Psychol. Inj.
and Law (2014) 7:245–254
DOI 10.1007/s12207-014-9201-3
Nocebo Effects and Mild Traumatic Brain Injury:
Legal Implications
Rodney D. Vanderploeg & Heather G. Belanger &
Paul M. Kaufmann
Received: 18 April 2014 / Accepted: 22 July 2014 / Published online: 5 August 2014
# Springer Science+Business Media New York (outside the USA) 2014
Abstract Expectations may play a large role in health-related
outcomes, but they may not be fully addressed or considered
in medical–legal contexts. Contextual factors can influence a
patient’s expectations for recovery following a concussion,
including explicit or implicit messages from the media,
healthcare providers and systems of care, and the forensic
arena. This article discusses these factors as nocebo effects,
that is, various inherently “inert” factors may create negative
expectancies for recovery and therefore impede a given pa-
tient’s progress and recovery. It is argued that the negligence
theory upon which the legal system is based tends to com-
pound these nocebo effects. In accident-related concussions,
both the accident itself and subsequent nocebo effects includ-
ing potential healthcare and medical–legal provider negli-
gence can create legal liability.
Keywords Brain concussion . Head injury . Concussion .
Forensic . Traumatic brain injury . Nocebo
R. D. Vanderploeg (*) : H. G. Belanger
MHBS/Psychology (116B), James A. Haley Veterans’ Hospital,
13000 Bruce B. Downs Blvd., Tampa, FL 33612, USA
e-mail: Rodney.Vanderploeg@va.gov
R. D. Vanderploeg : H. G. Belanger
Department of Psychology, University of South Florida, Tampa, FL,
USA
R. D. Vanderploeg : H. G. Belanger
Departments of Psychiatry and Behavioral Neurosciences,
University of South Florida, Tampa, FL, USA
R. D. Vanderploeg : H. G. Belanger
Defense and Veterans Brain Injury Center, Tampa, FL, USA
P. M. Kaufmann
University of Arizona, Tucson, AZ, USA
Traumatic brain injury (TBI) is typically defined as disrupted
brain functioning or damage from any force to the head as
evidenced by altered or lost consciousness, positive neurolog-
ical signs, or positive neuroimaging. An individual with a
mild TBI (also frequently called “concussion”) will by defi-
nition have a Glasgow Coma Scale score (GCS) (Teasdale &
Jennett, 1974) of 13–15 within 30 min of injury (American
Congress of Rehabilitation Medicine, 1993). Thus, within
30 min of injury, they obey commands and at worst may be
mentally confused and consequently be somewhat disoriented
or have inappropriate speech. Also by definition, post-injury
disorientation and confusion, if present, last less than a day.
However, other post-concussive symptoms such as head-
aches, dizziness, nausea, slowed thinking, difficulty concen-
trating, anxiety, and irritability or moodiness may last some-
what longer.
Multiple independent meta-analytic studies have shown
that the overwhelming majority of individuals who experi-
enced a concussion make excellent neurobehavioral recovery
within minutes to weeks (Belanger, Curtiss, Demery,
Lebowitz, & Vanderploeg, 2005; Binder, Rohling, &
Larrabee, 1997; Frencham, Fox, & Maybery, 2005; Rohling
et al., 2011; Schretlen & Shapiro, 2003). Although within a
few days of injury there is a neuropsychological performance
decrement of about half a standard deviation (i.e., perfor-
mance around the 25th to 30th normative percentile level),
performance is back to normal baseline by 1 month post-
injury (Schretlen & Shapiro, 2003).
In contrast to this typical pattern of excellent recovery
following concussion in the population at large (i.e., prospec-
tive or longitudinal studies), individuals with concussion who
present to clinics in the chronic phase for medical or neuro-
psychological evaluation or who are in litigation (i.e., groups
composed of individuals reporting ongoing symptoms and
problems) represent a different subsample of patients. At least
a portion of these individuals perform more poorly on
246
neuropsychological measures but in a manner not associated
with any specific pattern. Inconsistent with the natural course
of recovery, worse neuropsychological performance is seen
across time (Belanger et al., 2005). See Table 1 for the effect
size-associated, litigation-based, and clinic-based studies.
In terms of post-concussive symptoms (PCS), although
some individuals with concussion report symptoms months
and even years afterward, the available longitudinal literature
indicates that these symptoms are less likely to be related to
the concussion as time goes by (Meares et al., 2008, 2011;
Ponsford et al., 2012) and that the natural course of concus-
sion is recovery (Meares et al., 2011). As might be expected
with nonspecific symptoms (e.g., headaches, fatigue, insom-
nia, concentration problems, irritability), in the general popu-
lation, post-concussive-like symptoms following concussion
wax and wane over time (Meares et al., 2011). Further, these
studies show that post-concussive-like symptoms are general-
ly not related to brain injury, particularly as time goes by, but
instead are associated with accompanying acute post-
traumatic stress and depression or anxiety disorders (Boake
et al., 2005; Meares et al., 2008, 2011; Ponsford et al., 2012).
As such, the prevailing viewpoint appears to be that while
neurological factors contribute to acute PCS, psychological
factors likely account for ongoing symptoms. Longitudinal
studies with appropriate injured controls are critical in under-
standing etiology and time course of symptom complaints.
Understanding the factors accounting for the poorer out-
comes in this minority subset and what to do about them
represent the real challenge for both healthcare providers
and researchers (Carroll et al., 2004).
Expectations or Beliefs
Research has consistently shown the benefit of acute, brief
psychoeducational interventions for significantly reducing the
severity and duration of PCS. Mittenberg et al. demonstrated
that a psychoeducational intervention, which included giving
the patient a printed manual and having them meet with a
therapist for 1 h prior to hospital discharge, resulted in
Table 1 Neuropsychological performance effect sizes for time since injury by evaluation context
Litigation-based studies
Time since injury d (k)
<90 days 0.52* (2)
≥90 days 0.78* (6)
These are meta-analytic results from Belanger et al. (2005). Research studies were categorized into three contexts and the meta-analytic findings
separated by those studies conducted within 90 days of injury versus greater than 90 from injury. The natural course of recovery is seen in the population-
based studies, such as studies including everyone seen in an emergency department following a concussion
d effect size, k number of studies that contributed to the effect size
*p<0.05, significant
Psychol. Inj. and Law (2014) 7:245–254
significantly shorter symptom duration and significantly few-
er symptoms at 6-month follow-up compared to a matched
control group who received routine hospital care (Mittenberg,
Tremont, Zielinski, Fichera, & Rayls, 1996; Mittenberg,
Zielinski, & Fichera, 1993). The 1-h meeting included
reviewing the nature and incidence of expected symptoms,
providing a cognitive–behavioral model of symptom mainte-
nance and treatment, providing symptom-specific strategies,
and providing instructions for gradual resumption of activi-
ties. Two additional studies with prospective recruitment with-
in 1 week of injury (i.e., Ponsford et al., 2002; Wade, King,
Wenden, Crawford, & Caldwell, 1998) similarly demonstrat-
ed significantly reduced PCS at follow-up secondary to edu-
cational interventions.
Mittenberg et al. (1992) found that control subjects asked
to imagine symptoms following a head injury reported very
similar symptom profiles to individuals who actually experi-
enced a concussion. Twenty-two of the 30 symptoms were
anticipated by control subjects at frequencies comparable to
that reported following actual concussion. They suggested
that this “expectation” formed the basis for symptoms experi-
enced following a concussion.
This hypothesis was supported by a follow-up study in
sports concussion (Ferguson, Mittenberg, Barone, &
Schneider, 1999). Similar to the general population, before
experiencing a concussion, athletes expected that they would
have a significant increase in symptoms following a concus-
sion (102 % increase). An average of 6 months following a
sports concussion, concussed athletes reported experiencing
the same mean number of post-concussion symptoms reported
by unconcussed athletes at baseline. The researchers reasoned
that if athletes expect an increase in post-concussion symp-
toms but do not experience any actual increase, they might
underestimate pre-morbid symptom incidence as a means of
reconciling their perceptions and expectations. That was in
fact found. Concussed athletes underestimated their pre-injury
symptoms by 97 % compared with uninjured athletes, indi-
cating that they subjectively overestimated symptom change
in the absence of objective change. The symptom increases
perceived by the concussed athletes appear to be a direct result
Clinic-based studies Population-based studies
d (k) d (k)
No studies 0.63* (23)
0.74* (11) 0.04 (8)
Psychol. Inj. and Law (2014) 7:245–254
of the expectation that post-concussion symptoms will occur
following a concussion. Athletes are not the only individuals
who underestimate the extent to which they experienced
“post-concussion symptoms” prior to their TBI (Gunstad &
Suhr, 2001; Mittenberg et al., 1992). Attention to pre-existing
symptoms following a concussion and misattribution of those
symptoms to the concussion has been called the “expectation
as etiology” principal (Mittenberg et al., 1992). Commonly,
some percentage of alleged post-concussion symptoms are
likely falsely attributed to the concussion.
Nocebo Effects
“With placebos (‘I will please’ in Latin), the mere ex-
pectation that treatment will help brings a diminution of
symptoms, even if the patient is given a sugar pill. With
nocebos (‘I will harm’), dark expectations breed dark
realities. In clinical drug trials, people often report the
side effects they were warned about, even if they are
taking a placebo.” The New Yorker, April 3, 2013, The
Nocebo Effect: How We Worry Ourselves Sick. Posted
by Gareth Cook
In medicine, a nocebo is a harmless substance that creates
harmful effects in a patient who takes it. In contrast to the
placebo effect, the nocebo effect is a negative reaction expe-
rienced by a patient who receives an inert substance. For
example, in a review article of dropout rates in pain treatment
for fibromyalgia, it was reported that 9.6 % of participants
taking a placebo dropped out because of intolerable adverse
side effects (Hauser, Bartram, Bartram-Wunn, & Tolle, 2012).
Within the context of TBI, we might think of certain contexts
as causing nocebo effects (see also McCrea, 2008). This might
potentially explain why a minority of patients do not follow
the typical course of recovery following concussion.
Media Nocebo Effects on Beliefs/Expectations
Media plays a powerful role in setting expectations. To exper-
imentally investigate the effects of media messages on health
outcomes, Witthoft and Rubin (2013) randomly assigned
healthy university research volunteers (i.e., students and staff)
to watch either a real television report that promoted a link
between exposure to Wi-Fi and symptoms or to watch a
control film about the security of mobile phone data transmis-
sion. After watching their film, participants received a 15-min
sham exposure to a Wi-Fi signal. Over half of the participants
(54 %) reported symptoms which they attributed to the sham
exposure. These included tingling in fingers, hands, and feet;
pressure and tingling in the head; stomachaches; and trouble
concentrating. Two of the participants found the experience so
unpleasant that they had to stop the sham Wi-Fi exposure
247
before their time was up. Simply watching the television
report about the potential effects of Wi-Fi exposure increased
health worries. Sham Wi-Fi exposure subsequently increased
symptom levels. The media-based expectations interacted
with pre-existing personality characteristics such that those
with higher pre-exposure anxiety reported more severe symp-
toms and also were more likely to attribute their symptoms to
the sham Wi-Fi exposure.
Sensational media attention in recent years regarding the
adverse effects of sports-related concussions and resulting
behavioral deterioration, dementia, chronic traumatic enceph-
alopathy (CTE), and suicide, as well as similar attention to
concussions sustained by military personnel exposed to blasts,
may be creating iatrogenic scenarios, much like the media Wi-
Fi study described above. However, as Iverson notes (Iverson,
2014), there are no published cross-sectional, epidemiologi-
cal, or prospective studies showing a relation between contact
sports and risk of suicide. One published epidemiological
study suggests that retired National Football League players
actually have lower rates of death overall compared to the
general population, as well as lower rates of death by suicide.
Rates of death due to neurological conditions were compara-
ble to the general population (Baron, Hein, Lehman, & Gersic,
2012). Similarly, another study found that school students
who played American football from 1946 to 1956 did not
have an increased risk of later developing dementia,
Parkinson’s disease, or amyotrophic lateral sclerosis (ALS)
compared with non-football-playing high school males
(Savica, Parisi, Wold, Josephs, & Ahlskog, 2012). While the
evidence tying dramatic adverse outcomes (like suicide, CTE,
or dementia) to concussion is largely absent, the media and
even the actions of entire healthcare systems might suggest
otherwise.
These repeated media messages likely create a heightened
and biased perception that adverse health outcomes are more
likely than not, following a concussion. Additionally, the
Departments of Defense (DoD) and Veterans Affairs (VA)
population-based screening and evaluation programs for con-
cussion similarly set the stage for negative expectancies to
exert an adverse influence on the patient’s belief system. This
potentially results in increased symptoms and misattribution
of many or all difficulties to TBI, rather than to other potential
etiologies. Supporting this hypothesized worsening outcome
over time, Polusny et al. (2011) found rates of positive TBI
screens more than doubled between screens conducted in-
theater (9.2 % positive) and re-screens completed 1-year
post-deployment (22 % positive). In our own ongoing analy-
ses of VA TBI screening at the Tampa VA Medical Center,
rates of positive screens doubled between TBI screens con-
ducted as part of the Veterans’ healthcare (21 % positive) and
a subsequent re-screening done for research purposes (42 %
positive) conducted an average of 32 months later. In addition,
the rate of positive TBI re-screens compared to the original
248
clinical screen increased with longer time intervals between
screens. For re-screens completed within 24 months of the
original clinical screen, the rate of endorsement increased 1.6
times; for inter-screening intervals between 24 and 38 months,
the rate of endorsement increased 2.1 times; and for inter-
screening intervals between 38 and 57 months, the rate of
endorsement increased 2.4 times. With greater time between
screens, presumably there is increased exposure to environ-
mental factors, including media attention to TBI, which may
create negative expectancies related to concussion. This is of
course speculative. When compared to a criterion standard
semi-structured TBI identification interview (Vanderploeg,
Groer, & Belanger, 2012), the original clinical screens are
more accurate. In addition, the original clinical screens com-
pleted more than 24 months in the past were more consistent
with the criterion TBI diagnosis than screens completed with-
in the past 24 months. In other words, with the passage of
time, participants were less able to reliably report their de-
ployment experience and any associated TBI.
Stereotype/Diagnosis Threats Nocebo Effects
Another factor that can impact cognitive test performance as
well as symptomology is stereotype threat. Stereotype threat
occurs when individuals face a task or situation that is be-
lieved to be poorly performed or experienced in a certain
manner by members of those individuals’ self-identified
group, such as their ethnicity, gender, or socioeconomic
group. Many studies have found that individuals of stigma-
tized groups perform poorly in situations in which the stereo-
type is salient yet display no deficits in performance when the
stereotype is not salient (Aronson et al., 1999; Spencer, Steele,
& Quinn, 1999). Common examples of stereotype threat
include poorer performance on cognitive tasks by African
Americans who are made to believe the task is a measure of
intelligence (e.g., Katz, Roberts, & Robinson, 1965; McKay,
Doverspike, Bowen-Hilton, & Martin, 2002; Steele &
Aronson, 1995) and poorer performance by women on math
tests when their gender is emphasized (e.g., Keller &
Dauenheimer, 2003; Schmader, 2002). A recent meta-
analysis of stereotype threat effects on cognitive test perfor-
mance found an overall mean effect size of 0.26 (Nguyen &
Ryan, 2008), which can represent a clinically meaningful
effect.
Suhr and Gunstad (2002) proposed the use of the term
“diagnosis threat” (p. 450) to refer to the negative impact on
cognitive performance obtained by calling attention to one’s
history of concussion and its potential effects on cognition
(see also, Salazar, Cimino, Belanger, & Vanderploeg, 2013;
Suhr & Gunstad, 2005). Across studies, the effect size of
concussion diagnosis threat on cognitive performance has
ranged from 0.20 to 0.90 (Suhr & Gunstad, 2002, 2005;
Pavawalla et al., 2013). Diagnosis threat can also impact
Psychol. Inj. and Law (2014) 7:245–254
post-concussive symptoms (Ozen & Fernandes, 2011). TBI
or concussion diagnosis threat may occur presumably because
people associate a concussion with negative outcomes and as
a result experience a type of stereotype threat. The increased
rates of positive TBI re-screenings within DoD and VA
healthcare systems may in part be secondary to a diagnosis
threat effect, likely amplified by negative media messages
regarding the adverse effects of concussions.
Factors that modulate diagnosis threat include (a) strength
of the diagnosis threat cues influencing the examinees beliefs
or expectations and (b) group identification (i.e., how much
the examinee’s self-identity is tied to that “stigmatized” group)
(Pavawalla et al., 2013). Hou et al. (2012) found that negative
perceptions of concussion were the best predictor of PCS at
6 months post-injury. Snell et al. found that those individuals
endorsing (a) stronger injury identity beliefs (i.e., the extent to
which symptoms are attributed to concussion), (b) expecta-
tions of lasting severe consequences following injury, and (c)
greater distress at 3 months post-concussion had greater odds
of poor outcome at 6 months post-injury (Snell, Hay-Smith,
Surgenor, & Siegert, 2013).
In an interesting longitudinal study, Whittaker, Kemp, and
House (2007) found that PCS at 3 months post-injury was not
related to injury severity or psychological distress but rather
was related to what they termed “consequences” and “time-
line.” “Consequences” was the extent to which people be-
lieved that a concussion would have a negative impact on their
lives, while “timeline” was the extent to which people be-
lieved concussion-related symptoms would last. “Timeline”
beliefs significantly predicted symptomatic outcome while
“consequences” beliefs significantly predicted functional out-
come. When entered in a regression together, “consequences”
remained a significant predictor of post-concussion disorder.
Patients who believed that the symptoms they experi-
enced following a mild head injury had serious negative
consequences on their lives were at heightened risk of
experiencing enduring post-concussion symptoms. Initial
severity of PCS was not an independent predictor of
persisting symptoms. Furthermore, anxiety, depression,
and PTSD symptom severity did not significantly im-
prove the predictive model of chronic PCS. In summary,
what people believe about concussion plays an impor-
tant role in outcome, suggesting the need to assess and
manage patient perceptions and beliefs.
These factors may also reflect the “misattribution” of
symptoms to TBI discussed earlier and the “expectation as
etiology” principal (Mittenberg et al., 1992). Larson et al.
(2012) reported that attribution to concussion was associated
with more severe PCS symptom reporting in their sample of
Veterans. Similarly, Belanger et al. (2013) found that the most
potent predictor of PCS was attribution or the extent to which
one attributed symptoms to concussion versus other potential
causes. Importantly, work in other specialties suggests that
Psychol. Inj. and Law (2014) 7:245–254
attributional styles are mutable and can be modified (Peters,
Constans, & Mathews, 2011).
Healthcare Nocebo Effects
Belanger et al. (2005) in a meta-analytic study on concussion
found that clinically presenting samples in the post-acute
phase (i.e., more than 90 days after sustaining a concussion)
had a moderate to large negative neuropsychological effect
(i.e., d=0.74; see Table 1). It is unclear what accounts for this
differentially poor outcome in clinical groups, as compared to
the improvement over time found in prospectively followed
concussion cohorts (i.e., less than 90 days since concussion,
d=0.63; greater than 90 days, d=0.04). Factors such as ste-
reotype or diagnosis threat, anger/revenge, and loss aversion
likely play important roles (Silver, 2012). However, medically
induced iatrogenic effects might also be present.
The importance of the media message effects described
above cannot be minimized. If providers convey similar mes-
sages of negative expectation, symptoms may increase and
cognitive performance decrease as a result. Our society tends
to view medical providers and physicians in particular, as
omniscient. If medical providers explicitly or implicitly hold
negative expectations related to concussion, patients may
unknowingly internalize similar negative expectations. A neg-
ative message (nocebo effect) is conveyed if healthcare pro-
viders focus intensely on the injury and order tests and proce-
dures that “must be done to figure out what is wrong.” This
negative message would be amplified if any type of causality
message is conveyed such as, “your concussion is or may well
be the cause of your difficulties.”
The message is that the patient is damaged and that
the provider is uncertain regarding how best to handle
the clinical situation. Specialists must be brought it,
implying that something serious must be very wrong.
Such a message may increase patient fears and anxiety,
which in turn may increase stress-induced
symptomology, sustain existing symptoms entirely unre-
lated to concussion, and reinforce a false belief that
concussion is likely to have a problematic outcome.
Such a negative message may be reinforced by media
coverage of concussions in the sports and military arenas
and consequent implication that concussion causes CTE,
dementia, suicide, and other adverse long-term outcomes.
As a result, it is understandable that both patients and
providers may have internalized this negative message
and its nocebo effects.
Even use of the term “mild TBI” compared to “concussion”
can have adverse consequences. Indeed, there is empirical
evidence to suggest that poorer outcomes and more symptoms
are expected when the term “mild TBI” is used as opposed to
“concussion” when these labels are used to describe the same
249
injury (Dematteo et al., 2010; Sullivan, Edmed, & Kempe,
2014; Weber & Edwards, 2010).
For symptomatic patients presenting in a chronic
timeframe (several months to years following a concussion),
the research literature suggests that there is no reason for
healthcare providers to attribute the reported symptoms to
the remote concussion, even if patients attribute their symp-
toms to that TBI. Prospective longitudinal studies clearly
demonstrate that in the post-acute and chronic phases (i.e.,
two or more months following a concussion), PCS symptoms
are not related to concussion but instead are associated with
accompanying acute post-traumatic stress and depression or
anxiety disorders (Boake et al., 2005; Meares et al., 2008,
2011; Ponsford et al., 2012). Therefore, any clinical implica-
tion that these symptoms are directly related to the past con-
cussion is a negative message likely to sustain or worsen these
symptoms. It is possible that there may be individual excep-
tions to this natural history course, as suggested by Pertab
et al. (2009). However, Rohling et al. (2012) performed a
statistical analysis of this hypothesis and did not find support
for the existence of a “miserable minority” that is obscured in
larger meta-analytic studies of concussion neuropsychological
outcomes. If such an impaired subgroup existed, their
level of impairment would have to be so small as to be
undetectable in any type of clinical evaluation (i.e., less
than a tenth of a standard deviation). Attempting to
attribute mild deficits on neuropsychological testing or
chronic post-concussive-like symptoms to a remote con-
cussion would result in more false positives than true
positives. These authors argue that such a clinical prac-
tice would greatly increase the risk of misdiagnosis in
persons who are susceptible to misattribution, expectan-
cy effects, and “diagnosis threat,” thereby increasing the
risk of iatrogenic illness. We also have previously
discussed the potential for similar medical iatrogenic
effects following concussion in the VA and military
healthcare systems (Vanderploeg & Belanger, 2013).
Consistent with potential nocebo effects associated with
clinical evaluations and treatment, there is some evidence that
“greater treatment” is not helpful following concussion and
may even be harmful. One study (Ghaffar, McCullagh,
Ouchterlony, & Feinstein, 2006) found that multidisciplinary
treatment in the acute phase was not useful in reducing post-
concussive symptoms. It is also notable that Paniak et al.
(Paniak, Toller-Lobe, Durand, & Nagy, 1998; Paniak, Toller-
Lobe, Reynolds, Melnyk, & Nagy, 2000), in their randomized
controlled trial in the post-acute phase, found that there was no
added benefit in providing more extensive treatment (as is
typically provided following more severe TBI) as compared to
a single informational meeting during which patients’ post-
TBI experiences were legitimized, education was provided
about common symptoms and coping strategies, and reassur-
ance of positive outcomes was provided.
250
In contrast to clinically induced nocebo effects, a positive
message can be conveyed with potential beneficial effect.
Such a positive message would include providing accurate
information that acute symptoms after a concussion are ex-
pected but transient and will improve over days to weeks. A
positive healthcare response also would include offering in-
terventions to help the patient manage symptoms. These in-
ventions may include (a) acute headache and pain manage-
ment, (b) symptom/stress management techniques including a
period of rest with a gradual resumption of normal activities,
and perhaps (c) sleep hygiene or brief use of sleep medica-
tions. Here, the message is:
“You may well have some normal, expected symptoms
for a few days or so, but we can help you deal with them
during this transitional period. There are also things that
you can to do minimize or cope with these symptoms.
We will work together to get through this transitional
period as you recover.”
A more evidence-based approach would involve promot-
ing self-efficacy and health-promoting behavior. This message
and set of interventions, when delivered acutely, have been
demonstrated in multiple studies to reduce post-concussion
symptom intensity and duration (Mittenberg et al., 1993,
1996; Ponsford et al., 2002; Wade et al., 1998).
If patients present in the chronic phase following a concus-
sion and attribute their symptoms to a past concussion, this
positive message must be modified somewhat. The message
should be that:
“Many of the symptoms that occur following an acci-
dent or concussion are the same type of symptoms
everyone experiences at times in their everyday life.
These symptoms are also associated with and exacer-
bated by stress. Therefore postconcussion and stress-
related symptoms are easily confused with each other,
particularly with longer periods of time after a concus-
sion. Both postconcussion and stress symptoms ad-
versely affect one’s ability to pay attention and re-
member information. If you are several months or
even years after your concussion you likely have
noticed that as your stress levels go down, your
ability to pay attention and remember information
improves. During higher stress levels, you likely
experience pain and other symptoms as more severe
and distressing. If you think about it, you probably
would recognize that you are functioning better at
some times than others, and at those better times
have fewer symptoms and problems. As stress levels
decrease, that is what happens. We can help you
more effectively manage your symptoms and stress.
Any residual symptoms can be treated. We will work
together on these issues as you recover.”
Psychol. Inj. and Law (2014) 7:245–254
Litigation Nocebo Effects
Research has shown that compensation and litigation factors
are the single most stable predictor of prolonged post-
concussive symptoms in concussion samples (Carrol et al.,
2004). This is based in part on a meta-analysis by Binder and
Rohling (1996) that found financial compensation was a
strong risk factor for long-term disability, symptoms, and
objective cognitive decrements after concussion.
Importantly, financial incentives appeared to play a more
powerful role in patients with mild versus moderate/severe
head injuries. Subsequent to that meta-analysis, Paniak et al.
(2000, 2002) found that compensation-seeking strongly pre-
dicted delayed return to work, more long-term symptoms, and
greater symptom severity, independent of TBI injury severity.
Similarly, Cassidy et al. (2004) found that making tort claims
following motor vehicle accidents was one of the strongest
factors associated with slower recovery. In another meta-anal-
ysis, Belanger et al. (2005) also found greater neuropsycho-
logical impairment in the late stage of recovery among con-
cussion samples who were involved in litigation compared to
prospectively followed samples. As can be seen in Table 1,
worsening neuropsychological performance is seen across
time for those involved in litigation.
Litigation and secondary gain factors clearly negatively
affect both subjective PCS symptoms and objective neuropsy-
chological performance. It is tempting to attribute these neu-
ropsychological litigation effects, particularly in the post-
acute phase (>90 days post-injury), to test invalidity, symptom
exaggeration, or malingering. However, the use of perfor-
mance or symptom validity criteria did not moderate effect
sizes (no validity screening d=0.50; validity screening d=
0.66), in the Belanger et al. meta-analysis (2005). Therefore,
other litigation-related nocebo factors may account for the
performance decrement in the forensic arena. Silver (2012)
has discussed the contribution of stress, stereotype or diagno-
sis threat, anger/revenge, loss aversion, and cheating as factors
contributing to these litigation-setting nocebo performance
decrements.
One must consider that a person involved in the litigation
process may receive implicit messages that reinforce illness.
The litigation context also results in multiple medical specialty
assessments and diagnostic procedures. These multiple eval-
uations may inadvertently reinforce a negative message that
something serious must be wrong and the medical condition
must be complicated. Even patients/litigants who are not
malingering likely would, via repeated independent or com-
pulsory medical evaluations, experience a nocebo effect
resulting in an amplification of symptoms or a “decline” in
functioning.
The media and medical message nocebo effects likely are
amplified in litigation contexts in which attorneys, acute
healthcare providers, and plaintiff experts consciously or
Psychol. Inj. and Law (2014) 7:245–254
unconsciously convey the message that the concussion is the
primary or sole cause for most or all of the problems experi-
enced by the patient. To strengthen the legal suit, patients,
families, plaintiff attorneys, and medical experts look for data
to confirm that the concussion is the primary cause of current
problems. This “confirmatory bias” is a well-recognized psy-
chological phenomenon whereby people tend to favor infor-
mation that confirms their beliefs or hypotheses. Information
is gathered or remembered selectively or interpreted in a
biased way (Martindale, 2005; Nickerson, 1998; Greenwald,
Pratkanis, Leippe, & Baumgardner, 1986). The effect is stron-
ger for emotionally charged issues and for deeply entrenched
beliefs. Litigation contexts are often emotionally charged with
strong beliefs about blame and causation. In addition, a whole
set of professionals benefit financially from this system.
Causality Implications
This article has focused on and discussed group data as it
relates to cognitive functioning and symptom presentation in
individuals with a history of concussion. Unfortunately, in
both the clinical and the medical–legal context, it is not the
group but rather the individual who is of interest. The question
is not, “What factors influence outcome following concus-
sion?”, but rather, “What is causing the symptoms or problems
in this particular case?” The clinical arena can accommodate
an ambiguous interactive systemic model of causality.
Contrary to popular opinion, the legal arena also makes ad-
justments to manage ambiguity. In any given individual case,
it may be very difficult, if not impossible, to attribute ques-
tionably abnormal cognitive findings, complaints of dizziness
and balance problems, headaches, fatigue, and memory com-
plaints to a particular etiology. Such a pattern of symptoms
could represent (a) a normal population variant, (b) various
nocebo effects, (c) pre-existing mental health problems (e.g.,
depression and anxiety), (d) pre-existing or co-existing med-
ical problems (e.g., pain syndrome, multiple sclerosis, hyper-
tension, alcohol abuse-related complications, etc.), (e) inade-
quate patient effort on examination or outright malingering, (f)
brain dysfunction, or (g) a combination of these factors.
If an answer exists for the healthcare provider, it lies in
time-tested, clinically validated diagnostic evaluations, a care-
ful history of pre- and post-injury symptoms and functioning,
and a reliance on the linear medical model of causality.
However, the answer also relies on examination of multiple
potential predisposing factors, causative agents (including
nocebo effects), and perpetuating factors which interactively
influence each other (Vanderploeg, Belanger, & Curtiss,
2006). Causality determination requires (a) examination of
all relevant etiological events or factors; (b) investigation of
the initial clinical presentation as being more or less consistent
251
with those potential causative agents; (c) tracking ongoing or
emerging symptoms as being consistent with the medical
literature regarding potential causative agents and not consis-
tent with other potential etiological factors; and (d) examina-
tion of findings from diagnostic procedures as being consis-
tent with the clinical history, the nature and course of symp-
toms, and suspected explanatory causative factors. Only if a
chronologically consistent and clinically logical pattern of
results emerges can findings be attributed to potential etiolog-
ical factors.
The civil legal system addresses the causation problem
by lowering the standard of proof, considering competing
legal theories of causation, and establishing rules for
proximate cause. Briefly, expert opinions about causation
in civil cases do not require certainty or the absence of
reasonable doubt. Rather, tort law governing negligence
only requires an expert to identify “more likely than not”
what the cause(s) of symptoms are in the individual case.
Experts are there to assist the trier-of-fact to reduce, but
not necessarily eliminate, all doubt. Although many ex-
perts may apply a more stringent scientific standard, the
expert witness needs only be 51 % confident in her or his
opinions. Further, the law distinguishes cause-in-fact from
proximate cause, but unfortunately, this distinction is
poorly understood. Cause-in-fact is commonly referred
to as the “but-for” test. For example, but for the blow to
the head, these symptoms would not have occurred.
However, such statements are deceptively simple after
considering the cause-in-fact doctrine also analyzes con-
current causes and sufficient combined causes.
In the context of litigation, post-accident healthcare
and medical–legal provider interventions and behaviors
can have a nocebo effect. As such, provider negligence,
combined with the injury itself, may contribute to per-
sistent or worsening symptoms following motor vehicle
accident-related concussions. Both the driver responsible
for the accident and subsequent provider negligence can
create legal liability. Although the current authors would
prefer provider education rather than legal action against
a provider when nocebo effects might have arisen from
well-meaning actions, the fact remains that providers
can potentially be sued for making patients worse.
Legal Implications and Conclusions
The legal implications of nocebo effects after concussion
involve managing risk, determining liability, and assigning
blame for persistent symptoms. As such, courts inevitably
end up considering the proximate cause or chain of causal
events that perpetuate these vague symptoms.
Proximate cause is more complicated because legal
scholars have competing theories (e.g., relative risk,
252
foreseeability, presence of intervening causes) whose applica-
tion vary significantly among jurisdictions and judges. The
doctrine of proximate cause is notoriously confusing and
beyond the scope of this article. Perhaps, the most straightfor-
ward definition for proximate cause is any cause that is legally
sufficient to result in liability. However, to illustrate the in-
consistent approaches, two very different proximate cause
applications are summarized: (a) efficient proximate cause
and (b) the “egg shell skull” rule. Efficient proximate cause
arises out of insurance law and frames the causation question
in terms of whether the injury sustained was covered by the
insurance policy. Under this doctrine, if a covered act and a
non-covered act combine to “cause” injury, then the loss is not
covered by the insurance policy. Not surprisingly, insurance
companies tend to prefer the minority of jurisdictions that
adopt this rule. Some jurisdictions have found it void as
against public policy.
The “egg shell skull” rule holds parties liable for all con-
sequences resulting from negligence, even if the victim
(plaintiff) suffers a higher degree of damage due to a unique
pre-existing vulnerability or medical condition. The criminal
law maxim “take the victim as you find them” is often refer-
enced to understand the application of this rule. The public
policy underlying this rule reflects that courts do not want
defendants to use the victim’s own vulnerabilities to avoid
liability. Not surprisingly, the plaintiff bar tends to prefer this
formulation.
Finally, jurisdictional variations are also prominent in
pleading cases under state rules of civil procedure.
Here, if the liabilities of the driver responsible for the
accident and subsequent physician negligence (and other
potential nocebo effects) for persistent symptoms fol-
lowing concussion are not plead correctly, plaintiffs
may not recover for damages. State civil procedure
law governs how two or more individuals (joint
tortfeasors) may be held liable for the same injury. In
some states, these rules are addressed under joint and
several liability (e.g., 42 Pa. Cons. Stat. § 8322), using
the mechanisms of joinder and contribution (see
Lasprogata v. Qualls (1979) for historical discussion).
Under Pennsylvania law, there are special circumstances
that allow a driver and a doctor to be identified as joint
tortfeasors. The facts and circumstances must be
weighed carefully because the acts of the responsible
driver and the physician do not occur at the same time,
nor does either potential defendant have the opportunity
to guard against each other’s acts. Obviously, the duties
owed by the driver and the doctor to the plaintiff differ.
In the end, whether a reckless driver, a negligent doctor,
an exaggerating or malingering plaintiff, or some com-
bination thereof are responsible for persistent symptoms
is a question of fact for the jury to decide but only if a
case is properly plead. Some states such as Florida have
Psychol. Inj. and Law (2014) 7:245–254
essentially abolished joint and several liability claims
(Fla. Stat. § 768.31), requiring defendants to assert an
affirmative defense to include any subsequent negli-
gence of non-parties.
What are the legal implications for concussion cases that
show the following pattern of symptoms?
1. Initial alteration of consciousness due to a blow to the
head results in mild neuropsychological impairments dur-
ing the first 3 months post-injury.
2. By 3 months post-concussion, the neuropsychological test
results return to baseline and the individual returns to
work. However, a few vague mild somatic complaints
(e.g., headache, intermittent dizziness, and irritability)
are noted on self-report measures.
3. A newly consulted physician or therapist treating the
plaintiff attributes these symptoms to the TBI, evoking
patient concern and sympathy from family members.
4. The patient files a lawsuit.
In Pennsylvania, the plaintiff may assert driver–
doctor joint and several liability and name both as
defendants in the case. In Florida, the plaintiff would
file a lawsuit against the reckless driver and the
driver’s insurance company would have to evaluate
whether to assert a defense by naming a negligent
physician or psychotherapist.
Now that the lawsuit has been filed:
5. A follow-up defense neuropsychological evaluation re-
veals a return to pre-injury level of functioning, but var-
ious somatic complaints are worse than previously docu-
mented and inconsistent effort is noted during the
examination.
How should a neuropsychological evaluation address the
complex factors that may be supporting the continued or
worsened symptoms? More importantly, how should the neu-
ropsychologist report findings and formulate an expert causa-
tion opinion in this matter?
This article argues that multiple possible nocebo ef-
fects should be considered, along with the original in-
jury. Symptom onset and course would be crucial to
sorting through multiple potential causes for symptoms
or functional impairments by examining the scientific
literature regarding the natural course of possible ex-
planatory etiologies. Worsening or late onset symptoms
or functional impairments could not logically be attrib-
uted to the original injury, and other factors would need
to be considered as explanatory. The neuropsychologist
should clearly delineate the complex and interactive
factors involved in the case and offer a professional
opinion regarding impairments and their severity, func-
tional implications, etiological factors responsible, and
appropriate interventions, if any are indicated.
Psychol. Inj. and Law (2014) 7:245–254
References
42 Pa. Cons. Stat. § 8322. (2014).
American Congress of Rehabilitation Medicine. (1993). Report of the
Mild Traumatic Brain Injury Committee of the Head Injury
Interdisciplinary Special Interest Group. Journal of Head Trauma
Rehabilitation, 8, 86–87.
Aronson, J., Lustina, M. J., Good, C., Keough, K., Steele, C. M., &
Brown, J. (1999). When white men can’t do math: necessary and
sufficient factors in stereotype threat. Journal of Experimental
Social Psychology, 35(1), 29–46.
Baron, S. L., Hein, M. J., Lehman, E., & Gersic, C. M. (2012). Body mass
index, playing position, race, and the cardiovascular mortality of
retired professional football players. American Journal of
Cardiology, 109(6), 889–896. doi:10.1016/j.amjcard.2011.10.050
Belanger, H. G., Barwick, F. H., Kip, K. E., Kretzmer, T., & Vanderploeg,
R. D. (2013). Postconcussive symptom complaints and potentially
malleable positive predictors. Clinical Neuropsychologist, 27(3),
343–355. doi:10.1080/13854046.2013.774438
Belanger, H. G., Curtiss, G., Demery, J. A., Lebowitz, B. K., &
Vanderploeg, R. D. (2005). Factors moderating neuropsychological
outcomes following mild traumatic brain injury: a meta-analysis.
Journal of the International Neuropsychological Society, 11(3),
215–227.
Binder, L. M. & Rohling, M. L. (1996). Money matters: meta-analytic
review of the effects of financial incentives on recovery after closed-
head injury. The American Journal of Psychiatry, 153, 7–10.
Binder, L. M., Rohling, M. L., & Larrabee, J. (1997). A review of mild
head trauma. Part I: meta-analytic review of neuropsychological
studies. Journal of Clinical and Experimental Neuropsychology,
19(3), 421–431.
Boake, C., McCauley, S. R., Levin, H. S., Pedroza, C., Contant, C. F.,
Song, J. X., . . . Diaz-Marchan, P. J. (2005). Diagnostic criteria for
postconcussional syndrome after mild to moderate traumatic brain
injury. The Journal of Neuropsychiatry and Clinical Neurosciences,
17, 350–356. doi:10.1176/appi.neuropsych.17.3.350
Carroll, L. J., Cassidy, J. D., Peloso, P. M., Borg, J., von Holst, H., Holm,
L., et al. (2004). Prognosis for mild traumatic brain injury: results of
the WHO Collaborating Centre Task Force on Mild Traumatic Brain
Injury. Journal of Rehabilitation Medicine, 43, 84–105.
Cassidy, J. D., Carroll, L. J., Cote, P., Holm, L., & Nygren, A. (2004).
Mild traumatic brain injury after traffic collisions: a population-
based cohort study. Journal of Rehabilitation Medicine,
Supplement, 43, 15–21.
Dematteo, C. A., Hanna, S. E., Mahoney, W. J., Hollenberg, R. D., Scott,
L. A., Law, M. C., Xu, L. (2010). My child doesn’t have a brain
injury, he only has a concussion. Pediatrics, 125(2), 327–334. doi:
10.1542/peds.2008-2720
Ferguson, R. J., Mittenberg, W., Barone, D. F., & Schneider, B. (1999).
Postconcussion syndrome following sports-related head injury: ex-
pectation as etiology. Neuropsychology, 13(4), 582–589. doi:10.
1037/0894-4105.13.4.582
Fla. Stat. § 768.31. (2014).
Frencham, K. A., Fox, A. M., & Maybery, M. T. (2005).
Neuropsychological studies of mild traumatic brain injury: a meta-
analytic review of research since 1995. Journal of Clinical and
Experimental Neuropsychology, 27, 334–351.
Ghaffar, O., McCullagh, S., Ouchterlony, D., & Feinstein, A. (2006).
Randomized treatment trial in mild traumatic brain injury. Journal of
Psychosomatic Research, 61(2), 153–160.
Greenwald, A. G., Pratkanis, A. R., Leippe, M. R., & Baumgardner, M.
H. (1986). Under what conditions does theory obstruct research
progress? Psychological Review, 93, 216–229.
Gunstad, J., & Suhr, J. A. (2001). “Expectation as etiology” versus “the
good old days”: postconcussion syndrome symptom reporting in
253
athletes, headache sufferers, and depressed individuals. Journal of
the International Neuropsychological Society, 7(3), 323–333.
Hauser, W., Bartram, C., Bartram-Wunn, E., & Tolle, T. (2012). Adverse
events attributable to nocebo in randomized controlled drug trials in
fibromyalgia syndrome and painful diabetic peripheral neuropathy:
systematic review. Clinical Journal of Pain, 28, 437–451.
Hou, R., Moss-Morris, R., Peveler, R., Mogg, K., Bradley, B. P., & Belli,
A. (2012). When a minor head injury results in enduring symptoms:
a prospective investigation of risk factors for postconcussional syn-
drome after mild traumatic brain injury. Journal of Neurology,
Neurosurgery and Psychiatry, 83(2), 217–223.
Iverson, G. L. (2014). Chronic traumatic encephalopathy and risk of
suicide in former athletes. British Journal of Sports Medicine,
48(2), 162–165. doi:10.1136/bjsports-2013-092935
Katz, I., Roberts, S. O., & Robinson, J. M. (1965). Effects of task
difficulty, race of administrator, and instructions on digit-symbol
performance of negroes. Journal of Personality and Social
Psychology, 2(1), 53–59.
Keller, J., & Dauenheimer, D. (2003). Stereotype threat in the classroom:
dejection mediates the disrupting threat effect on women’s math
performance. Personality and Social Psychology Bulletin, 29(3),
371–381.
Larson, E. B., Kondiles, B. R., Starr, C. R., & Zollman, F. S. (2012).
Postconcussive complaints, cognition, symptom attribution and ef-
fort among veterans. Journal of the International
Neuropsychological Society, 19, 88–95.
Lasprogata v. Qualls, 263 Pa. Super. 174 (Pa. Super. Ct. 1979).
Martindale, D. A. (2005). Confirmatory bias and confirmatory distortion.
Journal of Child Custody, 2, 31–48. doi:10.1300/J190v02n01_03
McCrea, M. (2008). Mild traumatic brain injury and postconcussion
syndrome: the new evidence base for diagnosis and treatment.
New York, NY: Oxford University Press.
McKay, P. F., Doverspike, D., Bowen-Hilton, D., & Martin, Q. D. (2002).
Stereotype threat effects on the raven advanced progressive matrices
scores of African Americans. Journal of Applied Social Psychology,
32(4), 767–787.
Meares, S., Shores, E. A., Taylor, A. J., Batchelor, J., Bryant, R. A.,
Baguley, I. J., . . . Marosszeky, J. E. (2008). Mild traumatic brain
injury does not predict acute postconcussion syndrome. Journal of
Neurology, Neurosurgery, & Psychiatry, 79(3), 300–306.
Meares, S., Shores, E. A., Taylor, A. J., Batchelor, J., Bryant, R. A.,
Baguley, I. J., . . . Marosszeky, J. E. (2011). The prospective course
of postconcussion syndrome: the role of mild traumatic brain injury.
Neuropsychology, 25(4), 454–465.
Mittenberg, W., DiGiulio, D. V., Perrin, S., & Bass, A. E. (1992).
Symptoms following mild head injury: expectation as aetiology.
Journal of Neurology, Neurosurgery & Psychiatry, 55(3), 200–
204. doi:10.1136/jnnp.55.3.200
Mittenberg, W., Tremont, G., Zielinski, R. E., Fichera, S., & Rayls, K. R.
(1996). Cognitive-behavioral prevention of postconcussion syn-
drome. Archives of Clinical Neuropsychology, 11(2), 139–145.
Mittenberg, W., Zielinski, R. E., & Fichera, S. (1993). Recovery from
mild head injury: a treatment manual for patients. Psychotherapy in
Private Practice, 12, 37–52.
Nguyen, H. D., & Ryan, A. M. (2008). Does stereotype threat affect test
performance of minorities and women? A meta-analysis of experi-
mental evidence. Journal of Applied Psychology, 93(6), 1314–1334.
Nickerson, R. S. (1998). Confirmation bias: a ubiquitous phenomenon in
many guises. Review of General Psychology, 2, 175–220. doi:10.
1037/1089-2680.2.2.175
Ozen, L. J., & Fernandes, M. A. (2011). Effects of “diagnosis threat” on
cognitive and affective functioning long after mild head injury.
Journal of the International Neuropsychological Society, 17(2),
219–229.
Paniak, C., Reynolds, S., Toller-Lobe, G., Melnyk, A., Nagy, J., &
Schmidt, D. (2002). A longitudinal study of the relationship between
254
financial compensation and symptoms after treated mild traumatic
brain injury. Journal of Clinical & Experimental Neuropsychology,
24(2), 187–193. doi:10.1076/jcen.24.2.187.999
Paniak, C., Toller-Lobe, G., Durand, A., & Nagy, J. (1998). A random-
ized trial of two treatments for mild traumatic brain injury. Brain
Injury, 12, 1011–1023. doi:10.1080/026990598121927
Paniak, C., Toller-Lobe, G., Reynolds, S., Melnyk, A., & Nagy, J. (2000).
A randomized trial of two treatments for mild traumatic brain injury:
1 year follow-up. Brain Injury, 14(3), 219–226.
Pavawalla, S. P., Salazar, R., Cimino, C., Belanger, H. G., &
Vanderploeg, R. D. (2013). An exploration of diagnosis threat and
group identification following concussion injury. Journal of the
International Neuropsychological Society, 19(3), 305–313.
Pertab, J. L., James, K. M., & Bigler, E. D. (2009). Limitations of mild
traumatic brain injury meta-analyses. Brain Injury, 23, 498–508.
doi:10.1080/02699050902927984
Peters, K. D., Constans, J. I., & Mathews, A. (2011). Experimental
modification of attribution processes. Journal of Abnormal
Psychology, 120(1), 168–173.
Polusny, M. A., Kehle, S. M., Nelson, N. W., Erbes, C. R., Arbisi, P. A., &
Thuras, P. (2011). Longitudinal effects of mild traumatic brain injury
and posttraumatic stress disorder comorbidity on postdeployment
outcomes in national guard soldiers deployed to Iraq. Archives of
General Psychiatry, 68(1), 79–89. doi:10.1001/archgenpsychiatry.
2010.172
Ponsford, J., Cameron, P., Fitzgerald, M., Grant, M., Mikocka-Walus, A.,
& Schonberger, M. (2012). Predictors of postconcussive symptoms
3 months after mild traumatic brain injury. Neuropsychology, 26(3),
304–313.
Ponsford, J., Willmott, C., Rothwell, A., Cameron, P., Kelly, A. M.,
Nelms, R., & Curran, C. (2002). Impact of early intervention on
outcome following mild head injury in adults. Journal of Neurology,
Neurosurgery and Psychiatry, 73(3), 330–332.
Rohling, M. L., Binder, L. M., Demakis, G. J., Larrabee, G. J., Ploetz, D.
M., & Langhinrichsen-Rohling, J. (2011). A meta-analysis of neu-
ropsychological outcome after mild traumatic brain injury: re-
analyses and reconsiderations of Binder et al. (1997), Frencham
et al. (2005), and Pertab et al. (2009). Clinical Neuropsychologist,
25(4), 608–623.
Rohling, M. L., Larrabee, G. J., & Millis, S. R. (2012). The “Miserable
Minority” following mild traumatic brain injury: who are they and
do meta-analyses hide them? Clinical Neuropsychologist, 26, 197–
213. doi:10.1080/13854046.2011.647085
Savica, R., Parisi, J. E., Wold, L. E., Josephs, K. A., & Ahlskog, J. E.
(2012). High school football and risk of neurodegeneration: a
community-based study. Mayo Clinic Proceedings, 87(4), 335–
340. doi:10.1016/j.mayocp.2011.12.016
Schmader, T. (2002). Gender identification moderates stereotype threat
effects on women’s math performance. Journal of Experimental
Social Psychology, 38, 194–201.
Schretlen, D. J., & Shapiro, A. M. (2003). A quantitative review of the
effects of traumatic brain injury on cognitive functioning.
International Review of Psychiatry, 15, 341–349.
Silver, J. M. (2012). Effort, exaggeration and malingering after concus-
sion. Journal of Neurology, Neurosurgery & Psychiatry, 83, 836–
841. doi:10.1136/jnnp-2011-302078
Psychol. Inj. and Law (2014) 7:245–254
Snell, D. L., Hay-Smith, E. J., Surgenor, L. J., & Siegert, R. J. (2013).
Examination of outcome after mild traumatic brain injury: the con-
tribution of injury beliefs and Leventhal’s Common Sense Model.
Neuropsychological Rehabilitation, 23(3), 333–362. doi:10.1080/
09658211.2012.758419
Spencer, S. J., Steele, C. M., & Quinn, D. M. (1999). Stereotype threat
and women’s math performance. Journal of Experimental Social
Psychology, 35(1), 4–28.
Steele, C. M., & Aronson, J. (1995). Stereotype threat and the intellectual
test performance of African Americans. Journal of Personality and
Social Psychology, 69(5), 797–811.
Suhr, J. A., & Gunstad, J. (2002). “Diagnosis threat”: the effect of
negative expectations on cognitive performance in head injury.
Journal of Clinical and Experimental Neuropsychology, 24(4),
448–457.
Suhr, J. A., & Gunstad, J. (2005). Further exploration of the effect of
“diagnosis threat” on cognitive performance in individuals with mild
head injury. Journal of the International Neuropsychological
Society, 11(1), 23–29.
Sullivan, K. A., Edmed, S. L., & Kempe, C. (2014). The effect of injury
diagnosis on illness perceptions and expected postconcussion syn-
drome and posttraumatic stress disorder symptoms. Journal of Head
Trauma Rehabilitation, 29(1), 54–64. doi:10.1097/HTR.
0b013e31828c708a
Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired
consciousness. A practical scale. Lancet, 2(7872), 81–84.
Vanderploeg, R. D. & Belanger, H. G. (2013). Screening for a
remote history of mild TBI: when a good idea is bad. Journal
of Head Trauma Rehabilitation, 28, 211–218. doi:10.1097/
HTR.0b013e31828b50db
Vanderploeg, R. D., Belanger, H. G., & Curtiss, G. (2006). Mild
traumatic brain injury: neuropsychological causality modeling.
In G. Young, A. Kane, & K. Nicholson (Eds.), Psychological
knowledge in court: PTSD, pain and TBI (pp. 279–307). New
York: Springer.
Vanderploeg, R. D., Groer, S., & Belanger, H. G. (2012). Initial develop-
mental process of a VA semi-structured clinical interview for TBI
identification. Journal of Rehabilitation Research and Development,
49, 545–556.
Wade, D. T., King, N. S., Wenden, F. J., Crawford, S., & Caldwell, F. E.
(1998). Routine follow up after head injury: a second randomised
controlled trial. Journal of Neurology, Neurosurgery and Psychiatry,
65(2), 177–183.
Weber, M., & Edwards, M. G. (2010). The effect of brain injury termi-
nology on university athletes’ expected outcome from injury, famil-
iarity and actual symptom report. Brain Injury, 24(11), 1364–1371.
doi:10.3109/02699052.2010.507110
Whittaker, R., Kemp, S., & House, A. (2007). Illness perceptions and
outcome in mild head injury: a longitudinal study. Journal of
Neurology, Neurosurgery & Psychiatry, 78(6), 644–646.
Witthoft, M., & Rubin, G. J. (2013). Are media warnings about
the adverse health effects of modern life self-fulfilling? An
experimental study on idiopathic environmental intolerance
attributed to electromagnetic fields (IEI-EMF). Journal of
Psychosomatic Research, 74(3), 206–212. doi:10.1016/j.
jpsychores.2012.12.002