primary afferent neurons, cause them to fire as well. In addition, the dorsal horn neurons themselves become more excitable. They show an enlargement in their receptive field and become more sensitive to mechanical, thermal, and chemical stimulation. The result is an increase in the neuronal barrage into the CNS and the perception of pain with usually nonpainful stimuli.¹³

Complex regional pain syndrome (CRPS) is an example of pain that arises from abnormal activity within the ANS.⁴⁴ CRPS has been classified into two distinct types³⁹: CRPS type I (formerly reflex sympathetic dystrophy) follows mild trauma without nerve injury, and CRPS type II (formerly causalgia) follows trauma with nerve injury. CRPS type I generally begins within the month after the injury, whereas CRPS type II can occur any time after the injury.⁴⁵

The main features of CRPS type I are constant burning pain that fluctuates in intensity and increases with movement, constant stimulation, or stress. There are also allodynia and hyperalgesia, edema, abnormal sweating, abnormal blood flow and trophic changes in the area of pain, and impaired motor function. CRPS type I is relieved by blocking the SNS, indicating that the pain is sympathetically maintained.⁴⁵

CRPS type II occurs in the region of a limb innervated by an injured nerve. The nerves most commonly involved in CRPS type II are the median, sciatic, tibial, and ulnar; involvement of the radial nerve is rare. Pain is described as spontaneous, constant, and burning and is exacerbated by light touch, stress, temperature change, movement, visual and auditory stimuli, and emotional disturbances. Allodynia and hyperalgesia are common and may involve the distribution of more than one peripheral nerve. As with CRPS type I, edema, abnormal sweating, abnormal blood flow, trophic changes, and impaired motor function occur. The symptoms spread proximally and can involve other areas of the body. Evidence also points to sympathetic involvement in CRPS type II.⁴⁵

The treatment of CRPS is complex and must be carefully coordinated among members of an interdisciplinary team including the neurologist (medications), psychologist (behavior), anesthesiologist (injections), and therapist (functional recovery). The therapist provides the core treatment to improve function. Therapists need to pay close attention to the following aspects of the disorder: (1) the degree of motor abnormalities, including restricted active range of motion (ROM), abnormal posturing, spasm, tremor, and dystonia; (2) true passive range restriction; (3) hyperesthesia and allodynia; (4) swelling and vasomotor changes; and (5) evidence of osteoporosis by radiograph.⁴⁶ Please refer to Case Study 32-1 for interventions for clients with CRPS.

Peripheral pain results from noxious irritation of the nociceptors. The character of peripheral pain depends on the location and intensity of the noxious stimulation, as well as which fibers carry the information into the dorsal gray matter. As noted previously, information carried on A delta fibers is sharp and well localized, begins rapidly, and lasts only as long as the stimulus is present, whereas information carried on C fibers is dull and diffuse, has a delayed onset, and lasts longer than the duration of the stimulus. The treatment of peripheral pain is covered in detail in Chapter 18.

The management of central versus peripheral pain is determined by the type of pain—acute or chronic—and the clinical features present, including clinical localization; time of onset; laboratory study localization; response to analgesics, including narcotics; response to antidepressants; and response to nerve block or neurectomy.⁴¹ Differentiation among features will drive the treatment plan, but because some peripheral and central forms can coexist, diagnosis may be difficult.

The multidimensional aspects of chronic pain make it important to evaluate the causes as well as the emotional and cognitive sequelae.⁴⁷ Persistent pain is now considered to have a psychogenic component.⁴⁸ The longer an individual has pain, the more a psychological component may become dominant. Many emotional factors can strongly influence pain, such as pain thresholds, past experiences with pain, coping styles, and social roles. The emotional experience that we perceive with pain reflects the interaction of higher brain centers and subcortical regions, such as the amygdala and cingulate gyrus (limbic system).⁴⁹ Positron emission tomography of patients with chronic neuropathic pain demonstrates a shift of acute pain activity in the sensory cortex to regions such as the anterior cingulate gyrus.⁵⁰ Understanding the physical limitations imposed by chronic pain is an area that therapists commonly assess; it is the mind-body connection that is often less articulated by the client and more difficult for the practitioner.

Treatment of chronic pain should include a patient-centered approach, given the unique manifestations that occur in an individual’s response to pain. Patient-centered models, such as the ICF model, provide a framework that embraces a multidisciplinary team approach practiced in pain clinics. In such models, chronic pain has been noted to include psychological factors such as feelings of fear, anxiety, and depression,⁵¹ which are known to have the ability to modulate and exacerbate the physical pain experience.⁵² For example, a client with chronic pain who has the fear that movement will increase pain may alter his activity, causing muscular shortening, spasms, and a spiraling course of more pain and disability. The focus in treating clients with chronic pain should be on improving functional physical activity, decreasing peripheral nociception and central facilitation, and providing cognitive and behavioral strategies to help in resuming normal activities.

Examination of the client with pain

The examination of a client with pain can be challenging because the therapist must frequently weed through the individual’s emotions, behaviors, and secondary gains in an attempt to identify the source of the symptoms. Many clients are not referred to therapy until they have participated in weeks, months, or even years of failed interventions, and their expectations and patience are at low levels. They often approach therapy anticipating more instructions, more frustration, and more pain. Despite these obstacles, therapists must strive to complete pain evaluations that include measurable, reproducible information that identifies the source of pain and provides direction toward treatment that is both beneficial and cost-effective and that assists in establishing attainable goals. The time allotted for the examination may be dependent on the type of practice setting; many therapists send a comprehensive questionnaire to the client or ask the client to arrive early to complete important paperwork. It is essential to develop a trusting relationship, ensuring that the client feels that the therapist has listened to his or her concerns and has acknowledged his or her fears, and will participate in a plan for improving his or her physical, mental, and functional abilities.

Pain measurement

Research has shown that pain memory does not provide an accurate measure of pain intensity.⁵³ Therefore pain measurement tools are designed to provide information about the intensity, location, and character of a client’s symptoms at the time of the evaluation. This information can then be merged with the pain history, the disease or pathology history, and the physical findings to identify the cause of the pain. The disease or pathology management and its pain measurement will be the responsibility of the physician, whereas the movement limitations caused by the pain are the responsibility of the therapist. A number of pain measurement tools are available. These tools are used by professionals whose focus is pathology, as well as professionals whose responsibility is helping the patient to regain functional activities and life participation. The applications and limitations of several are discussed.

Measuring pain intensity

Pain intensity rating tools are scales that have the client rate the current level of pain by marking a continuum or assigning a numerical value to the pain intensity (Figure 32-3).

Each of the first three tools described here has been found to be reliable over time when used to measure pain that is present at the time of the rating. In general, however, clients who are depressed or anxious tend to report higher levels of pain and clients who are not depressed or anxious tend to report lower levels of pain on all three of these scales.⁵⁴

Visual analog scale.

With the visual analog scale (VAS), the client rates the pain on a continuum that begins with “no pain” and ends with “maximum pain tolerable.” This tool provides an infinite number of points between the extremes, making it sensitive to small changes in pain intensity. However, it has not been found reliable for individuals who have impaired abstract thinking skills⁵⁵ and may be unable to translate their pain intensity into a corresponding point on a line.

Simple descriptive pain scale.

With a simple descriptive pain scale (SDPS), the client rates the pain on a continuum that is subdivided using descriptors that gradually increase in intensity. Sample descriptors are “no pain,” “mild pain,” “moderate pain,” “severe pain,” and “maximum pain tolerable.” This tool is more useful than the VAS for clients with impaired abstract thinking because it is easier for them to identify with the pain descriptors than with the line found in the VAS. However, clients have been found to favor the points corresponding to each descriptor rather than points between, resulting in a less sensitive tool than the VAS.⁵⁶

Pain estimate.

With a pain estimate, the client assigns a numerical rating to the pain, staying within defined limits (most commonly between 0 and 100, where 0 represents no pain and 100 represents maximum pain tolerable). Because it provides a numerical range of scores, this tool is valuable for statistical analysis purposes. However, whereas some clients find assigning a numerical rating to their pain intensity easy, clients with impaired abstract thinking may have difficulty similar to that encountered with the VAS.

Faces pain scale.

With the Faces Pain Scale, the client selects one of seven schematic faces representing gradually increasing pain intensities. The scale begins with a face representing no pain and ends with a face representing the most pain possible. This tool is designed for use with young children who do not have the ability to use any of the three previous tools. The Faces Pain Scale has been found to be valid across cultural lines⁵⁷ and to have a strong correlation with other pain measures.⁵⁶ It is simple to use, does not require verbal skills, and requires little instruction. It has been used successfully with children as young as age 3 and with individuals who are limited in verbal expression.

Localizing pain symptoms

Pain drawings.

The client is asked to draw his or her symptoms on a schematic of the human body using a provided list of symbols (Figure 32-4). The result is a diagram describing the nature and location of the client’s pain, which can be compared with the client’s verbal report. In addition to providing a database, the pain drawing has been found to be useful in identifying individuals who have a heavy psychological or emotional component to their pain, making it helpful also in identifying clients who would benefit from further psychological evaluation.⁵⁸

Describing pain quality

Mcgill pain questionnaire (mpq).

One of the most popular scales to rate pain quality is the McGill Pain Questionnaire (MPQ), which includes 20 categories of descriptive words covering the sensory (numbers 1 to 10), affective (numbers 11 to 15), and evaluative (number 16) properties of pain (Figure 32-5). Sensory properties are measured using temporal, thermal, spatial, and pressure descriptors. Affective properties are measured using fear, tension, and autonomic descriptors. Evaluative properties are measured using pain experience descriptors.⁵⁹ Each word has a numerical value based on its position within its category.

The client is instructed to “select the word in each category that best describes the pain you have now. If there is no word in the category that describes the pain, skip the category. If there is more than one word that describes the pain, select the word that best describes the pain.”⁵⁹

The MPQ can provide the following types of information⁵⁹:

 A pain-rating index based on the sum of the values of all the words selected

 A pain-rating index based on the sum of the values of all the words in a given category

 The total number of words chosen

The MPQ has been studied extensively and found valid for adults with acute and chronic pain as well as for those with a variety of specific pathological states.60–62 It provides clues into the specific cause of pain because it describes the client’s symptoms.

However, the MPQ does pose some disadvantages. It is time-consuming, requiring more time to complete than any of the previously described rating scales. Thus it is not appropriate for quick estimates of pain after treatment. Clients, especially children, are frequently unfamiliar with some of the descriptors and ask the evaluator to assist by defining words. However, reliability and validity of this test are based on examiner objectivity, and care must be taken to avoid the introduction of evaluator bias by helping the client to select appropriate descriptors.⁵⁹ This issue can be dealt with by telling the client, “If you do not recognize a word, it probably does not apply to you.”

Pediatric verbal descriptor scale.

Because a child’s description of pain is limited by a smaller vocabulary, Wilkie and associates⁶³ have developed a verbal descriptor scale specifically for use with children (Table 32-1). Their list includes 56 words commonly used by children aged 8 to 17 to describe their pain experience. The word list is divided into the four categories found in the MPQ. The evaluators’ research has shown the list to be useful for children with a variety of diagnoses because it is relatively free of gender, ethnic, and developmental bias.

TABLE 32-1 

PEDIATRIC VERBAL DESCRIPTOR SCALE

DIMENSION	WORD	DIMENSION	WORD	DIMENSION	WORD	DIMENSION	WORD
A	Annoying Bad Horrible Miserable Terrible Uncomfortable

S

Biting

Cutting

Like a pin

Like a sharp knife

Pinlike

Sharp

Stabbing

S

Itching

Like a scratch

Like a sting

Scratching

Stinging

A

Crying

Frightening

Screaming

Terrifying

Caregiver checklist.

Clients who are unable to communicate verbally because of neurological disabilities may be unable to use any of the just-described pain measurement scales. However, because of pain associated with their medical conditions, extensive and repeated surgery, and behavioral oddities that might limit pain expression, these individuals are at high risk for having their pain go unrecognized. McGrath and colleagues⁶⁴ have attempted to develop and categorize a checklist of demonstrated pain behaviors identified by caregivers of severely handicapped individuals. Although their list did not pass validity criteria, the researchers propose that clinicians develop a client-specific checklist that could be used to gauge changes in the client’s pain from the information gained during the caregiver interview portion of the evaluation of nonverbal handicapped clients.

In addition to qualifying and quantifying the client’s pain, pain measurement tools have an additional value. They can be used to identify inconsistencies between a client’s pain report and the clinician’s objective findings. For example, a client with normal objective findings would not be expected to give a high pain report or draw symptoms over the entire pain drawing. Conversely, a client with a multitude of objective findings within the severe range would be expected to provide a high pain rating. In addition, as objective symptoms subside, it is expected that the client will report a similar decline on the rating scales. Inconsistencies between the client’s pain descriptions and the therapist’s findings should serve to alert the clinician that the client might require cognitive or affective intervention in addition to physical treatment.

Psychosocial assessment

Psychosocial factors are key variables in the comprehensive assessment of chronic pain. Davidson and colleagues⁶⁵ determined seven factors using a “prototypical” pain assessment battery that included pain and disability, pain description, affective distress, support, positive coping strategies, negative coping strategies, and activity. Irving and Squire⁶⁶ described two key individual personality features that affect pain: catastrophizing and health-related anxiety. Persons who catastrophically misinterpret innocuous bodily sensations, including pain, are likely to become fearful of pain, which results in pain-related fear. Pain-related fear is associated with avoidance of movement and physical activity, which directly affects recovery of function. Pain-related fear is also associated with increased pain levels and an exacerbated painful experience. Two validated tools to screen for these features include the Pain Catastrophizing Scale (PCS) and the Tampa Scale of Kinesophobia (TKS).⁶⁷

Examination of the client

The clinical examination should begin the moment the client enters the door. Clients frequently change posture and affect when they are being formally evaluated, and it is important to gain an accurate view of pain behavior during spontaneous activities to assess the validity of complaints. The following should be included in the examination:

It is not always possible to complete a pain evaluation in one session. Clients may not be able to tolerate all the required activities at one time, or there may be enough inconsistencies for the therapist to want a second appointment to refocus on specific tests. However, with the limitations on number of visits common with managed care, the therapist may feel pressured to identify a cause for the client’s pain in the initial visit. This is not necessary. It is far better to take more than one visit and be accurate than to take only one visit and develop a treatment plan that is not appropriate for the client’s needs.

Rehabilitation management of the client with pain

There are three broad avenues of intervention for pain management: physical interventions, cognitive strategies, and behavioral manipulations.⁷¹ Each avenue addresses a different aspect of the pain experience, and each requires a different level of participation from the client.

Physical interventions are directed at the client’s body with the goal of healing the tissue injury. Examples include medication, surgery, and the therapy modalities. Physical interventions are of use most frequently with acute pain or recurrent pain resulting from reinjury. Physical interventions are often passive and, for the most part, soothing. When used long term, they promote dependence on the clinician. Therefore it is best to use them as a short-term adjunct in the overall treatment program.

Cognitive strategies are directed at the client’s thoughts with the goal of changing the client’s pain paradigms. Cognitive strategies include body scanning and reinterpretation of self-statements. Cognitive strategies are self-initiated and performed independently; therefore they encourage personal responsibility and independence.

Behavioral manipulations involve a behavioral change on the part of the client to bring about the desired response. They include exercise, biofeedback, hypnosis, relaxation exercises, and operant conditioning. There is usually a brief learning period until the client becomes proficient with these techniques; however, once learned, behavioral manipulations can be initiated and performed independently. Behavioral manipulations also encourage personal responsibility and independence.

A brief review of the benefits, indications, contraindications, and precautions for many of the interventions provided by therapists should provide an overview of the complexity of pain management. The purpose of this section is to provide guidance in the selection of one treatment option over another so that intervention will be based on sound physiological principles. Readers who wish to explore an intervention in greater depth are directed to the references listed at the end of this chapter.

Physical interventions

Thermotherapy

The physiological effects of heat depend on the method of application, the depth of penetration, and the rate and magnitude of temperature change. In terms of the use of thermotherapy to control pain, several mechanisms have been established. Muscle spasm decreases as a result of decreased activity in gamma motor efferents, decreased excitability of muscle spindles, and increased activity of Golgi tendon organs.^72,73 This modality will often decrease peripheral pain. Ischemic pain is relieved by the influx of oxygen-rich blood into the dilated vessels, and muscle tension pain is decreased by interruption of the pain-spasm cycle. In addition, the pain threshold itself rises through gating at the spinal cord level.^74,75

Several textbooks76–80 on physical agents and rehabilitation discuss the physiological effects, precautions, contraindications, and method of application for these modalities. The reader is advised to refer to the textbooks for details.

Superficial heat can be applied by conduction, convection, or radiation. Conductive heating involves the exchange of heat down a temperature gradient by two objects that are in contact. The depth of penetration with conductive heating is usually 1 cm or less.⁸¹ Moist heat packs and paraffin are examples of therapeutic conductive heating. Convective heating involves heat transfer through the flow of hot fluid. Therapeutic convective heating takes place during hydrotherapy and Fluidotherapy (Encore Medical Corporation, Austin, Texas). Molecules with a temperature greater than absolute zero are in an excited state and emit energy, thus creating radiant heat. Objects that are warmed by the energy are heated by radiation. Therapeutic radiant heat is applied with infrared or ultraviolet light. Because of the contraindications of ultraviolet light, this type of radiant heat is seldom used by therapists today in rehabilitation settings.

Clients can be taught how and when to apply superficial heat independently. Once they have demonstrated independence, responsibility for the application of superficial heat should be transferred to the client or her or his caregiver.

The deeper tissues can be heated using conversion, the alteration of one form of energy into another. Examples of heating by conversion include use of shortwave diathermy or ultrasound.

During shortwave diathermy, the client is placed into an oscillating magnetic field. The systemic ions create friction as they attempt to line up with the continuously reversing current, resulting in an increase in tissue temperature deep within the body. Shortwave diathermy is contraindicated for clients with metal implants because of the potential for the implant to become hot and burn the surrounding tissues. It is also contraindicated for clients with cardiac pacemakers because of the pacemaker’s metal components and because the electromagnetic radiation may interfere with the pacemaker’s operation. Shortwave diathermy should not be used for clients with cancer or multiple sclerosis or who are pregnant, and it should not be used over the eyes, the reproductive organs, or growing epiphyses. Female therapists should avoid prolonged exposure to shortwave diathermy because some research has demonstrated a possible negative effect on pregnancy outcome and fetal development.⁸²

Ultrasound is another modality that heats deep tissues by conversion. As its name implies, ultrasound consists of sound waves delivered at a frequency too high to be perceived by human hearing. Sound waves are repeatedly refracted as they encounter tissues of differing acoustical resistance while traveling through the skin toward the bone (Figure 32-6). Tissues with high collagen content (tendon, ligament, fascia, and joint capsule) are heated more efficiently than tissues with low collagen content (fat, muscle). The extent of the temperature increase is related to the dose of ultrasound energy delivered. As the dose of ultrasound energy is increased by increasing the treatment duration or intensity, more energy is available to the tissues and the heating effect increases.²¹ Moreover, the higher the frequency of ultrasound delivered, the more superficial the effect. Ultrasound delivered at 1 MHz heats tissues at depths to 5 cm, whereas ultrasound delivered at 3 MHz heats tissues in the upper 2 cm.⁸³

The thermal effects of ultrasound can be used to increase tissue extensibility, cellular metabolic processes, and circulation; decrease pain and muscle spasm; and change nerve conduction velocity. The number of impulses traveling along the nerve decreases at low doses but begins to rise slowly beginning at 1.9 W/cm². Sounding of C fibers yields pain relief distal to the point of application, whereas sounding of large-diameter A fibers brings relief of spasm by changing gamma fiber activity, making the muscle fibers less sensitive to stretch.⁸⁴ Because it is impossible to treat C or A fibers selectively, ultrasound provides both pain relief and relief from muscle spasm, making it effective in the treatment of peripheral neuropathies, neuroma, and muscle spasm associated with musculoskeletal pathology, including sprains, strains, and contusions.⁸⁵

In addition to thermal effects, ultrasound has nonthermal effects that come from the mechanical effects of the ultrasound wave on the tissues. Ultrasound causes cavitation, the development and growth of gas-filled bubbles, in the tissues. Ultrasound also causes tissue fluid to move or stream. The movement of fluid around the gas bubbles formed by cavitation is called microstreaming, and the movement of fluid within the ultrasound delivery area is called acoustic streaming. The nonthermal effects of ultrasound include accelerating metabolic processes, enzyme activity, and the rate of ion exchange, as well as increasing cell membrane permeability and the rate and volume of diffusion across cell membranes. These effects are thought to explain the role of ultrasound in enhancing the healing of soft tissue and bone.86–88 The nonthermal effects of ultrasound can be achieved without raising tissue temperature by applying ultrasound in the pulsed mode.

Phonophoresis is the use of ultrasound to deliver pain-relieving chemicals to the tissues. Chemicals are delivered to the cells by the ultrasound wave, where they are broken down into ions and taken up into the cells (Figure 32-7). Common pain-relieving chemicals that can be administered with phonophoresis include 5% lidocaine ointment (Xylocaine) for acute conditions in which immediate pain relief is the primary goal, and 10% hydrocortisone cream or ointment for conditions in which pain is the result of inflammation.⁸⁹

After phonophoresis, measurable quantities of these molecules have been found at tissue depths of up to 2 inches.⁹⁰ The contraindication to use of any chemical during phonophoresis is having an allergy to that chemical. Clients should be questioned about any adverse reactions to dental local anesthesia (lidocaine) or aspirin.

Cryotherapy

The physiological effects of cold make it superior to heat for acute pain from inflammatory conditions, for the period immediately after tissue trauma, and for treating muscle spasm and abnormal tone. Peripheral nerve conduction velocity in both large myelinated and small unmyelinated fibers decreases 2.4 m per degree centigrade of cooling. As a result, pain perception and muscle contractility diminish.⁹¹ Peripheral receptors become less excitable.⁹¹ Muscle spindle responsiveness to stretch decreases; as a result, muscle spasm diminishes.⁸⁴

Local blood flow initially decreases, local edema decreases, the inflammatory response decreases, and hemorrhage is minimized. However, cold application for longer than 15 minutes results in increased local blood flow. Known as the “hunting response,” this protective mechanism brings core temperature blood to the surface and prevents tissue injury resulting from prolonged cooling.⁸¹ Cellular metabolic activities slow. The oxygen requirements of the cell decrease.⁹¹

As with heat, several precautions must be taken when using cold as a therapeutic modality. Cryotherapy is contraindicated in individuals with Raynaud phenomenon or cold allergy. Cryotherapy should not be used in individuals with rheumatic disease who, with the application of cold, have increased joint pain and stiffness. Cryotherapy should be used with caution in young, frail, or elderly individuals and those with peripheral vascular disease, circulatory pathological processes, or sensory loss.⁹²

Cryotherapy is applied in three ways. Convective cooling involves movement of air over the skin (fanning) and is rarely used therapeutically. Evaporative cooling results when a substance applied to the skin uses thermal energy to evaporate, thereby lowering surface temperature. Most commonly, this substance is a vapocoolant spray. Conductive cooling uses local application of cold via ice packs, ice massage, or immersion. Cooling is accomplished as heat from the higher-temperature object is transferred to the colder object down a temperature gradient. Conductive cooling is the most commonly used form of therapeutic cold application.

Because muscles, tendons, and joints respond differently, the best method of cold application depends on which tissues are causing the pain.⁹³ Acute injuries are best treated with cryotherapy along with rest, compression, and elevation (RICE). Muscle spasm is decreased with cold packs and stretching. Trigger points, irritable foci within muscles, are best treated with vapocoolant spray, deep friction massage, and stretching. Tendinitis responds well to ice massage and exercise. Cold packs are often the only source of pain relief in acute disc pathology. The inflamed joints of rheumatoid arthritis frequently respond to cold packs or ice massage with decreased inflammation, increased function, and long-lasting pain relief.^92,94

Clients and caregivers can be taught how and when to perform cryotherapy independently. Once they have demonstrated their proficiency, responsibility for the use of cryotherapy should be transferred to the client or the client’s caregiver.

Transcutaneous electrical nerve stimulation

TENS is the use of electricity to control the perception of pain. It appears that at a high rate TENS selectively stimulates the low-threshold, large-diameter A beta fibers, resulting in presynaptic inhibition within the dorsal horns,⁹⁵ either directly through the gating mechanism or indirectly through stimulation of the tonic descending pain-inhibiting pathways.⁹⁶ Research has shown that the neurons in the brain stem fire in synchrony with the TENS stimulation frequency,⁹⁷ and although the significance of this is not known at this time, it does indicate that the action of high-rate TENS is not limited to the dorsal columns. TENS delivered at a low rate is thought to facilitate elevation of the level of endogenous opiates in the CNS.⁹⁸

Stimulation frequencies of 1 to 250 pulses per second (pps) decrease pain. Frequencies of 50 to 100 pps have proven most effective for sensory-level (high-rate) TENS, and frequencies of 2 to 3 pps are most effective for motor level (low-rate) TENS.³¹ Stimulation at exactly 2 pps causes an increase in the pain threshold.⁵³ As the frequency is decreased, more time is needed before the onset of relief, but the effects are more long-lasting.⁹⁹ Pulse width duration determines which nerves are stimulated. Sensory nerves are stimulated at widths of 20 to 100 ms, and motor nerves at 100 to 600 ms.¹⁰⁰

There is a variety of modes of TENS delivery. Each mode relieves pain through a specific physiological mechanism and is therefore most beneficial for a specific type of pain.

When TENS impulses are generated at a high rate (greater than or equal to 50 pps) with a relatively short duration, the stimulation is referred to as sensory-level or conventional or high-rate TENS. Sensory-level TENS produces mild to moderate paresthesia without muscle contraction throughout the treatment area. Sensory-level TENS is thought to control pain through the gating mechanism in the spinal cord. The onset of relief is fast (seconds to 15 minutes)³¹ because the gate is closed at the onset of stimulation. The duration of relief after stimulation stops is short-lived (at best up to a few hours). Sensory-level TENS has been found to be beneficial for acute pain syndromes and for some deep, aching chronic pain syndromes. (Refer to Chapter 33.)

Stimulation using high-rate and long-duration impulses is called brief-intense TENS. Brief-intense TENS decreases the conduction velocity of A delta and C fibers, producing a peripheral blockade to transmission.³¹ Brief-intense TENS is useful in the clinical setting for short-term anesthesia during wound debridement, suture removal, friction massage, joint mobilization, or other painful procedures.

When the impulses are generated at a low rate (less than or equal to 20 pps) and have a relatively long duration (100 to 300 microseconds), the stimulation is referred to as motor-level or acupuncture-like or low-rate TENS. Motor-level TENS produces strong muscle contractions in the treatment area with or without the perception of paresthesia. Motor-level TENS is associated with deployment of endogenous opiates within the CNS. The onset of relief is delayed 20 to 30 minutes, presumably the time it takes to deploy the opiates. Relief frequently lasts hours or days after treatment. Because motor nerves are not stimulated in isolation, sensory fibers are also excited, causing the gating mechanism to come into play.¹⁰⁰ Motor-level TENS has been found to be beneficial for chronic pain syndromes and when sensory-level TENS has not been successful.

Modulating TENS parameters is one way to avoid the negative aspects of each of the treatment modes. Rate modulation is most commonly used to avoid neural accommodation during TENS. By setting the initial pulse rate so that, even with the programmed decrement, it will remain within the treatment range, there will be continuous variation in the stimulus, and neural accommodation will be avoided.

Width modulation is most commonly used with motor-level TENS. By setting the initial pulse duration so that, even with the programmed decrement, the impulses are able to recruit the desired motor units, there will be a continuous variation in perceived strength of the muscle contraction, rendering motor-level TENS more tolerable.

Stimulation in which the impulses are generated in pulse trains is called burst TENS. Burst TENS is another form of TENS modulation. The stimulator generates low-rate carrier impulses, each of which contains a series of high-rate pulses. Because burst TENS is a combination of high-rate and low-rate TENS, it provides the benefits of each. The low-rate carrier impulse stimulates endorphin release, and the high-rate pulse trains provide an overlay of paresthesia. The advantage to burst TENS is that muscle contractions occur at a lower, more comfortable amplitude, and accommodation does not occur. Burst TENS is beneficial whenever motor-level TENS cannot be tolerated and sensory-level TENS is ineffective because of neural accommodation.¹⁰¹

TENS, like all electrical stimulation, is contraindicated for clients with pacemakers, in the low back and pelvic regions of pregnant women, and over areas with thrombus. TENS should be used with caution for clients who have decreased sensation in the area being stimulated and for clients who have difficulty with understanding or expression. TENS electrodes should not be placed over areas of skin irritation, the eyes, or the carotid sinuses. It also should not be used in the immediate area of an operating diathermy unit.

TENS appears to be of greatest benefit for acute conditions with focal pain, chronic pain syndromes, postoperative incision pain, and during delivery. It has been found least effective with psychogenic pain¹⁰² and pain of central origin.¹⁰³ For additional information on TENS, see Chapter 33.

Clients and caregivers can be taught how and when to apply TENS independently. Once they have demonstrated independence, responsibility for the use of TENS can be transferred to the client or to the caregiver.

Iontophoresis

Iontophoresis is a process in which chemical ions are driven through the skin by a small electrical current. Ionizable compounds are placed on the skin under an electrode that, when polarized by a direct (galvanic) current, repels the ion of like charge into the tissues. Once subcutaneous, the ions are free to combine with the physiological ions, resulting in a physiological effect dependent on the characteristics of the ion (Figure 32-8). Ionizable substances that are known to be effective analgesics include the following¹⁰⁴:

 Five-percent lidocaine ointment (Xylocaine) administered under the positive electrode for an immediate, although short-lived, decrease in pain. Iontophoresis with lidocaine is recommended before ROM exercises, stretching, and joint mobilization and when immediate relief of acute pain (as in bursitis) is the object of treatment.

 One-percent to 10% hydrocortisone and dexamethasone administered under the positive electrode for relief of inflammatory pain in conditions such as arthritis, bursitis, or entrapment syndromes. Iontophoresis with hydrocortisone has a delayed onset but a prolonged effect, and it frequently eliminates the underlying cause of pain.

 Two-percent magnesium (from Epsom salts) administered under the positive electrode for relief of pain from muscle spasm or localized ischemia. High levels of extracellular magnesium inhibit muscle contraction, including the smooth muscle found in the walls of the vessels, leading to localized vasodilation.

 Iodine (from Iodex ointment [Lee Pharmaceuticals, South El Monte, California]) administered under the negative pole for relief of pain caused by adhesions or scar tissue. Iodine “softens” fibrotic, sclerotic tissue, thereby increasing tissue pliability.

 Salicylate (from Iodex with Methyl Salicylate [Lee Pharmaceuticals] or Gordogesic Creme [Gordon Laboratories, Upper Darby, Pennsylvania]) administered under the negative pole for relief of pain from inflammation. Salicylate is effective for arthritic joint inflammation, myalgia, and entrapment syndromes.

 Two-percent acetic acid administered under the negative pole to dissolve calcium deposits.

 Two-percent lithium chloride or lithium carbonate administered under the positive pole to dissolve gouty tophi. In both acetic acid and lithium iontophoresis, the insoluble radicals in the deposits are replaced by soluble chemical radicals so the deposits can be broken down through natural processes.

The contraindication to the use of any ion is an allergy to that ion. Because most clients will not have had iontophoresis previously, it is important to inquire about experiences that might indicate an allergy. For example, intolerance to shellfish may be the result of an allergy to iodine, and a poor reaction to dental local anesthesia may indicate a problem with lidocaine. Moreover, because iontophoresis involves the application of direct current, the likelihood of polar reactions under each electrode is greater than with electrical stimulations using alternating current (for example, TENS), and therefore the risk for skin burns is greater.

Massage

Massage has been recognized as a remedy for pain for at least 3000 years. Evidence of its beneficial effects first appeared in ancient Chinese literature, and then in the writings of the Hindus, Persians, Egyptians, and Greeks. Hippocrates advocated massage for sprains and dislocations as well as for constipation.¹⁰⁵

Massage decreases pain through both direct and indirect means. Massage movements increase circulation through mechanical compression of the tissues, resulting in reflex relaxation of muscle tissue and direct relief from ischemic pain. Massage also indirectly stimulates A delta and A beta fibers, causing activation of the gating mechanism and the descending pain-modulating system.³⁴

Massage movements are classified by pressure and the part of the hand that is used.¹⁰⁶ The two massage movements that may cause a decrease in pain include stroking (effleurage) and compression (kneading or pétrissage). Stroking involves running the entire hand over large portions of the body. Stroking causes muscle relaxation and elimination of muscle spasm or improved circulation depending on the depth and force of the strokes. Compression is applied with intermittent pressure using lifting, rolling, or pressing movements meant to stretch shortened tissues, loosen adhesions, and assist with circulation.

Massage is useful in any condition in which pain relief will follow the reduction of swelling or the mobilization of the tissues. These include arthritis, bursitis, neuritis, fibrositis, low back pain, hemiplegia, paraplegia, quadriplegia, and joint sprains, strains, and contusions. Massage is contraindicated over infected areas, diseased skin, and thrombophlebitic regions.

Clients or caregivers can be taught how and when to perform massage. Once they have demonstrated independence in the appropriate technique, responsibility for the performance of massage should be given to the client or caregiver.

A specialized massage technique is lymphatic massage, which consists of light-pressure rhythmic strokes to encourage organizational flow of the lymphatic system. This type of massage can be beneficial with clients who have peripheral swelling with or without pain. A popular form of lymph massage called manual lymphatic drainage (MLD) is used after surgical procedures to reduce swelling (for example, mastectomy for breast cancer). Evidence-based studies show conflicting results regarding the efficacy of this technique, and more research needs to be done to validate it.107–109

Myofascial release

Myofascial release (MFR) techniques are used to release the built-in imbalances and restrictions within the fascia and to reintegrate the fascial mechanism. The therapist palpates the various tissue layers, beginning with the most superficial and working systematically toward the deepest, looking for movement restrictions and asymmetry. Areas of altered structure and function are then “normalized” through the systematic application of pressure and stretching applied in specific directions to bring about decreased myofascial tension, myofascial lengthening, and myofascial softening,¹¹⁰ thereby restoring pain-free motion in normal patterns of movement. MFR is useful in treating musculoskeletal injuries, chronic pain, headaches, and adhesions or adherent scars.¹¹¹ MFR has been shown to be effective in the treatment of chronic prostatitis (CP) and chronic pelvic pain syndrome (CPPS) in conjunction with paradoxical relaxation therapy (PRT).¹¹² More research is needed to provide evidence regarding the efficacy of MFR in pain control.

MFR is contraindicated over areas with infection, diseased skin, thromboembolus, cellulitis, osteomyelitis, and open wounds. In addition, it should not be used with clients who have osteoporosis, advanced degenerative changes, acute circulatory conditions, acute joint pathology, advanced diabetes, obstructive edema, or hypersensitive skin.¹¹¹ (See Chapter 39 for more in-depth information regarding MFR.)

Joint mobilization

Joint mobilization consists of passive oscillations that restore normal accessory movements.¹¹³ In addition, the rhythmical repetition of the motions provides pain relief through the spinal gating mechanism.¹¹⁴

The oscillations involved in joint mobilization are presented in Chapters 9 and 18. Grades I and II oscillations are performed to maintain joint mobility and for pain relief, making them the choice for subacute conditions in which pain and potential loss of motion are the primary considerations. Grades III and IV oscillations are performed to increase joint mobility and are indicated for chronic conditions in which regaining lost motion is the goal. Grade V thrusts are performed to regain full joint mobility.¹¹³

Joint mobilization is contraindicated with rheumatoid arthritis, bone disease, advanced osteoporosis, and pregnancy (pelvic mobilization), as well as in the presence of malignancy, vascular disease, or infection in the area to be mobilized.⁵³

Light therapy

Light therapy is described by Bot and Bouter¹¹⁵ as a light source that generates extremely pure infrared light of a single wavelength. When applied to the skin, infrared laser light produces no sensation and it does not burn the skin. Because of the low absorption, it is hypothesized that the energy can penetrate deeply into the tissues, where it is assumed to have a biostimulative effect.^77,115,116 It has been suggested that laser therapy may act by stimulating ligament repair,^117,118 producing antiinflammatory effects,¹¹⁹ increasing production of endogenous opioids,¹²⁰ reducing swelling,¹²¹ and influencing nerve conduction velocity.¹²² To promote wound healing and manage pain, rehabilitation centers use lasers with power outputs less than 500 mW at a power density of 50 mW/cm² and wavelengths ranging from 600 to 1500 nm.⁷⁷ Contraindications to light therapy include exposing photosensitive areas, hemorrhagic areas, any area that has undergone 4 to 6 months of radiation treatment,¹¹⁶ neoplastic lesions, and unclosed fontanelles in children; the abdomen of pregnant women; areas over the heart, the vagus nerve, or sympathetic innervations routes to the heart of cardiac patients; or, locally, endocrine glands.^{77,116,123,124} In addition, exposure to the cornea of the eye is contraindicated, so protective eye equipment should be worn by the patient and the therapist. Caution should be used for areas with compromised somatosensation, the epiphyseal plates in children, the gonads, and infected areas and with patients displaying fever, epilepsy, or mental confusion.^77,116,123

Therapeutic touch

A description of therapeutic touch can be found in Chapter 39. Therapeutic touch has been effective in treating painful conditions resulting from anxiety and tension. In a report by Keller and Bzdek, 90% of individuals treated with therapeutic touch experienced tension headache relief, and 70% had continued relief for more than 4 hours; only 37% of the placebo group expressed sustained relief.¹²⁵ A meta-analysis and systematic review on therapeutic touch revealed that the available studies have varying approaches and protocols on therapeutic touch, subject selection, and description. Although most of these studies confirm the efficacy of the technique, several studies also have demonstrated negative or mixed results.¹²⁶ Therapeutic touch, as well as other approaches, are being more widely accepted; however, the therapist must continue to be diligent in using outcome studies to substantiate the use of any complementary therapy. (See Chapter 39 for additional information.)

Point stimulation

Refer to Chapter 39 for an in-depth discussion of point stimulation. It is interesting to note that acupuncture points frequently correspond in location to trigger points, which are tight, elevated bands of tissue that are extremely sensitive when palpated and have a characteristic pattern of radiation to remote regions of the body. Trigger points appear to be areas of “focal irritability” that are myofascial in origin and are usually the site of small aggregations of nerve fibers that produce continuous afferent input when stimulated.

Needling therapies include trigger point injections and trigger point dry needling and are used in myofascial pain conditions. Trigger point injections are usually restricted to medical doctors and their professional support staff.¹²⁷ Trigger point dry needling consists of superficial and deep dry needling, and the exact mechanism of pain relief is not known. It is thought that needling and injections may trigger changes in the end plate cholinesterase and ACh receptors,¹²⁷ may involve central pain mechanisms, and may activate enkephalinergic, serotonergic, and noradrenergic inhibitory systems in association with A delta fibers through segmental inhibition.¹²⁷ Acupressure (i.e., finger pressure applied to acupuncture or trigger points) is thought to decrease their sensitivity through the same mechanism. The therapist applies deep pressure in a circular motion to each point for 1 to 5 minutes, until the sensitivity subsides. Pressure must be applied directly to each point for the treatment to be effective. Acupressure can be accompanied by the use of a vapocoolant spray to provide additional sensory stimulation.

Sensitive points also can be stimulated using electricity. A point locator is used to identify points along the appropriate meridians that are sensitive to stimulation or more conductive to electricity. Each is then stimulated at the client’s level of pain tolerance for 30 to 45 seconds. The points farthest from the site of pain are treated first.

Points that are most sensitive to stimulation are beneficial sites for TENS electrode placement. When point stimulation alone does not provide sufficient pain relief, TENS can be used between sessions for continuous stimulation for more prolonged relief. (See Chapter 39 for additional information on electrical acupuncture.)

General treatment guidelines

As noted earlier, chronic pain management using the medical model has not been found effective. Treatment limited to correcting pathology promotes dependence on the therapist, as well as making full resolution of symptoms the measure of success.

The ICF model addresses the functional losses associated with impairments. Therapeutic interventions are not focused on pathology, but they are directed at improving the individual’s function and preventing or improving disability. This does not mean that the impairment is ignored, however. Most times, addressing the individual’s functional losses involves treating the impairments that caused them.

For example, clients with chronic pain frequently become sedentary, leading to the impairments of limited ROM, muscle weakness, and deconditioning. These factors can then, of themselves, cause pain, creating a cycle that spirals upward until the individual becomes disabled. During therapy, interventions are directed at the impairments with the goal of restoring function. Therapeutic interventions are selected based on their ability to improve functional outcome. Impairments that do not affect function do not become the focus of therapy; therapeutic interventions that do not address functional deficits are not used.

The development of an appropriate treatment plan may seem overwhelming when the therapist is confronted with a client who has chronic pain that has not responded to previous interventions or who has a chronic condition that has pain as one of its characteristics. The key is to identify the client’s functional deficits and then develop a treatment plan that addresses the causes of those deficits. In some cases this may mean not treating the pain itself but rather its causative factors.

For example, if the client has chronic pain because of joint hypomobility, the treatment plan includes interventions to increase joint mobility. Conversely, if the client’s pain is caused by joint hypermobility, the treatment plan includes interventions to increase support around the hypermobile joints. Merely addressing the joint pain by applying modalities will do little to resolve the pain because it does nothing to correct the precipitating cause.

When a client has pain because of a chronic disease and the treatment plan will include instruction in pain-relieving interventions, it is important for the therapist to understand the specific causes of the pain to select the appropriate intervention. For example, pain from rheumatoid arthritis most commonly is the result of either joint inflammation or biomechanical stress on unstable joints. A client would be instructed in pain-relieving modalities for the former and instructed to wear splints to support the joints for the latter. One intervention would not be appropriate for both causes.

Case studies

Case Studies 32-1, 32-2, and 32-3 demonstrate a problem-solving approach to the treatment of clients with chronic pain.