Miller was (mostly) right: Head injury severity inversely related to simulation

131 Legal and Criminological Psychology (2006), 11, 131 145 q 2006 The British Psychological Society The British Psychological Society www.bpsjournals.co.uk Miller was (mostly) right: Head injury severity inversely related to simulation Manfred F. Greiffenstein* and W. John Baker Psychological Systems Inc., Royal Oak, MI, USA Purpose. British neurologist Henry Miller (1961; Miller & Cartlidge, 1972) provoked controversy by asserting late post-concussion syndrome (LPCS) is explained by simulation. The present study examines Miller s inverse dose-response assertion; the more minor the compensable injury, the greater the likelihood of deficit simulation. Method. We examined the prevalence of three types of simulation (memory, motor, and psychiatric) in two archival cohorts of compensation seekers (N ¼ 391 and 368) representing a broad range of cranio-cervical injury severity. A moderate-severe brain injured group provided two sets of performance floors to establish possible or probable pseudoabnormalities. Instruments included the Rey word recognition list, the Smedley dynamometer, the Test of Memory Malingering, and the MMPI-2 infrequency scale. Results. Chronic whiplash and minor head-injury litigants produced more invalid signs than severely injured persons on measures of simulated memory and motor deficits irrespective of definitional stringency. ANOVA revealed striking inverse linear trends as a function of severity. Under a possible rule, at least one pseudoabnormality was present in 80% of LPCS claimants. Memory and motor pseudoabnormalities were more common than psychotic ones. Conclusions. These findings support Miller and Cartlidge s (1972) observations that embellishment rises as injury severity decreases in a compensable context. Simulating litigants may tailor performance to fit aetiological expectations, as we found a low prevalence of psychosis simulation. There is a general dose-response relationship between severity of brain trauma and neurocognitive outcome. Large inception cohort studies show worst neuropsychological outcome in severe head injury (Dikmen, Machamer, Winn, & Temkin, 1995; Kay, Kerr, & Lassman, 1971; Volbrecht, Meyers, & Kaster-Bundgaard, 2000) but rapid recovery in mild closed head injury (mchi) and no cognitive defect in cervical strain (Alexander, 1998, 2003; Gronwall & Wrightson, 1974; McCrea et al., 2003; Ruff, Levin, Mattis, High, & Tabaddor, 1989; Olsnes, 1989). Nonetheless, a small percentage of * Correspondence should be addressed to Manfred F. Greiffenstein, Psychological Systems Inc., Suite 103, Royal Oak, Michigan 48067, USA (e-mail: mfgreiff@yahoo.com). DOI:10.1348/135532505X49828

132 Manfred F. Greiffenstein and W. John Baker whiplash and mchi patients continue to report subjective disability collectively termed persistent (Luis, Vanderploeg, & Curtiss, 2003) or late post-concussion syndrome (LCPS; Greiffenstein & Baker, 2001). This non-specific complex includes pseudoneurologic, emotional, and cognitive complaints in the absence of objective neurological findings (Vanderploeg et al., 2003). Despite over a century of investigations since Sir John Erichsen coined the term railway spine (Benton, 1989), LPCS remains a controversial diagnosis for lack of any organic basis for subjective disability (Youngjohn, Burrows, & Erdal, 1995). Various neurogenic, psychogenic and multifactorial models of LPCS are reviewed elsewhere (Alexander, 1997; Binder, 1986; Brown et al., 1994; Lishman, 1988). British neurologist Henry Miller s published lectures (Miller, 1961; Miller & Cartlidge, 1972) provoked controversy by theorizing that simulation is the primary element of LPCS. His view rested on two observations. First, Miller reported most litigants originally suffering minor cervico-cranial injuries returned to work shortly after concluding litigation. Second, he described an inverse dose-response relationship in compensable injury (Miller & Cartlidge, 1972); the more minor the cervico-cranial injury, the more florid the later symptom production. The claim of high work return rates in LPCS was challenged by Australian psychiatrist George Mendelson s (1982) review of eight uncontrolled studies of post-litigation outcome. Mendelson (1995) later reported that 75% of traceable litigants were still not working 23 months after concluding litigation. Miller s second assertion of inverse dose-response relation has received no attention, although some studies bear indirectly on the issue. Workers with fewer years of solvent exposure report more symptoms than senior workers (Albers & Berent, 2000), and mildly shocked workers claim more frequent delayed symptoms than reported by severely shocked workers (Pliskin et al., 1998). Litigants with minor compensable injuries report more atypical symptoms than severely brain-injured litigants (Greiffenstein, Baker, Gola, Donders, & Miller, 2002; Miller & Donders, 2001) and more problems than non-litigating mchi patients (Paniak et al., 2002). Miller supported his conclusions with unaided clinical judgments, but the modern approach eschews clinical intuition (Faust, 1995; Heaton, Smith, Lehman, & Vogt, 1978), instead favouring direct measurement of simulation behaviour. There are two general approaches to detecting simulation symptom validity tests (SVT) specifically designed to detect manufactured cognitive defect (Frederick, 2003; Green, Lees-Haley, & Allen, 2002; Tombaugh, 1995) and detecting atypical response patterns on genuine neurocognitive measures (Ashendorf, O Bryant, & McCaffrey, 2003; Tenhula & Sweet, 1996). In this latter paradigm, deficit simulation is defined as atypically poor performance on common neuropsychological tasks relative to persons with substantial cortical damage (Greiffenstein, Baker, & Gola, 1994; Rogers, 1997) and is termed the floor effects strategy (Binder & Willis, 1991; van Gorp et al., 1999). Researchers have also moved away from a general malingering construct towards a multifaceted approach. Domain specific forms of simulation include somatic malingering (Larrabee, 1998), intellectual underperformance (Gudjonsson & Shackleton, 1986), non-anatomic motor deficits (Greiffenstein, Baker, & Gola, 1996; Rapport, Farchione, Coleman, & Axelrod, 1998), simulated memory and attention deficits (Green & Iversen, 2001), and exaggerated psychopathology (Greiffenstein et al., 2002). The focus of this paper is the inverse dose-response law proposed by Miller and Cartlidge (1972). To date, no study has directly tested Miller s inverse dose-response law by examining pseudoabnormality rate as a function of injury severity. Miller and Cartlidge defined simulation subjectively and did not specify the specific behavioural domain being simulated. We tested the inverse dose-response assertion

Simulation rates in late post-concussion 133 using both actuarial and frequentist statistics applied to two head-injury cohorts given a battery of measures from three functional domains (memory, motor, and psychiatric). Simulation rates were objectively established with a normative floor effects strategy. This involved comparing mildly injured litigant s scores to various performance limits of persons with substantial cerebral damage. A negligibly injured litigant scoring below defined floors is a reasonable operational definition of simulation. ANOVA with trend analysis was used to determine goodness of fit to an inverse dose-response model. A close reading of Miller and Cartlidge (1972) suggests the following three testable hypotheses: H1. LPCS litigants produce lower motor, memory, and psychiatric symptom scores than more severely injured claimants. H2. The majority of LPCS litigants will show simulation signs. H3. LPCS claimants producing the most complaints ( floridity ) will produce more pseudoabnormalities than will claimants with fewer complaints. Method Participants The participant data was archival and drawn from 759 neuropsychological examinations of head-injury claimants. The original data pool contained 1,027 claimants seen for insurance examinations but 268 cases had claims unrelated to head trauma. The data was further divided into two cohorts because of changes in battery composition, intelligence measures, and symptom coding. The 1990 1999 group (Cohort 1) consisted of 391 respondents and the 2000 2004 cohort (Cohort 2) consisted of 368 respondents undergoing medico-legal neuropsychological evaluations of remote head injuries. Referral sources included physicians, solicitors, insurers, and nurses. All were either receiving compensation or were involved in litigation for improved medical and care taking benefits, or both. Both cohorts were further subdivided into two major groupings a moderate-severe closed head-injury (MSCHI) reference group to establish floor effects and the LPCS for calculating simulation prevalence. Moderate-severe closed head-injury group (MSCHI) The MSCHI criteria were as follows: (1) Glasgow coma scale (GCS) of 12 or less on admission; (2) in-patient stays of a week or more; and (3) the presence of at least one acute focal neurological finding either on radiographic scanning or during the admission physical. Ninety-one persons from Cohort 1 and 68 persons from Cohort 2 were classified as MSCHI. CT scans demonstrated cerebral contusions and/or bleeds were seen in 83% of persons and 67% presented with either focal neurologic sensory or motor findings. These focal signs included hemiplegia, anosmia, and/or ataxia. Functionally, all MSCHI were community residing 2.1 years after injury. Late post-concussion syndrome (LPCS) The LPCS subgroup consisted of 607 claimants (300 from 1990 to 1999 and 307 from 2000 to 2004) alleging disability of more than 1 year duration following accidents with

134 Manfred F. Greiffenstein and W. John Baker minor injury characteristics, including classic concussion proven by medical records (N ¼ 106 in Cohort 1 and N ¼ 90 in Cohort 2), head trauma without altered mental status (N ¼ 123 in Cohort 1 and N ¼ 100 in Cohort 2), and common whiplash (N ¼ 71 in Cohort 1 and N ¼ 117 in Cohort 2). Classic concussion was defined as blunt head trauma associated with either brief (a) unresponsivity or (b) post-traumatic amnesia (Shaw, 2002). Whiplash was defined by a combination of self-report, absence of expected lordosis on radiography, and negative evidence for blunt trauma. There were minimal prospects for real cerebral dysfunction in this group. A few LPCS claimants showed minor abnormalities on their first CT scans but all showed normal CT scans at 1-year follow-up. None had diagnosable neuromuscular or orthopaedic disease. Procedure Both cohorts underwent structured interviews with one of the two authors, both board certified neuropsychologists. Ambulance and hospital records were available for all participants. Demographic and neurological variables collected during the history and records review included age, education, duration of illness, days in hospital, gender, handedness, ethnicity (e.g. black), civil status (e.g. marriage), CT/MRI findings (negative, abnormal), focal neurological findings, and admission/field GCS rankings from 3 to 15). Cranio-cervical injury was coded into a 3-level ordinal ranking for Cohort 1 (whiplash, mild concussion, and MSCHI) but in Cohort 2, whiplash was no longer coded separately; such patients were simply assigned GCS ratings of 15. Only four general symptom categories were coded for Cohort 1: cognitive, emotional, physical, and pseudoneurologic complaints (absent or present). The symptom coding for Cohort 2 was based on the 10 core post-concussive symptoms used by Fox, Lees-Haley, Earnest, and Dolezal-Wood (1995) in their adaptation of Diagnostic and Statistical Manual IV (American Psychiatric Association, 1994) criteria for PCS: memory, concentration, headaches, pain other than headache, sensory hyperacuity, insomnia, irritability, mood change (excluding irritability), dizziness, and fatigue. Both cohorts received neuropsychological and psychological testing including intelligence, achievement, and SVT. The 1990 1999 cohort received the Wechsler adult intelligence scale-revised (WAIS-R; Wechsler, 1980) as the measure of intelligence and the North American Adult Reading Test (Johnstone, Callahan, Kapila, & Bouman, 1996) as a measure of premorbid intelligence. To avoid generational cohort differences in intelligence ( Flynn Effect ; Kanaya, Scullin, & Ceci, 2003), we replaced the 20-year-old WAIS-R with the Wechsler abbreviated scales of intelligence (WASI; Wechsler, 2000) and the NAART with the Wechsler Test of Adult Reading (Wechsler, 2001). The WASI was selected because of its brevity and contemporary standardization sample. The SVTs were from three functional domains: memory, motor, and psychiatric deficit simulation. Memory simulation Cohort 1 received the Rey word recognition list (RWRL), an easy verbal recognition measure, consisting of 15 target and 15 foil words (Frederick, 2003; Lezak, 1983), was administered according to previously published guidelines (Greiffenstein et al., 1996). The score was the number of target words identified by pointing or circling (maximum ¼ 15 correct). We replaced the RWRL with the Test of Memory Malingering (TOMM; Tombaugh, 1995). The TOMM is a forced-choice visual memory test consisting of target-foil pairs presented over three test phases of 50 trials each (Tombaugh, 1995). Although Tombaugh recommends using the second or third trials for effort judgments,

Simulation rates in late post-concussion 135 we summed the correct choices over all three trials to increase the available variance for ANOVA (maximum ¼ 150). Psychiatric simulation Excessive psychiatric symptom report was measured with the Minnesota Multiphasic Personality Inventory-2 (MMPI-2) Infrequency scale (MMPI-F). The MMPI-F items represent complaints relatively uncommon in the general population and high scores generally indicate exaggerated psychosis (Greene, 2000; Greiffenstein et al., 2002) but not simulated cognitive defect (Greiffenstein, Baker, & Gola, 1995). All participants from both cohorts completed at least the first 370 items of the MMPI-2, necessary for scoring the three validity and ten basic clinical scales. The test was scored and plotted according to the test manual (Butcher, Dahlstrom, Graham, Tellegen, & Kaemmer, 1989) and the MMPI-F score coded in T score units (maximum ¼ 120 2 T). Motor simulation Simulated motor deficit was evaluated in both cohorts with the Smedley dynamometer, commonly referred to as grip strength (GS; Reitan & Wolfson, 1985). GS has proven relatively insensitive to cerebral dysfunction (Haaland & Delaney, 1981; Haaland, Temkin, Randahl, & Dikmen, 1994), but sensitive to atypical post-concussion histories (Greiffenstein et al., 1996; Pearce, 1994). The GS score represented the average of four trials (two for each hand) in kilograms. Results Group characteristics A summary of initial injury, neurological, and demographic characteristics are displayed in Table 1. Categorical variables were tested with Pearson s chi-square and continuous variables with student s t (two-tailed). There were no differences in demographic variables such as gender distribution, handedness, ethnicity, or Wechsler full scale IQ. The NAART and WTAR were not statistically comparable because the former is an IQ point estimate based on regression and the latter is a standard score. However, Cohort 1 was significantly older (t ¼ 27:8, df ¼ 757, p, :0001), and a significantly greater percentage was married (Pearson x 2 ¼ 53:3, df ¼ 5, p, :0001). Inter-cohort comparisons of neurological variables showed no significant differences in GCS distributions, post-injury durations, and CT abnormality rates. Among the two SVTs common to both cohorts, there was no difference in MMPI-F or GRIPSUM scores. Analysis of inverse dose-response prediction We tested Miller s inverse dose-response assertion by grouping participants into three groups reflecting increasing severity and examining the relationship to each simulation behaviour (memory, motor, psychiatric) through univariate ANOVA. To examine goodness of fit, all ANOVAs were followed by polynomial contrasts using weights (2 1, 0, and 1) reflecting an inverse relation. Because of unequal Ns, the weighted rather than unweighted sum of squares was used to calculate the F ratio. Recall that whiplash was coded separately for the Cohort 1 but assigned GCS ¼ 15 in Cohort 2.

136 Manfred F. Greiffenstein and W. John Baker Table 1. Demographic, neurological, performance, and symptom characteristics of the two cohorts and severity subgroups Groups 1991 1999 cohort 2000 2004 cohort Mod-severe CHI Late post-concussion Mod-severe CHI Late post-concussion Sample size 91 300 61 307 Age, MN years 33.14 (12.5) 35.89 (11.8) 38.02 (15.4) 42.7 (12.2) Gender % Female ¼ 26.3% Female ¼ 53% Female ¼ 29% Female ¼ 45.9% Education, MN years 11.36 (1.4) 12.9 (3.4) 11.96 (1.9) 11.4 (2.3) Hospital days, MN 81.92 (48.3).05 (.22) 48.3 0.4 (.23) Time after injury, MN months 21.1 (17.6) 23.7 (16.8) 33.45 (36) 23.5 (24.3) Abnormal first CT 83% 3% 68.8% 6.3% Motor/sensory signs 58% 0% 30.8%, 1% Admission GCS # 12 100% 0% 100% 0% Admission GCS 13 14 0% 23% 0% 30% Admission GCS ¼ 15 0% 77% 0% 70% Intelligence MN FSIQ WAIS-R WAIS-R WASI WASI 88.0 (11.3) 88.83 (12.6) 90.15 (16.4) 86.65 (15.1) Premorbid MN FSIQ estimate NAART NAART WTAR WTAR 90.74 (8.4) 95.18 (10.6) 85.00 (17.5) 85.99 (17.2) Grip strength, MN Kg 37.43 (12.3) 29.64 (15.1) 36.9 (12.6) 29.5 (14.3) Rey word recognition score, MN words 9.0 (2.4) 7.54 (2.9) TOMM sum, MN correct N/A N/A 139.5 (15.7) 122.4 (28.4) MMPI-2 F scale, MN T score 67.71 (21.7) 67.56 (22.5) 66.40 (22.5) 71.9 (22.0) Total head-injury symptoms reported, MN 3.64 (2.2) 6.21 (2.1) Note. Numbers in parentheses are standard deviations. FSIQ ¼ Full scale IQ; GCS ¼ Glasgow coma scale; MMPI-2 F scale ¼ Infrequency scale; NAART ¼ North American Adult Reading Test; TOMM ¼ Test of Memory Malingering, number correct out of 150 items; WAIS-R ¼ Wechsler adult intelligence scale, Revised; WASI ¼ Wechsler abbreviated scales of intelligence; WTAR ¼ Wechsler Test of Adult Reading.

Simulation rates in late post-concussion 137 Examining for inverse trends with the RWRL in Cohort 1 cohort showed both a significant group effect, Fð2; 388Þ ¼10:0, p, :0001, and weighted linear term, Fð1; 388Þ ¼ 18:75, p, :001. The polynomial contrast was significant at t ¼ 4:46, df ¼ 388, p, :0001. The inverse relationship between initial injury severity and RWRL performance is more easily visualized in Fig. 1. Both cohorts were combined to evaluate relations between injury severity and GS. There was a significant groups effect, Fð2; 756Þ ¼10:33, p, :0001, and a significant weighted linear term, F ¼ 17:03, p, :0001. Polynomial contrast testing showed a significant inverse linear trend, t ¼ 4:32, p, :0001. Figure 2 illustrates that more severe compensable injuries are associated with less weakness than more minor injuries. This result is especially powerful when one considers that some of the severely head injury showed focal motor signs at some point in their initial hospitalizations. The TOMM data from Cohort 2 showed significant group effects, Fð2; 365Þ ¼13:50, p, :0001, weighted linear term, F ¼ 26:97, p, :0001, and polynomial contrasts, t ¼ 5:02, df ¼ 365, p, :0001. Figure 3 depicts the mean sum of all TOMM trials plotted against increasing injury severity and shows improving performance as a function of compensable injury severity. Put differently, the more minor the initial injury, the greater the errors. Psychiatric embellishment trends were examined through use of the MMPI infrequency scale. There was no group effect for the MMPI-F scale, Fð2; 756Þ ¼:29, p ¼ :75, and polynomial contrasts did not reveal a trend in the expected direction, t ¼ 21:59, p ¼ :16. Within-cohort ANOVAs also did not reveal any significant trends either for MMPI-F. Figure 1. Percentage of claimants from 1990 to 1999 cohort scoring in the invalid range on the Rey Word Recognition List plotted against injury type.

138 Manfred F. Greiffenstein and W. John Baker Figure 2. Mean combined dominant and non-dominant handgrip strength (Smedley dynamometer) plotted against increasing injury severity for both cohorts. Prevalence of simulation hypothesis Frequentist statistics may not adequately characterize individual differences. Only an actuarial approach will determine whether test score irregularities are representative of any group. In order to calculate the prevalence of valid/invalid test signs, we tabulated the frequencies of single and combined simulation signs in the two LPCS cohorts. As prevalence estimates are dependent on the stringency of criteria, we examined invalid and valid performance under two certainty levels: probable and possible. Probable was defined as any score in the LPCS group # 2 1.0 SD below the MSCHI mean and possible invalid performance was defined as any score below the MSCHI group mean. Figure 3. Sum of all Test of Memory Malingering (TOMM) trials grouped by initial head-injury severity for the 2000 2004 cohort. The GCS ¼ 15 group includes persons with whiplash.

Simulation rates in late post-concussion 139 Table 2. Group means, standard deviations, and cut scores (floors) to calculate valid and invalid performances under two certainty levels (probable and possible) 1990 1999 cohort MSCHI group 2000 2004 cohort MSCHI group MN (SD) Prob. Floor Poss. Floor MN (SD) Prob. Floor Poss. Floor TOMM 139.49 (15.7) #124 #139 RWRL 9.0 (2.4) #6 words #8 words GRIP SUM 37.43 (12.3) 36.91 (12.6) Females 26.44 (10.5) #16 kg,26 kg 25.63 (10.0) #16 kg #25 kg Males 41.37 (10.3) #31 kg #41 kg 40.03 (11.5) #29 kg #40 kg MMPI-F 67.1 (21.8) $90 T. 68 T 66.46 (22.3) $89 T $67 T Note. Prob. Floor ¼ probable simulation defined by performance at or below 21 SD of the more seriously injured reference group (but at or above þ1 SD for the MMPI-2 infrequency scale); Poss. Floor ¼ possible simulation defined by performance at or below the reference group mean; GRIP SUM ¼ average of both hands on the Smedley dynamometer; MMPI-F ¼ infrequency scale T score from the MMPI-2; RWRL ¼ sum of all correct on the Rey word recognition list; TOMM ¼ sum of all three trials of the Test of Memory Malingering. Although weaker than probable simulation, it is still reasonable to expect a person with an old minor injury to score above the average performance of persons with definitive cortical damage (Dikmen et al., 1995). Table 2 summarizes the means, standard deviations, and cut scores for the two cohorts. Table 3 summarizes the probabilities for various combinations of valid and invalid test signs under two levels of certainty. The first row (any invalid sign) provides the best test of Miller and Cartlidge s (1972) contention that simulation dominates LPCS presentations. Table 3 suggests a majority of the LPCS claimants demonstrate at least one irregularity irrespective of stringency. Three-quarters of the combined cohorts showed at least one suspicious performance under the possible rule and roughly half showed a pseudoabnormality under the probable rule. Hence, simulation tendency appears to be the rule rather than the exception in LPCS, consistent with H2. The remainder of Table 3 provides evidence for type of simulated presentation. Inspection of the combined cohort s column indicates that 7% or 18% demonstrated diffusely poor performance (all three invalid signs present). Further, exaggeration of psychiatric symptoms (as measured by the MMPI-2 F scale) was rare under the probable rule but jumped under a possible rule. However, the mean MMPI-F score (see Table 1) was still far below the critical score of 100 T necessary to render an MMPI profile invalid (Greene, 2000). In descending order, under the more stringent probable rule, the most common presentation was a suspiciously poor memory presentation on very simple recognition tests (TOMM and RWRL), followed by exaggerated weakness (bilateral GS) with suspicious MMPI-F scores a distant third. This suggests the pseudoabnormalities may represent tailoring of performances to fit an internal stereotype of brain damage. In other words, few LPCS claimants present with implausible psychotic presentations. Floridity and simulation H3 is the florid assertion. Miller and Cartlidge (1972) described a subset of 50 workers with multiple diffuse complaints and concluded that the simulation rate was 100%.

140 Manfred F. Greiffenstein and W. John Baker Table 3. Prevalence of invalid and valid performances in late post-concussion compensation seekers for both and combined cohorts 1990 1999 LPCS cohort (N ¼ 300) 2000 2004 LPCS cohort (N ¼ 307) Combined cohorts (N ¼ 607) Pattern Probable simulation Possible simulation Probable simulation criterion Possible simulation criterion Probable simulation criterion Possible simulation criterion Any invalid sign(s) present 56.7% (170) 80.3% (241) 57.3% (176) 78.8% (222) 57% 76.2% All valid 43.3% (130) 19.7% (59) 42.7% (131) 21.2% (85) 31.1% 23.7% One invalid sign 34% (102) 34% (102) 28.9% (89) 25.4% (78) 31.5% 29.7% only Any two invalid signs All three invalid signs Memory sign present Motor sign present Psychiatric sign present 18.3% (55) 33.7% (101) 20.5% (63) 30.9% (95) 19.4% 63.8% 4.3% (13) 12.7% (38) 9.4% (29) 24.2% (73) 6.9% 18.3% 39.7% (119) 60.3% (181) 42% (130) 57.9% (178) 41% 59% 27.7% (83) 39% (117) 31.5% (97) 45.9% (141) 29.7% 42.5% 16.3% (49) 40% (120) 19.5% (60) 50.8% (156) 18% 45.5% Note. Figure in parentheses is number of participants in LCPS cohort showing the feature.

Simulation rates in late post-concussion 141 Table 4. Number of post-concussive complaints and frequency of cases showing invalid signs in all three functional domains as test of the floridity hypothesis Cases showing three atypical signs Symptoms reported Cases reporting Probable Possible 0 0 0 0 1 2 7 0 0 3 4 51 0 4 (7.8%) 5 6 95 2 (2%) 17 (17.8%) 7 8 109 15 (13.8%) 28 (25.7%) 9 10 45 12 (26.7%) 24 (53.3%) Note. The 2000 2004 cohort only. Number in parentheses is percentage of cases within each row. A conservative way to test this hypothesis is tabulate the total number of subjective complaints against the frequency of cases showing all three simulation signs. This could only be done with Cohort 2 with its improved symptom coding. The results are presented in Table 4. Those reporting no or few symptoms did not show the simulation triad. Although half the sample produced complaints ranging from 0 to 6, only 2% and 25.6% of this subgroup showed the simulation triad under probable and possible definitions. All three pseudoabnormalities were most frequent in those reporting seven or more symptoms, with more than half of those in the 9 10 symptom range, showing the simulation triad under the possible rule. The Kruskal-Wallis test for independence of symptom count versus probability of diffuse simulation was robustly significant (x 2 ¼ 38:1, df ¼ 5, p, :0001). This supports Miller and Cartlidge s contention that florid symptom production during history justifies concerns about protocol validity; however, diffuse simulation was not universal in those reporting extreme symptom counts. Discussion The results support the general contours of Miller and Cartlidge s (1972) positions. We found robust inverse dose-response relationships in two of three functional areas. Poorer performance on simple memory and motor tasks in persons with minor craniocervical injury. Examination of base rates for three types of simulated deficit (memory, motor, psychiatric) demonstrated that suspected simulation was the rule rather than the exception. Those reporting the most symptoms ( floridity in Miller s terms) showed the highest rates of egregious simulation, although not universally so. A comparison of present with earlier published findings is complicated because we examined three pseudoabnormalities across a broad injury range, which rendered our study unique. Our finding of 41% probable amnesia simulation is nearly identical to Mittenberg, Patton, Canyock, & Condit s (2002) report of 39% implausible cognitive patterns and Larrabee s (2003a) compilation showing 40% cognitive simulation (11 studies, 548/1363 subjects) in litigants. With respect to motor simulation, Peterson (1998) found 73% spurious weakness among 249 LPCS claimants during neurological examinations, which was markedly above the levels reported here. However, Peterson examined all muscle groups, not just the upper extremities. Pearce (1994) estimated 55% spurious grip strength is whiplash patients, a finding closer to the 43% rate reported here.

142 Manfred F. Greiffenstein and W. John Baker We doubt that our findings will resolve the long-standing debate over the meaning of LPCS. Simulation as sole causation for LPCS cannot be determined by a cross-sectional design. The best conclusion is that simulation is strongly associated with persistent postconcussion syndrome, but may not be the initial cause or the only association. Because this study supports the general contours of Miller and Cartlidge s (1972) theory, there is no support for the belief that simulation is rare or that litigants are not different than nonlitigants (Evans, 1994). We strongly urge formal effort testing in all compensation seekers. However, we do not believe that simulation is universal, and there is no basis for Sir Aubrey Lewis speculation that LPCS is a form of psychopathy (cited in Lishman, 1988). A multifactorial approach that considers multiple pre- and post-injury biopsychosocial factors is advisable even if simulation is present (Greiffenstein, 2000; Lishman, 1988). Limitations and future directions Criticisms of this study may focus on factors that under- or overestimate simulation rates. Factors underestimating rates may include test sensitivity and motivation levels of the reference group. We used the RWRL and TOMM as a simulation measure but there may be more sensitive measures (Gervais, Rohling, Green, & Ford, 2004; Green & Iverson, 2001). Similarly, there is growing evidence the MMPI-F scale is insensitive to the types of exaggerated symptoms seen in personal injury litigants (Greiffenstein et al., 2002; Larrabee, 2003a, 2003b). Exaggerated defect has also been documented in some severe CHI cases (Boone & Lu, 2003) and suboptimal performance in this group could have lowered the performance floors, making our prevalence rates too conservative. Factors potentially leading to overestimation include the specific floors chosen as cutting scores. Some may argue that choosing the MSCHI group mean as a cutting scores for possible simulation and,21 SD as the probable rule sets the cutting score too low, resulting in false positive conclusions. We argue that the differences in neurological defects between minor and major injury groups are substantial and it is reasonable to expect a person sustaining whiplash to perform above the mean of patients with low admitting GCS scores. The present study results should not be generalized to all mildly injured persons. Acute mchi and LCPS should not be lumped into a vague head-injury category. Our study focused only on persons who failed to recover after minor trauma, a small percentage of all minor injury patients (Gronwall, 1991). Our results would only be applicable to persons with medically unexplained chronic complaints. Miller s views of post-litigation return-to-work rates could not be addressed in this study because of its cross-sectional nature. The problem addressing this issue is methodological as both Miller and his critics never defined what was meant by settlement or finalization of claim. Does this mean a lump sum payout or recurrent benefits in perpetuity? This issue will remain unresolved until measurement of legal context and monetary contingencies improves (Mendelson, 1991). References Albers, J. W., & Berent, S. (2000). Controversies in neurotoxicology: Current status. Neurological Clinics, 18, 741 764. Alexander, M. P. (1997). Minor traumatic brain injury: A review of physiogenesis and psychogenesis. Seminars in Clinical Neuropsychiatry, 2, 177 187. Alexander, M. P. (1998). In the pursuit of proof of brain damage after whiplash injury. Neurology, 51, 336 340.

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