Transcript personal_injury_II_2014

Forensic Neuropsychology in
Personal Injury Cases II
Russell M. Bauer, Ph.D.
July 17, 2008
Summary from Last Week
 Persistent
deficits after mTBI are rare
 Even when present, severity of deficits
is small (<.5 SD)
 NP impairment is often the only
“objective” indicator of abnormality
 What to make of this?
 IMPORTANT REMINDER: SOME
PATIENTS DO SUFFER RESIDUAL
DEFICITS!!
“Noninjury” Contributors to
Neuropsychological Impairment in MHI


Adversarial patient-examiner relationship
Expectation/attributional processes
– Diagnosis threat, role stereotypes

Exaggeration or poor effort
– Impairment as communication
– Frank malingering for gain; financial incentives
– Factitious disorders


Fatigue, pain, other physical factors
Psychiatric/behavioral disturbance (e.g., psychosis, anxiety,
depression)
– Cogniform disorder/cogniform condition
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Pre-existing factors affecting neuropsychological performance (e.g.,
learning disability, limited education)
Occupational/life experience factors
Assessment of Malingering
and Poor Effort

Issues/problems with definition
– Intentional (intention)
– Fabrication or exaggeration (action)
– For purposes of gain (motive)

Explanatory models (Rogers, 1997)
– Pathological (mental disorder)
– Criminological (fake)
– Adaptational (meeting adversarial demands)

Cognitive vs. Somatic Malingering
Diagnosis Threat (Suhr &
Gunstad, 2002)
 37
MHI (17 in “diagnosis threat”
condition)
 Diagnosis threat: told selected because
of a MHI history; “a growing number of
studies show that many individuals
with head injury show cognitive deficits
in neuropsychological tests”
Suhr & Gunstad, 2002
*
Suhr & Gunstad, 2002
Cogniform Disorder/Cogniform Condition
 Patients
with excessive cognitive
complaints
 Difficulties with existing diagnostic
options
– Symptom specificity
– Intentionality
– Presence of external incentive
 COGNIFORM
PRESENTATION
Pain and NP Performance

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Pain itself associated with mild NP performance
decrements
Pain medications
– Opioids: attention/concentration (on dose
escalations)
Neurobiological systems
– ACC, NA, extended amygdala
Pain ALONE would not explain a -2SD discrepancy
in severity
Block & Cianfrini Neurorehabilitation, 2013; Moriarty, et al
Prog Neurobiol, 2011.
Depression and NP
 Moderate
effect sizes in executive
function, memory and attention (-.34 to
-.65)
 After treatment/remission,
– Executive/attention: -.52 to -.61 in patients
with depression relative to controls (sig)
– Memory: -.22 to -.54 (nonsig)
 Suggests
that “poor” cognition is a
central, core feature
Rock, et al., Psychological Medicine, 2013
Lim et al, Int Psychogeriatr,
2013
 Meta-analysis
of a total of 22 trials
involving 955 MDD patients and 7,664
healthy participants. MDD < healthy:
–
–
–
–
–
Digit Span, CPT (attention)
TMT-A, Digit Symbol (processing speed)
Stroop, WCST, Verbal Fluency (exec)
Immed verbal memory (memory)MDD
Other tests did not differentiate
Larrabee & Rohling, 2013
Effort, Motivation, & Response Styles
Frederick et al., 2000
Malingering Algorithms:
Slick (1999)
 Considers
report
 4 criteria
–
–
–
–
evidence from NP and self
Presence of incentive
Evidence from NP
Evidence from self-report
Not better accounted for by….
Slick et al. (1999; cont’d)
 NP
criteria
– Definite (below chance) or probable (low)
response bias on FC measures
– Discrepancies/inconsistencies between
 NP
data and patterns of brain functioning
 NP data and observed behavior
 NP data and reliable collateral reports
 NP data and past history
Slick et al. (1999; cont’d)

Self-report criteria
– Self-report discrepant with history
– Self-report discrepant with known patterns of
brain functioniong
– Self-report discrepant with behavioral
observations
– Self-report discrepant with collateral information
– Evidence of exaggerated or fabricated
psychological dysfunction
Slick et al, 1999 (cont’d)
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

DEFINITE MND
Presence of financial
incentive
Definite negative
response bias
Behaviors that meet
criteria for negative
response bias that are
not fully accounted for
by psychiatric,
neurological, or
developmental factors



PROBABLE MND
Presence of financial
incentive
Two or more types of
evidence from NP,
excluding definite
response bias, or one
piece of evidence from
NP and one from selfreport
Malingering Research Literature


Case study
Simulation studies
– Interpretive issues
– Appropriate designs

Differential prevalence design
– contrasting high and low baserate groups (e.g., groups with
and without financial incentives)
– Valuable mostly for determining average performances

Known-groups design
– Selecting groups on the basis of malingering criteria (e.g.,
Slick, et al)
– Examining differences between the groups
Selecting Specialized Cognitive
Effort Tests
 Ease
of use
 Credibility of rationale
 Operating Characteristics
– Incremental validity
– TBI vs. PPCS
 Coaching
issues
 There is not likely to be a “best” test in
all circumstances
Commonly Used Specialized
Tests
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Portland Digit Recognition
Digit Memory Test
Computerized Assessment of Response Bias (CARB)
Word Memory Test (WMT)
Victoria Symptom Validity Test
Test of Memory Malingering
Validity Indicator Profile
Rey 15-Item Test
Dot Counting Test
Detecting Anomalous Results with
Embedded Measures and Performance
Patterns
 Measures
within standard NP tests that
signify noncredible or ‘suspect’
performance
 Identification of such measures can be
“rational” or “empirical”
 May be less subject to coaching than
separate measures
Pattern Analysis
 Pattern
Analysis
– With HRNB, DFA outperforms clinicians
(80-90% v. 50-60%)
– Most DFA’s multivariate , consisting of
attention and memory measures
 Generally,
measures
malingers score better on hard
– DFA’s exist for WMS-R, WMS-III, WAIS-R,
WAIS-III and other tests
– Before using, investigate whether the DFA
was validated/cross validated with known
groups or simulators
Iverson & Binder, 2000; Larrabee, 2005
Common “suspect” neuropsychological
signs on NP testing
Recognition << recall (hits, discriminability)
 Extremely poor DS in the context of normal
auditory comprehension (RDS)
 Motor slowing (e.g., reduced tapping) relative
to overt motor disability
 Excessive failures-to-maintain-set on WCST
 Discrepancies between test level and level
during informal interaction
 Other “impossible” signs

Embedded Measures – Motor,
Sensory, and Perceptual-Motor


Perceptual-motor pseudoabnormality should not be
overlooked b/c of emphasis on “higher” cognitive
disabilities
Approaches
– Neurologic exam
– Sensorimotor impairments on NP exam

Findings
– RCFT copy 50% sensitive with lots of FP
– Malingering groups favor memory over visuoconstructive
impairment (e.g. memory trials of RCFT discriminate better)
– Generally large grip strength effect size in K-G designs
– Reduced FT speed in the context of MHI
Embedded Cognitive
Measures
– WMS-R/WMS-III
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Malingerers: Attention/Concentration < General Memory
Opposite pattern is more typical of head injury
Rarely-missed index on LM delayed recognition trials
– WAIS-R/WAIS-III: Digit Span
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Malingerers: Low digit span performance (ACSS < 5)
Reliable Digit Span (sum of longest correct span for both trials < 8)
Vocabulary – Digit Span (low digit span while vocabulary is high)
– CVLT
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Malingerers: Low recognition (hits & forced-choice)
Cutoff scores for recall trials produce variable false-positive rates
Variable results with most widely used cutoffs (Millis et al): Total < 35,
LDCR <7, delayed recognition <11, discriminability < 81; sensitivity in
question, not specificity
Malingering Patterns in NΨ Tests
 Pattern Analysis
– Word Memory Test
Malingerers: Inconsistent responding, poor initial
recognition
 Pattern should reflect severity of impairments

– Category Test

Malingerers: Poor performance on first 2 subtests
– Wisconsin Card Sorting Task

Malingerers: Poor ratios of categories completed compared
to both perseverative errors and failure to maintain set
Iverson & Binder, 2000; Larrabee, 2005
Why being a knowledgeable
neuropsychologist is important
 You
know likely patterns of impairment
 You know psychometric relationships
among tests
 You know course of recovery
 You know about contributory factors
(e.g., LD, depression, etc.)
 You can compare what you see to what
you expect
Some Take Home Messages
Use multiple measures (forced choice,
embedded, etc.)
 Clarify your goals: sensitivity, specificity, etc.
 Be aware of correlations among malingering
measures
 Look for emerging research on
sensitivity/specificity of multiple indicators

Symptom Exaggeration

Self-Report of Symptoms
– May be exaggerated due to other variables (depression, pain,
stress)


e.g., Post-Concussive Syndrome persisting for more than 3
months
MMPI-2
– Malingerers tend to show elevations in clinical scales 1, 2, 3, 7,
and 8, the Fake Bad Scale (FBS), VRIN, TRIN, the InfrequencyPsychopathology Scale [F(p)].
– The F Scale and F – K does not appear to be as sensitive, and
therefore “valid” profiles may be obtained.
– Caution should be given to interpreting the clinical scales and
F Scale derivatives, as these can be easily influenced by
psychiatric comorbidities.
Iverson & Binder, 2000; Larrabee, 2005
Detecting Somatic Malingering
Symptom report, as well as cognitive
performance, can be controlled by the litigant
 Use of MMPI-2

–
–
–
–
–
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F-scale, F(p)
VRIN, TRIN
Subtle-Obvious
F-K index
Revised Dissimulation Scales
These scales may not be sufficiently sensitive
to TBI-related claims, despite neuropsychological differences
MMPI Measures
 FBS: 43 items – honest with bad injury;
Originally the “Fake Bad Scale” and now the
“Symptom Validity Scale” (FBS)
 Response
Bias Scale (RBS): 28 items that
predicted failure on CARB and WMT
 Henry-Heilbronner
Index (HHI): 15
items sensitive to neurocognitive complaints
in the months following head trauma
FBS
 Model
of goal-directed behavior:
– Want to appear honest
– Want to appear psychologically normal
except for the influence of injury
– Avoid admitting longstanding problems
– Minimize pre-existing complaints
– Minimizing pre-injury antisocial or illegal
behavior
– Presenting plausible injury severity
Lees-Haley FBS (cont’d)
 18
“True” , 25 “False”
 Does not correlate very strongly with Fscale derivatives
 Most scale items overlap with
“neurotic” side of MMPI
 Cut-off mid 20’s, with varying false
positive rates; increasing security with
scores > 25-27
FBS Operating Characteristics
 Most
frequently failed indicator of
MND (Larrabee)
 FBS > 27 has Sn=.46 , Sp=.96, better than
F or Fb (Greve et al)
 Sensitive to symptom exaggeration in
personal injury, not just litigation
 Cutoffs determine TP, FP rate
Critical Studies

Butcher et al (2003)
– Unacceptably high FP of FBS (24% of males, 37.9% of females
exceeded cutoffs)
– Psychiatric, corrections, medical, pain, VA, personal injury litigants
– No measures of symptom validity external to the MMPI
– No report of who was litigating
– Can’t compute specificity or sensitivity without this information

Bury & Bagby (2002)
–
–
–
–
–
PTSD vs. students (standard and exaggeration instructions)
F family produced best overall classification rates
Entire PTSD sample were being evaluated for workplace disability
Mean PTSD FBS was 26.31
No independent measures of malingering or exaggeration
RBS
 Sensitivity
low (.34), specificity high
(.96-.98)
 Specifically designed to predict SVT
failure
 Outperforms F-family and FBS in doing
this
 Seems to measure more “cognitive”
than “somatic” factors
HHI
 Neurocognitive
complaints in the
immediate postinjury period.
 9 items overlap with FBS, 4 with
original “Pseudoneurologic Scale; PNS)
 Sensitivity 80%, Specificity 89% with a
cutoff of > 8
Classification Accuracy of FBS, RBS, and HHI
Dionysus et al., Arch Clin Neuropsychol, 2011

Neuropsychology for Physicists:

“Neuropsychological testing was highly consistent with her 2/8/97 automobile
accident. That is, she showed evidence suggestive of significant shearing damage, the
frontal system being damaged bilaterally, with relative sparing of the intentional
memory system structures and posterior brain areas, a pattern expected with an injury
in which the brain is spun and then violently counterspun within the skull. She also
showed significant deficits with passive attention plus more problems with incidental
than intentional memory. This suggests reticular activating system damage such as
would occur with significant shearing and/or when the brain is slammed down
against the tentorium. Hypothalamic symptoms were numerous. Damage to this
nucleus is quite common in this type of injury as well. Finally, Ms. X showed some
right posterior deficits, but sparing of left posterior function. This suggests a possible
right posterior/left frontal coup/contracoup pattern overlaying the bilateral frontal
system shearing. This dual pattern can occur in an accident such as hers where the
driver is seat-belt restrained and the left front of her car is hit. Ms. X reported
symptoms consistent with mild to moderate depression. The pattern of her
neuropsychological deficits was inconsistent with scores of non-head-injured patients
suffering from depression. The pattern of Ms. X’s neuropsychological damage and
residual strengths, the nature of her 2/8/97 MVA, and the timing of symptom onset all
indicate the cause of her present brain damage to be the 2/8/97 accident.
Patient after MVA, with no LOC, undergoes neuropsychological testing, has a normal neuropsychological
evaluation. He has a VIQ of 106 and a PIQ of 89. On WMS, he has an MQ of 108, but only remembers
an average of 6 items on Logical Memory. Other verbal memory tests are normal. The patient is mildly
depressed and faces several orthopedic surgeries for lower extremity injuries. The neuropsych is
summarized:
“Based on the present test results there is evidence that Mr. X is experiencing significant cortical
dysfunctioning. His organic deficits appear to be highly lateralized and focal in nature. Specifically, he is
manifesting significantly impaired visual motor skills relative to verbal skills. This finding is consistent
with Organic Brain Dysfunction and in particular consistent with Nondominant Hemisphere Dysfunction.
In addition, when one compares Mr. X’s premorbid level of intellectual functioning to his present level of
intellectual functioning it is clear that his overall intelligence has declined (no records obtained by him,
attentional problems/poor school attendance later discovered from records I obtained). In addition, test
results indicate localized organic impairment for both short term verbal memory functioning as well as
delayed verbal memory functioning. This finding is highly consistent with dominant temporal cortex
lesioning. With regard to psychological functioning, there is evidence of clinically significant levels of
depression (MMPI 2-scale at 68, no other scales elevated, patient reports loss of interest and mild
dysphoria). It is strongly believed that the patient’s organic dysfunctioning and depression are directly
related to the automobile accident on February 8, 1997.”