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Neuropathic pain: A guide to comprehensive assessment
Neuropathic Pain: A Guide to Comprehensive Assessment yyy Keela Herr, PhD, RN, FAAN
y
From Adult and Gerontological Nursing Area, College of Nursing, University of Iowa, Iowa City, IA. Address correspondence and reprint requests to Keela Herr, PhD, RN, FAAN, Professor and Chair, Adult and Gerontological Nursing Area, College of Nursing, 452 NB, The University of Iowa, Iowa City, IA 52242. E-mail: [email protected] 1524-9042/$30.00 © 2004 by the American Society for Pain Management Nursing doi:10.1016/j.jpmn.2004.10.004
ABSTRACT:
Patients with neuropathic pain present a clinical challenge. Neuropathic pain, when chronic, often leads to disability. Diagnosis can be difficult because both positive and negative sensory and motor signs and symptoms may be present, as well as a variety of comorbid conditions. In addition, there may be a high degree of interpatient variability. Currently, clinical evaluation, rather than diagnostic tests, is one of the best available tools for assessment and diagnosis. As with all chronic pain conditions, the key to a thorough assessment is a thorough history that includes medical, functional, and psychosocial evaluations. Currently available pain assessment tools, which are widely used in nursing practice, are still inadequate for use in patients with neuropathic pain. The physical and neurologic examination remains a critical element for patient evaluation. This includes an assessment of spontaneous pain (continuous or intermittent), pain evoked by daily activities (allodynia), and other abnormal sensations that are not necessarily painful (paresthesias, dysesthesias). Sensitivity to pinprick, touch, pressure, cold, heat, and vibration are measured, often confirming the suspected diagnosis. Patients may be confused by the unusual sensations they are experiencing and unable to effectively describe or communicate their symptoms. This communication barrier may contribute to an inadequate physical examination. With improved skills in patient assessment and through enhanced communication with patients, nurses can make an important contribution to treatment outcomes in patients with neuropathic pain. © 2004 by the American Society for Pain Management Nursing
Neuropathic pain has been defined by the International Association for the Study of Pain (IASP) as pain “initiated or caused by a primary lesion or dysfunction in the nervous system” (Merskey & Bogduk, 1994). Depending on the location of the lesion or dysfunction, neuropathic pain can be categorized as primarily peripheral or central in origin. Peripheral neuropathic pain is more prevalent than central neuropathic pain (Dworkin, 2002). Neuropathic pain syndromes are long-lasting and often disabling. Diagnostically, they present a challenge. Clinical manifestations often include both negative and positive sensory symptoms and signs. Motor signs and symptoms are often present, but subtle (Dworkin et al., 2003). No single symptom is diagnostic for neuropathic Pain Management Nursing, Vol 5, No 4, suppl 1 (December), 2004: pp 9-18
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pain, and there may be a high degree of interpatient variability in presentation. Moreover, not all patients with nerve damage will experience neuropathic pain. Some may have only sensory loss, for example. If such a patient presents with pain, it may be due to the damaged nerve or to a different cause. He or she may be misdiagnosed with neuropathic pain and consequently mistreated. At the same time, in other patients, the signs and symptoms of nerve dysfunction may be subtle and go unrecognized, leading to underdiagnosis and undertreatment (Chong & Bajwa, 2003). For these and other reasons, a thorough and focused assessment is important. Ideally, this elicits information about the patient’s medical history, associated comorbid conditions, and prior response to treatment, and concludes with the physical examination. The present article outlines the key components and rationale of a thorough assessment and the role of pain assessment in clinical practice.
PAIN QUALITY A brief guide to the assessment of the patient with neuropathic pain is shown in Table 1. This guide is targeted for use in nursing practice and includes examples of typical questions for patients. In the assessment of neuropathic pain, information on pain quality is critical. Most patients have more than one pain quality (e.g., constant “burning” pain plus intermittent “shooting” or “electric shock-like” pain). It has been demonstrated clinically (Boureau, Dubrere, & Luu, 1990) that patients with neuropathic pain are significantly more likely to use six particular sensory adjectives (“electric-shock,” “burning,” “tingling,” “cold,” “pricking,” and “itching”) to describe their pain. “Electric shock,” “burning,” and “tingling” were the most common terms, reported by 53%, 54%, and 48%, respectively, of patients with neuropathic pain. Other adjectives, including “lancinating” and “shooting,” were not useful to distinguish neuropathic from nonneuropathic pain. It should be noted that if the patient reports “aching” pain, this does not necessarily rule out neuropathic pain as a possible diagnosis. Aching pain is a frequent complaint of patients with central pain due to multiple sclerosis and syringomyelia (Hansson, 2002). In addition, the patient may report spontaneous abnormal sensations (paresthesias and dysesthesias) including crawling, numbness, itching, and tingling. Although overlap in descriptor use exists between nociceptive and neuropathic pain, an accurate assessment of pain quality in pain of neuropathic origin is important to provide a guide to the underlying etiology and pain mechanisms, and to evaluate the response to treatment.
IMPACT The impact of the pain on the patient’s activities of daily living and quality of life is also important to assess. Various measures of physical and emotional function can be used to evaluate pain impact (e.g., the Brief Pain Inventory; Cleeland et al., 1996). The presence of depression or anxiety, sleep disturbance, work-related issues, treatment expectations, rehabilitative needs, and the availability of social support from family and friends are important areas to explore (Dworkin et al., 2003), especially psychiatric comorbidities, which are common in patients with chronic pain (Harden & Cohen, 2003). Psychosocial factors are a major component of the experience of chronic pain. They should be addressed when patients are evaluated and included in the treatment plan. Table 1 shows related assessment questions. LOCATION The location and distribution of the pain is important clinical information because it often correlates with the degree of neural lesion (Chong & Bajwa, 2003). All neuropathic pains are projected and, with few exceptions, the pain distribution matches the level of the lesion (Hansson, 2002). A dermatome chart can be most useful in recognizing referral patterns that are nerve related. The topographic distribution is especially helpful in guiding the neurologic examination. Patients with chronic pain are often asked to complete a body diagram to document pain distribution, which has been shown to be useful in elders, as well as younger patients (Weiner et al., 1998). One approach is to use color coding to indicate different types of sensations (e.g., burning, numbness, increased sensitivity; Figure 1).
PAIN INTENSITY AND THE ROLE OF PAIN ASSESSMENT SCALES Evaluation of pain intensity or severity is always an important aspect of any complete pain assessment and should be conducted in a manner appropriate to the population. In other words, approaches for assessing pain intensity should be valid and reliable for the patient’s age and other potential factors that may impact successful and accurate reporting of pain (e.g., sex, race, education, sensory capability) (Herr & Mobily, 1993; Herr, Spratt, Mobily, & Richardson, 2004; Merkel & Malviya, 2000). Several tools are available for the clinical assessment of neuropathic pain. These include the Visual Analog Scale (VAS), Verbal Descriptor Scales (VDS), McGill Pain Questionnaire and Short Form (MPQ, MPQ-SF; Melzack,
TABLE 1. Pain Assessment Mnemonic “QISS TAPED” and Examples of Potentially Useful Questions Quality
I
Impact
S
Site
S
Severity
T
Temporal Characteristics
A
Aggravating and Alleviating Factors
P
Past Response, Preferences
E
Expectations, Goals, Meaning
D
Diagnostics & Physical Exam
What were your first symptoms? Pain? Tingling? Numbness? Weakness? What does the pain feel like? What words would you use to describe the pain? (achy, sharp, burning, squeezing, dull, icy, etc) Besides sensations you consider “pain,” are there other abnormal sensations? How does the pain affect you? How does the pain impact your sleep, activity, mood, appetite (other: work, relationships, physical therapy, etc.) What does the pain prevent you from doing? What is your typical day like? How much time in bed or reclined? (It is often very helpful to ask a significant other about daily functioning). Do you feel sad or blue? Crying often: Loss of interest in life? Loss of or increased appetite? Do you feel stressed or nervous? Have you been particularly anxious about anything? Show me where you feel the pain.-Can you put your hand on it? Or show me on a body diagram? Does the pain move/radiate anywhere? Has the location changed over time? Is it local or diffuse? On a 0–10 scale with 0 ⫽ no pain and 10 ⫽ the worst pain possible, how much pain are you in right now? What is the least or lowest pain you’ve had in the past (24 hours, one week, month)? What is the highest or worst pain you have had in the past (24 hours, one week, month)? How often are you in severe pain? (percentage of day, or how many days a week are you without pain)? When did the pain start? Was it sudden? Gradual? Is the pain constant or intermittent? Is there a predictable pattern? (e.g., always worse in the morning or in the evening? Does it suddenly flare up?) What makes the pain better? What makes the pain worse? If you are currently taking pain medicine: How long until it starts working? When do you get the best relief? How much relief do you get? How long does it last? How have you managed your pain in the past? (Ask about both drug and non-drug methods) What worked? What did not help? What medications have you tried? Was the dose increased until you had pain relief or side effects? How long did you take the drug? Are there any pain medicines you are aware of that you should not be given because of allergy or bad reaction? How do you feel about taking medications? What nerve blocks have you had? What physical or occupational therapy have you had? What would you like to try now to treat this pain? What can we do to help you? What are the results you hope to receive from the pain treatment? What number (on the pain intensity scale) would allow you to (sleep, eat, participate in physical therapy, etc.)? What do you think is causing the pain? What are you most afraid of? Examine and inspect site (view and feel) Perform a systems assessment and neurologic examination as indicated Review radiologic or laboratory test results as indicated
A Guide to Comprehensive Assessment
Q
Note: Adapted and used with permission from mnemonic developed by M. Backonja, MD.
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FIGURE 1. y Body diagrams illustrating neuropathic pain as completed by patients. Yellow, aches; blue, burning; red, stabbing; black, numbness; green, pins and needles. (Reprinted with permission from the University of Wisconsin Pain Treatment and Research Center, Madison, WI.)
1975; Melzack, 1987), the Neuropathic Pain Scale (NPS; Galer & Jensen, 1997), the Neuropathic Pain Questionnaire (NPQ; Krause & Backonja, 2003) and the Leeds Assessment of Neuropathic Symptoms and Signs Pain Scale (LANSS; Bennett, 2001). The VAS, VDS and MPQ are currently commonly used to measure pain intensity. The patient rates pain intensity using some type of continuum (e.g., “no pain” to “worst possible pain”). These tools have been validated for use with older adults, as well as the general adult population (Herr et al., 2004; Gagliese & Melzack, 2003). Other approaches may be more appropriate when assessing pain intensity in children (Merkel & Malviya, 2000). Available measures of pain intensity are generally inadequate assessment tools for patients with neuropathic pain because they do not measure individual pain qualities that may be present, and this omission has clinical significance. For example, in one trial, patients with painful diabetic polyneuropathy who described their pains as “sharp” or “shooting” were more likely to respond to transdermal clonidine than
those who did not describe their pain in this way (Byas-Smith, Max, Muir, & Kingman, 1995). If a single global pain intensity rating were taken for these patients, it would most likely fail to detect a response to clonidine because it would not specifically measure a change in the intensity of “sharp” and “shooting” pains. The MPQ is useful to distinguish between neuropathic and nonneuropathic types of pain, however, with up to 66% accuracy, based only on patient descriptors (Melzack, Terrence, Fromm, & Amsel, 1986; Masson, Hunt, Gem, & Boulton, 1989; Boureau et al., 1990). The MPQ-SF (Melzack, 1987) is easier for older patients to complete and combines the qualitative descriptors with intensity ratings (Herr & Garand, 2001). The NPS and NPQ are two newer assessment tools. Both tools measure individual pain qualities and abnormal sensations reported by patients with neuropathic pain. In initial studies, the NPS was useful to distinguish postherpetic neuralgia (PHN) from other types of neuropathic pain (Galer & Jensen, 1997),
A Guide to Comprehensive Assessment
although it may be less useful to distinguish neuropathic from nonneuropathic pain. The NPQ and the LANSS are intended to provide a general assessment of neuropathic pain symptoms, as well as to allow for differentiation between neuropathic and nonneuropathic pain (Krause & Backonja, 2003). Use of a pain diary can be a helpful tool in collecting information from the patient about their pain and its characteristics, as well as response to treatment options. Most pain diaries include a scale that can be used to determine the severity of pain, as well as options for identifying pain qualities.
TEMPORAL CHARACTERISTICS Temporal aspects include the duration of the pain; whether its onset was sudden or gradual; and whether the pain is intermittent, continuous, or paroxysmal. Neuropathic pain may have one or more of these characteristics. Moreover, there may be several different components to the patient’s pain, including spontaneous pain, evoked pain, and abnormal sensations (paresthesias and dysesthesias). These are further discussed below. Each component may have different characteristics and temporal aspects, and their intensity frequently varies from time to time (Krause & Backonja, 2003). In two common neuropathic pain syndromes, trigeminal neuralgia and glossopharyngeal neuralgia, pain is typically solely intermittent and/or paroxysmal, suggesting a diagnosis based on temporal characteristics. Most other neuropathic pain syndromes, however, cannot be diagnosed in this way (Hansson, 2002).
AGGRAVATING AND ALLEVIATING FACTORS Pain reported by patients is often described clinically as either spontaneous or evoked pain. An alternative terminology seen in the literature is that of stimulusindependent (spontaneous) or stimulus-dependent (evoked) pain. Separation into these two types of pain is clinically useful because it allows a separate consideration of pain that is ongoing from that which is provoked by some activity (Jensen & Baron, 2003). These characteristics of neuropathic pain may be used to differentiate the pain etiology. Table 2 presents a list of commonly used IASP pain terms and their definitions, which are used in the following discussion. Spontaneous Pain Spontaneous pain may be continuous or intermittent. Either type typically varies in its intensity over time. Spontaneous continuous pain is present all or almost
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all of the time, whereas spontaneous intermittent pain is episodic (paroxysmal) and typically is of relatively short duration. Spontaneous intermittent pain is often described as “shooting,” “stabbing,” “burning,” “throbbing,” or “electric shock–like” in quality. It may have several of these qualities (Dworkin, 2002). Evoked Pain Evoked pain is also typically of two types, allodynia or hyperalgesia. Allodynia is a term that describes pain due to a stimulus which does not normally provoke pain. For example, patients may report pain caused by gentle touch, the friction of clothing or wind against the skin, or riding in a car (Dworkin et al., 2003). Allodynia may be further categorized as dynamic or static, each evoked by different types of stimuli. Dynamic allodynia may be observed if the patient experiences pain when, for example, the clinician lightly moves a paint brush or cotton swab across the skin. Static allodynia may be observed if pain is caused by light blunt pressure (e.g., with a finger or pencil eraser tip), light punctate pressure (e.g., with a pinprick or von Frey filament) or application of heat or cold stimuli (e.g., by heating or cooling a tuning fork, or by a brief application of ice) (Dworkin, 2002). In many neuropathic pain conditions, allodynia is seen in response to cold. Patients may describe their pain as cold, wet, ice-like or, paradoxically, as burning hot or ice burning (similar to holding a snowball in the hand). Hyperalgesia describes an increased response to a stimulus that is normally painful. Hyperalgesia may occur in response to cold, heat, touch, pressure, pinprick, or even the application of topical capsaicin. Additional types of evoked pain include aftersensation (the persistence of pain after termination of a painful stimulus) and sympathetically maintained pain. Some patients with central pain complain of pain caused by movement in which the movement itself elicits a tightening, squeezing, or burning sensation in the skin (Jensen & Baron, 2003). Patients may also report abnormal sensations (i.e., dysesthesias, paraesthesias), which may be spontaneous or evoked. Dysesthesias are unpleasant abnormal sensations, and paresthesias are abnormal sensations, not necessarily unpleasant. Examples of paresthesias/ dysesthesias include feelings of itching, crawling, numbness, tingling, and pins-and-needles sensations.
PAST RESPONSES TO AND PREFERENCES FOR TREATMENT Additional relevant history includes information about prior treatments and their efficacy. Current and past medication use should be fully evaluated. It is critically
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TABLE 2. A Selection of Pain Terms Plus Definitions from the Published IASP List of Pain Terms Pain Term
Definition
Pain
An unpleasant sensory and emotional experience associated with actual or potential tissue damage
Allodynia
Pain due to a stimulus that does not normally provoke pain
Causalgia
A syndrome of sustained burning pain, allodynia, and hyperpathia after a traumatic nerve lesion
Central pain
Pain initiated or caused by a primary lesion or dysfunction in the central nervous system
Dysesthesia
An unpleasant abnormal sensation, whether spontaneous or evoked
Hyperalgesia
An increased response to a stimulus that is normally painful
Hyperesthesia
Increased sensitivity to stimulation, excluding the special senses
Hyperpathia
A painful syndrome characterized by an abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold
Neuralgia
Pain in the distribution of a nerve or nerves
Neuropathic pain
Pain initiated or caused by a primary lesion or dysfunction in the nervous system
Neuropathy
A disturbance or pathologic change in a nerve; in one nerve, mononeuropathy; in several nerves, monooneuropathy multiplex; if diffuse and bilateral, polyneuropathy
Nociceptor
A receptor preferentially sensitive to a noxious stimulus or to a stimulus that would become noxious if prolonged
Noxious stimulus
A noxious stimulus is one that is damaging to normal tissues
Paresthesia
An abnormal sensation, whether spontaneous or evoked
Peripheral neuropathic pain
Pain initiated or caused by a primary lesion or dysfunction in the peripheral nervous system
Note: IASP ⫽ International Association for the Study of Pain. (Adapted from Chong, M. S., & Bajwa, Z. H. (2003). Diagnosis and treatment of neuropathic pain. Journal of Pain and Symptom Management, 25, S4-S11 (used with permission).
important to ascertain whether prior treatments were titrated until pain relief or unacceptable side effects occurred (Galer & Dworkin, 2000). Clinical surveys have shown that a large majority of patients with neuropathic pain or chronic pain received the wrong type of drug or the right type of drug in doses that were too low. The use of interventional techniques (e.g., nerve blocks) and nondrug treatments should be explored. In addition, the use and effectiveness of prior physical or occupational therapy modalities (e.g., active exercise, stretching, massage, myofascial release, craniosacral manipulation, ultrasound) should be determined and considered in the plan of care. The four primary reasons for failed treatment in neuropathic pain include inadequate diagnosis, inadequate management of comorbid conditions, incorrect choice of treatment options, and the use of inappropriate outcome measures (Harden & Cohen, 2003). Nurses can make an important contribution to improved pain management by alleviating these failures through eliciting comprehensive information about the patient’s history and prior treatment and by facilitating im-
proved communication between the patient and clinician.
EXPECTATIONS, GOALS, MEANING In a patient-centered approach, the goals of treatment should be identified. The patient may have specific goals for treatment, such as sleeping through the night, improving the ability to eat or participate in physical therapy, resuming a hobby or social activity, or returning to work. These goals should be identified, and the feasibility of achieving them discussed. In addition, it may be useful to explore the patient’s fears and beliefs regarding his or her pain.
PHYSICAL EXAMINATION The Role of Communication The physical examination is important to confirm or reject the suspected anatomic location of the lesion identified from the history. The patient’s report of symptoms is key to an adequate physical examination. The clinician
A Guide to Comprehensive Assessment
should provide reassurance that symptoms may be (and usually are) complex. Patients might be confused by their unusual sensory experiences. For example, along the same nerve distribution, a patient may be numb to pinprick, yet unusually sensitive to light touch. Communication may be hampered for two reasons: first, it might be difficult for the patient to describe his or her symptoms; and second, the patient may fear he or she is not believed because of the unusual sensations that may be experienced. In particular, it might be difficult for some patients to recognize and report changes in pain sensation. A limited ability to use language may hamper the ability of children to verbalize pain sensations. The same may be true for patients who do not use English as a first language. In addition, elderly patients may have cognitive and sensory losses due to aging that impact their ability to recognize and report changes in neuropathic pain sensations (Herr & Garand, 2001). All patients should be encouraged to provide all the necessary information for an adequate assessment. They should be reassured that their pain is taken seriously and that some pain problems of neuropathic origin may present with unusual sensations and patterns of sensation. The clinician should elicit a careful description of symptoms and of the severity of abnormal sensations. Communication, encouragement, and reassurance can help increase the reliability of the physical examination. To enhance and facilitate communication during the examination, simple queries should precede more complex ones. For example, the clinician may apply a specific stimulus to the unaffected area and then to the area affected by pain. First, patients should be asked whether or not the stimulus causes the same sensation in both areas (e.g., “Does this feel the same or different?”). If it is not experienced as the same sensation, the patient should then be asked whether the sensation in the area affected by pain is more or less intense than the sensation in the unaffected area (e.g., “Does it feel stronger or weaker?”). Lastly, the patient should be asked to describe his or her perception of the quality of the sensation (e.g., “What does it feel like?”). For example, a pinprick might be more painful (hyperalgesia) in the affected area but less sharp in quality because of an underlying sensory deficit (Dworkin et al., 2003).
THE NEUROLOGIC EXAMINATION The neurologic examination should be the last part of the assessment process focused on somatosensory function in the area identified through the history and pain characteristics. One can be most certain of a diagnosis of neuropathic pain if sensory abnormalities are observed in the area that corresponds to the inner-
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vation of a nerve. The sensory examination will often evaluate the response to pinprick, touch, pressure, cold, heat, and vibration. Sensitivity to cold or warm stimuli can be assessed using thermorollers kept at 20°C and 45°C. In addition, sensitivity to cold can be assessed by the response to acetone or menthol. Vibration can be assessed by use of a tuning fork placed at strategic anatomic points (e.g., malleoli, interphalangeal joints). A camel hair brush or cotton swab may be used for touch sensations and a pin for pain sensation. Use of multiple tools is important because sensory abnormalities may be limited to one or a few of these tools. The borders of the dysfunction should be determined using the different tools available (Hansson, 2002).
CLASSIFICATION AND DIAGNOSIS In neuropathic pain, both positive and negative symptoms and signs are observed, and these correlate with clinical assessments on physical examination of normal, decreased, or increased sensations. Positive sensory phenomena include spontaneous and evoked pain (including allodynia and hyperalgesia), and paresthesias (Chong & Bajwa, 2003). Negative sensory symptoms and signs include reduced sensitivities to touch, pinprick, cold/warm sensations, or vibration (Jensen & Baron, 2003). If hyperesthesia is present, this may be classified as dysesthesia, hyperalgesia, or allodynia. The intensity, threshold for elicitation of response, duration of response, and the area of allodynia or hyperalgesia should be noted. In addition, nonsensory neurologic symptoms and signs may be present to some degree. Examples include weakness, fatigability, hypotonia, tremor, dystonia, spasticity, ataxia, apraxia, and motor neglect (Dworkin et al., 2003). Depending on the underlying cause of neuropathic pain, there may be decreased range of motion, stiffness of joints, spontaneous muscle spasms, localized muscle tenderness, and myofascial trigger points, each of which may contribute to pain and disability. Abnormal motor function can be an important factor in the patient’s status and may require therapy. In addition, many patients with neuropathic pain develop a secondary myofascial pain syndrome (tight, spastic, and/or painful muscles, ligaments, and tendons) (Galer & Dworkin, 2000). Clinically, different findings might be expected for peripheral versus central neuropathic pain syndromes. Paroxysmal pain is often seen in peripheral syndromes, but it may also occur in central syndromes. In peripheral neuropathic pain syndromes due to nerve damage, typical findings include paroxysms with hypoesthesia/hypoalgesia in combination with hyperesthesia (i.e., an
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increased sensitivity to stimulation), hyperalgesia, and allodynia. Temporal and spatial sensory abnormalities may be found as well. An abnormal delay in response to a stimulus (abnormal latency) or aftersensations (sensory experience after removal of the stimulus) may occur. There might be faulty localization of a stimulus or the spread of a sensation beyond the territory of innervation. In studies of patients with central pain due to stroke or multiple sclerosis, patients exhibited signs of an altered sensibility to temperature and/or painful stimuli (Boivie, Leijon, & Johansson, 1989; Leijon, Boivie, & Johansson, 1989; Osterberg, Boivie, Holmgren, Thuomas, & Johansson, 1994). Occasionally, central sensitization may be present if pain and/or sensory dysfunction are observed in area(s) outside the distribution of the damaged nerve. Diagnostically, this should be carefully distinguished from symptoms that may be caused by nonneurologic conditions (Hansson, 2002). The mechanisms underlying central neuropathic pain are still unclear (Dworkin et al., 2003). Further information on this topic is available in a recent review (Jensen & Baron, 2003).
DIAGNOSTIC TESTS Diagnostic testing that is sometimes used for neuropathic pain conditions includes nerve conduction velocity testing, electromyography, magnetic resonance imaging, and quantitative sensory testing (QST). The current evaluation tools are not yet capable of accurately identifying the mechanisms underlying neuropathic pain. Laboratory tests are often normal in many neuropathic pain syndromes, and no diagnostic test can identify the source of the pain with great accuracy. Occasionally, however, laboratory tests may be informative in the diagnosis of neuropathic pain. Rather than measuring the lesion or dysfunction, diagnostic testing usually provides correlates to clinical information. Often, no lesion can be demonstrated, yet neuropathic pain cannot be excluded as a diagnosis (Dworkin et al., 2003). In rare instances, diagnostic testing can be used to confirm or exclude the presence of a nerve lesion or dysfunction. Frequently, however, neuropathic pain remains a subjective phenomenon reported by the patient (Jensen & Baron, 2003). If laboratory testing fails to provide validation of patient reports, a tendency to discount patient complaints or attribute complaints to malingering or to psychogenic causes must be avoided. NEUROPHYSIOLOGIC TESTS Nerve conduction velocity tests or electromyography can be used to assess nerve function in large, myelinated peripheral nerves but provide no information about smaller myelinated or unmyelinated nerve fibers
carrying pain and temperature sensory information. Magnetic resonance imaging is used to assess the anatomic integrity of thermonociceptive sensory processing regions, such as the brainstem, thalamus, sensory cortex, anterior cingulate, and insular cortex, which can contribute to central neuropathic pain when injured. Functional magnetic resonance imaging can provide further information about these and other pain-related structures, although its role in clinical practice is limited at present. It does not provide information about the functional state of the structure or its role in causing pain (Galer & Dworkin, 2000). Although not widely used in clinical practice, QST is assuming a greater role in neuropathic pain research. In QST, a computer-controlled device is used to provide a stimulus (for example, a heat probe providing heat sensory input). The level of stimulus needed to produce a particular sensation is measured (e.g., the temperature at which a patient reports pain due to heat). In this way, the sensory threshold is measured, and the function of peripheral nerve fibers and their central components can be measured. QST relies on the patient’s psychophysical ability to discriminate between fine changes in thermal stimuli. It is not widely used clinically because it requires specialized equipment and training (Dworkin et al., 2003). PHARMACOLOGIC TESTS Pharmacologic tests have been used to classify mechanisms involved in neuropathic pain. In these tests, the same agent may be administered by different routes (e.g., topical, systemic, epidural, intrathecal) to determine the pain-generating site. The use of topical lidocaine has been one of the tools used to classify mechanisms in PHN (Fields, Rowbotham, & Baron, 1998). Intravenous phentolamine or epidural opioid administration has also been used this way clinically. The N-methyl-D-aspartate antagonist ketamine, administered systemically in subanesthetic doses, has been shown to reduce ongoing spontaneous pain (brushand pinprick-evoked pain) in patients with amputations, traumatic nerve injuries, and PHN (Jensen & Baron, 2003). In two studies, a brief intravenous infusion of opioid or lidocaine was useful to predict a patient’s subsequent response to long-term treatment with an opioid or mexiletine (Dellimijn, van Duijn, & Vanneste, 1998; Galer, Harle, & Rowbotham, 1996).
CONCLUSIONS Traditionally, neuropathic pain has been diagnosed based on the underlying disease or etiology (e.g., painful diabetic neuropathy). As presented elsewhere in this supplement (Pasero, 2004), pain syndromes iden-
A Guide to Comprehensive Assessment
tified by disease most likely have multiple distinct mechanisms that account for chronic pain. For example, in PHN, nerve damage is caused by a virus and perhaps inflammation, whereas in painful diabetic neuropathy, it is caused by ischemia and perhaps altered metabolism. It would be expected that these processes are associated with different symptoms. Although not possible at present, a goal for the future is to identify specific pathophysiologic mechanisms associated with specific symptoms of neuropathic pain. For example, one patient with PHN may have mechanical allodynia, which indicates central sensitization, but another may not. Clinical researchers are seeking to meet this challenge by identifying pain mechanisms using combined information about symptoms, signs, QST, and the response to pharmacologic challenges (Dworkin, 2002). In nursing practice, patients with neuropathic pain remain a challenge. Neuropathic pain is often
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chronic and is difficult to diagnose because of the presence of positive and negative sensory and motor symptoms and signs, comorbid conditions, psychosocial issues, and interpatient variability. Pain assessment tools, commonly used in nursing practice, are able to provide information on some aspects of the pain and its characteristics. However, a thorough and focused clinical evaluation, including a thorough history, physical examination, and neurologic examination is key for adequate assessment and accurate diagnosis. Empathy and therapeutic communication with the patient are ever important elements of nursing practice. Patients with neuropathic pain experience unusual, uncommon sensations and may have difficulty communicating these to the clinician. Nurses with improved diagnostic skills, together with a greater knowledge base and empathy for the patient, can make significant contributions to the well-being of their patients with neuropathic pain.
REFERENCES Bennett, M. (2001). The LANSS pain scale: The Leeds assessment of neuropathic symptoms and signs. Pain, 92, 147-157. Boivie, J., Leijon, G., & Johansson, I. (1989). Central post-stroke pain & A study of the mechanisms through analyses of the sensory abnormalities. Pain, 37, 173-185. Boureau, F., Doubrere, J. F., & Luu, M. (1990). Study of verbal description in neuropathic pain. Pain, 42, 145-152. Byas-Smith, M. G., Max, M. B., Muir, J., & Kingman, A. (1995). Transdermal clonidine compared to placebo in painful diabetic neuropathy using a two-stage “enriched enrollment” design. Pain, 60, 267-274. Chong, M. S., & Bajwa, Z. H. (2003). Diagnosis and treatment of neuropathic pain. Journal of Pain and Symptom Management, 25, S4-S11. Cleeland, C. S., Nakamura, Y., Mendoza, T. R., Edwards, K. R., Douglas, J., & Serlin, R. C. (1996). Dimensions of the impact of cancer pain in a four country sample: New information from multidimensional scaling. Pain, 67, 267-273. Dellemijn, P. L., van Duijn, H., & Vanneste, J. A. (1998). Prolonged treatment with transdermal fentanyl in neuropathic pain. Journal of Pain and Symptom Management, 16, 220-229. Dworkin, R. H. (2002). An overview of neuropathic pain: Syndromes, symptoms, signs, and several mechanisms. Clinical Journal of Pain, 18, 343-349. Dworkin, R. H., Backonja, M., Rowbotham, M. C., Allen, R. R., Argoff, C. R., Bennett, G. J., et al. (2003). Advances in neuropathic pain. Diagnosis, mechanisms and treatment recommendations. Archives of Neurology, 60, 1524-1534. Fields, H. L., Rowbotham, M., & Baron, R. (1998). Postherpetic neuralgia: Irritable nociceptors and deafferentation. Neurobiology of Disease, 5, 209-227. Galer, B. S., Harle, J., & Rowbotham, M. C. (1996). Response to intravenous lidocaine infusion predicts subse-
quent response to oral mexiletine: A prospective study. Journal of Pain and Symptom Management, 12, 161-167. Galer, B. S., & Jensen, M. P. (1997). Development and preliminary validation of a pain measure specific to neuropathic pain: The neuropathic pain scale. Neurology, 48, 332-338. Galer, B. S., & Dworkin, R. H. (2000). A clinical guide to neuropathic pain. Minneapolis, MN: Healthcare Information Programs. Hansson, P. (2002). Neuropathic pain: Clinical characteristics and diagnostic workup. European Journal of Pain, 6(Suppl. A), 47-50. Harden, N., & Cohen, M. (2003). Unmet needs in the management of neuropathic pain. Journal of Pain and Symptom Management, 25, S12-S17. Herr, K., & Garand, L. (2001). Pain assessment and measurement in older adults. Clinics in Geriatric Medicine, 17, 457-478. Herr, K. A., & Mobily, P. R. (1993). Comparison of selected pain assessment tools for use with the elderly. Applied Nursing Research, 6, 39-46. Herr, K., Spratt, K., Mobily, P., & Richardson, G. (2004). Pain intensity assessment in older adults: Use of experimental pain to compare psychometric properties and usability of selected scales in adult and older populations. Clinical Journal of Pain, 20, 207-219. Gagliese, L., & Melzack, R. (2003). Age-related differences in the qualities but not the intensity of chronic pain. Pain, 104, 597-608. Jensen, T. S., & Baron, R. (2002). Translation of symptoms and signs into mechanisms in neuropathic pain. Pain, 102, 1-8. Krause, S. J., & Backonja, M. (2003). Development of a neuropathic pain questionnaire. Clinical Journal of Pain, 19, 306-314.
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Leijon, G., Boivie, J., & Johansson, I. (1989). Central post-stroke pain—Neurological symptoms and pain characteristics. Pain, 36, 13-25. Masson, E. A., Hunt, L., Gem, J. M., & Boulton, A. J. (1989). A novel approach to the diagnosis and assessment of symptomatic diabetic neuropathy. Pain, 38, 25-28. Melzack, R. (1975). The McGill Pain Questionnaire: Major properties and scoring methods. Pain, 1, 277-299. Melzack, R. (1987). The short-form McGill Pain Questionnaire. Pain, 30, 191-197. Melzack, R., Terrence, C., Fromm, G., & Amsel, R. (1986). Trigeminal neuralgia and atypical facial pain: Use of the McGill Pain Questionnaire for discrimination and diagnosis. Pain, 27, 297-302. Merkel, S., & Malviya, S. (2000). Pediatric pain, tools and assessment. Journal of Perianesthesia Nursing, 15, 408-414.
Merskey, H., & Bogduk, N. (Eds.). (1994). Classification of chronic pain: descriptions of chronic pain syndromes and definitions of pain terms (2nd ed.). Seattle, Washington: International Association for the Study of Pain Press. Osterberg, A., Boivie, J., Holmgren, H., Thuomas, K-A., & Johansson, I. (1994). The clinical characteristics and sensory abnormalities of patients with central pain caused by multiple sclerosis. In G. F. Gebhart, D. L. Hammond, & T. S. Jensen (Eds.), Proceedings of the 7th World Congress on Pain. Progress in pain research and management, Vol. 2 (pp. 789-796). Seattle Washington: International Association for the Study of Pain Press. Pasero, C. (2004). Pathophysiology of neuropathic pain. Pain Management Nursing, 5(Suppl. 1), 3-8
y
From Adult and Gerontological Nursing Area, College of Nursing, University of Iowa, Iowa City, IA. Address correspondence and reprint requests to Keela Herr, PhD, RN, FAAN, Professor and Chair, Adult and Gerontological Nursing Area, College of Nursing, 452 NB, The University of Iowa, Iowa City, IA 52242. E-mail: [email protected] 1524-9042/$30.00 © 2004 by the American Society for Pain Management Nursing doi:10.1016/j.jpmn.2004.10.004
ABSTRACT:
Patients with neuropathic pain present a clinical challenge. Neuropathic pain, when chronic, often leads to disability. Diagnosis can be difficult because both positive and negative sensory and motor signs and symptoms may be present, as well as a variety of comorbid conditions. In addition, there may be a high degree of interpatient variability. Currently, clinical evaluation, rather than diagnostic tests, is one of the best available tools for assessment and diagnosis. As with all chronic pain conditions, the key to a thorough assessment is a thorough history that includes medical, functional, and psychosocial evaluations. Currently available pain assessment tools, which are widely used in nursing practice, are still inadequate for use in patients with neuropathic pain. The physical and neurologic examination remains a critical element for patient evaluation. This includes an assessment of spontaneous pain (continuous or intermittent), pain evoked by daily activities (allodynia), and other abnormal sensations that are not necessarily painful (paresthesias, dysesthesias). Sensitivity to pinprick, touch, pressure, cold, heat, and vibration are measured, often confirming the suspected diagnosis. Patients may be confused by the unusual sensations they are experiencing and unable to effectively describe or communicate their symptoms. This communication barrier may contribute to an inadequate physical examination. With improved skills in patient assessment and through enhanced communication with patients, nurses can make an important contribution to treatment outcomes in patients with neuropathic pain. © 2004 by the American Society for Pain Management Nursing
Neuropathic pain has been defined by the International Association for the Study of Pain (IASP) as pain “initiated or caused by a primary lesion or dysfunction in the nervous system” (Merskey & Bogduk, 1994). Depending on the location of the lesion or dysfunction, neuropathic pain can be categorized as primarily peripheral or central in origin. Peripheral neuropathic pain is more prevalent than central neuropathic pain (Dworkin, 2002). Neuropathic pain syndromes are long-lasting and often disabling. Diagnostically, they present a challenge. Clinical manifestations often include both negative and positive sensory symptoms and signs. Motor signs and symptoms are often present, but subtle (Dworkin et al., 2003). No single symptom is diagnostic for neuropathic Pain Management Nursing, Vol 5, No 4, suppl 1 (December), 2004: pp 9-18
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pain, and there may be a high degree of interpatient variability in presentation. Moreover, not all patients with nerve damage will experience neuropathic pain. Some may have only sensory loss, for example. If such a patient presents with pain, it may be due to the damaged nerve or to a different cause. He or she may be misdiagnosed with neuropathic pain and consequently mistreated. At the same time, in other patients, the signs and symptoms of nerve dysfunction may be subtle and go unrecognized, leading to underdiagnosis and undertreatment (Chong & Bajwa, 2003). For these and other reasons, a thorough and focused assessment is important. Ideally, this elicits information about the patient’s medical history, associated comorbid conditions, and prior response to treatment, and concludes with the physical examination. The present article outlines the key components and rationale of a thorough assessment and the role of pain assessment in clinical practice.
PAIN QUALITY A brief guide to the assessment of the patient with neuropathic pain is shown in Table 1. This guide is targeted for use in nursing practice and includes examples of typical questions for patients. In the assessment of neuropathic pain, information on pain quality is critical. Most patients have more than one pain quality (e.g., constant “burning” pain plus intermittent “shooting” or “electric shock-like” pain). It has been demonstrated clinically (Boureau, Dubrere, & Luu, 1990) that patients with neuropathic pain are significantly more likely to use six particular sensory adjectives (“electric-shock,” “burning,” “tingling,” “cold,” “pricking,” and “itching”) to describe their pain. “Electric shock,” “burning,” and “tingling” were the most common terms, reported by 53%, 54%, and 48%, respectively, of patients with neuropathic pain. Other adjectives, including “lancinating” and “shooting,” were not useful to distinguish neuropathic from nonneuropathic pain. It should be noted that if the patient reports “aching” pain, this does not necessarily rule out neuropathic pain as a possible diagnosis. Aching pain is a frequent complaint of patients with central pain due to multiple sclerosis and syringomyelia (Hansson, 2002). In addition, the patient may report spontaneous abnormal sensations (paresthesias and dysesthesias) including crawling, numbness, itching, and tingling. Although overlap in descriptor use exists between nociceptive and neuropathic pain, an accurate assessment of pain quality in pain of neuropathic origin is important to provide a guide to the underlying etiology and pain mechanisms, and to evaluate the response to treatment.
IMPACT The impact of the pain on the patient’s activities of daily living and quality of life is also important to assess. Various measures of physical and emotional function can be used to evaluate pain impact (e.g., the Brief Pain Inventory; Cleeland et al., 1996). The presence of depression or anxiety, sleep disturbance, work-related issues, treatment expectations, rehabilitative needs, and the availability of social support from family and friends are important areas to explore (Dworkin et al., 2003), especially psychiatric comorbidities, which are common in patients with chronic pain (Harden & Cohen, 2003). Psychosocial factors are a major component of the experience of chronic pain. They should be addressed when patients are evaluated and included in the treatment plan. Table 1 shows related assessment questions. LOCATION The location and distribution of the pain is important clinical information because it often correlates with the degree of neural lesion (Chong & Bajwa, 2003). All neuropathic pains are projected and, with few exceptions, the pain distribution matches the level of the lesion (Hansson, 2002). A dermatome chart can be most useful in recognizing referral patterns that are nerve related. The topographic distribution is especially helpful in guiding the neurologic examination. Patients with chronic pain are often asked to complete a body diagram to document pain distribution, which has been shown to be useful in elders, as well as younger patients (Weiner et al., 1998). One approach is to use color coding to indicate different types of sensations (e.g., burning, numbness, increased sensitivity; Figure 1).
PAIN INTENSITY AND THE ROLE OF PAIN ASSESSMENT SCALES Evaluation of pain intensity or severity is always an important aspect of any complete pain assessment and should be conducted in a manner appropriate to the population. In other words, approaches for assessing pain intensity should be valid and reliable for the patient’s age and other potential factors that may impact successful and accurate reporting of pain (e.g., sex, race, education, sensory capability) (Herr & Mobily, 1993; Herr, Spratt, Mobily, & Richardson, 2004; Merkel & Malviya, 2000). Several tools are available for the clinical assessment of neuropathic pain. These include the Visual Analog Scale (VAS), Verbal Descriptor Scales (VDS), McGill Pain Questionnaire and Short Form (MPQ, MPQ-SF; Melzack,
TABLE 1. Pain Assessment Mnemonic “QISS TAPED” and Examples of Potentially Useful Questions Quality
I
Impact
S
Site
S
Severity
T
Temporal Characteristics
A
Aggravating and Alleviating Factors
P
Past Response, Preferences
E
Expectations, Goals, Meaning
D
Diagnostics & Physical Exam
What were your first symptoms? Pain? Tingling? Numbness? Weakness? What does the pain feel like? What words would you use to describe the pain? (achy, sharp, burning, squeezing, dull, icy, etc) Besides sensations you consider “pain,” are there other abnormal sensations? How does the pain affect you? How does the pain impact your sleep, activity, mood, appetite (other: work, relationships, physical therapy, etc.) What does the pain prevent you from doing? What is your typical day like? How much time in bed or reclined? (It is often very helpful to ask a significant other about daily functioning). Do you feel sad or blue? Crying often: Loss of interest in life? Loss of or increased appetite? Do you feel stressed or nervous? Have you been particularly anxious about anything? Show me where you feel the pain.-Can you put your hand on it? Or show me on a body diagram? Does the pain move/radiate anywhere? Has the location changed over time? Is it local or diffuse? On a 0–10 scale with 0 ⫽ no pain and 10 ⫽ the worst pain possible, how much pain are you in right now? What is the least or lowest pain you’ve had in the past (24 hours, one week, month)? What is the highest or worst pain you have had in the past (24 hours, one week, month)? How often are you in severe pain? (percentage of day, or how many days a week are you without pain)? When did the pain start? Was it sudden? Gradual? Is the pain constant or intermittent? Is there a predictable pattern? (e.g., always worse in the morning or in the evening? Does it suddenly flare up?) What makes the pain better? What makes the pain worse? If you are currently taking pain medicine: How long until it starts working? When do you get the best relief? How much relief do you get? How long does it last? How have you managed your pain in the past? (Ask about both drug and non-drug methods) What worked? What did not help? What medications have you tried? Was the dose increased until you had pain relief or side effects? How long did you take the drug? Are there any pain medicines you are aware of that you should not be given because of allergy or bad reaction? How do you feel about taking medications? What nerve blocks have you had? What physical or occupational therapy have you had? What would you like to try now to treat this pain? What can we do to help you? What are the results you hope to receive from the pain treatment? What number (on the pain intensity scale) would allow you to (sleep, eat, participate in physical therapy, etc.)? What do you think is causing the pain? What are you most afraid of? Examine and inspect site (view and feel) Perform a systems assessment and neurologic examination as indicated Review radiologic or laboratory test results as indicated
A Guide to Comprehensive Assessment
Q
Note: Adapted and used with permission from mnemonic developed by M. Backonja, MD.
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FIGURE 1. y Body diagrams illustrating neuropathic pain as completed by patients. Yellow, aches; blue, burning; red, stabbing; black, numbness; green, pins and needles. (Reprinted with permission from the University of Wisconsin Pain Treatment and Research Center, Madison, WI.)
1975; Melzack, 1987), the Neuropathic Pain Scale (NPS; Galer & Jensen, 1997), the Neuropathic Pain Questionnaire (NPQ; Krause & Backonja, 2003) and the Leeds Assessment of Neuropathic Symptoms and Signs Pain Scale (LANSS; Bennett, 2001). The VAS, VDS and MPQ are currently commonly used to measure pain intensity. The patient rates pain intensity using some type of continuum (e.g., “no pain” to “worst possible pain”). These tools have been validated for use with older adults, as well as the general adult population (Herr et al., 2004; Gagliese & Melzack, 2003). Other approaches may be more appropriate when assessing pain intensity in children (Merkel & Malviya, 2000). Available measures of pain intensity are generally inadequate assessment tools for patients with neuropathic pain because they do not measure individual pain qualities that may be present, and this omission has clinical significance. For example, in one trial, patients with painful diabetic polyneuropathy who described their pains as “sharp” or “shooting” were more likely to respond to transdermal clonidine than
those who did not describe their pain in this way (Byas-Smith, Max, Muir, & Kingman, 1995). If a single global pain intensity rating were taken for these patients, it would most likely fail to detect a response to clonidine because it would not specifically measure a change in the intensity of “sharp” and “shooting” pains. The MPQ is useful to distinguish between neuropathic and nonneuropathic types of pain, however, with up to 66% accuracy, based only on patient descriptors (Melzack, Terrence, Fromm, & Amsel, 1986; Masson, Hunt, Gem, & Boulton, 1989; Boureau et al., 1990). The MPQ-SF (Melzack, 1987) is easier for older patients to complete and combines the qualitative descriptors with intensity ratings (Herr & Garand, 2001). The NPS and NPQ are two newer assessment tools. Both tools measure individual pain qualities and abnormal sensations reported by patients with neuropathic pain. In initial studies, the NPS was useful to distinguish postherpetic neuralgia (PHN) from other types of neuropathic pain (Galer & Jensen, 1997),
A Guide to Comprehensive Assessment
although it may be less useful to distinguish neuropathic from nonneuropathic pain. The NPQ and the LANSS are intended to provide a general assessment of neuropathic pain symptoms, as well as to allow for differentiation between neuropathic and nonneuropathic pain (Krause & Backonja, 2003). Use of a pain diary can be a helpful tool in collecting information from the patient about their pain and its characteristics, as well as response to treatment options. Most pain diaries include a scale that can be used to determine the severity of pain, as well as options for identifying pain qualities.
TEMPORAL CHARACTERISTICS Temporal aspects include the duration of the pain; whether its onset was sudden or gradual; and whether the pain is intermittent, continuous, or paroxysmal. Neuropathic pain may have one or more of these characteristics. Moreover, there may be several different components to the patient’s pain, including spontaneous pain, evoked pain, and abnormal sensations (paresthesias and dysesthesias). These are further discussed below. Each component may have different characteristics and temporal aspects, and their intensity frequently varies from time to time (Krause & Backonja, 2003). In two common neuropathic pain syndromes, trigeminal neuralgia and glossopharyngeal neuralgia, pain is typically solely intermittent and/or paroxysmal, suggesting a diagnosis based on temporal characteristics. Most other neuropathic pain syndromes, however, cannot be diagnosed in this way (Hansson, 2002).
AGGRAVATING AND ALLEVIATING FACTORS Pain reported by patients is often described clinically as either spontaneous or evoked pain. An alternative terminology seen in the literature is that of stimulusindependent (spontaneous) or stimulus-dependent (evoked) pain. Separation into these two types of pain is clinically useful because it allows a separate consideration of pain that is ongoing from that which is provoked by some activity (Jensen & Baron, 2003). These characteristics of neuropathic pain may be used to differentiate the pain etiology. Table 2 presents a list of commonly used IASP pain terms and their definitions, which are used in the following discussion. Spontaneous Pain Spontaneous pain may be continuous or intermittent. Either type typically varies in its intensity over time. Spontaneous continuous pain is present all or almost
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all of the time, whereas spontaneous intermittent pain is episodic (paroxysmal) and typically is of relatively short duration. Spontaneous intermittent pain is often described as “shooting,” “stabbing,” “burning,” “throbbing,” or “electric shock–like” in quality. It may have several of these qualities (Dworkin, 2002). Evoked Pain Evoked pain is also typically of two types, allodynia or hyperalgesia. Allodynia is a term that describes pain due to a stimulus which does not normally provoke pain. For example, patients may report pain caused by gentle touch, the friction of clothing or wind against the skin, or riding in a car (Dworkin et al., 2003). Allodynia may be further categorized as dynamic or static, each evoked by different types of stimuli. Dynamic allodynia may be observed if the patient experiences pain when, for example, the clinician lightly moves a paint brush or cotton swab across the skin. Static allodynia may be observed if pain is caused by light blunt pressure (e.g., with a finger or pencil eraser tip), light punctate pressure (e.g., with a pinprick or von Frey filament) or application of heat or cold stimuli (e.g., by heating or cooling a tuning fork, or by a brief application of ice) (Dworkin, 2002). In many neuropathic pain conditions, allodynia is seen in response to cold. Patients may describe their pain as cold, wet, ice-like or, paradoxically, as burning hot or ice burning (similar to holding a snowball in the hand). Hyperalgesia describes an increased response to a stimulus that is normally painful. Hyperalgesia may occur in response to cold, heat, touch, pressure, pinprick, or even the application of topical capsaicin. Additional types of evoked pain include aftersensation (the persistence of pain after termination of a painful stimulus) and sympathetically maintained pain. Some patients with central pain complain of pain caused by movement in which the movement itself elicits a tightening, squeezing, or burning sensation in the skin (Jensen & Baron, 2003). Patients may also report abnormal sensations (i.e., dysesthesias, paraesthesias), which may be spontaneous or evoked. Dysesthesias are unpleasant abnormal sensations, and paresthesias are abnormal sensations, not necessarily unpleasant. Examples of paresthesias/ dysesthesias include feelings of itching, crawling, numbness, tingling, and pins-and-needles sensations.
PAST RESPONSES TO AND PREFERENCES FOR TREATMENT Additional relevant history includes information about prior treatments and their efficacy. Current and past medication use should be fully evaluated. It is critically
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TABLE 2. A Selection of Pain Terms Plus Definitions from the Published IASP List of Pain Terms Pain Term
Definition
Pain
An unpleasant sensory and emotional experience associated with actual or potential tissue damage
Allodynia
Pain due to a stimulus that does not normally provoke pain
Causalgia
A syndrome of sustained burning pain, allodynia, and hyperpathia after a traumatic nerve lesion
Central pain
Pain initiated or caused by a primary lesion or dysfunction in the central nervous system
Dysesthesia
An unpleasant abnormal sensation, whether spontaneous or evoked
Hyperalgesia
An increased response to a stimulus that is normally painful
Hyperesthesia
Increased sensitivity to stimulation, excluding the special senses
Hyperpathia
A painful syndrome characterized by an abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold
Neuralgia
Pain in the distribution of a nerve or nerves
Neuropathic pain
Pain initiated or caused by a primary lesion or dysfunction in the nervous system
Neuropathy
A disturbance or pathologic change in a nerve; in one nerve, mononeuropathy; in several nerves, monooneuropathy multiplex; if diffuse and bilateral, polyneuropathy
Nociceptor
A receptor preferentially sensitive to a noxious stimulus or to a stimulus that would become noxious if prolonged
Noxious stimulus
A noxious stimulus is one that is damaging to normal tissues
Paresthesia
An abnormal sensation, whether spontaneous or evoked
Peripheral neuropathic pain
Pain initiated or caused by a primary lesion or dysfunction in the peripheral nervous system
Note: IASP ⫽ International Association for the Study of Pain. (Adapted from Chong, M. S., & Bajwa, Z. H. (2003). Diagnosis and treatment of neuropathic pain. Journal of Pain and Symptom Management, 25, S4-S11 (used with permission).
important to ascertain whether prior treatments were titrated until pain relief or unacceptable side effects occurred (Galer & Dworkin, 2000). Clinical surveys have shown that a large majority of patients with neuropathic pain or chronic pain received the wrong type of drug or the right type of drug in doses that were too low. The use of interventional techniques (e.g., nerve blocks) and nondrug treatments should be explored. In addition, the use and effectiveness of prior physical or occupational therapy modalities (e.g., active exercise, stretching, massage, myofascial release, craniosacral manipulation, ultrasound) should be determined and considered in the plan of care. The four primary reasons for failed treatment in neuropathic pain include inadequate diagnosis, inadequate management of comorbid conditions, incorrect choice of treatment options, and the use of inappropriate outcome measures (Harden & Cohen, 2003). Nurses can make an important contribution to improved pain management by alleviating these failures through eliciting comprehensive information about the patient’s history and prior treatment and by facilitating im-
proved communication between the patient and clinician.
EXPECTATIONS, GOALS, MEANING In a patient-centered approach, the goals of treatment should be identified. The patient may have specific goals for treatment, such as sleeping through the night, improving the ability to eat or participate in physical therapy, resuming a hobby or social activity, or returning to work. These goals should be identified, and the feasibility of achieving them discussed. In addition, it may be useful to explore the patient’s fears and beliefs regarding his or her pain.
PHYSICAL EXAMINATION The Role of Communication The physical examination is important to confirm or reject the suspected anatomic location of the lesion identified from the history. The patient’s report of symptoms is key to an adequate physical examination. The clinician
A Guide to Comprehensive Assessment
should provide reassurance that symptoms may be (and usually are) complex. Patients might be confused by their unusual sensory experiences. For example, along the same nerve distribution, a patient may be numb to pinprick, yet unusually sensitive to light touch. Communication may be hampered for two reasons: first, it might be difficult for the patient to describe his or her symptoms; and second, the patient may fear he or she is not believed because of the unusual sensations that may be experienced. In particular, it might be difficult for some patients to recognize and report changes in pain sensation. A limited ability to use language may hamper the ability of children to verbalize pain sensations. The same may be true for patients who do not use English as a first language. In addition, elderly patients may have cognitive and sensory losses due to aging that impact their ability to recognize and report changes in neuropathic pain sensations (Herr & Garand, 2001). All patients should be encouraged to provide all the necessary information for an adequate assessment. They should be reassured that their pain is taken seriously and that some pain problems of neuropathic origin may present with unusual sensations and patterns of sensation. The clinician should elicit a careful description of symptoms and of the severity of abnormal sensations. Communication, encouragement, and reassurance can help increase the reliability of the physical examination. To enhance and facilitate communication during the examination, simple queries should precede more complex ones. For example, the clinician may apply a specific stimulus to the unaffected area and then to the area affected by pain. First, patients should be asked whether or not the stimulus causes the same sensation in both areas (e.g., “Does this feel the same or different?”). If it is not experienced as the same sensation, the patient should then be asked whether the sensation in the area affected by pain is more or less intense than the sensation in the unaffected area (e.g., “Does it feel stronger or weaker?”). Lastly, the patient should be asked to describe his or her perception of the quality of the sensation (e.g., “What does it feel like?”). For example, a pinprick might be more painful (hyperalgesia) in the affected area but less sharp in quality because of an underlying sensory deficit (Dworkin et al., 2003).
THE NEUROLOGIC EXAMINATION The neurologic examination should be the last part of the assessment process focused on somatosensory function in the area identified through the history and pain characteristics. One can be most certain of a diagnosis of neuropathic pain if sensory abnormalities are observed in the area that corresponds to the inner-
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vation of a nerve. The sensory examination will often evaluate the response to pinprick, touch, pressure, cold, heat, and vibration. Sensitivity to cold or warm stimuli can be assessed using thermorollers kept at 20°C and 45°C. In addition, sensitivity to cold can be assessed by the response to acetone or menthol. Vibration can be assessed by use of a tuning fork placed at strategic anatomic points (e.g., malleoli, interphalangeal joints). A camel hair brush or cotton swab may be used for touch sensations and a pin for pain sensation. Use of multiple tools is important because sensory abnormalities may be limited to one or a few of these tools. The borders of the dysfunction should be determined using the different tools available (Hansson, 2002).
CLASSIFICATION AND DIAGNOSIS In neuropathic pain, both positive and negative symptoms and signs are observed, and these correlate with clinical assessments on physical examination of normal, decreased, or increased sensations. Positive sensory phenomena include spontaneous and evoked pain (including allodynia and hyperalgesia), and paresthesias (Chong & Bajwa, 2003). Negative sensory symptoms and signs include reduced sensitivities to touch, pinprick, cold/warm sensations, or vibration (Jensen & Baron, 2003). If hyperesthesia is present, this may be classified as dysesthesia, hyperalgesia, or allodynia. The intensity, threshold for elicitation of response, duration of response, and the area of allodynia or hyperalgesia should be noted. In addition, nonsensory neurologic symptoms and signs may be present to some degree. Examples include weakness, fatigability, hypotonia, tremor, dystonia, spasticity, ataxia, apraxia, and motor neglect (Dworkin et al., 2003). Depending on the underlying cause of neuropathic pain, there may be decreased range of motion, stiffness of joints, spontaneous muscle spasms, localized muscle tenderness, and myofascial trigger points, each of which may contribute to pain and disability. Abnormal motor function can be an important factor in the patient’s status and may require therapy. In addition, many patients with neuropathic pain develop a secondary myofascial pain syndrome (tight, spastic, and/or painful muscles, ligaments, and tendons) (Galer & Dworkin, 2000). Clinically, different findings might be expected for peripheral versus central neuropathic pain syndromes. Paroxysmal pain is often seen in peripheral syndromes, but it may also occur in central syndromes. In peripheral neuropathic pain syndromes due to nerve damage, typical findings include paroxysms with hypoesthesia/hypoalgesia in combination with hyperesthesia (i.e., an
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Keela Herr
increased sensitivity to stimulation), hyperalgesia, and allodynia. Temporal and spatial sensory abnormalities may be found as well. An abnormal delay in response to a stimulus (abnormal latency) or aftersensations (sensory experience after removal of the stimulus) may occur. There might be faulty localization of a stimulus or the spread of a sensation beyond the territory of innervation. In studies of patients with central pain due to stroke or multiple sclerosis, patients exhibited signs of an altered sensibility to temperature and/or painful stimuli (Boivie, Leijon, & Johansson, 1989; Leijon, Boivie, & Johansson, 1989; Osterberg, Boivie, Holmgren, Thuomas, & Johansson, 1994). Occasionally, central sensitization may be present if pain and/or sensory dysfunction are observed in area(s) outside the distribution of the damaged nerve. Diagnostically, this should be carefully distinguished from symptoms that may be caused by nonneurologic conditions (Hansson, 2002). The mechanisms underlying central neuropathic pain are still unclear (Dworkin et al., 2003). Further information on this topic is available in a recent review (Jensen & Baron, 2003).
DIAGNOSTIC TESTS Diagnostic testing that is sometimes used for neuropathic pain conditions includes nerve conduction velocity testing, electromyography, magnetic resonance imaging, and quantitative sensory testing (QST). The current evaluation tools are not yet capable of accurately identifying the mechanisms underlying neuropathic pain. Laboratory tests are often normal in many neuropathic pain syndromes, and no diagnostic test can identify the source of the pain with great accuracy. Occasionally, however, laboratory tests may be informative in the diagnosis of neuropathic pain. Rather than measuring the lesion or dysfunction, diagnostic testing usually provides correlates to clinical information. Often, no lesion can be demonstrated, yet neuropathic pain cannot be excluded as a diagnosis (Dworkin et al., 2003). In rare instances, diagnostic testing can be used to confirm or exclude the presence of a nerve lesion or dysfunction. Frequently, however, neuropathic pain remains a subjective phenomenon reported by the patient (Jensen & Baron, 2003). If laboratory testing fails to provide validation of patient reports, a tendency to discount patient complaints or attribute complaints to malingering or to psychogenic causes must be avoided. NEUROPHYSIOLOGIC TESTS Nerve conduction velocity tests or electromyography can be used to assess nerve function in large, myelinated peripheral nerves but provide no information about smaller myelinated or unmyelinated nerve fibers
carrying pain and temperature sensory information. Magnetic resonance imaging is used to assess the anatomic integrity of thermonociceptive sensory processing regions, such as the brainstem, thalamus, sensory cortex, anterior cingulate, and insular cortex, which can contribute to central neuropathic pain when injured. Functional magnetic resonance imaging can provide further information about these and other pain-related structures, although its role in clinical practice is limited at present. It does not provide information about the functional state of the structure or its role in causing pain (Galer & Dworkin, 2000). Although not widely used in clinical practice, QST is assuming a greater role in neuropathic pain research. In QST, a computer-controlled device is used to provide a stimulus (for example, a heat probe providing heat sensory input). The level of stimulus needed to produce a particular sensation is measured (e.g., the temperature at which a patient reports pain due to heat). In this way, the sensory threshold is measured, and the function of peripheral nerve fibers and their central components can be measured. QST relies on the patient’s psychophysical ability to discriminate between fine changes in thermal stimuli. It is not widely used clinically because it requires specialized equipment and training (Dworkin et al., 2003). PHARMACOLOGIC TESTS Pharmacologic tests have been used to classify mechanisms involved in neuropathic pain. In these tests, the same agent may be administered by different routes (e.g., topical, systemic, epidural, intrathecal) to determine the pain-generating site. The use of topical lidocaine has been one of the tools used to classify mechanisms in PHN (Fields, Rowbotham, & Baron, 1998). Intravenous phentolamine or epidural opioid administration has also been used this way clinically. The N-methyl-D-aspartate antagonist ketamine, administered systemically in subanesthetic doses, has been shown to reduce ongoing spontaneous pain (brushand pinprick-evoked pain) in patients with amputations, traumatic nerve injuries, and PHN (Jensen & Baron, 2003). In two studies, a brief intravenous infusion of opioid or lidocaine was useful to predict a patient’s subsequent response to long-term treatment with an opioid or mexiletine (Dellimijn, van Duijn, & Vanneste, 1998; Galer, Harle, & Rowbotham, 1996).
CONCLUSIONS Traditionally, neuropathic pain has been diagnosed based on the underlying disease or etiology (e.g., painful diabetic neuropathy). As presented elsewhere in this supplement (Pasero, 2004), pain syndromes iden-
A Guide to Comprehensive Assessment
tified by disease most likely have multiple distinct mechanisms that account for chronic pain. For example, in PHN, nerve damage is caused by a virus and perhaps inflammation, whereas in painful diabetic neuropathy, it is caused by ischemia and perhaps altered metabolism. It would be expected that these processes are associated with different symptoms. Although not possible at present, a goal for the future is to identify specific pathophysiologic mechanisms associated with specific symptoms of neuropathic pain. For example, one patient with PHN may have mechanical allodynia, which indicates central sensitization, but another may not. Clinical researchers are seeking to meet this challenge by identifying pain mechanisms using combined information about symptoms, signs, QST, and the response to pharmacologic challenges (Dworkin, 2002). In nursing practice, patients with neuropathic pain remain a challenge. Neuropathic pain is often
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chronic and is difficult to diagnose because of the presence of positive and negative sensory and motor symptoms and signs, comorbid conditions, psychosocial issues, and interpatient variability. Pain assessment tools, commonly used in nursing practice, are able to provide information on some aspects of the pain and its characteristics. However, a thorough and focused clinical evaluation, including a thorough history, physical examination, and neurologic examination is key for adequate assessment and accurate diagnosis. Empathy and therapeutic communication with the patient are ever important elements of nursing practice. Patients with neuropathic pain experience unusual, uncommon sensations and may have difficulty communicating these to the clinician. Nurses with improved diagnostic skills, together with a greater knowledge base and empathy for the patient, can make significant contributions to the well-being of their patients with neuropathic pain.
REFERENCES Bennett, M. (2001). The LANSS pain scale: The Leeds assessment of neuropathic symptoms and signs. Pain, 92, 147-157. Boivie, J., Leijon, G., & Johansson, I. (1989). Central post-stroke pain & A study of the mechanisms through analyses of the sensory abnormalities. Pain, 37, 173-185. Boureau, F., Doubrere, J. F., & Luu, M. (1990). Study of verbal description in neuropathic pain. Pain, 42, 145-152. Byas-Smith, M. G., Max, M. B., Muir, J., & Kingman, A. (1995). Transdermal clonidine compared to placebo in painful diabetic neuropathy using a two-stage “enriched enrollment” design. Pain, 60, 267-274. Chong, M. S., & Bajwa, Z. H. (2003). Diagnosis and treatment of neuropathic pain. Journal of Pain and Symptom Management, 25, S4-S11. Cleeland, C. S., Nakamura, Y., Mendoza, T. R., Edwards, K. R., Douglas, J., & Serlin, R. C. (1996). Dimensions of the impact of cancer pain in a four country sample: New information from multidimensional scaling. Pain, 67, 267-273. Dellemijn, P. L., van Duijn, H., & Vanneste, J. A. (1998). Prolonged treatment with transdermal fentanyl in neuropathic pain. Journal of Pain and Symptom Management, 16, 220-229. Dworkin, R. H. (2002). An overview of neuropathic pain: Syndromes, symptoms, signs, and several mechanisms. Clinical Journal of Pain, 18, 343-349. Dworkin, R. H., Backonja, M., Rowbotham, M. C., Allen, R. R., Argoff, C. R., Bennett, G. J., et al. (2003). Advances in neuropathic pain. Diagnosis, mechanisms and treatment recommendations. Archives of Neurology, 60, 1524-1534. Fields, H. L., Rowbotham, M., & Baron, R. (1998). Postherpetic neuralgia: Irritable nociceptors and deafferentation. Neurobiology of Disease, 5, 209-227. Galer, B. S., Harle, J., & Rowbotham, M. C. (1996). Response to intravenous lidocaine infusion predicts subse-
quent response to oral mexiletine: A prospective study. Journal of Pain and Symptom Management, 12, 161-167. Galer, B. S., & Jensen, M. P. (1997). Development and preliminary validation of a pain measure specific to neuropathic pain: The neuropathic pain scale. Neurology, 48, 332-338. Galer, B. S., & Dworkin, R. H. (2000). A clinical guide to neuropathic pain. Minneapolis, MN: Healthcare Information Programs. Hansson, P. (2002). Neuropathic pain: Clinical characteristics and diagnostic workup. European Journal of Pain, 6(Suppl. A), 47-50. Harden, N., & Cohen, M. (2003). Unmet needs in the management of neuropathic pain. Journal of Pain and Symptom Management, 25, S12-S17. Herr, K., & Garand, L. (2001). Pain assessment and measurement in older adults. Clinics in Geriatric Medicine, 17, 457-478. Herr, K. A., & Mobily, P. R. (1993). Comparison of selected pain assessment tools for use with the elderly. Applied Nursing Research, 6, 39-46. Herr, K., Spratt, K., Mobily, P., & Richardson, G. (2004). Pain intensity assessment in older adults: Use of experimental pain to compare psychometric properties and usability of selected scales in adult and older populations. Clinical Journal of Pain, 20, 207-219. Gagliese, L., & Melzack, R. (2003). Age-related differences in the qualities but not the intensity of chronic pain. Pain, 104, 597-608. Jensen, T. S., & Baron, R. (2002). Translation of symptoms and signs into mechanisms in neuropathic pain. Pain, 102, 1-8. Krause, S. J., & Backonja, M. (2003). Development of a neuropathic pain questionnaire. Clinical Journal of Pain, 19, 306-314.
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Leijon, G., Boivie, J., & Johansson, I. (1989). Central post-stroke pain—Neurological symptoms and pain characteristics. Pain, 36, 13-25. Masson, E. A., Hunt, L., Gem, J. M., & Boulton, A. J. (1989). A novel approach to the diagnosis and assessment of symptomatic diabetic neuropathy. Pain, 38, 25-28. Melzack, R. (1975). The McGill Pain Questionnaire: Major properties and scoring methods. Pain, 1, 277-299. Melzack, R. (1987). The short-form McGill Pain Questionnaire. Pain, 30, 191-197. Melzack, R., Terrence, C., Fromm, G., & Amsel, R. (1986). Trigeminal neuralgia and atypical facial pain: Use of the McGill Pain Questionnaire for discrimination and diagnosis. Pain, 27, 297-302. Merkel, S., & Malviya, S. (2000). Pediatric pain, tools and assessment. Journal of Perianesthesia Nursing, 15, 408-414.
Merskey, H., & Bogduk, N. (Eds.). (1994). Classification of chronic pain: descriptions of chronic pain syndromes and definitions of pain terms (2nd ed.). Seattle, Washington: International Association for the Study of Pain Press. Osterberg, A., Boivie, J., Holmgren, H., Thuomas, K-A., & Johansson, I. (1994). The clinical characteristics and sensory abnormalities of patients with central pain caused by multiple sclerosis. In G. F. Gebhart, D. L. Hammond, & T. S. Jensen (Eds.), Proceedings of the 7th World Congress on Pain. Progress in pain research and management, Vol. 2 (pp. 789-796). Seattle Washington: International Association for the Study of Pain Press. Pasero, C. (2004). Pathophysiology of neuropathic pain. Pain Management Nursing, 5(Suppl. 1), 3-8