APPLIED NEUROPSYCHOLOGY: ADULT, 22: 227–232, 2015 Copyright # Taylor & Francis Group, LLC ISSN: 2327-9095 print=2327-9109 online DOI: 10.1080/23279095.2014.910213
The Effects of Cold Pressor-Induced Pain on PASAT Performance Brian E. Tapscott Department of Psychology, The University of Rhode Island, Kingston, Rhode Island
Joseph Etherton Department of Psychology, Texas State University, San Marcos, Texas
Although clinicians have frequently observed that patients with chronic pain experience cognitive deficits related to memory and concentration, research on these deficits is equivocal, with some studies showing significant impairment and others suggesting minimal deficits. As such, the present study sought to examine the relationship between laboratory-induced pain and performance on the Paced Auditory Serial Addition Test (PASAT) using a mixed factorial design. Seventy-two nonclinical volunteers were randomly assigned to a pain group, who took the PASAT while experiencing cold pressor-induced pain, or a control group, who took the PASAT while experiencing painless room-temperature water immersion. To account for practice effects, all participants were administered 1 practice trial and 3 standard trials of the PASAT, with the final trial administered in cold pressor-induced pain or painless water immersion. The results revealed a significant interaction between condition and PASAT performance, F(1, 64) ¼ 23.63, p < .001, partial g2 ¼ .27. The control group increased performance by 6 items while the pain group showed no such improvement. The results suggest that because the pain group did not demonstrate the same practice effects relative to the control group, their performance was impaired by cold pressor-induced pain. However, the impairment was relatively mild (about 0.5 standard deviation) and did not occur in all participants.
Key words:
assessment, chronic pain, PASAT
INTRODUCTION Patients with chronic pain often complain of cognitive problems associated with attention and memory. Research has reported that chronic pain is associated with impairment to some cognitive processes (Eccleston, 1994; Hart, Wade, & Martelli, 2003; Sjøgren, Olsen, Thomsen, & Dalberg, 2000). Specifically, chronic pain has been associated with impaired memory (Oosterman, Derksen, van Wijck, Veldhuijzen, & Kessels, 2011; Address correspondence to Brian E. Tapscott, MA, Department of Psychology, The University of Rhode Island, 142 Flagg Road, Kingston, RI 02881. E-mail: [email protected]
Sjøgren, Thomsen, & Olsen, 2000), impaired executive functioning (Abeare et al., 2010; Glass et al., 2011), impaired processing speed (Grigsby, Rosenberg, & Busenbark, 1995), impaired psychomotor speed (Sjøgren, Thomsen, et al., 2000), and impaired attention (Moore, Keogh, & Eccleston, 2012). As noted by Kreitler and Niv (2007), these impairments warrant closer inspection because they may contribute to further suffering and reduce quality of life. Although the precise neurophysiological mechanisms that lead to such impairments are not fully understood, research suggests that pain may utilize many of the same mechanisms necessary for certain cognitive processes (Sanchez, 2011), leading to deterioration in task
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performance. For example, Eccleston and Crombez (1999) postulate that physical pain is a stimulus that demands attention. This distraction from our normal thought processes orients us toward the problem (e.g., a sprained ankle) and motivates us to take action toward relief. Because attention is a limited-capacity resource (e.g., Norman, 1968), pain-related distraction presumably leaves less attention available for other cognitive processes. As a result, cognitive performance may be impaired when one is in pain. However, when acute pain extends into chronic pain, additional factors other than pain may influence cognitive performance. A host of psychosocial variables may impact the experience of pain including beliefs about pain, perceived social support, coping styles, and pain-related catastrophizing (Sullivan, Bishop, & Pivik, 1995), which have been shown to contribute to pain intensity, pain-related interference, and psychological functioning (Osborne, Jensen, Ehde, Hanley, & Kraft, 2007). In addition, one study reported that psychological distress (an amalgam of anxiety, depression, irritability, and energy levels) and lower ratings of emotional well-being were significantly related to cognitive impairment in patients with chronic pain (Grace, Nielson, Hopkins, & Berg, 1999; Kewman, Vaishampayan, Zald, & Han, 1991; Landrø, Stiles, & Sletvold, 1997; Radanov, Dvora´k, & Valach, 1992). Although the relationship between psychosocial factors and cognitive deficits in patients with chronic pain is not entirely understood, researchers have suggested that emotional distress may contribute independently to reduced cognitive performance. Further, additional factors commonly observed in patients with chronic pain may also affect cognition, including fatigue, apathy, disordered sleep, or medication effects (Kreitler & Niv, 2007). Although many studies have compared patients with chronic pain to healthy controls, this methodology involves extraneous psychosocial variables other than pain that are frequently present in patients with chronic pain. Eccleston (1995) suggests that laboratory-induced pain has been the most effective at parsing pain control and pain processing. This experimental paradigm allows researchers to enhance internal validity by isolating the effects of pain while controlling for confounding variables. In contrast to research reporting significant cognitive impairments due to pain (e.g., Eccleston, 1994; Hart et al., 2003; Sjøgren, Olsen, et al., 2000), other studies have reported that neither induced nor chronic pain led to substantial impairments on standard clinical measures of processing speed and working memory (Etherton, Bianchini, Ciota, Heinly, & Greve, 2006; Etherton, Bianchini, Heinly, & Greve, 2006). Further research has revealed that many cognitive tasks are not impaired by induced pain in healthy volunteers (Buhle & Wager, 2009). Although the literature clearly
shows some pain-related impairment in some cognitive functions for certain populations (Kewman et al., 1991), the extent to which pain per se may be expected to impair performance on different types of cognitive tasks remains relatively understudied. As such, the present study examines the relationship between induced pain and performance on the Paced Auditory Serial Addition Test (PASAT; Gronwall, 1977).
METHODS Approval for this study was granted by the institutional review board (IRB) of the authors’ university. Participants Seventy-two nonclinical undergraduate participants were recruited via e-mail from introductory psychology courses and received extra credit from their instructor as an incentive to participate. Exclusion criteria included hearing impairments, pain-related or neurological disorders, current use of analgesic medication or psychiatric medication, a history of traumatic brain injury (TBI) or stroke, Raynaud’s disease, or the presence of a skin disease. Five participants withdrew from the study because the severity of pain exceeded tolerable limits, leaving a final sample of 67 participants. The majority of participants had 13 years of education (N ¼ 23, 34.3%), followed by 14 years (N ¼ 13, 19.4%), 15 years (N ¼ 10, 14.9%), 12 years (N ¼ 9, 13.4%), 16 years (N ¼ 9, 13.4%), and 17 or more years (N ¼ 3, 4.5%). Additionally, most participants were 18 to 19 years old (N ¼ 38, 56.7%), followed by 20 to 21 years of age (N ¼ 17, 25.4%), 22 to 23 years of age (N ¼ 8, 11.9%), and 24 years old or older (N ¼ 4, 6.0%). Caucasian=White was the most common selfidentified ethnicity (N ¼ 30, 44.8%), followed by Hispanic=Latino (N ¼ 24, 35.8%), African American= Black (N ¼ 9, 13.4%), Asian=Pacific Islander (N ¼ 2, 3.0%), and Mix=Other (N ¼ 2, 3.0%). Eighty-seven percent of the sample was right-handed (N ¼ 58). Instruments PASAT. The PASAT requires participants to listen to a standardized audio-recording of a series of singledigit numbers, add the two most recently heard numbers, and say aloud the sum (Cardinal, Wilson, Giesser, Drain, & Sicotte, 2008). The time between digits being read may be as long as 3 s for some versions, with the shortest standard version being a delay of 0.8 s between digits. The PASAT is regarded as a difficult task, particularly as the delay between numbers decreases. It is a
EFFECTS OF COLD PRESSOR-INDUCED PAIN ON THE PASAT
highly sensitive instrument originally developed for patients with TBI as a measure of processing speed (Tombaugh, 2006). Subsequent research, however, has revealed it to be appropriate for assessing a range of neuropsychological conditions, which is likely due to its ability to tap into multiple constructs including attention, working memory, processing speed, and mathematics abilities (Chronicle & MacGregor, 1998; Crawford, Obonsawin, & Allan, 1998; Lockwood, Linn, Szymanski, Coad, & Wack, 2004; Sherman, Strauss, & Spellacy, 1997; Tombaugh, 2006). Despite evidence suggesting limited utility, particularly for individuals with low IQ (Crawford et al., 1998; Egan, 1988), high self-reported nervousness (Rosti, Ha¨ma¨la¨inen, Koivisto, & Hokkanen, 2007a), and low mathematic abilities (Chronicle & MacGregor, 1998), as well as the elderly (Tombaugh, 2006), the PASAT is commonly used in clinical settings and is a core measure of cognitive impairment in patients with multiple sclerosis (MS; Rosti, Ha¨ma¨la¨inen, Koivisto, & Hokkanen, 2007b). However, as noted by Tombaugh (2006), caution must be exercised when interpreting the significance of a low score. Criticism of the instrument stems from the fact that it has been shown to induce autonomic arousal (Mathias, Stanford, & Houston, 2004) and contribute to negative mood (Holdwick & Wingenfeld, 1999). Although this has not been shown to modulate performance in healthy populations, the concern is that it may confound the interpretability of results in sensitive populations, especially considering that it is a difficult task even for intelligent individuals (Bidin-Brooks et al., 2011). Conversely, it has been shown to be a reliable instrument with high internal consistency (Tombaugh, 2006) and adequate sensitivity in detecting cognitive impairment in patients with MS (Rosti et al., 2007a, 2007b). In the current study, the interstimulus interval between digits was limited to 2 s for all trials (as opposed to the 3-s trial) to minimize the amount of time participants in the pain group were exposed to pain, in accordance with IRB recommendations. Pain rating. During pain induction, participants were asked to rate their level of pain on an 11-point scale (0 ¼ no pain, 10 ¼ very strong pain). Pain ratings were collected at two time intervals during pain induction: immediately before administering the PASAT and immediately after. These pain ratings are labeled Pain Rating 1 and Pain Rating 2, respectively. Procedures The experiment was administered by three undergraduate psychology students and two master’s-level
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psychology graduate students. All students had received thorough training on PASAT procedures and protocols prior to beginning the present study. Informed consent was obtained from all participants. Cold pressor task. The cold pressor task is a method for inducing nonharmful and quickly reversible pain, commonly used in research settings to simulate the conditions of chronic pain (Peckerman, Saab, & McCabe, 1991). Participants place their hand or foot in a container holding a mixture of ice and water, which rapidly induces pain of typically moderate severity. In the current study, participants placed their left hand into the ice water. All participants were informed that they could discontinue the pain-inducing procedure at any time without penalty. Conditions. Participants were randomly assigned to either a pain condition or control condition. Both groups received identical treatment (i.e., completed the same instruments and were administered the PASAT in the same way) except that those in the pain condition took the PASAT while experiencing cold pressor-induced pain. Because the cold pressor procedure involves potentially distracting variables other than pain, such as holding one’s hand in water and being asked to provide a pain rating verbally, participants in the control condition underwent procedurally equivalent, but nonpainful, room temperature water immersion in place of the cold pressor procedure (Etherton, Bianchini, Ciota, et al., 2006; Etherton, Bianchini, Heinly, et al., 2006). That is, they were asked to place their hands in roomtemperature water and to provide pain ratings, matching the conditions of the pain group in all respects except for the absence of pain induction. Participants first completed a demographic questionnaire. Next, one practice trial (10 items) and three standard trials (60 items) of the 2-s PASAT (Gronwall, 1977) were administered to both groups (in that order), of which only the final two standard trials were scored. This approach was used because research has shown that, although practice effects occur with the PASAT (Barker-Collo, 2005), they are most pronounced from the first to second administration (Solari, Radice, Manneschi, Motti, & Montanari, 2004), suggesting a ceiling effect for practice. Thus, to minimize the confounding nature of practice effects, participants were administered a 10-item practice trial and one 60-item standard trial prior to the scored trials. The second standard administration served as a ‘‘baseline’’ and the third standard administration was recorded as the ‘‘experimental administration,’’ involving either the presence or absence of induced pain. These administrations are reported as ‘‘Trial 1’’ and ‘‘Trial 2.’’ The control group
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was administered Trial 2 with their hand in a bucket of room-temperature water (procedural distraction). The pain group was administered Trial 2 while experiencing cold pressor-induced pain. For both groups, Pain Rating 1 was collected immediately prior to Trial 2 and Pain Rating 2 was collected immediately after Trial 2. To protect against familiarity with the numbers being used, alternate forms were used. Half of the participants were administered the PASAT in the order of Form A, Form B, and Form A, and the other half were administered the test in the order of Form B, Form A, Form B. Participants in the pain group generally did not experience cold pressor-induced pain for more than 130 s.
RESULTS Prior to the analyses, 1 participant’s data were removed as an extreme outlier on the PASAT and another participant’s pain ratings were removed for potentially misrepresenting pain levels. The final sample consisted of 66 participants (52 female, 14 male), including 34 in the control group (5 male, 29 female) and 32 in the pain group (9 male, 23 female). For the pain group and the control group, the mean scores for Trial 2 of the PASAT were 28 (SD ¼ 10.36) and 33.15 (SD ¼ 9.88), respectively. The means of Pain Rating 1 were 0.63 (SD ¼ 0.83) for the control group and 3.5 (SD ¼ 2.1) for the pain group, while the means of Pain Rating 2 were 1.2 (SD ¼ 1.7) for the control group and 7.2 (SD ¼ 2.1) for the pain group. A mixed-measures analysis of variance was performed to assess the effects of pain on PASAT performance as well as to assess potential interactions. The results are reported in Table 1. No significant differences were found between the control and pain conditions for Trial 1 (which did not involve pain induction), F(1, 64) ¼ 0.64, p ¼ .43. However, a significant difference was found between the Trial 1 and Trial 2 PASAT administrations, F(1, 64) ¼ 15.42, p < .05, partial g2 ¼ .19, as was a significant interaction effect between group and PASAT performance, F(1, 64) ¼ 23.63, p < .001, partial g2 ¼ .27. The control group improved their performance from Trial 1 to Trial 2 by roughly six items, presumably reflecting continued practice effects; in contrast, the pain group showed no TABLE 1 Number of Correct PASAT Items by Group for Trials 1 and 2 Trial 1
Trial 2
Condition
N
Mean (SD)
N
Mean (SD)
Control Group Pain Group
34 32
27.26 (9.86) 28.63 (9.75)
34 32
33.15 (9.88) 28.00 (10.36)
TABLE 2 Correlations for Pain Group Variable
Trial 2 Pain Rating 1 Pain Rating 2 Pain Mean
1. 2. 3. 4.
.37 .12 .26
Trial 2 Pain Rating 1 Pain Rating 2 Pain mean
.48 .84
.88
Correlation is significant at the .05 level (two-tailed). Correlation is significant at the .01 level (two-tailed).
improvement in performance from Trial 1 to Trial 2, suggesting pain-related reduction in performance relative to the control group. Based on Cohen’s guidelines for interpreting effect size, the partial g2 value of .27 for the interaction is considered a large effect size (Cohen, 1977). To assess the relationship between pain ratings and PASAT performance, the correlation coefficients were computed for the pain group only. The results are reported in Table 2. A negative correlation was found between Pain Rating 1 and Trial 2 of the PASAT (r ¼ .37, p < .05). However, Pain Rating 2 and the mean of Pain Rating 1 and 2 (listed as ‘‘pain mean’’) were not significantly correlated with Trial 2, indicating that pain severity is moderately but inconsistently associated with poorer PASAT performance.
DISCUSSION The present study further contributes to the overall understanding of the effects of pain on cognition. Previous research has shown mixed results on how pain affects cognition, with some research suggesting significant cognitive impairment (Hart et al., 2003; Sjøgren, Olsen, et al., 2000), while other research suggest minimal or no deficits (Etherton, Bianchini, Ciota, et al., 2006; Etherton, Bianchini, Heinly, et al., 2006). Additional research has shown that cognitive task impairment only occurs with high-severity pain ratings or for particularly difficult cognitive tasks (Eccleston, 1994). Further contributing to the difficulty in assessing the effects of pain on cognition is the well-established relationship between psychosocial factors and cognitive impairment in patients with chronic pain (Kreitler & Niv, 2007). The present study utilized laboratory-induced pain to examine the relationship between pain and PASAT performance. In contrast to research with chronic pain samples, laboratory-induced pain in nonclinical volunteers allows an examination of the degree of impairment exclusively attributable to pain, rather than to extraneous nonpainful variables frequently observed in patients with chronic pain (e.g., mood disturbance, sleep impairment).
EFFECTS OF COLD PRESSOR-INDUCED PAIN ON THE PASAT
The results of the present study suggest that induced pain impairs performance on the PASAT (partial g2 ¼ .27). Whereas participants in the control group showed continued improvement in performance from Trial 1 to Trial 2 (mean improvement of six correct items), presumably attributable to continued practice effects, participants in the pain group showed no such improvement. This absence of expected improvement in the pain condition relative to the control group may be viewed as indicative of impairment in that it reflects failure to benefit from practice in a manner equivalent to the control group. The six-item discrepancy between the pain group and control group is roughly equivalent to 0.5 standard deviation (SD) based on PASAT norms (M ¼ 39.4, SD ¼ 10.2; Rao, Leo, Bernardin, & Unverzagt, 1991). Of particular importance in the present study is the role of practice effects in the interpretation of the results. Despite measures to minimize practice effects, notable increases between each administration were observed in both groups, although this was not observed in all participants (26.5% of the control group showed 1 SD improvement from Trial 1 to Trial 2, 18.2% of the pain group showed 0.5 SD improvement from Trial 1 to Trial 2). In the pain group, the largest increase for a single participant from Trial 1 to Trial 2 with induced pain was 15 items, while the largest decrease was 17 items. In the control group, participants increased their performance from Trial 1 to Trial 2 by 0 to 15 items. No participants in the control group decreased their performance. It should be noted, however, that the largest increase from Trial 1 to Trial 2 (15 items) was observed in both conditions. A review of the data suggests that although some are strongly influenced by the effects of induced pain, many participants did not display difficulty redirecting their attention toward the PASAT and away from the induced pain; as a result, they did not show impairment in their performance. This is consistent with the literature showing that the scores of some patients with chronic pain demonstrate attentional impairment (Etherton, Bianchini, Ciota, et al., 2006; Etherton, Bianchini, Heinly, et al., 2006); but most patients with chronic pain, as most participants in the present study, show minimal or no impairment due to pain. Abnormally low scores may be indicative of lack of motivation, misrepresentation of abilities, or other pathology. The clinical implications of the present study suggest that although pain itself may impact PASAT performance, the impairment is relatively mild (about 0.5 SD) and does not occur for all individuals. Strengths and Limitations A strength of the present study is the use of laboratory-induced pain and a mixed factorial design,
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which enhances internal validity and allows for greater control of potential confounds. In addition, the present study used a measure widely used in clinical settings, which allows for greater generalizability to clinical practice. Although the PASAT is frequently used in neuropsychological evaluations, to the authors’ knowledge, no study has evaluated the relationship between induced pain and PASAT performance. Notwithstanding the strengths of the present study, limitations should be noted. First, the sample consisted of nonclinical, healthy volunteers who experienced temporary, localized pain. Accordingly, these results may not fully generalize to patients with chronic pain. Second, as the sample was disproportionately female, it is possible that gender influenced the results. Research shows that women do not typically tolerate pain as well as men, which may be related to a reduced pain tolerance when menstruating and reduced padding in the fingers (Ravn, Frederiksen, Skovsen, Christup, & Werner, 2012). Third, because the present study isolated the effects of pain, the potential influence of salient psychosocial variables (e.g., anxiety, depression, fatigue, hope, and social support) that could impact performance was not measured. Research shows that college students high in hope are more tolerant of pain than their less hopeful peers (Snyder et al., 2005), and students who volunteer early in the school year have higher hope levels than students who volunteer late in the semester (Navarick & Bellone, 2010). However, presumably, effects of the construct of hope would be randomly distributed across both the control group and pain group, such that observed differences between the two groups would be attributable to effects of pain rather than differences in level of hope. Nonetheless, it is possible that hope influenced the results of the present study. Future research should replicate these findings with particular focus given to pain ratings and the influence of psychosocial variables in the relationship between pain and PASAT performance. Additionally, future research should aim to identify which individuals are cognitively impacted by pain.
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The Effects of Cold Pressor-Induced Pain on PASAT Performance Brian E. Tapscott Department of Psychology, The University of Rhode Island, Kingston, Rhode Island
Joseph Etherton Department of Psychology, Texas State University, San Marcos, Texas
Although clinicians have frequently observed that patients with chronic pain experience cognitive deficits related to memory and concentration, research on these deficits is equivocal, with some studies showing significant impairment and others suggesting minimal deficits. As such, the present study sought to examine the relationship between laboratory-induced pain and performance on the Paced Auditory Serial Addition Test (PASAT) using a mixed factorial design. Seventy-two nonclinical volunteers were randomly assigned to a pain group, who took the PASAT while experiencing cold pressor-induced pain, or a control group, who took the PASAT while experiencing painless room-temperature water immersion. To account for practice effects, all participants were administered 1 practice trial and 3 standard trials of the PASAT, with the final trial administered in cold pressor-induced pain or painless water immersion. The results revealed a significant interaction between condition and PASAT performance, F(1, 64) ¼ 23.63, p < .001, partial g2 ¼ .27. The control group increased performance by 6 items while the pain group showed no such improvement. The results suggest that because the pain group did not demonstrate the same practice effects relative to the control group, their performance was impaired by cold pressor-induced pain. However, the impairment was relatively mild (about 0.5 standard deviation) and did not occur in all participants.
Key words:
assessment, chronic pain, PASAT
INTRODUCTION Patients with chronic pain often complain of cognitive problems associated with attention and memory. Research has reported that chronic pain is associated with impairment to some cognitive processes (Eccleston, 1994; Hart, Wade, & Martelli, 2003; Sjøgren, Olsen, Thomsen, & Dalberg, 2000). Specifically, chronic pain has been associated with impaired memory (Oosterman, Derksen, van Wijck, Veldhuijzen, & Kessels, 2011; Address correspondence to Brian E. Tapscott, MA, Department of Psychology, The University of Rhode Island, 142 Flagg Road, Kingston, RI 02881. E-mail: [email protected]
Sjøgren, Thomsen, & Olsen, 2000), impaired executive functioning (Abeare et al., 2010; Glass et al., 2011), impaired processing speed (Grigsby, Rosenberg, & Busenbark, 1995), impaired psychomotor speed (Sjøgren, Thomsen, et al., 2000), and impaired attention (Moore, Keogh, & Eccleston, 2012). As noted by Kreitler and Niv (2007), these impairments warrant closer inspection because they may contribute to further suffering and reduce quality of life. Although the precise neurophysiological mechanisms that lead to such impairments are not fully understood, research suggests that pain may utilize many of the same mechanisms necessary for certain cognitive processes (Sanchez, 2011), leading to deterioration in task
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performance. For example, Eccleston and Crombez (1999) postulate that physical pain is a stimulus that demands attention. This distraction from our normal thought processes orients us toward the problem (e.g., a sprained ankle) and motivates us to take action toward relief. Because attention is a limited-capacity resource (e.g., Norman, 1968), pain-related distraction presumably leaves less attention available for other cognitive processes. As a result, cognitive performance may be impaired when one is in pain. However, when acute pain extends into chronic pain, additional factors other than pain may influence cognitive performance. A host of psychosocial variables may impact the experience of pain including beliefs about pain, perceived social support, coping styles, and pain-related catastrophizing (Sullivan, Bishop, & Pivik, 1995), which have been shown to contribute to pain intensity, pain-related interference, and psychological functioning (Osborne, Jensen, Ehde, Hanley, & Kraft, 2007). In addition, one study reported that psychological distress (an amalgam of anxiety, depression, irritability, and energy levels) and lower ratings of emotional well-being were significantly related to cognitive impairment in patients with chronic pain (Grace, Nielson, Hopkins, & Berg, 1999; Kewman, Vaishampayan, Zald, & Han, 1991; Landrø, Stiles, & Sletvold, 1997; Radanov, Dvora´k, & Valach, 1992). Although the relationship between psychosocial factors and cognitive deficits in patients with chronic pain is not entirely understood, researchers have suggested that emotional distress may contribute independently to reduced cognitive performance. Further, additional factors commonly observed in patients with chronic pain may also affect cognition, including fatigue, apathy, disordered sleep, or medication effects (Kreitler & Niv, 2007). Although many studies have compared patients with chronic pain to healthy controls, this methodology involves extraneous psychosocial variables other than pain that are frequently present in patients with chronic pain. Eccleston (1995) suggests that laboratory-induced pain has been the most effective at parsing pain control and pain processing. This experimental paradigm allows researchers to enhance internal validity by isolating the effects of pain while controlling for confounding variables. In contrast to research reporting significant cognitive impairments due to pain (e.g., Eccleston, 1994; Hart et al., 2003; Sjøgren, Olsen, et al., 2000), other studies have reported that neither induced nor chronic pain led to substantial impairments on standard clinical measures of processing speed and working memory (Etherton, Bianchini, Ciota, Heinly, & Greve, 2006; Etherton, Bianchini, Heinly, & Greve, 2006). Further research has revealed that many cognitive tasks are not impaired by induced pain in healthy volunteers (Buhle & Wager, 2009). Although the literature clearly
shows some pain-related impairment in some cognitive functions for certain populations (Kewman et al., 1991), the extent to which pain per se may be expected to impair performance on different types of cognitive tasks remains relatively understudied. As such, the present study examines the relationship between induced pain and performance on the Paced Auditory Serial Addition Test (PASAT; Gronwall, 1977).
METHODS Approval for this study was granted by the institutional review board (IRB) of the authors’ university. Participants Seventy-two nonclinical undergraduate participants were recruited via e-mail from introductory psychology courses and received extra credit from their instructor as an incentive to participate. Exclusion criteria included hearing impairments, pain-related or neurological disorders, current use of analgesic medication or psychiatric medication, a history of traumatic brain injury (TBI) or stroke, Raynaud’s disease, or the presence of a skin disease. Five participants withdrew from the study because the severity of pain exceeded tolerable limits, leaving a final sample of 67 participants. The majority of participants had 13 years of education (N ¼ 23, 34.3%), followed by 14 years (N ¼ 13, 19.4%), 15 years (N ¼ 10, 14.9%), 12 years (N ¼ 9, 13.4%), 16 years (N ¼ 9, 13.4%), and 17 or more years (N ¼ 3, 4.5%). Additionally, most participants were 18 to 19 years old (N ¼ 38, 56.7%), followed by 20 to 21 years of age (N ¼ 17, 25.4%), 22 to 23 years of age (N ¼ 8, 11.9%), and 24 years old or older (N ¼ 4, 6.0%). Caucasian=White was the most common selfidentified ethnicity (N ¼ 30, 44.8%), followed by Hispanic=Latino (N ¼ 24, 35.8%), African American= Black (N ¼ 9, 13.4%), Asian=Pacific Islander (N ¼ 2, 3.0%), and Mix=Other (N ¼ 2, 3.0%). Eighty-seven percent of the sample was right-handed (N ¼ 58). Instruments PASAT. The PASAT requires participants to listen to a standardized audio-recording of a series of singledigit numbers, add the two most recently heard numbers, and say aloud the sum (Cardinal, Wilson, Giesser, Drain, & Sicotte, 2008). The time between digits being read may be as long as 3 s for some versions, with the shortest standard version being a delay of 0.8 s between digits. The PASAT is regarded as a difficult task, particularly as the delay between numbers decreases. It is a
EFFECTS OF COLD PRESSOR-INDUCED PAIN ON THE PASAT
highly sensitive instrument originally developed for patients with TBI as a measure of processing speed (Tombaugh, 2006). Subsequent research, however, has revealed it to be appropriate for assessing a range of neuropsychological conditions, which is likely due to its ability to tap into multiple constructs including attention, working memory, processing speed, and mathematics abilities (Chronicle & MacGregor, 1998; Crawford, Obonsawin, & Allan, 1998; Lockwood, Linn, Szymanski, Coad, & Wack, 2004; Sherman, Strauss, & Spellacy, 1997; Tombaugh, 2006). Despite evidence suggesting limited utility, particularly for individuals with low IQ (Crawford et al., 1998; Egan, 1988), high self-reported nervousness (Rosti, Ha¨ma¨la¨inen, Koivisto, & Hokkanen, 2007a), and low mathematic abilities (Chronicle & MacGregor, 1998), as well as the elderly (Tombaugh, 2006), the PASAT is commonly used in clinical settings and is a core measure of cognitive impairment in patients with multiple sclerosis (MS; Rosti, Ha¨ma¨la¨inen, Koivisto, & Hokkanen, 2007b). However, as noted by Tombaugh (2006), caution must be exercised when interpreting the significance of a low score. Criticism of the instrument stems from the fact that it has been shown to induce autonomic arousal (Mathias, Stanford, & Houston, 2004) and contribute to negative mood (Holdwick & Wingenfeld, 1999). Although this has not been shown to modulate performance in healthy populations, the concern is that it may confound the interpretability of results in sensitive populations, especially considering that it is a difficult task even for intelligent individuals (Bidin-Brooks et al., 2011). Conversely, it has been shown to be a reliable instrument with high internal consistency (Tombaugh, 2006) and adequate sensitivity in detecting cognitive impairment in patients with MS (Rosti et al., 2007a, 2007b). In the current study, the interstimulus interval between digits was limited to 2 s for all trials (as opposed to the 3-s trial) to minimize the amount of time participants in the pain group were exposed to pain, in accordance with IRB recommendations. Pain rating. During pain induction, participants were asked to rate their level of pain on an 11-point scale (0 ¼ no pain, 10 ¼ very strong pain). Pain ratings were collected at two time intervals during pain induction: immediately before administering the PASAT and immediately after. These pain ratings are labeled Pain Rating 1 and Pain Rating 2, respectively. Procedures The experiment was administered by three undergraduate psychology students and two master’s-level
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psychology graduate students. All students had received thorough training on PASAT procedures and protocols prior to beginning the present study. Informed consent was obtained from all participants. Cold pressor task. The cold pressor task is a method for inducing nonharmful and quickly reversible pain, commonly used in research settings to simulate the conditions of chronic pain (Peckerman, Saab, & McCabe, 1991). Participants place their hand or foot in a container holding a mixture of ice and water, which rapidly induces pain of typically moderate severity. In the current study, participants placed their left hand into the ice water. All participants were informed that they could discontinue the pain-inducing procedure at any time without penalty. Conditions. Participants were randomly assigned to either a pain condition or control condition. Both groups received identical treatment (i.e., completed the same instruments and were administered the PASAT in the same way) except that those in the pain condition took the PASAT while experiencing cold pressor-induced pain. Because the cold pressor procedure involves potentially distracting variables other than pain, such as holding one’s hand in water and being asked to provide a pain rating verbally, participants in the control condition underwent procedurally equivalent, but nonpainful, room temperature water immersion in place of the cold pressor procedure (Etherton, Bianchini, Ciota, et al., 2006; Etherton, Bianchini, Heinly, et al., 2006). That is, they were asked to place their hands in roomtemperature water and to provide pain ratings, matching the conditions of the pain group in all respects except for the absence of pain induction. Participants first completed a demographic questionnaire. Next, one practice trial (10 items) and three standard trials (60 items) of the 2-s PASAT (Gronwall, 1977) were administered to both groups (in that order), of which only the final two standard trials were scored. This approach was used because research has shown that, although practice effects occur with the PASAT (Barker-Collo, 2005), they are most pronounced from the first to second administration (Solari, Radice, Manneschi, Motti, & Montanari, 2004), suggesting a ceiling effect for practice. Thus, to minimize the confounding nature of practice effects, participants were administered a 10-item practice trial and one 60-item standard trial prior to the scored trials. The second standard administration served as a ‘‘baseline’’ and the third standard administration was recorded as the ‘‘experimental administration,’’ involving either the presence or absence of induced pain. These administrations are reported as ‘‘Trial 1’’ and ‘‘Trial 2.’’ The control group
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was administered Trial 2 with their hand in a bucket of room-temperature water (procedural distraction). The pain group was administered Trial 2 while experiencing cold pressor-induced pain. For both groups, Pain Rating 1 was collected immediately prior to Trial 2 and Pain Rating 2 was collected immediately after Trial 2. To protect against familiarity with the numbers being used, alternate forms were used. Half of the participants were administered the PASAT in the order of Form A, Form B, and Form A, and the other half were administered the test in the order of Form B, Form A, Form B. Participants in the pain group generally did not experience cold pressor-induced pain for more than 130 s.
RESULTS Prior to the analyses, 1 participant’s data were removed as an extreme outlier on the PASAT and another participant’s pain ratings were removed for potentially misrepresenting pain levels. The final sample consisted of 66 participants (52 female, 14 male), including 34 in the control group (5 male, 29 female) and 32 in the pain group (9 male, 23 female). For the pain group and the control group, the mean scores for Trial 2 of the PASAT were 28 (SD ¼ 10.36) and 33.15 (SD ¼ 9.88), respectively. The means of Pain Rating 1 were 0.63 (SD ¼ 0.83) for the control group and 3.5 (SD ¼ 2.1) for the pain group, while the means of Pain Rating 2 were 1.2 (SD ¼ 1.7) for the control group and 7.2 (SD ¼ 2.1) for the pain group. A mixed-measures analysis of variance was performed to assess the effects of pain on PASAT performance as well as to assess potential interactions. The results are reported in Table 1. No significant differences were found between the control and pain conditions for Trial 1 (which did not involve pain induction), F(1, 64) ¼ 0.64, p ¼ .43. However, a significant difference was found between the Trial 1 and Trial 2 PASAT administrations, F(1, 64) ¼ 15.42, p < .05, partial g2 ¼ .19, as was a significant interaction effect between group and PASAT performance, F(1, 64) ¼ 23.63, p < .001, partial g2 ¼ .27. The control group improved their performance from Trial 1 to Trial 2 by roughly six items, presumably reflecting continued practice effects; in contrast, the pain group showed no TABLE 1 Number of Correct PASAT Items by Group for Trials 1 and 2 Trial 1
Trial 2
Condition
N
Mean (SD)
N
Mean (SD)
Control Group Pain Group
34 32
27.26 (9.86) 28.63 (9.75)
34 32
33.15 (9.88) 28.00 (10.36)
TABLE 2 Correlations for Pain Group Variable
Trial 2 Pain Rating 1 Pain Rating 2 Pain Mean
1. 2. 3. 4.
.37 .12 .26
Trial 2 Pain Rating 1 Pain Rating 2 Pain mean
.48 .84
.88
Correlation is significant at the .05 level (two-tailed). Correlation is significant at the .01 level (two-tailed).
improvement in performance from Trial 1 to Trial 2, suggesting pain-related reduction in performance relative to the control group. Based on Cohen’s guidelines for interpreting effect size, the partial g2 value of .27 for the interaction is considered a large effect size (Cohen, 1977). To assess the relationship between pain ratings and PASAT performance, the correlation coefficients were computed for the pain group only. The results are reported in Table 2. A negative correlation was found between Pain Rating 1 and Trial 2 of the PASAT (r ¼ .37, p < .05). However, Pain Rating 2 and the mean of Pain Rating 1 and 2 (listed as ‘‘pain mean’’) were not significantly correlated with Trial 2, indicating that pain severity is moderately but inconsistently associated with poorer PASAT performance.
DISCUSSION The present study further contributes to the overall understanding of the effects of pain on cognition. Previous research has shown mixed results on how pain affects cognition, with some research suggesting significant cognitive impairment (Hart et al., 2003; Sjøgren, Olsen, et al., 2000), while other research suggest minimal or no deficits (Etherton, Bianchini, Ciota, et al., 2006; Etherton, Bianchini, Heinly, et al., 2006). Additional research has shown that cognitive task impairment only occurs with high-severity pain ratings or for particularly difficult cognitive tasks (Eccleston, 1994). Further contributing to the difficulty in assessing the effects of pain on cognition is the well-established relationship between psychosocial factors and cognitive impairment in patients with chronic pain (Kreitler & Niv, 2007). The present study utilized laboratory-induced pain to examine the relationship between pain and PASAT performance. In contrast to research with chronic pain samples, laboratory-induced pain in nonclinical volunteers allows an examination of the degree of impairment exclusively attributable to pain, rather than to extraneous nonpainful variables frequently observed in patients with chronic pain (e.g., mood disturbance, sleep impairment).
EFFECTS OF COLD PRESSOR-INDUCED PAIN ON THE PASAT
The results of the present study suggest that induced pain impairs performance on the PASAT (partial g2 ¼ .27). Whereas participants in the control group showed continued improvement in performance from Trial 1 to Trial 2 (mean improvement of six correct items), presumably attributable to continued practice effects, participants in the pain group showed no such improvement. This absence of expected improvement in the pain condition relative to the control group may be viewed as indicative of impairment in that it reflects failure to benefit from practice in a manner equivalent to the control group. The six-item discrepancy between the pain group and control group is roughly equivalent to 0.5 standard deviation (SD) based on PASAT norms (M ¼ 39.4, SD ¼ 10.2; Rao, Leo, Bernardin, & Unverzagt, 1991). Of particular importance in the present study is the role of practice effects in the interpretation of the results. Despite measures to minimize practice effects, notable increases between each administration were observed in both groups, although this was not observed in all participants (26.5% of the control group showed 1 SD improvement from Trial 1 to Trial 2, 18.2% of the pain group showed 0.5 SD improvement from Trial 1 to Trial 2). In the pain group, the largest increase for a single participant from Trial 1 to Trial 2 with induced pain was 15 items, while the largest decrease was 17 items. In the control group, participants increased their performance from Trial 1 to Trial 2 by 0 to 15 items. No participants in the control group decreased their performance. It should be noted, however, that the largest increase from Trial 1 to Trial 2 (15 items) was observed in both conditions. A review of the data suggests that although some are strongly influenced by the effects of induced pain, many participants did not display difficulty redirecting their attention toward the PASAT and away from the induced pain; as a result, they did not show impairment in their performance. This is consistent with the literature showing that the scores of some patients with chronic pain demonstrate attentional impairment (Etherton, Bianchini, Ciota, et al., 2006; Etherton, Bianchini, Heinly, et al., 2006); but most patients with chronic pain, as most participants in the present study, show minimal or no impairment due to pain. Abnormally low scores may be indicative of lack of motivation, misrepresentation of abilities, or other pathology. The clinical implications of the present study suggest that although pain itself may impact PASAT performance, the impairment is relatively mild (about 0.5 SD) and does not occur for all individuals. Strengths and Limitations A strength of the present study is the use of laboratory-induced pain and a mixed factorial design,
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which enhances internal validity and allows for greater control of potential confounds. In addition, the present study used a measure widely used in clinical settings, which allows for greater generalizability to clinical practice. Although the PASAT is frequently used in neuropsychological evaluations, to the authors’ knowledge, no study has evaluated the relationship between induced pain and PASAT performance. Notwithstanding the strengths of the present study, limitations should be noted. First, the sample consisted of nonclinical, healthy volunteers who experienced temporary, localized pain. Accordingly, these results may not fully generalize to patients with chronic pain. Second, as the sample was disproportionately female, it is possible that gender influenced the results. Research shows that women do not typically tolerate pain as well as men, which may be related to a reduced pain tolerance when menstruating and reduced padding in the fingers (Ravn, Frederiksen, Skovsen, Christup, & Werner, 2012). Third, because the present study isolated the effects of pain, the potential influence of salient psychosocial variables (e.g., anxiety, depression, fatigue, hope, and social support) that could impact performance was not measured. Research shows that college students high in hope are more tolerant of pain than their less hopeful peers (Snyder et al., 2005), and students who volunteer early in the school year have higher hope levels than students who volunteer late in the semester (Navarick & Bellone, 2010). However, presumably, effects of the construct of hope would be randomly distributed across both the control group and pain group, such that observed differences between the two groups would be attributable to effects of pain rather than differences in level of hope. Nonetheless, it is possible that hope influenced the results of the present study. Future research should replicate these findings with particular focus given to pain ratings and the influence of psychosocial variables in the relationship between pain and PASAT performance. Additionally, future research should aim to identify which individuals are cognitively impacted by pain.
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