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RESEARCH Open Access
Potential impact of propofol immediately after
motor vehicle accident on later symptoms of
posttraumatic stress disorder at 6-month follow
up: a retrospective cohort study
Masato Usuki1,2,3,4, Yutaka Matsuoka1,2,3,5*, Daisuke Nishi1,2,3,4, Naohiro Yonemoto3,5, Kenta Matsumura1,3,
Yasuhiro Otomo6, Yoshiharu Kim1 and Shigenobu Kanba4
Abstract
Introduction: Critically injured patients are at risk of developing posttraumatic stress disorder (PTSD). Propofol was
recently reported to enhance fear memory consolidation retrospectively. Thus, we investigated here whether
administration of propofol within 72 h of a motor vehicle accident (MVA) affects the subsequent development of
PTSD symptoms.
Methods: We examined data obtained from a prospective cohort study of MVA-related injured patients, admitted
to the intensive care unit of a general hospital. We investigated the effect of propofol administration within 72 h
of MVA on outcome. Primary outcome was diagnosis of full or partial PTSD as determined by the ClinicianAdministered PTSD Scale (CAPS) at 6 months. Secondary outcomes were diagnosis of full or partial PTSD at 1
month and CAPS score indicating PTSD at 1 and 6 months. Multivariate analysis was conducted adjusting for being
female, age, injury severity score (ISS), and administration of ketamine or midazolam within 72 h of MVA.
Results: Among 300 patients recruited (mean ISS, 8.0; median Glasgow Coma Scale (GCS) score, 15.0; age, 18 to 69
years), propofol administration showed a higher risk for full or partial PTSD as determined by CAPS at 6 months
(odds ratio = 6.13, 95% confidence interval (CI): 1.57 to 23.85, P = 0.009) and at 1 month (odds ratio = 1.31, 95% CI:
0.41 to 4.23, P = 0.647) in the multivariate logistic regression. Multivariate regression analysis showed a trend
toward adverse effects of propofol on PTSD symptom development at 6 months after MVA (b = 4.08, 95% CI: -0.49
to 8.64, P = 0.080), but not at 1 month after MVA (b = -0.42, 95% CI: -6.34 to 5.51, P = 0.890).
Conclusions: These findings suggest that using propofol in the acute phase after MVA might be associated with
the development of PTSD symptoms 6 months later. However, since the design of this study was retrospective,
these findings should be interpreted cautiously and further study is warranted.
Introduction
Critically injured patients are at risk of developing posttraumatic stress disorder (PTSD), particularly those
injured in a motor vehicle accident (MVA) [1-10]. MVA
survivors with psychiatric morbidity such as PTSD have
also been found to have significantly lower quality of life
and post-accident work potential than those without
psychiatric morbidity [11,12]. Thus, it is important to
detect MVA survivors at risk of developing later PTSD
and prevent it when feasible.
In general, MVA survivors are administered sedatives
for agitation while in the intensive care unit (ICU) or in
perioperative management after a traumatic experience.
The American College of Critical Care Medicine, clinical
practice guidelines recommend use of intravenous propofol, midazolam, or lorazepam for sustaining sedation in
the ICU [13]. Some researchers have examined whether
sedative drugs affect memory function and the subsequent
* Correspondence: yutaka@ncnp.go.jp
1National Institute of Mental Health, National Center of Neurology and
Psychiatry, Tokyo 187-8553, Japan
Full list of author information is available at the end of the article
Usuki et al. Critical Care 2012, 16:R196
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© 2012 Usuki et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited.
development of PTSD symptoms. Fisher et al. reported
that midazolam exposure resulted in antegrade memory
loss in humans [14]. McGee et al., working on the
assumption that midazolam decreases fear memory, examined the effectiveness of midazolam for later PTSD, but
found the prevalence of PTSD did not differ between
injured soldiers who received the drug intraoperatively,
and those who did not [15].
Recently, Hauer et al. reported that retrospectively propofol enhances consolidation of fear memory in rats [16].
Their experiment, using a well-characterized animal
model of aversive training, showed results similar to
those for MVA survivors who were administered propofol during acute trauma care and later presented with
PTSD. It is speculated that the core mechanism behind
the development of PTSD is excessive consolidation of
and failure to extinguish fear memory; therefore, modulating consolidation of fear memory as part of early intervention after a traumatic experience would be a potential
strategy to prevent PTSD symptoms from developing
later [17]. However, the findings of Hauer et al. were
obtained in an animal model, and it is still unclear
whether administration of propofol for MVA survivors in
the clinical setting is related to later PTSD development.
We hypothesized that administration of propofol at an
early stage after a traumatic experience might increase
the risk for PTSD symptoms later, and investigated here
whether such administration within 72 h of MVA is associated with the development of PTSD symptoms 6
months later.
Materials and methods
Participants
Overview of the Tachikawa cohort of the Motor Vehicle
Accident Study
This study was performed as a part of the Tachikawa
cohort of the MVA (TCOM) Study [10], a prospective
cohort study which was conducted in accordance with
the Declaration of Helsinki and approved by the Ethics
Committee of the National Disaster Medical Center
(NDMC), Tokyo. NDMC serves a population of approximately 1.7 million and its acute critical care center is
responsible for level-I trauma service provision. Participants in the present study were patients consecutively
admitted to the ICU of NDMC with MVA-related injury
between 30 May 2004 and 8 January 2008. During this
period, 344 patients met the eligible criteria and were
asked to participate in the study. After receiving a
description of the study, 300 patients (87.2%) provided
written informed consent. The median number of days
between the time of MVA (confirmed from ambulance
service records) and baseline assessments was 2.3 days
(range 0 to 23).
Study participants
The inclusion criteria were as follows: i) MVA-related
severe physical injury causing a life-threatening or critical
condition; ii) consecutive admittance to the NDMC acute
critical care center (ICU); iii) age between 18 and 69 years,
and iv) native Japanese speaking ability. The exclusion criteria were as follows: i) diffuse axonal injury, brain contusion, or subdural or subarachnoidal bleeding detected by
computed tomography and/or magnetic resonance imaging (with the exception of concussion), because the presence of traumatic brain injury creates considerable
difficulties when assessing psychological responses to
injury; ii) cognitive impairment, defined as a score < 24 on
the Mini-Mental State Examination (MMSE); iii) currently
suffering from schizophrenia, bipolar disorder, drug (nonalcohol) dependence or abuse, or epilepsy before the
MVA; iv) marked serious symptoms such as suicidal ideation, self-harm behavior, dissociation, or a severe physical
condition preventing the patient from tolerating the interview, and v) living or working at a location more than
40 km from the NDMC. Whether patients met the inclusion or exclusion criteria was clinically assessed by a
trained research nurse or psychiatrist.
Assessments
Baseline and follow-up assessments
The following baseline data were gathered: general sociodemographics, past history of psychopathology as determined in a structured interview, detailed information
about the MVA, vital signs first recorded on admission to
the emergency room, injury severity score (ISS) [18],
Glasgow Coma Scale (GCS) score [19], MMSE score [20],
pain on admission as measured subjectively, consumption of alcohol and tobacco prior to the MVA as determined in the structured interview, and other clinical
information. These assessments were performed by a
trained research nurse or psychiatrist.
To assess PTSD symptoms at follow-up, trained psychiatrists conducted the Clinician-Administered PTSD
Scale (CAPS) at 1 and 6 months after the MVA injury.
CAPS is the gold standard for assessing PTSD and
involves a structured interview in which a Likert-type
rating of frequency (0 to 4) and a separate rating of
intensity (0 to 4) for each symptom is assigned [21]. To
constitute a symptom, frequency must be ≥ 1 (once or
twice a month) and intensity ≥ 2 (moderate). Full PTSD
was diagnosed if patients fulfilled all of the symptom
criteria (A-1, stressor; B, re-experiencing; C, avoidance;
D, hyperarousal; E, duration; and F, impairment) according to the Diagnostic and Statistical Manual of Mental
Disorders (DSM), Fourth Edition, Text Revision [22].
Partial PTSD was diagnosed if they fulfilled two of
the three symptom criteria B, C, and D, and the criteria
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A-1, E, and F. A random sample of 30 patients assessed
by two raters (YM and DN) was used to assess interrater reliability. The calculated intraclass correlation
coefficient was 1.0.
Administration of propofol
The clinical practice guidelines of the American College
of Critical Care Medicine recommend that propofol is
administered for ongoing sedation within the first 3
days [13]; therefore, we retrospectively collected data
from the medical records on the total dose of propofol
over the initial 72-h period and the route of administration. We used propofol (2,6-disopropyl phenol) purchased from AstraZeneca Japan (Osaka, Japan).
Confounding factors
We investigated eight potential confounding variables,
namely, female sex, age, ISS, GCS score, pain on admission, and administration of midazolam, morphine, or ketamine, for the following reasons. A meta-analysis revealed
that civilian women were consistently at higher risk than
men for PTSD [23]. In an epidemiological study, younger
persons showed an increased risk of PTSD compared to
elderly persons [24]. ISS was chosen as the objective accident-related variable, and GCS score was chosen as a surrogate marker of traumatic brain injury as more severe
traumatic brain injury was found to be associated with a
diminished risk of PTSD [25]. ISS and GCS score were
determined by an emergency physician on admission.
Some studies have indicated that the level of pain is significantly associated with subsequent risk of PTSD [26,27]
and therefore we investigated whether or not patients
complained of pain on admission.
The clinical practice guidelines of the American College
of Critical Care Medicine recommend midazolam for
short-term use (within 48 to 72 h) and lorazepam for sedation in most patients via intermittent intravenous (i.v.)
administration or continuous infusion [13]. Benzodiazepines such as midazolam and lorazepam could affect
PTSD symptoms by creating an amnesic effect [15,28,29].
Therefore, we checked administration of midazolam
within 72 h of MVA, but not i.v. administration of lorazepam, which is not approved in Japan. Other studies have
suggested that morphine administered in the acute stage
of trauma may reduce the risk of subsequent development
of PTSD [30,31]. Moreover, single-dose ketamine affected
the severity and duration of posttraumatic stress symptoms in injured accident victims [32] and perioperative
ketamine was associated with a lower prevalence of PTSD
in burned soldiers than in those not receiving it [33].
Therefore, we also investigated the administration of morphine and ketamine within 72 h of MVA.
However, three potential covariates - GCS, pain on
admission, and morphine administration - were excluded
from the multivariate regression analysis because of zero,
small, or sparse data for these covariates.
Statistical analysis
We performed logistic regression analysis with diagnosis
of full or partial PTSD at 6 months after the MVA as
the primary outcome. Secondary outcomes were diagnosis of full or partial PTSD at 1 month and a CAPS score
indicating PTSD at 1 month and 6 months after the
MVA. We performed logistic regression analysis and
calculated odds ratios (ORs) and 95% confidence intervals (95% CIs) for full and partial PTSD. Univariate
regression analysis and multivariate regression analysis
were used to examine the effect of using propofol on
the CAPS score, accounting for the five potential covariates described above. Additionally, we calculated regression coefficients (b) and 95% CIs in the regression
analysis as secondary outcomes. All analyses were performed using SPSS statistical software version 17.0J for
Windows (SPSS, Tokyo, Japan).
As missing values were present at 1 and 6 months due
to dropout and other reasons, we performed multiple
imputations with SAS 9.1.3 via procedure MI (SAS System for Windows, version 9.1, SAS Institute, Cary, NC).
Results
The demographics and clinical characteristics of participants who were administered propofol within 72 h of an
MVA are shown in Table 1. Sixty-seven (22.3%) were
women and the mean age of all participants was 36.5 (SD
15.0) years. The median ISS was 8.0 (range 1 to 48) and
the median GCS score was 15.0 (range 3 to 15). Twentysix (9.7%) participants were administered propofol within
72 h of MVA, at an average dose of 942.2 mg (median
155 mg, 25th percentile 142.5 mg, 75th percentile 477.3
mg, range 60 to 6650 mg). Of the 300 participants, 155
(51.7%) completed the CAPS at the 1-month follow-up
and 106 (35.3%) completed it at the 6-month follow-up
(Figure 1). Reasons for dropout were as follows: refused
to participate in follow-up (n = 24), no response to telephone and mail (n = 126), moved to an unknown address
(n = 9), questionnaire data alone (n = 33), or excluded
due to serious psychiatric symptoms (n = 2). None of the
participants had died up to the 6-month follow-up. With
the imputed data, the mean CAPS score was 18.2 points
at 1 month and 14.0 points at 6 months. Ten participants
(3.3%) were deemed to have full PTSD at 1 month and 8
(2.7%) were deemed to have full PTSD at 6 months [34].
Forty-two participants (14.0%) had full or partial PTSD at
1 month, with 21 participants (7%) having the same
symptom level at 6 months.
Table 2 shows that the participants who were administered propofol had a higher risk of meeting the criteria for
full or partial PTSD at 1 month and 6 months after an
MVA: on univariate logistic regression, the OR at 1 month
was 2.52 (95% CI 0.99 to 6.42, P = 0.053) and at 6 months
was 5.18 (95% CI 1.81 to 14.81, P = 0.002); on multivariate
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logistic regression, the OR at 1 month was 1.31 (95% CI
0.41 to 4.23, P = 0.647) and at 6 months was 6.13 (95% CI
1.57 to 23.85, P = 0.009).
Table 3 shows the relationship between CAPS score at
1 month and 6 months after an MVA and administration of propofol. Univariate regression analysis revealed
that participants who received propofol had more severe
PTSD symptoms at 6 months (b = 4.84, P = 0.045, 95%
CI 0.01 to 9.58), whereas multivariate regression analysis
showed a non-significant trend toward adverse effects of
propofol on PTSD symptom development (b = 4.08, P =
0.080, 95% CI -0.49 to 8.64).
Discussion
The findings of the present study suggest that the
administration of propofol for MVA victims in the acute
trauma stage could have adversely affected the later
development of PTSD. In logistic regression analysis,
use of propofol showed a higher risk for developing full
or partial PTSD at 1 and 6 months after injury. However, the association seen on univariate logistic regression was not apparent on multivariate logistic regression
at 1 month after MVA. The reasons for this lack of
association on multivariate logistic regression might be
explained by the confounding factor of physical condition (assessed by the ISS) and the clinical course. Some
previous studies have suggested that injury-related
PTSD symptoms tend to develop late [35,36]. For
instance, 22% of MVA victims have been shown to meet
DSM-III-R criteria for PTSD at 6 months after injury
and 30% were diagnosed with PTSD at 12 months [35].
Further, 4.2% of US soldiers were found to have problematic PTSD at 1 month after injury compared with
12.0% at 7 months [36]. In the present study, in relation
to secondary outcome, the b-value of regression analysis
was over 4 points at 6 months after MVA. This value
was comparable to having one further clinical PTSD
symptom. This result suggests that propofol administration has adverse effects on not only categorical PTSD
diagnosis but also continuous PTSD symptom level.
Several risk factors for PTSD have been reported in a
meta-analysis [23]. However, few studies have examined
whether propofol is one of these risk factors, and in this
respect our findings offer new insight when considering
the risk factors for PTSD. Our results are similar to those
of Hauer et al. in that propofol enhanced consolidation
of retrograde fear memory in rats [16]. They suggested
that enhancement of retrograde memory by propofol
depends on an indirect activation of CB1 cannabinoid
receptors [16]. Their hypothesis was based on the fact
that administration of propofol indirectly increases anandamide (one of the main endocannabinoids) within the
Table 1 Demographics and clinical profile of participants critically injured in motor vehicle accidents
Clinical profile and administered drugs Propofol used
(n = 26)
Propofol not used
(n = 274)
All participants
(n = 300)
Age, years (range) 36.0 (18, 69) 36.6 (18, 65) 36.5 (18, 69)
Women, % (n) 23.1 (6) 22.3 (61) 22.3 (67)
Pain on admission, % (n) 88.5, 23 93.1, 255 92.7, 278
Glasgow Coma Scale score (range) 14.0 (3, 15) 14.6 (3, 15) 14.6 (3, 15)
Injury Severity Score (range) 18.1 (4, 41) 8.2 (1, 48) 9.1 (1, 48)
Heart rate on admission, bpm (range) 87.7 (52, 114) 84.7 (52, 140) 84.9 (52, 140)
History of self-reported psychiatric illness, % (n) 11.5 (3) 10.2 (28) 10.3 (31)
Smoker, % (n) 53.8 (14) 52.9 (145) 53.0 (159)
Alcohol consumption, % (n)
Never drinker or past drinker 19.2 (5) 18.2 (50) 18.3 (55)
Occasional drinker/drinks 1 to 3 days/month 42.3 (11) 29.6 (81) 30.7 (92)
Drinks 1 to 2 days/week to almost every day 38.5 (10) 52.2 (143) 51.0 (153)
Midazolam used within 72 h, % (n) 50.0 (13) 8.0 (22) 11.7 (35)
Morphine used within 72 h, % (n) 11.5 (3) 1.0 (2) 1.7 (5)
Ketamine used within 72 h, % (n) 34.6 (9) 10.9 (30) 13 (39)
Figure 1 Flow chart of enrollment and follow-up.
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mouse brain by inhibiting fatty acid amide hydrolase,
which degrades endocannabinoids [37]. It is well known
that endocannabinoids adversely affect a hippocampaldependent memory task [38]. However, recent studies
have demonstrated that endocannabinoids could facilitate
emotionally charged memories [38,39]. Accordingly, the
formation of emotional memory is similar to the development of PTSD. Patel et al. showed that other intravenous
general anesthetics, including midazolam, ketamine, etomidate, and thiopental, did not affect fatty acid amide
hydrolase activity at sedative-relevant concentrations
[37]. This also raises the possibility that propofol specifically facilitated formation of retrograde fear memory in
our study by excluding the effect of other sedative drugs.
In addition, our findings might support the previous
observation that propofol use in the ICU was associated
with delusional memory and PTSD symptoms after discharge [40].
The present study has several limitations. First, the
observational design of this study meant we could not
divide patients into two groups in regard to the use of propofol and the sample size of patients who were administered propofol was modest. Second, previous studies have
pointed out that the length of ICU stay is a predictor of
PTSD, a factor we did not investigate due to insufficient
data. Third, we wanted to adjust for three potential covariates, namely GCS, pain on admission, and morphine
administration, in the multivariate analysis, but could not
do so due to data problems. Further studies of these potential confounders are warranted. Fourth, the response rate
was low, especially at 6 months. Weisaeth had pointed out
that the high potential loss to follow-up would reduce the
predictor value, thus the response rates need to be high in
a longitudinal trauma study [41]. In addition, the risk of
either type I or II errors increase as time passes. We should
evaluate the present results with these points in mind.
Conclusions
The findings of this study indicate that administration of
propofol during the acute trauma stage after an MVA
may adversely affect the development of later PTSD.
However, a retrospective design tends to overestimate
the treatment effects, and therefore the findings should
be interpreted with caution. Clearly these results are not
definitive, but they do provide supplementary evidence to
animal studies and could be helpful for emergency physicians to consider. Studies on PTSD risk factors as a result
of drug administration for trauma are still relatively few;
in particular, the effects of anesthetic drugs on fear memory remained to be investigated. To clarify the correlation
Table 2 Multivariate analysis of propofol administration and diagnosis of full or partial posttraumatic stress disorder
(PTSD) at 1 and 6 months after a motor vehicle accident
PTSD diagnosis Logistic regression at 1 month Logistic regression at 6 months
Covariates OR 95% CI P-value OR 95% CI P-value
Full or partial Propofol 1.31 0.41, 4.23 0.647 6.13 1.57, 23.85 0.009
Age 0.99 0.97, 1.01 0.397 1.04 1.00, 1.07 0.032
Female 10.02 4.33, 23.17 < 0.001 5.76 1.97, 16.78 0.001
ISS 1.10 1.05, 1.15 < 0.001 1.04 0.98, 1.11 0.217
Midazolam 0.46 0.12, 1.69 0.240 0.40 0.06, 2.73 0.349
Ketamin 1.91 0.62, 5.94 0.262 1.15 0.20, 6.51 0.878
Full Propofol 0.90 0.09, 8.98 0.928 14.63 2.07, 103.29 0.007
Age 1.04 0.99, 1.08 0.128 1.01 0.96, 1.06 0.819
Female 7.53 1.65, 34.44 0.009 5.16 0.99, 27.04 0.052
ISS 1.07 0.98, 1.17 0.112 0.94 0.82, 1.07 0.352
Midazolam 0.42 0.02, 7.61 0.555 0.51 0.02, 12.08 0.673
Ketamine 0.96 0.07, 14.00 0.974 1.19 0.06, 23.97 0.909
The independent variable was use of propofol within 72 h of a motor vehicle accident (MVA); n = 300 participants analyzed by multivariate logistic regression
analysis of age, female sex, and administration of ketamine or midazolam within 72 h of an MVA. OR, odds ratio; ISS, injury severity score.
Table 3 Propofol administration and Clinician-Administered posttraumatic stress disorder (PTSD) Scale score 1 and 6
months after a motor vehicle accident (MVA).
Univariate regression Multivariate regression
b 95% CI P-value b 95% CI P-value
1 month 4.10 -1.67, 9.88 0.163 -0.42 -6.34, 5.51 0.890
6 months 4.84 0.10, 9.58 0.045 4.08 -0.49, 8.64 0.080
The independent variable was use of propofol within 72 h of an MVA; n = 300 participants analyzed by multivariate logistic regression analysis of age, female
sex, and administration of ketamine or midazolam within 72 h of an MVA.
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between the administration of sedative drugs and development of PTSD, further collaborative research from
bench to bedside, and between critical care medicine and
psychiatry are needed.
Key messages
• Modulating the formation of fear memory after
trauma is an important strategy to prevent the subsequent development of PTSD symptoms.
• Administration of propofol within 72 h of trauma
could adversely affect the development of PTSD
symptoms at 6-month follow-up.
• Propofol administration was shown to have adverse
effects not only on categorical PTSD diagnosis, but
also on continuous PTSD symptom levels.
• The present results support the findings that propofol enhances consolidation of retrograde fear
memory via the endocannabinoid system.
Abbreviations
CAPS: Clinician-Administered PTSD Scale; DSM: Diagnostic and Statistical
Manual of Mental Disorders; GCS: Glasgow Coma Scale; ICU: intensive care
unit; ISS: injury severity score; i.v.: intravenous; MMSE: Mini-Mental State
Examination; MVA: motor vehicle accident; NDMC: National Disaster Medical
Center; PTSD: posttraumatic stress disorder.
Acknowledgements
We thank Dr T Hifumi for useful advice on the drug assessment; Dr T Takagi
for his valuable advice on anesthesiology; Mss Noguchi, Kawase, Sano,
Hasegawa, and Takahashi for careful recruitment of and communication
with the participants, and Mss. Akutsu, Kamoshida, and Suzuki for data
management. The authors thank Ms T Usuki for her general support and
warm encouragement.
This study was supported by grants (16190501, 19230701 and 20300701)
from the Japanese Ministry of Health, Labor, and Welfare (Research on
Psychiatric and Neurological Disease and Mental Health) and CREST, the
Japan Science and Technology Agency. The funding body did not play any
role in the writing of the manuscript or in the decision to submit the
manuscript for publication.
Author details
1National Institute of Mental Health, National Center of Neurology and
Psychiatry, Tokyo 187-8553, Japan. 2Department of Psychiatry, National
Disaster Medical Center, Tokyo 190-0014, Japan. 3CREST, Japan Science and
Technology Agency, Tokyo 102-0075, Japan. 4Department of
Neuropsychiatry, Graduate School of Medical Science, Kyushu University,
Fukuoka 812-8582, Japan. 5Department of Clinical Epidemiology,
Translational Medical Center, National Center of Neurology and Psychiatry,
Tokyo 187-8551, Japan. 6Department of Acute Critical Care and Disaster
Medicine, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
Authors’ contributions
MU designed this secondary analysis, participated in data collection,
performed statistical analysis and wrote the manuscript. YM conceived the
original cohort study, wrote the protocol, recruited and interviewed the
participants and revised the manuscript critically for important intellectual
content. DN joined the preparation of the original protocol, recruited and
interviewed the participants and revised the manuscript critically for
important intellectual content. NY performed statistical analysis for multiple
imputations and reviewed the study design and statistical analysis. KM
performed interpretation of data and revised the manuscript critically for
important intellectual content. YO and YK joined the preparation of the
original protocol and revised the manuscript critically for important
intellectual content. SK has made contributions to analysis and interpretation
of data and revised the manuscript critically for important intellectual
content. All authors read and approved the final manuscript.
Competing interests
There are no competing interests to disclose related to this manuscript.
Other financial disclosures are as follows: MU has no financial competing
interests; YM has received research support from the Japan Science and
Technology Agency, CREST and the Ministry of Health, Labor, and Welfare of
Japan, Intramural Research Grant for Neurological and Psychiatric Disorders
of NCNP and lecture fees from Suntory Wellness Ltd., Eli Liliy Japan KK, and
Otsuka Pharmaceutical Co., Ltd. DN has received research support from
Toray Industries, Inc. and the Foundation for Total Health Promotion, and
lecture fees from Qol Co., Ltd, DHA & EPA Association and NTT DoCoMo,
Inc. NY has received research support from the Japan Society for the
Promotion of Science and the Japanese Ministry of Health, Labor and
Welfare. KM has received research support from the Japan Society for the
Promotion of Science, the 26th Research Grant in Medical and Health
Science of Meiji Yasuda Life Foundation of Health and Welfare. YO has
research support from the Japanese Ministry of Health, Labor, and Welfare.
YK has received research support from the Japanese Ministry of Health,
Labor, and Welfare, Japan Science and Technology Agency, CREST, and
received a grant from GlaxoSmithKline, Japan; he has been a speaker for
GlaxoSmithKline, Pfizer, Meiji Seika Pharma, Yoshitomi Pharmaceutical and
Meiji Yasuda Insurance Co. SK has received a grant from GlaxoSmithKline,
Pfizer and Shionogi Pharmaceutical Co. and received research support from
the Ono Pharmaceutical Co.; he has been a speaker for Mochida
Pharmaceutical, Astellas, GlaxoSmithKline, Asahi Kasei Pharma and Mitsubishi
Tanabe Pharma Co.
Received: 12 April 2012 Revised: 14 September 2012
Accepted: 11 October 2012 Published: 28 October 2012
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Cite this article as: Usuki et al.: Potential impact of propofol
immediately after motor vehicle accident on later symptoms of
posttraumatic stress disorder at 6-month follow up: a retrospective
cohort study. Critical Care 2012 16:R196.
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