Electroconvulsive Therapy for Traumatic Memories: A Randomized Controlled Clinical Trial
Phase: NA
Conditions: Post Traumatic Stress Disorder, Depression
Sponsor: Centre for Addiction and Mental Health

       
 
 
 
 
 
 
 
 
 
 
ECT for Traumatic Memories: A Randomized Controlled Clinical Trial 
 
 
PROTOCOL 
 
 
 
 
 
Electroconvulsive Therapy for Traumatic Memories: A Randomized Controlled Clinical Trial
PROTOCOL
Date: Sept 30, 2016

ECT for traumatic memories: an RCCT                                                                                     Albert Wong 
2 
 
Summary 
 
Specific Aim: The goal of this trial is to test whether electroconvulsive therapy (ECT) can 
reduce the intensity and distress caused by traumatic memories, when administered immediately 
after reactivation of those memories.  
Background: Traumatic events contribute to the genesis of disorders such as post-traumatic 
stress disorder (PTSD) and depression, and memories of the event can cause ongoing distress. 
Short-term episodic memories are encoded by the hippocampus and gradually become 
consolidated through reciprocal connections with the cortex, resulting in long-term memories 
being stored in a distributed network throughout the cerebral cortex. There are no effective 
treatments currently for specifically targeting traumatic memories and reducing the distress they 
cause.  
ECT is the most effective treatment for improving mood in patients with depression and 
there is new evidence emerging that suggests ECT can also improve PTSD symptoms 
independently of co-morbid depression. In addition, the main side-effect of ECT is memory loss, 
specifically for autobiographical details surrounding the course of ECT, but not typically 
affecting long-term episodic memory, nor procedural memories. Memories stored in the 
hippocampus are vulnerable to disruption by ECT because they rely on synaptic changes that are 
mediated by relatively unstable modifications in AMPA receptor and metabotropic glutamate 
receptor density. We propose to exploit this feature of ECT, which normally is considered an 
undesirable side-effect of treatment, in an attempt to selectively reduce traumatic memories and 
the distress associated with them.  
Our hypothesis is in part based on a recent study that demonstrated that ECT can 
significantly disrupt the recall of an emotionally aversive story if it was re-activated immediately 
before each ECT treatment session. (The difference between that study and our proposal is that 
the stories in that study were created by the experimenters and were not part of the subjects’ real 
life experience.) Moreover, there is good evidence in the literature that the physiological 
responses to the recall of a traumatic memory can be halted if intervention occurs immediately 
after the trauma itself: the administration of propranolol in one trial given during traumatic 
memory reactivation was sufficient to reduce autonomic responses to the traumatic memory one 
week later. Therefore, we want to test if reactivation of traumatic memories coupled with ECT 
treatment can similarly reduce the effect of those memories in PTSD patients. 
Methods: We propose to recruit 40 CAMH patients referred for ECT, who also have traumatic 
memories that are causing distress. These patients will be asked to write two narratives, one of 
the traumatic memory, and the other of a trivial, non-traumatic remote event. Patients will then 
be asked to listen to an audio recording of either the traumatic memory or the neutral memory 
(control group) immediately before their ECT sessions. The severity of the traumatic memory-
related symptoms will be assessed before and after the course of ECT using the Modified PTSD 
Symptom Scale (MPSS-SR) and the Clinician Administered PTSD Scale for DSM-5 (CAPS-5). 
Data will be analyzed by comparing the change in overall MPSS-SR scores and CAPS-5 scores 
pre- and post-ECT between the experimental and control groups.  
Expected outcome: We predict that patients with traumatic memories who hear a narrative of 
their traumatic memory immediately before ECT will experience a significant reduction in 
distressing symptoms related to the traumatic memory, compared to patients who hear a neutral, 
non-traumatic memory. 

ECT for traumatic memories: an RCCT                                                                                     Albert Wong 
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Significance: This study will demonstrate, for the first time, the efficacy of a treatment 
specifically targeted at reducing the intensity of traumatic memories, and the distress they cause. 
ECT for Traumatic Memories: A Randomized Controlled Clinical Trial 
 
Hypothesis  
This proposal will test the hypothesis that the reconsolidation of traumatic memories can be 
disrupted by ECT, when administered immediately after re-activation of the traumatic memory 
through listening to a recorded description of the subject’s own trauma. 
 
Specific Aim 
The specific aim of this proposal is to perform a randomized controlled clinical trial with patients 
receiving ECT who have distressing traumatic memories, including patients with or without 
psychiatric comorbidities. The specific intervention to be tested is reactivation of the traumatic 
memory 15 minutes before each ECT treatment, compared with control subjects who will instead 
reactivate a neutral, non-traumatic memory.  
 
Background 
Epidemiology of PTSD 
 
PTSD was originally described in soldiers exposed to horrific battlefield events, but the 
conception of psychological trauma has since been expanded to include any life or limb-
threatening events in either the military or civilian population. PTSD symptoms include 
flashbacks and nightmares of the traumatic event, avoidance of reminders of the trauma, negative 
mood or thoughts including blaming oneself for the trauma, withdrawal from previous interests 
and feeling detached. Hyperarousal is also common, and manifests as irritability, poor 
concentration, insomnia, hypervigilance and being easily startled (American Psychiatric 
Association, 2013).  
 
PTSD affects up to 18% of military combat veterans (Lawson, 2014), with about the 
same percentage (19%) of victims of physical assault similarly affected (Johansen et al., 2013). 
Approximately 2% of US military personnel report having PTSD symptoms (Smith et al., 2009). 
There is considerable overlap in symptoms between patients with Major Depressive Disorder (or 
simply depression) and PTSD (Gros et al., 2012). The majority of PTSD patients have a co-
morbid psychiatric diagnosis, most commonly depression (Brady et al., 2000). Patients who 
engage in deliberate self-harm are also likely to have had a history of trauma and current PTSD 
and depression symptoms (Jaquier et al., 2013).  
 
Existing treatments for PTSD 
 
The most effective current treatment for PTSD is cognitive-behavioural psychotherapy, 
with an average effect size of 1 to 1.27 (Cohen’s d on the Clinician-Administered PTSD Scale or 
CAPS) (Jonas et al., 2013), depending on the specific type of CBT. Exposure therapy is the most 
effective, and is aimed at desensitizing the patient to cues related to the traumatic even through 
gradual and repeated exposure. Cognitive restructuring consists of identifying and modifying 
cognitive distortions of the trauma, while stress inoculation training consists of teaching 
techniques to reduce anxiety and improve coping skills. In general, clinical trials assessing 
psychological treatments for PTSD have been of low quality (Bisson et al., 2013). However, 
there is some evidence to support that trauma-focused cognitive behavioural therapy, eye 

ECT for traumatic memories: an RCCT                                                                                     Albert Wong 
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movement desensitisation and re-processing, and non-trauma-focused cognitive behavioural 
therapy can be helpful for PTSD symptoms (Bisson et al., 2013).  
 
Medications are generally less effective than CBT, with an effect size about half that of 
CBT (Jonas et al., 2013). There are only two medications currently approved by the U.S. Food 
and Drug Administration (FDA) for the treatment of PTSD: sertraline and paroxetine, both of 
which are selective serotonin re-uptake inhibitor antidepressants. A recent Cochrane Database 
systematic review evaluated combined therapy and medication treatment for PTSD. “There is not 
enough evidence available to support or refute the effectiveness of combined psychological 
therapy and pharmacotherapy compared to either of these interventions alone. Further large 
randomised controlled trials are urgently required” (Hetrick et al., 2010). All the trials surveyed 
consisted of combined SSRI and cognitive behavioural or exposure-based interventions.  
 
A significant proportion of patients with PTSD have spontaneous remission of symptoms, 
depending on a number of factors, such as the nature of the trauma and the time interval since the 
trauma (Morina et al., 2014). Despite the treatments reviewed above, overall functioning and 
outcomes for patients with PTSD remains poor (Murdoch et al., 2011). The presence of PTSD 
significantly reduces the rate at which patients suffering physical traumatic injury can return to 
work (Zatzick et al., 2008). Stable remission of chronic PTSD is rare (Shalev, 2009), and thus 
there is a need for additional and better treatments for PTSD symptoms.  
 
Emerging new treatments for PTSD 
 
Several experimental treatments for PTSD that are relevant to this proposal include 
prazosin, D-cycloserine and propranolol. Prazosin reduced the psychological distress induced by 
a trauma-related word list when given during the day in addition to a bedtime dose to suppress 
trauma-related nightmares (Taylor et al., 2006). D-cylcoserine activates the glycine binding site 
at the NMDA receptor that enhances channel opening in addition to glutamate. D-cycloserine 
can enhance extinction of fear memories in rodents. It is also able to amplify the effects of 
exposure therapy in patients with phobia (Ressler et al., 2004), and thus has promise as an 
adjunctive treatment for PTSD (Choi et al., 2010). Propanolol has been shown to reduce both 
consolidation and reconsolidation of emotional memories such as words with negative valence, 
stories and cued fear responses (Lonergan et al., 2013). There is good evidence that propranolol 
can reduce the physiological responses to the recall of a traumatic memory if administered 
immediately after the trauma itself. There is one clinical trial with propranolol given during 
traumatic memory reconsolidation (Brunet et al., 2008). In that small study of 9 propanolol and 
10 control subjects, one reactivation session with a traumatic script, followed by a single dose of 
propanolol was sufficient to reduce autonomic responses to the traumatic memory one week 
later. However, the data supporting these novel pharmacological treatments remains preliminary, 
and there are no definitive clinical trial results available. It is likely that no single new treatment 
will be effective in every patient. It would be prudent to explore a number of different 
therapeutic approaches to optimize overall outcome for patients with PTSD symptoms. 
 
Memory consolidation, reconsolidation and ECT 
 
Short-term episodic memories are stored first in the hippocampus, which makes 
reciprocal connections throughout the cerebral cortex. Over time, memories that are retained 
become increasingly dependent on these cortical areas for maintenance (Frankland and 
Bontempi, 2005). This process is referred to as memory consolidation, which in addition to 
changing the physical location of the memory, also involves different cellular and molecular 

ECT for traumatic memories: an RCCT                                                                                     Albert Wong 
5 
 
mechanisms of memory storage than short-term memories (McGaugh, 2000). Protein synthesis 
and the modification of synaptic connections is required for establishing long-term memories 
(Kandel, 2001), while short-term memories are stored by more rapid modifications of AMPA 
receptor expression and glutamate release (Kauer and Malenka, 2007). Protein synthesis 
inhibitors and ECT can both disrupt consolidation of memories (Frankland et al., 2004; Fraser et 
al., 2008). When a memory is retrieved in the present, it again becomes liable to disruption by 
the same interventions that impair consolidation (Nader et al., 2000; Kroes et al., 2014). Thus, 
re-activated memories undergo a reconsolidation, or updating consolidation when new 
information modifies the original memory (Rodriguez-Ortiz and Bermúdez-Rattoni, 2007). 
 
The encoding of traumatic memories can be modeled in rodents using fear conditioning 
paradigms. These procedures pair the delivery of an unconditioned fear-inducing stimulus like a 
mild foot shock, with a conditioned stimulus such as the context of a particular cage, or a 
discrete stimulus such as an auditory tone or flashing light. Using this kind of behavioural 
paradigm, it is now known that specific neurons in the amygdala encode specific fear-context 
associations in a CREB (cAMP response element-binding protein)-dependent manner (Han et al., 
2007), and that removal of these neurons is sufficient to permanently erase the fear memory (Han 
et al., 2009). Thus, if the neurons encoding a specific memory trace can be targeted for a 
memory disrupting intervention, it is possible in principle to selectively reduce or remove that 
particular memory. The reconsolidation of an aversive memory was successfully impaired using 
localized intracranial electrical stimulation in the rat (Stehberg et al., 2009). The methods used 
experimentally in animals are of course not suitable for human clinical use, but ECT is an 
existing clinical treatment that has powerful effects on memory.  
 
ECT is the most effective treatment for depression, and the evidence for this comes from 
many well-designed, high-quality randomized clinical trials (Eranti and McLoughlin, 2003; UK 
ECT Review Group, 2003). There is a case report (Helsley et al., 1999), a retrospective chart 
review (Watts, 2007) and an open clinical trial (Margoob et al., 2010) suggesting that ECT can 
improve PTSD symptoms independently of co-morbid depression. However, none of those 
studies used a memory re-activation strategy, nor were they prospective randomized clinical 
trials. The main side-effect of ECT is memory loss, specifically for autobiographical details 
surrounding the course of ECT, but not typically affecting long-term episodic memory, nor 
procedural memories (Fink and Taylor, 2007). Here we propose to exploit this feature of ECT, 
which normally is considered an undesirable side-effect of treatment, in an attempt to selectively 
reduce traumatic memories and the distress associated with them. A recent paper demonstrated 
that ECT can significantly disrupt the recall of an emotionally aversive story only if it was re-
activated immediately before each ECT treatment (Kroes et al., 2014). The control comparison 
was a similar, but not re-activated memory of a different story. Both stories were created by the 
experimenters and were not part of the subjects’ real life experience, which is the main 
difference between that study and this current proposal.  
 
Standard care and treatment milieu for study patients 
 
Subjects for this study will be recruited from the Women’s Inpatient Unit on the 9th floor 
of the Centre for Addiction and Mental Health, College Street site (9-WIU). 9-WIU is a short-
stay 18-bed inpatient unit for women with severe mental illness or mood and anxiety disorders 
who may have experienced trauma (childhood sexual, physical and emotional abuse and/or 
sexual or physical assault in adulthood) and /or addiction. Individualized treatment includes 

ECT for traumatic memories: an RCCT                                                                                     Albert Wong 
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assessment, diagnostic clarification, stabilization, focused treatment interventions and facilitation 
of community linkages.  
 
9-WIU provides treatment based on the Sanctuary model of care, in which all staff are 
trained in trauma informed care and use dialectic behavioral therapy principles. 9-WIU is rated 
as a stage 1 trauma treatment program. Most admissions come from the emergency department 
and the prime goal of the admission is to have patients attain stability. Developing the patient’s 
narrative is part of the work that is done in the inpatient 9-WIU setting. As a starting point, 
patients are asked to just list their traumatic memories and experiences. The most bothersome 
memory is then suggested to be described in some detail. Patients are assessed for safety 
throughout this process, are supported and validated. Their thoughts and feelings around the 
trauma are encouraged to be expressed. There is evidence that writing about emotional or 
traumatic experiences can be helpful in a number of mental health domains (Pennebaker, 1997). 
  
Since the patients are already reflecting and thinking about their traumatic experience(s) 
as part of their treatment, involvement in this study should not generate additional stress. 
However, trained staff from 9-WIU will be available at all times, in case the process of writing a 
detailed narrative of the traumatic experience(s) or listening to the recording is found to be 
distressing. Having a staff member from 9-WIU present during the process will help support the 
patients, as well as assess their safety. If at any time the staff from 9-WIU believes a patient is 
too distressed or unsafe to continue in the study, the patient will be removed from the study.  
 
Trial design 
 
We propose a randomized controlled trial in which 40 patients referred for ECT who also 
have distressing traumatic memories will be invited to participate. Subjects meeting the inclusion 
criteria below will undergo a structured evaluation of their diagnosis using the MINI, and 
quantification of their trauma-related symptoms using the scales listed below, both before and 
after their course of ECT, will be done. To re-activate the traumatic experience(s), we will be 
using script-driven imagery (SDI), a method previously used to study or treat PTSD (Pitman et 
al., 1987; Rauch et al., 1996; Isserles et al., 2013). Each subject will be asked to complete a 
script preparation form, which includes a section for describing the traumatic experience (or the 
most traumatic experience) as well as a list of physical symptoms that may have accompanied 
the experience. Subjects will then complete this same form again, however this time describing a 
neutral experience.  
 
Each patient’s script will be prepared according to a published procedure (Pitman et al., 
1987). The script will be approximately 30 seconds in length, written in second person and 
present tense, and will incorporate 5 of the physical symptoms selected by the patient. A CAMH 
clinician from 9-WIU who is not directly involved in the study will record the scripts in a neutral 
voice. The two recordings will be randomly labeled as “A” or “B” by the individual who 
recorded the scripts. Subjects will then be randomized to either group A or B, and will then be 
asked to listen to the recording immediately before each ECT treatment session. The study 
personnel are thus blind to the intervention group (re-activation of the traumatic memory vs. re-
activation of a non-traumatic memory). The subjects themselves will not be blind to the 
intervention being investigated since they must actively listen to the script describing the 
traumatic or non-traumatic event.  
 
Traumatic memory-related symptoms will be assessed with the Modified PTSD 
Symptom Scale (MPSS-SR) and the Clinician Administered PTSD Scale for DSM-5 (CAPS-5). 
The MPSS-SR is a 17-item self-report measure that assesses the DSM-III-R symptoms of PTSD, 

ECT for traumatic memories: an RCCT                                                                                     Albert Wong 
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and it is a modification of the PTSD Symptom Scale (PSS). The MPSS-SR records symptoms 
that are not specific to a particular traumatic event and includes severity ratings in addition to the 
PSS frequency ratings for each item. This is useful for our study, as subjects may have single or 
multiple event traumas. The MPSS-SR can be used to assess response to treatment in its total 
score or its sub-domain scores (re-experiencing; avoidance-numbing and hyperarousal). It can 
also be used to make a preliminary determination of the diagnosis of PTSD using dichotomous 
scoring. We have chosen a MPSS-SR re-experiencing score (items 1-4, 17) cut-off score of 20 
since 23 on this subset of items is the approximate threshold for a PTSD diagnosis. We are 
attempting to select patients who have definite re-experiencing symptoms of trauma, but who 
may not necessarily meet the formal criteria for PTSD.  
  
The Clinician-Administered PTSD Scale for DSM-5 (CAPS-5) is a 30-item semi-
structured interview that is used to make a current (past month) or lifetime diagnosis of 
posttraumatic stress disorder (PTSD) and to provide a continuous index of PTSD severity. It also 
can be used to assess PTSD symptoms over the past week. In addition to assessing the 20 DSM-5 
PTSD symptoms, questions target the onset and duration of symptoms, subjective distress, and 
impact of symptoms on social and occupational functioning, improvement in symptoms since a 
previous CAPS administration, overall response validity, and features for the dissociative 
subtype (depersonalization and derealization). Administration requires identification of an index 
traumatic event to serve as the basis for symptom inquiry. The Life Events Checklist for DSM-5 
(LEC-5, see Trauma Adversity and Exposure) is recommended prior to the Criterion A inquiry 
included in the CAPS-5. Standardized questions and probes are provided for each symptom. 
 
Subjects 
 
Patients with depression and traumatic memory symptoms who have been approved for 
ECT treatment at CAMH will be screened for eligibility to participate in this study. Patients must 
be adults (aged 18+), be capable of informed consent, and be approved for ECT treatment 
according to standard clinic procedures, through a formal consultation with an ECT psychiatrist 
and an anesthesiologist on the ECT service. Other psychiatric diagnoses are not part of the 
inclusion criteria, but will be assessed and recorded. 
 
Inclusion criteria:  
1) Patient referred and accepted for ECT treatment at CAMH 
2) Presence of traumatic memories 
3) Able to write about their traumatic experience(s) 
4) Capable of informed consent to participate in this study 
5) Age 18 or greater 
6) MPSS-SR re-experiencing score (items 1-4, 17) ≥ 20  
 
Exclusion criteria: 
1) History of neurological or developmental disorder, including seizures 
2) ECT treatment already started 
 
Recruitment 
 
After approval to proceed with ECT has been granted, the ECT or 9-WIU staff will 
identify potentially eligible subjects. During the consultation with the ECT psychiatrist, it is 
standard practice to mention studies that are currently being conducted in our clinic, including 

ECT for traumatic memories: an RCCT                                                                                     Albert Wong 
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magnetic seizure therapy (MST) or transcranial magnetic stimulation (TMS) studies. Similarly, 
the consulting psychiatrist may describe this ECT-PTSD study to the patient and ask if they are 
interested in participating. If the patient expresses interest, the ECT clinic or 9-WIU staff will 
then notify the graduate student assigned to this study, who will approach the patients to ask 
whether they might be interested in participating.  
 
Study visits and schedule 
Visit 1: Patients will be screened for eligibility and consent obtained. If eligible and enrolled, the 
patient will be asked to complete the MINI, the Modified PTSD Symptom Scale (MPSS-SR) and 
the Clinician Administered PTSD Scale for DSM-5 (CAPS-5). Subjects will also be asked to 
write two script preparation forms, with instructions to write an approximately one-page 
recounting of:  
(1) the most problematic and prominent traumatic memory on one piece of paper, and  
(2) a neutral, non-traumatic memory of no emotional significance on the other paper.  
Patients will also be asked to identify physical symptoms associated with both of the narratives 
described. Trained staff from 9-WIU will be available at all times, in case the process of writing 
a detailed narrative of the traumatic experience(s) is found to be distressing. The non-traumatic 
memory will consist of a description of a typical and unremarkable sequence of events, such as 
the patient’s morning routine (e.g. a narrative of making breakfast and personal hygiene 
procedures). A study investigator will then transform the subject’s written descriptions into about 
125 word long “exposure scripts” in the second person, present tense. These exposure scripts will 
be then given to a CAMH clinician from 9-WIU not directly involved in the study, who will 
record the scripts in a neutral tone. The same CAMH clinician will narrate all the recordings in 
order to standardize the scripts in tone and length. All recordings will be approximately 30 
seconds in length and the traumatic script will include five of the physical symptoms described 
by the patient. The script recording is preceded with short instructions for the subject to 
concentrate on the script and to imagine the described experience for additional 30 seconds right 
after the script until a short beep sounds. Each recording will be stored as an MP3 file and 
labelled randomly as “A” or “B” and with the patient’s study identifier number. This process will 
help to maintain anonymity for the subjects and also blind the research team to the content of the 
recordings. No other subject identifiers will be stored on the MP3 player. 
 
Each patient will then be randomized to listen to either recording A or B for the duration of the 
study. 
 
ECT session visits: Approximately 15 minutes before each ECT treatment session, subjects will 
be asked to sit briefly in an assessment room in the Brain Stimulation Clinic with a member of 
the research or clinical team. The researcher will go over the protocol, and answer any questions 
the subject may have. When the subject enters the treatment room, they will be handed an MP3 
player with either recording A or B, depending on the intervention group. The patient will have 
several minutes to listen to the recording while the standard pre-ECT procedures are conducted. 
Subjects will have the option to use their own headphones, plugged into the study MP3 player, or 
will be provided with headphones. Trained staff from 9-WIU will be available during the process 
of script driven imagery. ECT will then proceed as usual.  
 

ECT for traumatic memories: an RCCT                                                                                     Albert Wong 
9 
 
Visit 2: Subjects will complete the MPSS-SR and the CAPS-5 again, immediately after the last 
ECT treatment session. This should take about 45-60 minutes. 
 
Visit 3, three-month follow-up: Subjects are asked to complete the MPSS-SR and the CAPS-5 
again. This should take about 45-60 minutes. 
 
The study will not interfere with standard of care in any way. Patients will come to the ECT 
sessions as they normally would and after listening to the recording, ECT will proceed as usual. 
All staff will be blind to the intervention group, including the physician overseeing the patient’s 
ECT treatment. 
 
 
Data analysis plan 
 
The change in MPSS-SR scores and CAPS-5 scores between subjects reactivating the 
traumatic memory and subjects reactivating the non-traumatic memory will be compared with a 
repeated measures ANOVA, after testing for normal distribution of the data using the Shapiro-
Wilk test. Based on the reported effects of ECT on memory reconsolidation (Kroes et al., 2014), 
and the magnitude of other treatment effects on the psychological distress associated with 
traumatic memories (Taylor et al., 2006), we estimate that 15 patients in each group should be 
sufficient to detect significant effects of memory reactivation before ECT. Kroes et al. found 
significant effects of ECT on memory reconsolidation with 13 subjects per group. Thus, we aim 
to recruit a total of 40 patients for this study (20 per group), with the expectation that at least 30 
will complete the entire protocol. ECT variables might affect the outcomes, and we will collect 
data on the number and type of ECT treatments, the frequency of ECT visits, seizure duration 
and anesthetic medication doses, to be included as covariates in our statistical analyses. 
 
Significance and Impact 
 
If successful, this study has the potential to contribute very significantly to the 
understanding of PTSD, and to advance the treatment of this important psychiatric disorder. The 
traumatic memory reactivation procedure is a very feasible and practical intervention that could 
easily and quickly be translated into clinical practice. The effect of memory reactivation in 
combination with ECT would also advance our general understanding of traumatic memory and 
memory reconsolidation. This knowledge will help in the exploration of other PTSD treatments 
aimed at disrupting traumatic memories through exploiting the reconsolidation mechanism. 
 
 
 
 

ECT for traumatic memories: an RCCT                                                                                     Albert Wong 
10 
 
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ECT for traumatic memories: an RCCT                                                                                     Albert Wong 
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