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Every year an estimated 42 million individuals worldwide experience a
mild traumatic brain injury (TBI) (Gardner & Yaffe, 2015). Most people who experience
a mild TBI tend to recover without any major complications, however, there is a
minority that still display adverse symptoms 1 year after the injury occurs.
There are many factors that influence symptom formation and persistence
following the acute period of mild TBI, such as premorbid psychological issues,
misattribution bias, and underestimating pre-injury symptoms. This essay will
discuss the different theories associated with symptom generation and
persistence, considering the biological, psychological, social, and iatrogenic
factors and how understanding the interaction of these can help clinicians in
diagnosing and devising treatment strategies to improve symptom outcome in mild


Mild TBI is a medical diagnosis which is
problematic to precisely define. It can be attributed to a traumatically
induced structural injury that often includes physiological disruption of brain
function, because of an external force (Otis et al., 2015). It is typically
classified into mild, moderate, and severe categories. Mild TBI is often
referred to as a concussion. The definition of mild TBI was first established
by Head (1993) in the American Congress of Rehabilitation Medicine as an alteration
of brain function due to external forces with one or more of:

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Loss of consciousness that
does not exceed 30 minutes.
Post traumatic amnesia before
or after the event lasting less than 24 hours.
Neurological deficits, that
may include but is not limited to an alteration in vision, sensory loss,
aphasia, or loss of balance.
Variation in mental state at
the time of the injury which may lead the patient to feel disorientated,
confused, and have slowed thinking.

These symptoms are typically assessed by the
Glasgow Coma Scale and must have a score between 13-15 to be considered a mild
TBI. Even with these guidelines of defining a mild TBI, confounding factors can
make diagnosis a challenge, such as the presence of other psychological issues
(Menon et al., 2010). Many clinicians struggle with unreliable self or witness
reports of loss of consciousness or post-traumatic amnesia. Other factors such
as substance abuse or medications can also alter an individual’s memory and
function which could disrupt accurate diagnosis.


Symptoms of mild TBI fall into three domains:
cognitive, somatic, and affective, yet there is no set list of specific
symptoms that must be present. In the cognitive domain, most complaints refer
to difficulty concentrating, losing track of thoughts, and memory problems.
However, there may be no correlation between cognitive test scores and symptoms
(Katz et al., 2015). A meta-analysis focusing on cognitive dysfunction after
sustaining a mild TBI revealed the effect of mild TBI on neuropsychological
functioning was much lower than the effect a variety of psychiatric conditions imposed
(Iverson et al., 2013). In terms of somatic complaints, headaches and dizziness
are the most frequently reported symptoms. Headache frequency typically
diminishes over time, however Kraus et al. (2005) conducted a longitudinal
study in which 36% of participants still reported frequent headaches 1-year
post-TBI. Emotional symptoms, particularly depression, are more evident after
the acute period following mild TBI, with rates of depression between 11-44% 3
months post-injury. (Levin et al., 2005). The symptoms of mild TBI typically
resolves in several days or weeks, and the vast majority do not display any
symptoms of mild TBI at 3 months post-injury (Yang et al., 2007). However, a
variety of studies shoe that approximately 15% of people with a mild TBI still
experience symptoms 1 year after the initial trauma occurred (Valente &
Fisher, 2011). Many somatic, cognitive, and emotional symptoms resulting from
mild TBI interact with and impair each other, which results in the persistence
of these symptoms, otherwise known as post-concussion syndrome (PCS) (Prince
& Bruhns, 2017).


Mild TBI is often the source of structural changes
in the brain and could possibly be directly related to the onset of
neuropsychiatric symptoms, the most widespread disorder being depression. In
the first three months following mild TBI, approximately 12-44% of individuals display
indicators of depression (Lange et al., 2011). The theory of medial temporal
vulnerability states that subcortical structures involved in depression are
located in the frontal and temporal lobes, in particular the hippocampus, and
are vulnerable to adverse effects following a mild TBI (Umile et al., 2002).
Given the location of the frontal and temporal lobes, damage is likely to occur
in these areas if a brain injury occurs. This theory is strongly supported by
physiological and imaging evidence, and from individuals reporting persistent
symptoms. A meta-analysis carried out by Eireud et al. (2014) reported
significant task-related activity in the hippocampus and thalamus in
participants with mild TBI symptoms and symptoms of depression, relative to
individuals with mild TBI who did not display depressive symptoms, and healthy
controls. Imaging also provides evidence for reductions in grey matter in
medial temporal areas in individuals with mild TBI reporting depressive
symptoms (Chen et al., 2009). There is typically evidence of reduced grey
matter in mild TBI however the volume of the grey matter in areas associated
with depression were significantly more reduced. It was concluded that
structural damages observed were likely caused by the mild TBI, but signs of
depression were associated with dysfunction of subcortical areas involved in
the brain injury


It is accepted that certain factors that are likely
to contribute to the persistence of adverse symptoms beyond the brain injury
itself. Premorbid psychological issues are a predictor of symptom persistence
after sustaining a mild TBI. Kashluba et al. (2008) compared 2 groups of mild
TBI patients, one group with premorbid psychiatric issues and the other group
who didn’t report any psychiatric issues prior to the injury. Participants with
previous psychiatric issues reported more complications following their injury.
They had a higher PCS symptom incidence, and they reported higher symptom
persistence after 3 months compared with the group with no previous psychiatric
issues. An important limitation of this study is the lack of non-brain injury
control groups, for example, spinal cord injury. Future studies could assess
the roles of premorbid psychiatric issues in recovery from trauma in general. Waljas
et al. (2015) also reported that mental health issues prior to the injury were
a predictor of persistent symptoms following mild TBI, yet 31% of the uninjured
control group also reported symptoms that fit the criteria of PCS syndrome,
indicating a high false-positive rate. There is evidently a correlation between
premorbid psychological issues and symptom generation and persistence with mild
TBI, however there are issues with the validity of symptom reporting of control
and injured groups (Kashluba et al., 2008). The use of valid scales to assess
personality and psychiatric characteristics would likely prove useful in the
interpretation of self-report measures in the recovery period of mild TBI
(Greiffenstein & Baker, 2006).


Symptom persistence following mild TBI can be
influenced by involvement in litigation in a variety of ways. One common theory
states that symptom complaints and poor results on neuropsychological tests are
a sign of deception and exaggeration, but that is not always the case.
Litigation itself may be a source of mental stress that can amplify and prolong
pre-existing symptoms (Katz et al., 2015). Attitudes and motivations of injured
patients can often shift due to the pressures involved in litigation. Those
involved in the process may directly or indirectly influence statements
regarding severity of symptoms, performance on tests, and decisions to delay
returning to everyday activities such as work or sport. Belanger et al. (2005)
found that involvement in litigation predicts poorer cognitive outcomes in the
recovery period of a mild TBI. To provide further evidence of this population
studies in Lithuania were carried out, where the litigation factor is not
present. Reports of postinjury symptoms and delay to return to work had much
lower rates than comparison controls (Mickeviciene et al., 2004). Some
individuals may exaggerate their symptoms and problems with different levels of
intent. Mittenberg et al. (2002) meta-analysis estimated that as many as 39% of
individuals with mild TBI exaggerated their symptoms over a variety of disorders.
This may imply a high level of intent but there are other factors which may
lead to emphasising symptoms and poor results on neuropsychological
examinations. Individuals may be motivated to exaggerate so they delay their
return to work, or receive legal compensation they feel they’re entitled to
(Iverson et al., 2013). Although many individuals appear to exaggerate their
symptoms with intent, it must always be considered that they may have a true
underlying impairment.


The role of attribution or expectation in symptom
generation and persistence is of great significance in some individuals.
Patients anticipate that certain cognitive or somatic symptoms will be a
natural part of the recovery from a mild TBI and attribute any perceived struggles
or changes to the brain injury (Ferguson et al., 1992). This theory is known as
‘Expectation as Etiology’ and was first devised by Mittenberg (1992). He compared individuals with a mild TBI to
a control group on several cognitive, affective, and somatic symptoms. Those
with a previous head injury had to give current symptoms and symptoms before
the injury, whereas the control group were asked to give current symptoms and
what symptoms they would expect to have if they sustained a head injury.
Participants with a mTBI reported 60% fewer symptoms relative to the control
group before the injury, and both groups anticipated or experienced extra symptoms
post-injury. It was concluded that most individuals expect to experience specific
symptoms when recovering from a mild TBI, and this results in the
misattribution of common symptoms to the injury. Individuals also tend to
underestimate symptoms prior to the injury and other confounding factors such
as stress. To counteract this misattribution, educating individuals on what to
expect post-injury can be an important intervention to reduce the role that
expectation plays in the persistence of symptoms (Broshek et al., 2015).


A psychological misconception known as the
‘good-old-days’ bias influences symptom reporting and persistence after sustaining
a mild TBI. This theory suggests that individuals underestimate their past
problems which can impact their perceived level of current symptoms (Yang et
al., 2014). To examine the impact of this bias on symptom reporting, Iverson et
al. (2010) asked individuals recovering from a mild TBI, who were receiving
compensation and taking time off work to estimate their symptoms prior to the
brain injury and describe their current state of symptoms. Consistent with the
‘good-old-days’ bias, the participants reported fewer pre-injury symptoms when
compared to an uninjured control group. However, methodological limitations may
diminish the validity of this theory as the participants symptoms were recorded
only once up to 4 months after the injury. Most patients with a mild TBI
exhibit adverse symptoms within the first month of the trauma. In addition, this
study failed take into account the potentially unstable psychological processes
or personality characteristics that could influence the misperception of
symptoms experienced (Furnham & Chamorro-Premuzic, 2004). If the
‘good-old-days’ bias can be identified in the early phase of recovery of a mild
TBI and clinicians focus on understanding the processes underlying this bias,
then an appropriate intervention program to improve the symptoms can be
introduced to decrease the likelihood of symptom persistence (Yang et al.,


Treatment strategies for mild TBI can contribute to
symptom generation and persistence. In recent years clinical pathways have been
developed using a multidisciplinary team (MDT) approach to set standards,
assess quality of care, ensure patient satisfaction, and make efficient use of
resources available (Davies & Gray, 2009). This approach is attractive
because it can improve the quality of care and improve the outcome of patients.
MDTs have recently theorised that early rehabilitation of mild TBI can improve
patient outcomes and reduce the impact of persistent cognitive, somatic, or
affective symptoms (Borg et al., 2004). This theory was supported by Singh et
al. (2013) who looked at the effect of early rehabilitation on 674 patients
after 6 months. 52% of participants’ symptoms had improved at the 6-month
follow-up period and overall the majority of patients were satisfied with their
progress. Although this study demonstrated a positive effect of early
rehabilitation, it only examined patients after 6 months. Research has shown
that at 10 years post-injury approximately 40% of patients require more support
than before the injury (Ponsford et al., 2014). The research literature on
early rehabilitation for mild TBI is limited by methodological inconsistency
and there is a lack of research on the long-term influence or early
rehabilitation on recovery from brain injury. Future research should focus on
the long-term follow-up of patients to determine if early rehabilitation
affects symptom generation and persistence. Early rehabilitation of mild TBI
could have future implications on costs of treatment. The associated cost of
care for individuals with persistent symptoms following mild TBI are
significantly high.  It is estimated that the cost of treatment and
follow-up care per individual with mild TBI is £28,300 (Humphreys et al.,
2013). Introducing early rehabilitation could result in substantial savings to
the individual through successful rehab of persistent symptoms.


The role of education and support is crucial in alleviating
persistent symptoms when recovering from a mild TBI. Reports have shown that even
one treatment session involving education, reassurance and explanation of
symptoms were effective at reducing persistent symptom incidence (Mittenberg et
al., 2001). Research addressing whether education and support interventions can
impact symptom generation and persistence has produced small, yet significant
results. These interventions are linked with the theory that persistent
symptoms can be a result of expected outcomes of the injury, and negative prospects
about recovery (Belanger et al., 2013). Educational interventions include
education on post-injury symptoms, reassurance on recovery, and guidance on
rest and return to work/activity timelines. Educational interventions have the
strongest empirical evidence, with several systematic reviews concluding they
are well supported, for example, psychoeducational interventions for treatment
of veterans with mild TBI resulted in a reduced incidence of persistent
symptoms when compared to previous studies that did not incorporate education
into treatments (Cooper et al., 2015). At present, individuals are not usually
seen by a specialist in neuropsychology or neurorehabilitation until their
symptoms persist beyond the normal period of recovery. However, early
consultations with neuropsychologists may be beneficial to those at risk of
developing persistent symptoms following mild TBI (Prince & Bruhns, 2017).
Neuropsychologists can offer educational support on somatic, cognitive, and
affective symptoms they may experience. They can inspire hope in patients who
experience anxiety about their recovery. Application of these educational
services on a broad scale would be beneficial for preventing persistent
symptoms in patients, and decrease costs and the burden of providing more
resource-intensive services.


To conclude, it is evident that there are multiple
factors contributing to symptom generation and persistence. Much of the current
research focuses on specific biological, psychosocial, or iatrogenic factors,
however, the etiology of symptom generation and persistence is likely diverse,
multifactorial, and characterised by individual variability. Therefore, a
perspective that integrates all of these factors mentioned into a
biopsychosocial framework may be useful in understanding symptom formation and
persistence. A MDT approach to treating the persistent symptoms of mild TBI has
proven to be the most effective when taking these factors into account.