Address for correspondence: Leonardo Baldaçara. Universidade Federal de São Paulo, LiNC. Rua Pedro de Toledo, 669, 3 andar fundos. Vila Clementino. 04039-032 – São Paulo, SP, Brazil.
Telephones: (+55 11) 5084-7060 / (+55 63) 9964-9744. Fax: (+55 11) 5084-7061. Email: firstname.lastname@example.org
Reduction of prefrontal thickness in military police ofcers with post-traumatic stress
Leonardo BaLdaçara1,2, CéLia araújo1, idaiane assunção1, ivaLdo da siLva1, andrea ParoLin jaCkowski1
1 Federal University of São Paulo (Unifesp), São Paulo, SP, Brazil.
2 Federal University of Tocantins (UFT), Palmas, TO, Brazil.
Received: 12/14/2016 – Accepted: 06/04/2017
Background: Brain-imaging studies in post-traumatic stress disorder (PTSD) have consistently revealed alterations in brain structure and function and this
is correlated to symptomatology. However, few studies have investigated the role of biomarkers in PTSD some specic groups, as police ocers. Objective: To
evaluate prefrontal and limbic volumes, and cortical thickness of police ocers exposed to trauma during work who developed post-traumatic stress disorder,
resilient matched controls (without PTSD), and compared to healthy civilians. Methods: Prefrontal and limbic volumes, and cortical thickness of 12 police
ocers with PTSD, 12 resilient police ocers, and 12 healthy civilians who underwent brain MRI were analyzed. Results: Dierences in limbic structures volume
were not signicative aer Bonferroni correction. A signicant reduction in cortical thickness on right rostral cingulate, right and le middle frontal gyrus, le
superior frontal, le lingual, calcarine and cuneus were observed in PTSD group in comparison to controls was observed. Discussion: Although preliminary,
our results suggested not only the association between cortical thickness and PTSD, but also indicated that patients and controls have anatomical dierences.
Baldaçara L et al. / Arch Clin Psychiatry. 2017;44(4):94-8
Keywords: Post-traumatic stress disorder, cortical thickness, limbic system, police ocers, trauma.
Post-traumatic stress disorder (PTSD) is a psychiatric condition
experienced by individuals aer suering psychological trauma.
PTSD symptoms include avoidance of trauma-related stimuli,
emotional numbing, re-experiencing the traumatic event,
hyperarousal, and cognitive decits1-3. Data from a large sample
that the lifetime prevalence of PTSD in general population is
approximately range from 1.3% to 9.2%4, worldwide, and 11.1% to
14.7% in Brazil5, with symptoms being triggered by many dierent
types of events4,5.
Brain-imaging studies in PTSD have consistently revealed
alterations in brain structure and function and this is correlated
to the PTSD symptomatology6. e most replicated ndings are
reduced volume in regions of the limbic system, such as amygdala7,8,
hippocampus9, and anterior cingulate cortex (ACC)1. Other studies
have found a thinner cortex in frontal and temporal areas10,11, and
in a longitudinal assessment conducted in a recovered group of
PTSD showed a greater dorsolateral prefrontal cortex associated to
improvement in PTSD symptoms12.
Studies in adult PTSD have revealed altered function in several
dierent areas of the prefrontal cortex including the dorsolateral
prefrontal cortex, the ventrolateral prefrontal cortex, the medial
prefrontal cortex, the anterior cingulate cortex, and the orbital frontal
cortex compared to controls13,14.
e medial prefrontal cortex (mPFC) seems to play a key role
in fear extinction of neurocircuitry models in anxiety and PTSD15
Studies in both humans and animals reinforce the involvement
and interaction among amygdala, hippocampus and mPFC in fear
e presence of an adverse event is necessary but not sucient for
the development of PTSD. In fact, only one in 10 subjects will develop
the disorder16,17, stressing that there are genetic and environmental
factors predisposing certain patients to PTSD. e study of biological
markers associated with PTSD is an extensive research eld with
promising results for both basic and clinical knowledge1,17. Brazil
has a unique environment to conduct translational research about
psychological trauma and posttraumatic stress disorder, since urban
violence became a Brazilian phenomenon, being particularly related
to the rapid population growth of its cities1,18.
e causes of posttraumatic stress disorder are many, including
the dierent types of traumatic events each person can be exposed
to. In turn, police ocers are a group that is continually exposed to
stressful and traumatic factors. At the same time, they are expensive
to train and require quick return when they are ill, given their role in
population safety. However, few studies have investigated the role of
biomarkers in PTSD police ocers19,20. Reduced amygdala, thalamus
and globus pallidus volumes were observed in police ocers with
chronic PTSD that had higher re-experiencing scores associated to
higher arousal ratings of negative pictures during trauma related
Compared with other occupational groups, police ocers face
an increased and anticipated risk of exposure to life-threatening and
potentially traumatic events in their work environments (for example,
when intervening in violent situations or witnessing suering and
death of others22). It has been found that the organizational and
psychosocial work environment of police ocers may aect the
degree and strength of PTSD symptoms23. e diagnosis of PTSD
is intrinsically linked to the presence of a traumatic event, but the
traumatic event per se is not sucient for the disease development.
In fact, only one in ten people will develop PTSD aer experiencing
trauma indicating that genetic and environmental factors contribute
to the onset of PTSD24.
In this study we hypothesized that the volumes of the cingulum
and amygdala, and thickness of frontal cortex are lower in police
officers exposed to traumatic situations who developed PTSD
compared to those exposed to the same situation but did not develop
PTSD and to healthy civilians. In this context, the goal of the present
study was to investigate alterations in limbic structures and frontal
cortex police ocers exposed to traumatic events during work and
compared to resilient military police and healthy civilians.
Baldaçara L et al. / Arch Clin Psychiatry. 2017;44(4):94-8
irty-six subjects matched by gender (all males) and age (mean age:
35, standard deviation [SD] ± 4 years old) were divided into three
groups: 12 police ocers exposed to trauma with PTSD, 12 police
ocers exposed to trauma without PTSD (resilient ocers), and 12
civilians without a history of trauma exposure. Police ocers with
at least 10 years of work experience were recruited from the General
Command of the Military Police of Tocantins, Brazil. Healthy civilian
subjects (controls) were recruited from the same community.
Traumatic experiences considered for the present study were
dened as duty-related urban violence, and included the following
experiences: being threatened, being shot, being beaten, witnessing
a death, witnessing a beating, experiencing a car accident, witnessing
the death a friend.
Patients were eligible for study participation if they met the
following inclusion criteria: 1) DSM-IV criteria for a diagnosis of
PTSD25; 2) aged between 18 and 60 years; 3) male gender; and 4) the
experience of a traumatic event, as previously dened, during duty.
Participant exclusion criteria included the following: 1) a history of
bipolar, psychotic, or borderline personality disorder; 2) substance
dependence or abuse (excluding nicotine and caeine); 3) severe or
unstable concurrent illness; 4) psychotropic medication use less than
four weeks prior to MRI, 5) current suicidal ideation or the presence
of psychotic symptoms; 6) use of psychoactive medications such as
antidepressants, neuroleptics, anxiolytics or sedative hypnotics and
mood stabilizers within the last eight weeks, 7) a Beck Depression
Inventory (BDI) score of more than 11 points.
Participants were informed about the research procedures and
risks of this study, and signed an informed consent form that was
fully approved by the Ethical Committee of the Federal University
of Tocantins (014/2012).
For the diagnosis of mental health disorders according to DSM-IV
criteria, we used the Structured Clinical Interview for DSM-IV I26,27.
To assess the presence of PTSD in patients, we used the Clinician-
Administered PTSD Scale (CAPS)28, a 30-item scale that investigates
the frequency and intensity of PTSD symptoms and traumatic
life experiences. Scores ranged from 0 to 136, with the following
classications: subclinical, 0 to 19; mild, 20 to 39; moderate, 40 to 59;
severe, 60 to 79; and extreme, 80 and above. Symptoms were divided
into the following clusters: re-experiencing symptoms, avoidance and
numbing symptoms, and hyperarousal symptoms.
To assess depressive symptoms in clinical settings, we used the
Beck Depression Inventory (BDI)29, a self-administered 21-item
questionnaire, which has been validated for the Brazilian population.
Scores ranged from 0 to 63, with depression classied according to
the following score categories: minimal, between 0 and 11; mild,
between 12 and 19; moderate, between 20 and 35; and severe, between
36 and 63. Subjects with scores more than 11 points were excluded.
Image acquisition and analysis
Imaging data were acquired using a Philips 1.5T Sigma scanner.
Structural MRI images were acquired using a sagittal T1 acquisition
series (TR = 9.8 ms, TE = 3.1 ms, ip angle = 30°, NEX = 1, matrix size
= 256 × 256, FOV = 24 cm, thickness = 1.0 mm), yielding 160 slices.
We used an automated, non-biased atlas-based Bayesian
segmentation method, applied in Freesurfer v.5.0 (http://surfer.
nmr.mgh.harvard.edu/). Too derive quantitative estimates of brain
structure and to label cortical and subcortical tissue classes Freesurfer
processing for volumetric T1-weighted images included: motion
correction, brain extraction and removal of non-brain tissue using a
hybrid watershed/surface deformation procedure, automated spatial
transformation and white matter (WM) segmentation of subcortical
volumetric structures, intensity normalization, tessellation of grey
matter GM/WM boundary and automated topology correction and
surface deformation, following intensity gradients to place optimally
GM/WM and GM/CSF borders at the location where the greatest
shi in intensity denes the transition to the other tissue class.
Image outputs from each stage of Freesurfer processing were visually
inspected. Freesurfer automatically assigns a neuroanatomical place
to each location on a cortical surface model based on probabilistic
information estimated from a manually labeled training set (made
using FreeSurfer). This method incorporates both geometric
information derived from the cortical model, and neuroanatomical
convention, as nding in the training set. e result is a complete
labeling of cortical sulci and gyri. e resulting segmentation and
parcellation was inspected by one of the authors and no adjustment
or reprocessing was needed. No manual region of interest (ROI) was
outlined in this study.
To account for inter-individual differences in head size,
intracranial and cerebral volumes were corrected by dividing by
each subject’s intracranial volume and multiplying this ratio by
1000 (Figure 1).
Figure 1. Regions analysed in the study.
Structural volume analysis
Data were codied and analyzed using the Statistical Package for
the Social Sciences (IBM SPSS for Windows, version 15.0). Prior to
analyses, measures were examined for normality using the Shapiro-
Wilk test. Signicance levels were set at p < 0.05, using a two-tailed
Group dierences in volumes were investigated using the general
linear model (Multivariate analysis of covariance – MANCOVA).
Results were corrected for multiple comparisons using Dunnet’s
post-hoc test (p ≤ 0.05), however to improve analysis all values were
corrected by Bonferroni method (p ≤ 0.0028). MANOVA eect sizes
were calculated using eta partial squared (h2), and compared between
groups using Cohen’s d method (d).
Cortical thickness analysis
e Query Design Estimate Contrast (QDEC) interface of FreeSurfer
was used to carry out a general linear model (GLM) analysis at each
vertex of the cortical surface.
Cortical thickness was considered as the dependent variable;
group (patients vs healthy controls), age, and their interaction
were explanatory variables, and intracranial volume was a nuisance
variable. Results were corrected for multiple comparisons at the
cluster level using the Monte Carlo approach for p-cluster < 0.05.
96 Baldaçara L et al. / Arch Clin Psychiatry. 2017;44(4):94-8
PTSD subjects has total mean CAPS score of 64.9 (SD ± 28.5) and
mean time to trauma of 2945 days (SD ± 2721). Mean time to trauma
for resilient group was 3630 days (SD ± 2654).
A signicant reduction in cortical thickness on le rostral cingulate, le
middle frontal gyrus, right middle frontal gyrus, right superior frontal,
and right lingual were observed in PTSD group in comparison to controls
survived Monte Carlo null-Z correction for multiple comparisons at p
< 0.05. No dierences between PTSD, healthy controls and resilient
controls survived multiple comparison correction (Figures 2 and 3).
A signicant reduction in cortical thickness on right rostral cingulate,
right and le middle frontal gyrus, le superior frontal, le lingual
were observed in PTSD group in comparison to controls survived
Monte Carlo null-Z correction for multiple comparisons at p < 0.05.
No dierences between PTSD, healthy controls and resilient controls
survived multiple comparison correction (Figures 2 and 3).
Not all individuals exposed to traumatic events develop PTSD.
Biological measures of PTSD should reect predictive markers of
risk/resilience (pre- or posttrauma exposure), or disease markers
indicating diagnostic status or symptom severity. More rened
applications include prognostic markers of therapy response that may
inform treatment choice or monitor response30. Once the biological
correlates of these constructs are identied, such biomarkers may
help identify those at highest risk following trauma exposure, target
prevention eorts, aid in diagnosis, treatment planning, and recovery
assessment for patients, and ultimately inform the development of
safe and eective pharmacological treatments for PTSD.
Table 1. Group differences in volumes of the Regions of Interest (cm3)
Variables (volume in cm3)PTSD group
F, df = 2 ph2
Intracranial volume 1637.53 (1558.62-1716.45) 1542.17 (1469.32-1615.01) 1578.77 (1489.27-1668.28) 1.721 0.195 0.094
Left hippocampus 2.56 (2.41-2.71) 2.64 (2.48-2.79) 2.66 (2.50-2.81) 0.435 0.651 0.026
Right hippocampus 2.65 (2.52-2.77) 2.60 (2.48-2.73) 2.59 (2.46-2.71) 0.239 0.789 0.014
Left parahippocampus 1.24 (1.10-1.38) 1.45 (1.32-1.59) 1.21 (1.07-1.35) 4.005 0.028* 0.195
Right parahippocampus 1.17 (1.07-1.27) 1.28 (1.19-1.38) 1.25 (1.16-1.35) 1.582 0.221 0.088
Left amygdala 0.94 (0.85-1.02) 0.94 (0.85-1.02) 0.93 (0.84-1.01) 0.011 0.989 0.001
Right amygdala 0.976 (0.91-1.04) 0.98 (0.92-1.05) 1.02 (0.96-1.09) 0.653 0.527 0.038
Left rostral anterior cingulate 1.62 (1.48-1.76) 1.87 (1.73-2.01) 1.88 (1.74-2.03) 4.389 0.020** 0.210
Right rostral anterior cingulate 1.32 (1.14-1.50) 1.36 (1.18-1.54) 1.48 (1.30-1.67) 0.876 0.426 0.050
Left dorsal anterior cingulate 1.20 (1.00-1.39) 1.30 (1.11-1.49) 1.22 (1.03-1.41) 0.350 0.707 0.021
Right dorsal anterior cingulate 1.39 (1.22-1.57) 1.34 (1.16-1.52) 1.43 (1.25-1.61) 0.271 0.765 0.016
Left isthmus cingulate 1.94 (1.77-2.12) 1.81 (1.64-1.99) 1.80 (1.62-1.97) 0.841 0.440 0.049
Right isthmus cingulate 1.75 (1.61-1.89) 1.65 (1.51-1.78) 1.67 (1.53-1.80) 0.692 0.508 0.040
Left posterior cingulate 2.05 (1.86-2.24) 2.15 (1.95-2.34) 2.12 (1.93-2.32) 0.273 0.763 0.016
Right posterior cingulate 2.12 (1.96-2.27) 2.07 (1.91-2.22) 2.17 (2.01-2.32) 0.450 0.642 0.027
Left lateral orbitofrontal 4.83 (4.57-5.10) 5.25 (5.00-5.52) 4.98 (4.72-5.24) 2.783 0.076 0.144
Right lateral orbitofrontal 4.73 (4.46-5.00) 5.06 (4.78-5.31) 4.88 (4.61-5.14) 1.461 0.247 0.081
Left medial orbitofrontal 3.52 (3.28-3.77) 3.73 (3.48-3.98) 3.88 (3.63-4.13) 2.150 0.133 0.115
Right medial orbitofrontal 3.25 (3.07-3.43) 3.55 (3.37-3.73) 3.50 (3.32-3.68) 3.226 0.053 0.164
cm3: cubic centimeters. p threshold was set at p < 0.05
* Post-hoc control x PTSD left parahippocampus p = 0.929 (d = 0.127), resilient x PTSD left parahippocampus p = 0.054 (d = 0.933).
** Post-hoc control x PTSD left rostral anterior cingulate p = 0.024 (d = 1.04), resilient x PTSD left rostral anterior cingulate p = 0.032 (d = 1.15).
Figure 2. Reduced cortical thickness on right middle frontal gyrus, right
superior frontal, and right lingual.
Figure 3. Reduced cortical thickness on left middle frontal gyrus and left
Baldaçara L et al. / Arch Clin Psychiatry. 2017;44(4):94-8
In this present study, we investigated possible alterations in brain
volume and thickness of police ocers with PTSD secondary to
traumatic events during duty. Our results showed reduced cortical
thickness in prefrontal area of PTSD group when compared to
resilient police ocers and healthy civilians.
Due to the cross-sectional nature of this study we can not state
whether the changes were present before or aer the disorder. For
a while the results suggests involvement of the frontal region in
individuals who develop PTSD.
On the other hand, the results also demonstrated lack of
evidences of alterations in the frontal and limbic volumes in PTSD
group compared to resilient police ocers and controls.
Literature remains contradictory about neurobiological ndings
in PTSD. Previous studies have found reduced volume and gray
matter of hippocampus and amygdala31,32 related to PTSD. We
previously observed that enlargement of hippo campus and amygdala
was related to early trauma in subjects exposed to urban violence1
which corroborates to the ndings of Kuo et al.33 that observed
larger amygdala volumes among patients with PTSD with a positive
correlation between early trauma and severity of adult trauma
exposure. However, no volumetric dierences in these structures
were found in this study.
Despite our results regarding to the volume of brain structures
did not reach statistical signicance, others studies that investigated
ACC volumes in patients with PTSD using MRI have yielded
conicting ndings. For instance, one study using the conventional
manual tracing method found signicant volume reductions in the
pregenual, but not dorsal, ACC34. A voxel-based analysis found gray
matter volume reductions in the dorsal ACC among patients with
PTSD35. Additionally, no dierences were found in ACC volume
between patients with acute PTSD and healthy subjects; however,
structural dissimilarities were reported35.
Few studies have assessed cortical thickness in PTSD. Corbo
et al.36 found a positive association between thickness of the le
posterior cingulate/paracentral area and PTSD symptoms severity in
veterans exposed to early trauma. On the other hand, this association
was negative in the veterans without history of trauma in childhood37.
Woodward (2009), also investigated the cortical thickness in adult
combat-related PTSD and found thinner cortex in participants
with PTSD at superior temporal cortex in comparison with healthy
controls37. The study of Kuhn reported a reduction of cortical
thickness of right medial orbitofrontal cortex negatively associated
to trait anxiety in a healthy sample38.
It has been suggested that the neurobiology of PTSD involves
circuitry pathology, rather than implication of a single brain
structure. In patients with PTSD, the default mode network, a set of
structures including the medial prefrontal cortex and the posterior
cingulate cortex (believed to be more “active” during the resting
state) is believed to be aected by the pathology underlying the
disorder39. Specically, the resting-state functional connectivity of
the posterior cingulate cortex, perigenual anterior cingulate cortex,
and the right amygdala is associated with current PTSD symptoms,
whereas functional correlation with the right amygdala is predictive
of future PTSD symptoms40. ere is also evidence using diusion
tensor imaging that white matter structural integrity in the cingulate
bundle is compromised in PTSD patients compared with that of
healthy individuals41. erefore, in addition to functional impairment
of the amygdala, mPFC and ACC, functional connectivity may be
disrupted in PTSD1.
Strengths and limitations
e primary strength of the current study is that the sample was
well selected: we used paired groups, including only males, excluded
those with alcohol abuse, and recruited subjects from the same site.
Secondly few studies have investigated morphometric brain
alterations in police ocers related PTSD and the result of this study
may contribute to the understanding of PTSD in occupations with
high stress levels.
is study has a few limitations that should be noted: rst, the
cross-sectional study design precludes determination whether the
observed changes are cause or consequence of PTSD; secondly, the
sample size in the present study was not suciently large to expand
Our results suggest that police ocers with PTSD has reduce cortical
thickness in prefrontal area compared to resilient police ocers and
healthy controls. is nding adds that the prefrontal region may
be aected in police exposed to traumatic situations. Since this is
an area involved in cognitive functions such impairment may have
direct implications on the performance of this profession. Also, the
results demonstrated lack of evidences of alterations in the frontal
and limbic volumes in PTSD group compared to resilient police
ocers and controls.
However, these results need to be conrmed by studies with larger
samples and dierent methods. Moreover, ours results compared
to literature suggested that neuroimaging findings in PTSD is
heterogeneous, and multiple factors (including individual factors)
are related to this disorders.
Role of funding sources
is study was supported by the State of São Paulo Funding Agency
(Fapesp) by the Grant: 2004/15039-0, and the National Research
Council (CNPq) by the grant: 476537/2011-8, and by Millenium
Institute of Violence and Mental Health by the grant: 420122/2005-2.
e Fapesp and CNPq had no further role in the study design; in
the collection, analysis and interpretation of the data; in the writing
of the report; or in the decision to submit the paper for publication.
e manuscript submission was supported by Federal University of
São Paulo (Unifesp).
ere are no contributors to declare.
Conict of interest
e authors report no nancial or other relationship relevant to the
subject of this article.
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