PRIVATE: HOMEPAGE
ECT: Life saving or brain frying?!
The aims of our SSC2a website are:
1. To gain a brief understanding of the history of ECT and the legal process.
2. To explore the theories surrounding the mechanism of action of ECT.
3. To examine the potential side effects of ECT.
4. To see whether ECT remains a viable mode of treatment for depression and its
efficacy versus pharmacotherapy.
5. To compare the efficacy of right unilateral versus bilateral ECT.
This site is made by a group of University of Edinburgh medical students who studied
this subject over 10 weeks as part of the Student Selected Component.
This website has not been peer reviewed.
We certify that this website is our own work and that we have authorisation to use all
content (e.g. figures/images) used in this website.
We would like to thank our tutor Dr Zara Bagot for her help and support with this
project.
Total Website Word count: 9729
Word count minus appendices: 5420
PRIVATE: A BRIEF HISTORY OF ECTThe history of electroconvulsive therapy (ECT) is convoluted and disputed; there is
no clear starting point. As with many areas of medical research, a universally agreed
consensus as to the the original founder simply does not exist. [1]
The idea of inducing seizure to treat psychiatric illness was introduced years before
using electricity was considered. Manfred Sakel and Ladislas Meduna developed
insulin and cardiozol shock therapy respectively. Although both were designed to
induce epileptic seizures and were developed around the same time in the 1930s, the
psychiatric community was more receptive to Meduna’s method as it was not as
costly nor as dangerous and Sakel’s.[2]
In 1934, Meduna began administering camphol to induce seizures, though he quickly
moved on to cardiozol as it was faster acting with fewer side effects – although these
did include joint dislocation and vertebral fractures.[3] In later years, barbiturates,
sedatives and EEG were used to counteract and monitor these.[4] Despite unconvincing
results, he continued his work due to a belief in a biological antagonism; a sort of
protective factor between epilepsy and schizophrenia. Eventually he concluded that
his treatment merely sped up recovery in acute cases, which generally had good
prognoses anyway.
In the following years, it became clear that affective disorder was in fact a far better
indication for shock therapy.[3]
In 1935, Ugo Cerletti was elected chair of psychiatry at the University of Rome. He
opened a clinic, dedicated entirely to the research of modern treatments. It was here
that both insulin and cardiozol therapy continued to be researched, soon leading to the
introduction of electricity to induce seizures. Experiments were carried out on animals
for almost two years, before Professor Lucio Bini, a student of Cerletti’s, carried out
the first ever human electroconvulsive therapy experiment in 1938.[2]
According to Bini’s notes, the patient was shocked 3 times, finding it unpleasant and
resisting treatment on the third attempt.[5] One of the students who witnessed the
experiment, Ferdinando Accornero, stated that the patient was initially passive and
showed no emotion. Following treatment he seemed more interested in his
surroundings and became clear-headed and healthy.
There are reports that this story may not be true, and that in fact it took several failed
attempts to achieve this success. This would explain why, in Accornero’s account, the
patient was shouting not to administer “the deadly shake”, as if he already knew what
was coming.
Regardless of this, the experiment was announced as a success and many models of
the Cerletti-Bini ECT machine were sold worldwide, leading to its use in a vast
selection of mental illnesses.[6,7]
However, by the late 1950s ECT had been largely discontinued in favour of new
psychotropic drug treatments which were easier to administer.[7]
Despite the steep decline in ECT use, a few scientists persisted with studies,
comparing it with these new drugs. Some found that ECT could be used where the
patient did not respond adequately to pharmacotherapy.[8]
As a result, it began to reappear in the mid-1970s, triggering a significant backlash,
led in particular by the newly founded Church of Scientology. Media portrayal of
ECT, such as in the film One Flew Over the Cuckoo’s Nest further aggravated the
situation, leading to serious legal restrictions on the use of ECT.[7]
The controversy surrounding ECT, created in part by the media and the uncertainty of
its mechanism of action, continues to this day. Despite this, ECT is still a highly
effective and relevant treatment. It will likely remain so as it continues to be fine-
tuned and tailored to fit specific patient needs.[9,10]
Word count: 595
PRIVATE: PATIENT JOURNEY
THROUGH ECT AND THE
ASSOCIATED LAW
Electroconvulsive therapy is usually done of a course of two treatments per week over
6 weeks, giving 12 treatments in total. On the day of ECT, the patient is taken to the
waiting room (Fig. 1) by their nurse and is met by the lead ECT nurse who will
perform a routine physical check, including questions about when they last ate, if they
have any false teeth, and if they have any other physical conditions. They will also
check the patient is still consenting, should they be an informal patient.
Once this is done, the patient is then taken into the ECT suite (Fig. 2) and laid down
on a bed where they are given Propofol (a general anaesthetic) and Suxamethasone (a
muscle relaxant) so that they don’t feel the shock or hurt themselves by convulsing
too violently. The psychiatrist places 5 EEG electrodes on the patient’s head to allow
for seizure monitoring. Once the patient is asleep, the psychiatrist places the ECT
electrodes, which have conductance gel on them, either bitemporally – to give
bilateral, or more unusually on the same side of the head, with one electrode at the
temporal region and the other over the posterior lobe – to give unilateral. The ECT
machine is then activated and an electric shocked given through the electrodes. If it is
the patient’s first session then the psychiatrist will need to titrate the dose by applying
up to 3 shocks of increasing voltage to determine a seizure threshold, with a seizure
ideally lasting between 20 and 50 seconds[11]. To monitor for seizure length, the ECT
machine will provide a print out of the EEG recording as soon as the shock has been
administered, and any witnessed convulsion objectively measured in seconds via a
stopwatch.
Once the patient has received their treatment, they are taken into the recovery room
(Fig. 3) where further physical observations are taken as they come round from the
anaesthetic. They will remain in the recovery room until staff are happy for them to
return to the ward.
The following flow charts demonstrate what happens on the legal and ethical side of
ECT when a patient is being considered for treatment.
T2-4 refer to treatment forms that need to be filled in if treating anyone under the
Mental Health act.[12,13]
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PRIVATE: THE MECHANISM OF
ACTION OF ECTWhen considering the mechanism of action of ECT there has been very little
conclusive evidence established, and so it has become widely accepted that the
therapeutic mechanisms involved in ECT are simply unknown. The issue with this is
that it makes it very easy to neglect the theories that have been established thus far
and the findings from various seminal studies that have been carried out with the aim
of validating these theories.[14]
By collating the findings of each of these seminal studies, the wider theory of the
mechanism of action of ECT has been hypothesised by Andrade:
Delivery of a small but adequate dose of electricity to the brain results in the
elicitation of seizure activity in the brain; higher electrical doses elicit a better quality
of seizure.
The seizure releases a large number of signalling chemicals that, in turn, produce
changes on the surface and then within nerve and glial cells in target areas of the
brain such as the hippocampus, amygdala, and prefrontal cortex.
Genes in these cells are activated or suppressed, which in turn leads to increase or
decrease in the number, activity, and connectivity of these cells.
Increased number and connectivity of cells in the hippocampus and prefrontal cortex
probably improve thinking and coping abilities, whereas decreased number and
connectivity of cells in the amygdala reduce negative emotions attached to unpleasant
memories; both effects can be expected to be therapeutic in depressed patients.
The time course of recovery from depression seems to parallel the time course of
occurrence of these cellular changes.[15]
Generalised Seizure Activity
This explanation reflects the findings of a significant number of seminal studies
carried out to date. The studies mentioned by Scott (2011) identified that generalised,
symmetrical seizure activity, reaching cortical and subcortical regions of both
hemispheres, is a crucial therapeutic mechanism in ECT. The induction of the seizure
was shown to have significant bearing on its generalization.[14] In Malitz (1986), an
investigation was conducted using the xenon inhalation technique to measure regional
cerebral blood flow in 32 depressed inpatients referred for ECT. The rCBF
measurements were taken 25 minutes before and 50 minutes after a single ECT
session. It was found that rCBF flow was generally reduced following ECT, and that
whilst bilateral stimulation resulted in symmetrical reduction, the reduction of rCBF
following threshold right unilateral ECT was restricted to the right hemisphere.[16]
Therefore threshold bilateral seizure induction was found to be more effective than
unilateral, because it led to more symmetrical seizure activity and so a greater rate of
recovery/remission.[14] However, these finding are only preliminary and should be
interpreted with caution because there was the possibility of inappropriate funding in
this study and the sample size was small and could be subject to chance effect.
Neuroanatomy and the Generalised Seizure
The therapeutic nature of generalised seizure activity was speculated to be due to the
selective involvement of specific networks of neurons in the propagation of the
seizure activity through the brain matter.[14] A node of particular importance is the
subgenual anterior cingulate cortex, which is one of the largest components of the
limbic system, playing a crucial role in goal-directed behaviours and the modulation
of negative mood states.[14] It has then been found that 4 in 6 patients with treatment-
resistant depression have been found to remit following chronic electrical stimulation
of the left subgenual anterior cingulate cortex, and metabolism of glucose increases in
this region of white matter in correlation with the antidepressant effect of an episode
of ECT.[14]
Role of Neurotransmitter Systems
It has also been found that following an episode of ECT, changes in
neurotransmission occur which are similar to the mechanism of action of
antidepressant drugs. There has been particular reference to the monoamine
hypothesis; that ‘depression is caused by a functional deficit of the monoamine
transmitters, noradrenaline and 5-hydroxytryptamine (5-HT) at certain sites in the
brain'[17] In animal studies it has been found that a single seizure can increase
functional measures of dopamine and, following patient studies, it was found that the
concentration of homovanillic acid, which is a major dopamine metabolite, in patient
CSF increased significantly following eight unilateral ECT sessions.[14]
SPECT imaging techniques have been used in a small sample of drug-resistant in-
patients with primary depressive illness to show that enhanced GABA function is
linked with remission following a course of ECT.[18] However, as this is a small, pilot
study, the findings must be interpreted with caution due to the poor statistical power
of the sample.
It seems to be that the key issues with establishing a mechanism of action of ECT lie
with the poor quality of the investigations carried out thus far. A large proportion of
these investigations are animal studies, and so the implications of the findings in
everyday clinical practice are limited. Where it has been possible to carry out patient
studies, the majority of these investigations have lacked statistical power due to small
participation rates, and so are likely to be influenced by chance effect. Therefore, the
majority of studies carried out to date must be viewed as preliminary and as such
should be interpreted with great caution until further research is able to validate these
findings.
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PRIVATE: INDICATIONS AND
EFFICACY OF ECT
NICE Clinical Guidelines recommend ECT for use in severe depressive illness,
prolonged/severe mania and catatonia.[19] It is recommended as a first-line treatment
only in cases where there is a clear and immediate risk of harm to the patient, such as
in suicidal patients.[19,20]
The guidelines set in 2003 by NICE may be considered to be quite conservative;
indeed they repeatedly specify the need for exhaustive use of antidepressants before
ECT should be considered. In these guidelines they conclude that ECT is not
advisable for use in treatment of schizophrenia, as ‘evidence for the effectiveness of
ECT in schizophrenia in general was not conclusive and therefore ECT is not
recommended’.[19 (p14)] However, some studies[21] have suggested that ECT can be an
efficacious treatment. The American Psychiatric Association’s (APA) guidelines are
more lenient on the matter, and although ECT use in treating schizophrenia is not
standard practice, the APA recommend its use cautiously.[22]
NICE and APA also differ in opinion on whether ECT is contraindicated in pregnancy
and elderly patients or not. NICE recommends caution in its use in these groups,
because complications can be more frequent. However APA considers ECT as safer
than the alternative treatments available.[19,22] The stance of NICE is perhaps justified,
as there have been few studies conducted on the developing brain.[19]
ECT has also been suggested as a treatment for many other psychological disorders,
notably in Multiple Sclerosis and Parkinson’s disease, although this is associated with
greater cognitive impairment, and its use is not as well researched as in other diseases.[20,22]
Indication for ECT in the three conditions listed at the top of the page is not widely
disputed.[19,20,22]
ECT has been shown to be of benefit to people suffering from a depressive illness.
Studies have investigated outcomes of patients with depressive disorders undergoing
real ECT compared with simulated ECT. Patients undergoing simulated ECT received
all the same treatment, including anaesthesia and after care, as those undergoing real
ECT, the only varied factor being the presence or absence of electrical stimulation.
The UK ECT Review Group analysed 6 such trials and found that in all studies real
ECT performed better than simulated ECT (measured using the Hamilton Depression
Rating Scale) in the treatment of depressive disorders. It must be noted however that
in some cases patients undergoing simulated ECT recovered.[23]
One such study looking into the efficacy of real ECT is the Nottingham trial[24]. Using
a double-blind randomised controlled trial, patients were assigned to receive
simulated ECT, bilateral (BL) ECT or right unilateral (RUL) ECT. Although the
initial group of patients referred for ECT was large (n=234) the study proceeded with
69 patients – only 29% of potential candidates. This was due in part to the lack of
consent and also patients not meeting inclusion criteria for the study. The use of strict
inclusion criteria is a blessing and a curse in the study of the effectiveness of ECT.
Although it normalises the group and reduces variables from the study, it also
distances the results from the clinical scenarios in which ECT is prescribed. For
example one of the inclusion criteria for the study was right-handedness. This is
important particularly for the comparison with RUL ECT and is a standard
consideration in neuropsychology, but not all patients with a depressive illness who
are started on ECT are right handed.
Another limitation of the study was that of the 69 participants, 25 received fewer than
6 treatments and so were not considered to have completed the trial (all other data
being analysed after the 6th session of ECT). Of those withdrawn from the study some
were removed due to failure to show any improvement, some because they had
become well, and some for other reasons (withdrawal of consent, physical illness). It
is understandable from an ethical standpoint to remove patients from a trial, as care
and treatment should be the primary concern of their medical practitioner, however I
feel it is a shame, given the nature of the study’s question, to remove candidates for
reasons that would have been of use in the analysis of data. It also cut down the final
number of analysed participants even further.
Despite these limitations the study is able to provide a placebo by which to compare
the effectiveness of ECT, and appears thorough in its attempts to reduce confounding
variables.
The data from the Nottingham trial was then reassessed to consider just those over the
age of 60 years to determine the effectiveness of ECT in older people [25]. The analysis
supported the results found in the Nottingham trial with ECT being more effective
than no ECT. This is important as ECT may be considered the treatment of preference
in older people who may be more sensitive to the side effects of psychotropic
medications. The analysis showed ECT to be effective in older age groups. As these
results were based on the same data as the Nottingham trial they share the same
shortcomings, however the small sample size is even more relevant in this case with
only 23 participants completing 6 sessions of ECT (35 participants over 60 years with
12 withdrawn).
As real ECT has been shown to be more effective than simulated ECT the next
question is to what extent is it effective, how many people benefit from treatment?
The Scottish ECT Accreditation Network (SEAN), which audits all ECT treatment in
Scotland, reported 67% of people undergoing ECT during 2012 showed a “definite
improvement” (>50% reduction in the Montgomery-Asberg Depression Rating Scale
(MADRS)) following a period of treatment, and 64% were rated as “much improved”
or “very much improved” based on the Clinical Global Impression[26]. These numbers
are slightly lower than those reported in previous years (2008-2011) where ≥70% of
patients have shown “definite improvement”. SEAN data also suggests that efficacy
of treatment is proportional to level of illness, with 80% of those who were considered
too ill to have capacity to consent achieving “definite improvement”.
SEAN data is collected for patients of all diagnoses undergoing ECT throughout the
year. The majority of patients undergoing ECT have a depressive disorder and
annually less than 10% of patients receiving ECT were classed as having an illness
other than a depressive illness (e.g. Schizophrenia, Schizoaffective disorder, persistent
affective disorders…etc). As patients representing “other” diagnoses is such a small
group their presence shouldn’t alter the analysis of efficacy of ECT in treating
depression, particularly considering that entrance and exit MADRS scores were used
in determining outcomes.
However, SEAN data is open to bias in that patients undergoing ECT will have been
referred because the consultant in charge of their care has concluded that they may
benefit from ECT.
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PRIVATE: SIDE EFFECTS OF ECTAlthough electroconvulsive therapy is a low risk procedure with very few incidences
of complications,[27] it inevitably brings some unwanted adverse effects. The most
common side effects include general somatic complaints. However there also exists
worry over cognitive impairment.[28]
Memory disturbances often receive the greatest concern when considering cognitive
changes. These involve both anterograde amnesia (loss of ability to create new
memories) and retrograde amnesia (loss of memory access to events before the ECT
episode).[29] While anterograde amnesia often disappears days to weeks after
completion of the ECT episode,[27] retrograde amnesia can persist for longer than four
weeks and is often more for immediate time prior to ECT.[30] Indeed, retrograde
amnesia may never completely resolve despite improvement during the first few
months after ECT.[29] The memory of autobiographical information has been shown to
be less affected by ECT than the memory of events of an impersonal nature.[31] It is
also important to note that self-reports of retrograde amnesia tend to be more highly
correlated with therapeutic outcome than with objective test results.[32]
The mode of delivery of ECT has an impact on the extent of memory impairment, and
the UK ECT Review Group has identified some of these impacts. For example,
bilateral ECT produces greater impairment than unilateral ECT. Treatment three times
a week causes more impairment than bi-weekly treatment, and high dose ECT
produces more impairment than low dose ECT. Despite discussion that sine wave
treatment produces greater memory impairment than brief pulse, the evidence is too
little and insignificant to be confirmed.
In addition to memory dysfunction, postictal (after seizure) disorientation and
interictal (between seizures) confusion can also occur in patients.[28] While the former
is experienced in all patients and lasts from a few minutes to hours, the latter happens
occasionally and rapidly disappears over a period of days following completion of
ECT.
The exact mechanism of how ECT leads to cognitive change is not fully understood.
It was suggested that seizure induced during ECT can lead to neuronal atrophy in the
hippocampus, however, no hippocampal atrophy or cell death was found in patients
receiving ECT in a magnetic resonance spectroscopic imaging (MRS) study.[30]
Headaches, nausea and muscle soreness are frequent side effects of ECT and they
usually last up to several hours.[28] Headaches are believed to be the result of
superficial vasodilation whereas muscle pain is caused by the depolarising action of
muscle relaxant used in ECT. They can be both managed with analgesics for
prophylactic purpose.
Other less common side effects include cardiovascular complication (e.g. cardiac
arrhythmias, ischaemia and hypertension), which can be the main cause of mortality
and serious morbidity with ECT, and of adverse psychological reaction to ECT.[32]
Lastly, there is a small physical risk from having a general anaesthetic, with death or
serious injury occurring in approximately 1 in 80000 treatments. As ECT is given in a
course of treatments, the risk per course will be around 1 in 10 000.[33]
In conclusion, it is worth mentioning that when ECT is used, it usually bears the full
burden of public fear of cognitive effects related to psychiatric treatment, as people
often forget the fact that severe depressive illness and psychotropic drugs can also
affect memory.[32] As a result, any detrimental effects should not be blamed solely on
ECT.
Word count: 549
PRIVATE: ECT VS.
PHARMACOLOGICAL
INTERVENTIONSMost modern research into ECT is centred on its efficacy versus pharmacotherapy
including selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants.
These clinical trials investigate the different modes of treatment and measure their
efficacy through how quickly remission is achieved and how long this period lasts
until relapse. Pharmacotherapy is often used concomitantly with ECT, meaning there
are few trials where ECT is compared against pharmacotherapy alone.
Some trials have concluded that there is no difference in efficacy between
antidepressants and ECT. In 2006, Kellner et al.[34] found that although there was a
trend for patients with continuation ECT to take longer to relapse, it was not
statistically significant.[34] They also found that there was no significant difference in
relapse rates between either the ECT or antidepressant groups, with a rate of 37.1%
and 31.6% respectively.[34] One of the strengths of this trial was its statistical power
due to its large sample size compared to most modern literature with n=148
completers.[34]
However several clinical trials have found ECT to be more efficacious than
antidepressants. One study found that after six weeks, patients receiving ECT had an
average Montgomery-Asberg Depression Rating Scale score 6.6 points lower than
patients receiving pharmacological therapy alone (p=0.002).[35] A weakness of this trial
was the lack of blinding of the psychiatrists involved, which may have caused the data
to be biased. The study was also carried out with a relatively small sample size and it
suffered from a high dropout rate. This means the trial may lack statistical power,
meaning their data is less reliable.
A trial by Folkerts et al.[36] reached a similar conclusion, after results showed that there
was a 59% reduction in Hamilton Rating Scale for Depression scores of patients who
received ECT versus a control (the SSRI paroxetine) and that this effect was greater in
the first three weeks of treatment. [36] However, this effect decreased by the end of the
study period. The design of this trial made the data more reliable. A clear case
definition to identify patients (WHO criteria, Hamilton Rating Scale for Depression
and independent psychiatrists) and a control group were used. [36]
Other clinical trials have shown that ECT combined with pharmacotherapy is more
effective in preventing relapse long term than pharmacological alternatives alone. An
American study found that ‘rates of survival without relapse or recurrence for patients
who received continuation ECT and long-term antidepressant treatment were nearly
doubled (93% versus 52%) at 2 years’.[37]The strengths of this study were the long
follow up time of up to five years and the range of antidepressants ECT was compared
favourably against. These results show how in combination with other treatments,
ECT can prolong remission and prevent relapse in patients in the long term.
One of the main weaknesses of the majority of clinical trials investigating the efficacy
of ECT is that they remain chronically underpowered. As ECT is often used only after
pharmacological intervention has failed, there is only a small population available to
study. In addition to this, the nature of the depressive conditions being studied results
in a high dropout rate, often due to comorbidities. This again causes many studies to
be statistically underpowered meaning their reliability is in question. [35,38] Other
weaknesses of some studies include: self-reporting, a lack of control groups, and poor
randomisation. [35,37–39] This reduces the reliability and reproducibility of many trials’
results.
Another critical weakness of many of the clinical trials is the lack of blinding. The
practicalities of ECT means that it is not always possible to blind patients, therefore
the placebo effect may take place. In some cases weak study design means the
psychiatrists, interviewers and statisticians involved in data collection are not blinded
to the patients’ treatment group. [34,35,38] The lack of blinding at this level may promote
biased results.
Overall, there is evidence to suggest that ECT is effective as an acute treatment of
many depressive disorders.[36] However, it is in combination with pharmacotherapy that
ECT has the best long-term effects in maintaining remission. [40] This is reflected in
clinical practice today, where treatment resistant depression is ideally improved with
ECT, then sustained with pharmacotherapy.
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PRIVATE: UNILATERAL VS
BILATERAL ECTThere have been many discussions and trials trying to determine the efficacy of two
methods of ECT; unilateral and bilateral. The studies we have researched focused on
right sided unilateral (RUL) ECT versus bilateral (BI) ECT. The main difference
between the two treatment methods fall in the placement of electrodes (Figure 1).
One particular study was conducted in Scotland, trying to identify which method of
ECT is most often applied. The results showed that out of the 62% of clinics that
conduct ECT, 79% of them favoured bilateral ECT.[41] The 2003 UK ECT review
noted that BI ECT is moderately more effective, thus clinics tend to favour it, rather
than the less effective, but safer alternative, RUL ECT. [23] However it is important
to note that the stimulus intensities used were combined, including optimal dosages,
which makes the evidence for the advantage of BI ECT inaccurate and dubious.
In 2007, a study by Sackheim and Prudic[42] sought to find the difference in efficacy
and side effects of the two methods. It was discovered that the efficacy of RUL ECT
is contingent on electrical dosage. A higher dosage RUL ECT was considerably more
effective than a low dose. Although the high dose RUL ECT did not match efficacy of
BI ECT, it provided less severe cognitive effects.
After the 6th treatment, both methods of ECT showed superior antidepressant
response. Measured using the Hamilton Rating Scale for Depression (HRSD), both
groups (n=20) showed significant improvements in their rating.[42]
Patients who underwent BI ECT showed 6 times greater prolonged disorientation
compared to the other group who underwent RUL ECT. BI ECT also resulted in
greater amnesia for the recall and recognition of words and geometric shapes. Across
every test of retention of new information, the group for BI ECT had poorest absolute
performance.[42]
The findings in Sackheim's study reflects a similar study conducted in 1984 by
Rosenburg and Pettinati.[43] This study was conducted in largely the same manner as
the 2007 study. Although slightly more BI ECT patients than RUL ECT patients felt
that treatment helped, it was not statistically significant. However, the difference in
memory complaints were apparent. More BI ECT patients were unable to remember
specific sessions, and described general difficulty in remembering things. 62% of BI
ECT compared to 14% of RUL patients complained of memory difficulty.
Although not many studies have been conducted on this topic, the similarities between
the 2 studies, conducted so many years apart, shows that results of the two methods of
ECT have not altered much. However, one major disadvantage faced by all the studies
were the small sample sizes. Small sample sizes increases the risk of false positives
and introduces a chance effect. More studies will have to be conducted, using larger
sample sizes, to see if RUL ECT at optimum or higher doses is as effective, while
retaining better adverse effects. This would greatly influence future prescribing
practices.
Word Count: 498
PRIVATE: CONCLUSIONSDespite being one of the oldest forms of psychiatric treatment, there are still many
unresolved questions regarding electroconvulsive therapy today. It is still unclear how
and why it works, and some argue that it does not in fact work at all. It is also not
agreed in which conditions it should be used, and how to deliver the treatment is still
not clear.
We have been able to gain an understanding of the position of ECT literature, and
hence have been able to reflect upon our aims and objectives set at the embarkment of
our study.
We believe that ECT is still a highly useful treatment of depression, and although its
adverse effects are undeniable and inevitable, they must be compared with the effects
of depressive illness, as well as noting that concomitant antidepressant medication
may be causing any adverse effects present. It can provide rapid recovery for severely
depressed patients, in a far shorter time-scale than antidepressant medications alone. It
is unlikely however, to provide lasting remission, and ECT must therefore be used in
conjunction with antidepressants to prevent relapse. We have found that use of both in
conjunction is far more efficacious than either used alone.
After extensive research we can conclude that there is too little evidence to reliably
support one individual theory for the mechanism of action of ECT, however three of
the more convincing theories have been discussed on our webpage. Discovering the
mechanism of action is of clinical relevance, as it may allow the treatment to be given
more safely, and it may uncover the aetiology of psychiatric disorders. If the
mechanism was understood, stigma towards electroconvulsive therapy may be
reduced also.
Unfortunately, there is a lack of reliable literature upon which to draw conclusions,
and this thwarted our study on several occasions. This does however mean that ECT is
a very relevant area of research. The literature related to ECT is notoriously
unreliable, with small sample sizes and serious design flaws being commonplace. It is
rare to find trials that compare ECT versus placebo and modern ECT research in this
area is constrained by ethical issues.
The debate over whether to administer treatment bilaterally or unilaterally is
especially clinically relevant. There is a lack of reliable patient-based studies
available, and no consensus has been achieved. Other areas require further research,
for example into its mechanism of action, and indeed most areas of research could be
improved with greater sample sizes.
After conducting our research, we support the use of ECT as a treatment for
psychiatric illnesses, especially in treatment of depression. This historic and
controversial treatment remains an efficacious form of therapy, and most likely will
do for the foreseeable future.
Word Count: 451
PRIVATE: APPENDIX 1 –
REFERENCESA Brief History of ECT
1. Berrios G. The scientific origins of electroconvulsive therapy: a conceptual
history. History of Psychiatry. 1997;8(29 pt 1):105-119.
A short article from a reliable journal, giving a brief outline of the key points
in ECT development
2. Passione R. Italian psychiatry in an international context: Ugo Cerletti and the case
of electroshock. History of psychiatry.2004;15(1):83-104.
A more recent article from the same journal, looking at the origins of ECT in
Italy, where many believe the therapy originated.
3. Gazdag G, Bitter I, Ungvari G, Baran B. Convulsive therapy turns 75. The British
Journal of Psychiatry. 2009;194(5):387-388.
A recent anniversary article from a very reliable, British journal. The piece
uses a storyline style approach to explain the journey of ECT from it's
primitive origins, to widespread controversy, to continued use 75 years later.
4. Fink M. Induced Seizures as Psychiatric Therapy: Ladislas Meduna’s
Contributions in Modern Neuroscience. The Journal of ECT.2004;20(3):133-136.
An article detailing the views of Professor Max Fink, a key figure in American
psychiatry, on the contributions of the commonly accepted "founders" of ECT.
5. Bini L. Professor Bini’s Notes on the First Electro-Shock Experiment. The Journal
of ECT. 1995;11(4):260-261.
Professor Bini's original notes from the first use of Electro-Shock therapy in
humans.
6. Aruta A. Shocking Waves at the Museum: The Bini-Cerletti Electro-shock
Apparatus. Medical history. 2011;55(03):407-412.
An article based around the original ECT apparatus, present at the a museum
in Rome. This piece also includes details of an eyewitness account of its first
use.
7. Fink M. Convulsive therapy: a review of the first 55 years. Journal of affective
disorders. 2001;63(1):1-15.
A detailed article by Max Fink, a renowned figure in ECT. It covers the
development of ECT over its first 55 years.
8. Fink M. History of Convulsive Therapies. In: Fink M (ed.) Convulsive Therapy
Theory and Practice. 1st ed. New York: Raven Press; 1979. p. 5-17.
An older article, describing the practice of ECT at that time.
9. Loo C. ECT in the 21st Century: Optimizing Treatment: State of the Art in the 21st
Century. The Journal of ECT. 2010;26(3):157.
A review of ECT as it is in modern times, from a reliable and relevant Journal.
10. Lerer B, Isserles M. From Meduna to ultrabrief: New directions for the oldest
brain stimulation therapy. Brain Stimulation.2008;1(2):84-85.
An article contrasting modern theories and research in ECT to the very first
steps taken by Meduna.
Patient Journey Through ECT and Law
11. Royal College of Psychiatrists’ Special Committee on ECT and related treatments
and Public Education Editorial Board. Information about ECT (Electro-convulsive
therapy).http://www.rcpsych.ac.uk/healthadvice/treatmentswellbeing/ect.aspx
(accessed 10 Oct 2014).
The RCPsych’s webpage on the basic information for ECT
12. Mental Health (Care and Treatment) (Scotland) Act 2003, Part
16. http://www.legislation.gov.uk/asp/2003/13/part/16 (accessed 10 Oct 2014).
The section of the Mental Health Act that applies to treatment of patients under its
jurisdiction.
13. The Scottish Government. Mental Health Treatment
Forms.http://www.scotland.gov.uk/Topics/Health/Services/Mental-Health/Law/
Forms/Treatment (accessed 10 Oct 2014).
A link to all the different forms that may need to be filled in when treating
someone under the MHA.
The Mechanism of Action of ECT
14. Scott AIF. Mode of action of electroconvulsive therapy: an update. Advances in
Psychiatric Treatment 2011; 17: 15-22
A literature review exploring the development of the hypotheses surrounding the
mechanism of action of ECT, developed through the implementation of seminal
studies, animal studies and patient treatment studies.
15. Andrade C. A primer for the conceptualization of the mechanism of action of
electroconvulsive therapy, 2: Organising the Information.The Journal of Clinical
Psychiatry 2014; 75(6): 548-551
A literature review published in the Journal of Clinical Psychiatry, which suggests
how the large quantity of information regarding the mechanism of action of ECT
could be organised to provide more accessible explanations for its therapeutic
nature.
16. Malitz S, Sackeim HA (eds) Electroconvulsive Therapy: Clinical and Basic
Research Issues. Annals of the New York Academy of Sciences1986; 462: 236-248
A collection of relevant academic research articles, which have been explored with
the intent to identify the issues associated with research aimed at establishing a
valid mechanism of action for ECT.
17. Rang HP, Dale MM, Ritter JM, Flower RJ, Henderson G (eds.)Rang and Dale’s
pharmacology. 7th ed. Edinburgh: Churchill Livingston; 2012
A core pharmacological textbook.
18. Mervaala E, Könönen M, Föhr J, et al. SPECT and neuropsychological
performance in severe depression treated with ECT. Journal of Affective
Disorders 2001; 66: 47–58
An observational study employing the use of single photon-emission computed
tomography (SPECT) and comprehensive neurological testing to investigate the
relationship between changes in regional cerebral blood flow and cognitive
behavioural changes, following a single ECT treatment.
Indications and Efficacy of ECT
19. National Institute for Health and Care Excellence (2003) Guidance on the use of
electroconvulsive therapy. NICE. [TA59]. London: National Institute for Health and
Care Excellence.
Guidance on the use of ECT for the NHS. Provides analysis of the evidence for its
indication, and discusses recommendations for further research.
20. Fink M. 6.2.10.1: Electroconvulsive therapy, In: Gelder M, Andreasen N, Lopez-
Ibor J, Geddes J (Eds.) New Oxford Textbook of Psychiatry. 2nd ed. Oxford: Oxford
University Press; 2012. p. 1251 – 1260
Provides an overview of ECT, including history, suggested mechanisms of action,
future use, and focussing especially on its indications.
21. Tharyan P, Adams CE. Electroconvulsive therapy for schizophrenia. Cochrane
Database of Systematic Reviews 2005, Issue 2. Art. No.: CD000076. DOI:
10.1002/14651858.CD000076.pub2.
A Cochrane systematic review of randomised control trials concerning ECT and its
efficacy in schizophrenia.
22. American Psychiatric Association. The Practice of Electroconvulsive Therapy:
Recommendations for Treatment, Training, and Privileging (A Task Force Report of
the American Psychiatric Association). 2nd ed. Washington: American Psychiatric
Association; 2008.
Handbook providing recommendations for the use of ECT in the USA, produced
as a resource for practitioners and trainees in psychiatry and related disciplines. Its
bibliography is an exhaustive search of ECT literature over the decade prior to
publication.
23. UK ECT review group. Efficacy and safety of electroconvulsive therapy in
depressive disorders: a systematic review and meta-analysis. The Lancet [Internet].
2003 [cited 12 October 2014];361(9360):799-808. Available from:
http://dx.doi.org/10.1016/s0140-6736(03)12705-5
Gold standard ECT paper. Meta-analysis bringing together a wealth of information
on various topics related to ECT.
24. Gregory S, Shawcross C, Gill D. The Nottingham ECT Study. A double-blind
comparison of bilateral, unilateral and simulated ECT in depressive illness. The
British Journal of Psychiatry. 1985;146(5):520–524.
Double-blinded randomised control trial. Valuable in that it is an approach that
would be unlikely to get approval in this day and age.
25. O’Leary D, Gill D, Gregory S, Shawcross C. The effectiveness of real versus
simulated electroconvulsive therapy in depressed elderly patients. International
journal of geriatric psychiatry. 1994;9(7):567–571.
A look at the data from the Nottingham trial with a particular interest in efficacy in
those greater than 60 years.
26. NHS Scotland. Scottish ECT Accreditation Network Annual Report 2013
[Internet]. 1st ed. Edinbugh; 2013 [cited 18 October 2014]. Available from:
http://www.sean.org.uk/AuditReport/SEAN-Report-2013-web.pdf
Collection of ECT data from around Scotland during the year 2012
Side Effects of ECT
27. Nuttall G, Bowersox M, Douglass S, McDonald J, Rasmussen L, Decker P et al.
Morbidity and mortality in the use of electroconvulsive therapy. The journal of ECT.
2004;20(4):237–241.
This paper indicates the very low risk of complication from ECT.
28. Mankad M, Weiner R. Adverse effect. In: Mankad M, ed. by. Clinical Manual of
Electroconvulsive therapy. 1st ed. Washington, DC: American Psychiatric Pub.; 2010.
p. 139-148.
It lists some general adverse effects discovered from ECT patients, including
cognitive change and somatic complaints.
29. UK ECT review group. Efficacy and safety of electroconvulsive therapy in
depressive disorders: a systematic review and meta-analysis. The Lancet [Internet].
2003 [cited 12 October 2014];361(9360):799-808. Available from:
http://dx.doi.org/10.1016/s0140-6736(03)12705-5
It compared the extent of memory impairment from different ECT methods.
30. Merkl A, Heuser I, Bajbouj M. Antidepressant electroconvulsive therapy:
mechanism of action, recent advances and limitations. Experimental neurology.
2009;219(1):20–26.
It suggested how ECT could lead to cognitive change in patients.
31. Lisanby S, Maddox J, Prudic J, Devanand D, Sackeim H. The effects of
electroconvulsive therapy on memory of autobiographical and public events. Archives
of General Psychiatry. 2000;57(6):581–590.
It showed autobiographical memory is less affect by ECT than memory of
impersonal memory.
32. Benbow S. Adverse effect of ECT. In: Scott A, ed. by. The ECT handbook. 2nd
ed. London: Royal College of Psychiatrist; 2005. p. 170-174.
It showed some common adverse effect of ECT and suggested the correlation of
the extent of amnesia with different research method.
33. Royal College of Psychiatrists, (2014). Electroconvulsive Therapy (ECT).
[online] Rcpsych.ac.uk. Available at:
http://www.rcpsych.ac.uk/healthadvice/treatmentswellbeing/ect.aspx [Accessed 2 Oct.
2014].
It gives general information about ECT and also side effects of ECT.
ECT vs Pharmacological Interventions
34. Kellner C, Knapp R, Petrides G, Rummans T, Husain M, Rasmussen K, Mueller
M, Bernstein H, O’Connor K, Smith G, Biggs M, Bailine S, Malur C, Yim E,
McClintock S, Sampson S, Fink M. Continuation Electroconvulsive Therapy vs
Pharmacotherapy for Relapse Prevention in Major Depression : A Multisite Study
From the Consortium for Research in Electroconvulsive Therapy. JAMA
Psychiatry 2006;62(12):1337-
1344.http://archpsyc.jamanetwork.com.ezproxy.is.ed.ac.uk/article.aspx?
articleid=209924 (Accessed 11/10/14).
Study had a good sample size and attempts were made to control bias. However
serious flaws in study design remained, so bias may still have affected the results.
35. Schoeyen H, Kessler U, Andreasses O, Auestad B, Bergsholm P, Malt U, Morken
G, Oedegaard K, Vaaler A. Treatment-Resistant Bipolar Depression: A Randomized
Controlled Trial of Electroconvulsive Therapy Versus Algorithm-Based
Pharmacological Treatment. The American Journal of Psychiatry (in advance)
2014.http://ajp.psychiatryonline.org/Article.aspx?ArticleID=1906047(Accessed
11/10/14).
Although the study was representative of the general population, poor blinding and
lack of statistical power means bias and chance may have affected their data.
36. Folkerts HW, Michael N, Tolle R, Schonauer K, Mucke S, Schulze-Monking H.
Electroconvulsive therapy vs. paroxetine in treatment-resistant depression – a
randomized study. Acta Psychiatrica Scandinavica 1997;96(5):334-
42.http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0447.1997.tb09926.x/pdf (Acce
ssed 11/10/14).
Although it was over a short time period, a strong case definition and use of
controls increases the reliability of their results.
37. Gagne G, Furman M, Carpenter L, Price L. Efficacy of Continuation ECT and
Antidepressant Drugs Compared to Long-Term Antidepressants Alone in Depressed
Patients. The American Journal of Psychiatry 2000;157(12):1960-
1965.http://ajp.psychiatryonline.org/article.aspx?articleid=174483 (Accessed
11/10/14).
A long period of follow up, good standardisation of populations and a broad range
of antidepressants were used. However, a lack of randomisation means chance and
confounding may still have affected their results.
38. Nordenskjold A, von Knorring L, Ljung T, Carlborg A, Brus O, Engstrom I.
Continuation Electroconvulsive Therapy with Pharmacotherapy Versus
Pharmacotherapy Alone for Prevention of Relapse of Depression: A Randomised
Controlled Trial. The Journal of ECT 2013;29(2):86-
92.http://journals.lww.com/ectjournal/Fulltext/2013/06000/
Continuation_Electroconvulsive_Therapy_With.3.aspx#R9 (Accessed 12/10/14).
Trial lacked statistical power and was unblinded, therefore data may be affected by
chance.
39. Prudic J, Olfson M, Marcus S, Fuller R, Sackeim H. Effectiveness of
electroconvulsive therapy in community settings. Biological
Psychiatry 2004;55(3):301-312.http://www.sciencedirect.com.ezproxy.is.ed.ac.uk/
science/article/pii/S0006322303010461 (Accessed 12/10/14).
The trial had adequate statistical power, meaning results due to chance are less
likely. However the populations were not standardised between sites.
40. Sackeim H, Dillingham E, Prudic J, Cooper T, McCall V, Rosenquist P, Isenberg
K, Garcia K, Benoit M, Haskett R. Effect of Concomitant Pharmacotherapy on
Electroconvulsive Therapy Outcomes. JAMA Psychiatry 2009;66(7): 729-
737.http://archpsyc.jamanetwork.com/article.aspx?articleid=483117(Accessed
12/10/14).
The study had a large sample size, was a randomised controlled trial and had
suitable blinding. Therefore it is likely that their data and conclusions are reliable.
Unilateral vs Bilateral ECT
41. Brown K. Unilateral and Bilateral Electro convulsive therapy: What informs
Scottish Psychiatry choices? Psychiatric Bulletin2009;33: 95-98.
Statistics on the use of ECT in Scottish psychiatric practices and preference of
bilateral vs. unilateral ECT.
42. Sackheim H, Prudic J, Devanand DP et al. A Prospective, Randomized, Double-
blind comparison of bilateral and right unilateral electroconvulsive therapy at
different stimulus intensities. Arch Gen Psychiatry 2000;57: 425-434.
A study comparing the two methods of ECT we have researched. Results were
used to establish the advantages and disadvantages of each method.
43. Rosenberg J, Pettinati H. Differential Memory complaints after bilateral and
unilateral ECT. Am J Psychiatry 1984;141: 1071-1074.
A study comparing the difference in adverse effects between bilateral and
unilateral ECT.
44. Gregory S, Shawcross CR, Gill D. The Nottingham ECT Study: A Double-Blind
Comparison of Bilateral, Unilateral and Simulated ECT in Depressive Illness. British
Journal of Psychiatry 1985;146: 520–524.
PRIVATE: APPENDIX 2 – GROUP
CRITICAL APPRAISALThe Nottingham ECT Study [44]
Aims of the study
To investigate the efficacy of Electroconvulsive therapy (ECT) and to resolve any
controversy between unilateral and bilateral ECT.
Patient group
564 patients with depression as defined by ICD-9 were admitted to Mapperly Hospital
from 1981-1983. Study criteria were:
Practitioner and patient consent
Right handedness
No severe physical illness
Physician referral
Had received no ECT for this current episode
Met Medical Research Council’s (MRC) criteria for depression of more than 1
month
Patients could not be detained
69 patients were suitable.
Study design
Double blind, randomised controlled trial.
Size of study
Intent to treat n=69. Withdrawals n=25. Completers n=44.
Intervention
Patients were divided randomly into 3 groups; bilateral, unilateral or simulated ECT.
Each received a standardised anaesthetic regime and a standard ECT machine was
used.
51 patients continued to receive benzodiazepines. A few patients remained on lithium,
antidepressants and major tranquilisers as it was deemed unethical to withdraw these.
Randomisation process or blinding
A randomisation process existed, but was not explicitly stated. Patients, Raters and
clinical teams were blind to the treatment group. Patient evaluation did not take place
on day of treatment in an attempt to reinforce blinding.
Statistical tests
Group comparisons:
Student t-test (two tailed)
Chi-square
One way analysis of variants with Scheffe’s Multiple Range test (AOVS) for
continuous variables.
Comparing treatment outcome:
Student t-test (two tailed) – to compare Montgomery – Asberg Depression Rating
Scale (MADRS) scores.
AOVS for continuous variants – To analyse change in MADRS, Hamilton
Depression Rating Scale (HDRS) and Psychological Impairment Rating schedule
(PIRS) scores.
Outcome measure
To compare efficacy of various ECT methods with several depressive scales:
MADRS
HDRS
Behavioural items from PIRS
Present state examination
Percentage change was measured after every 2 treatments, at the end of the trial, and
at 1, 3 and 6 months after the last treatment.
Main results
Real ECT had significantly more improvement in MADRS, HDRS and PIRS
scores compared to simulated ECT.
No significant difference between Unilateral and Bilateral ECT groups.
Bilateral ECT was superior to simulated ECT after 2 treatments, unilateral ECT
took 4 treatments to reach that stage.
Weaknesses – design flaws, sources of bias, confounding factors
Small sample size – increased chance effect and type 1 errors.
Use of Cuff method increases the chance of false negatives. Convulsions do not
always accompany seizure activity.
Confined to Nottingham
Patients were not on standardised medication during the trial – confounding factor
Selection bias:
Practitioners possibly gave consent to patients who would benefit the most from
ECT.
Mapperly Hospital only admitted patients under 65
Only informal patients were included meaning that very unwell and depressed
detained patients were excluded.
Comments
Aims are clear, well addressed and assessed – Multiple tests were used for
evaluation
There is an ethical concern with control group (simulated ECT) – Patients were
exposed to dangers of anaesthetic whilst not receiving treatment.
Very high and questionable withdrawal rate
Blinding was potentially unreliable as it is easy to tell if someone has had ECT or
not.
The results of the study agree with most papers published at that time.
Conclusion
On the surface, the study met its objectives and aims. It provides a randomised and
double-blind approach – which has never been applied to different methods of ECT.
However, there were no new or ground breaking results. There were also several
design flaws which detract from the quality and validity of the paper. This paper
measured an outcome that would be difficult to do ethically
presently. Although the study was flawed, we feel it contributed to the progression of
clinical knowledge in ECT.
Word Count: 582
PRIVATE: APPENDIX 3 –
INFORMATION SEARCH REPORTRecognising and addressing the information gap
We used Medline and Scopus to find studies regarding ECT and its efficacy in
treating depression. Together, we identified 7 areas of the main topic we wanted to go
further in depth. We then distributed the work load and thoroughly researched each
area.
After going through many papers, our tutor highlighted a paper by the UK ECT
review group that would help us with our research.
Search Strategies
We began by browsing the research concerning our particular aim. Subsequently, we
used Medline and Scopus for a more detailed and specific search.
We used Boolean operators such as ‘AND’ to link ECT with depression, or link
depressive disorders with electro-shock therapy. Since ECT has different identifying
terms, we ‘exploded’ the search to account for all forms, instead of using ‘OR’.
Challenges
It was hard to find suitable articles that were related to our topic. ECT is an area of
research that has not been extensively covered
It was hard to find studies with reliable results due to small sample sizes and a
range of other factors like poor methods of study.
It was difficult to find studies that were carried out in the UK
Many mechanistic studies were carried out on animals. Results may not be
transferable to humans.
Locating and assessing information
PRIVATE: APPENDIX 4 –
CONTRIBUTIONSContributions:
Mark Beeston researched, wrote and co-edited the ECT Versus Pharmacological
Interventions section of the website. He was responsible for the contributions page.
He also contributed towards the weekly diary and the group critical appraisal.
Hou in Chio researched, wrote and co-edited The Side Effects of ECTsection of the
website. He also contributed towards the weekly diary and the group critical appraisal.
Patrick Dodd researched, wrote and co-edited The Patient Journey through ECT and
the Associated Law section of the website and provided the photography. He also
contributed towards the weekly diary and group critical appraisal.
Calvin Eng researched, wrote and co-edited the Unilateral versus Bilateral
ECT section of the website. He was responsible for the information search report. He
also contributed towards the weekly diary and the group critical appraisal.
Conor Foley researched, co-wrote and co-edited the Indications and Efficacy of
ECT section of the website. He was responsible for formatting and ordering the
referencing and he wrote the conclusion. He also contributed towards the weekly
diary and the group critical appraisal.
Joseph James researched, co-wrote and co-edited the Indications and Efficacy of
ECT section of the website. He was responsible for website design and formatting. He
also contributed towards the weekly diary and the group critical appraisal.
Zoe Johnston researched, wrote and co-edited the History of ECTsection of the
website. She also contributed towards the weekly diary and the group critical
appraisal.
Shanon McAllister researched, wrote and co-edited the Mechanism of Action of
ECT section of the website. She also contributed towards the weekly diary and the
group critical appraisal.
Acknowledgements:
The group would like to acknowledge and thank our tutor Dr Zara Bagot and the
ECT staff at the Royal Edinburgh Hospital for their help and support with this project.
PRIVATE: APPENDIX 5 – WEEKLY
DIARY29/09/14 - We met for the first time as a group and with Dr Bagot. We talked about
what ECT actually is and what we already knew about it. We discussed why we chose
the topic and what we hoped to get out of the project. We then all went and had a look
at what an ECT looks like and saw the various bits of equipment.
We decided on some topics that we wanted to look into and then we allocated
ourselves a topic each to go away and do some research on. We also decided to start
putting drafts down on the website.
We arranged to meet as a group without Dr Bagot on the 5th of October to see what
we had done and a couple of the members of the group also arranged to go and watch
some ECT being done.
05/10/14 – This week we met up without the presence of Dr Bagot. We discussed the
different readings that everyone had covered over the week. We now have a much
better understanding of ECT, the processes and the different methods of administering
it. Everyone contributed and read a decent amount into their individual topics.
We then talked about focusing our SSC into using ECT as a treatment for depression,
as we found most of the trials were conducted on patients with depression.
We also created the different pages we would require on our wordpress website. We
planned for our next meeting to be on the 13th of Oct, 10am, and for everyone to enter
a draft of their respective webpages onto the website.
13/10/14 – We met to present to each other our webpage drafts. Everyone had
completed their pages and we agreed to go through them as a group to ensure
consistency of writing style and double check grammar etc.
We had organised to meet with Zara on the 20th already, to inform her of the group’s
progress thus far. For next week, we have agreed to:
1. collate all references into one list in the References Appendix
2. search for papers to present an appraisal of to the group, and
3. consider further which paper we should critically appraise as a group.
20/10/14 – Met with Dr Bagot at the Royal Edinburgh Hospital. Each member
presented to Dr Bagot the sections they were currently writing and any issues they had
come up against.
Some suggestions from Dr Bagot were:
1. To poll a group of students/consultants/non-medics as to their opinions on ECT.
2. To contact SEAN regarding indications for ECT data.
3. To focus mechanism of action on neurogenesis, blood flow
and neurotransmitter hypothesis.
Critical Appraisal was discussed (both individual appraisals and group appraisal). It
was suggested that we appraise the UK ECT review group’s meta-
analysis [UPDATE: Following a discovery that we need to appraise primary
research the new paper is the 1985 Nottingham Trial]. Individual appraisals will
be presented informally to Dr Bagot in early November, date tbd.
Tasks for this week:
1. Appraise paper using SSC2 handbook suggested headings.
2. Email individual articles to Dr Bagot (and post on Facebook page)
Next meeting will be Monday 27th October in the David Hume tower.
27/10/14 – We met to discuss and combine our individual work on the group critical
appraisal of The Nottingham Trial. Using the suggested headings in the SSC guide we
completed an initial draft of our critical appraisal.
Tasks for next session:
1. Continue work on the group appraisal and have some thoughts about the structure
of the report and the key points we need to include about this paper.
2. Begin work on our individual critical appraisals.
The next meeting will be on Thursday 30th October in Appleton Tower.
30/10/14 – We completed our group critical appraisal of The Nottingham Trial based
on our draft from the previous session. However, we went over the limit of 600
words. Therefore we need to make our appraisal more concise before we can have it
checked by Dr Bagot and add it to the website.
Tasks for next session:
1. Have some ideas about how we can make our appraisal more concise in order to
meet the word limit.
2. Continue work on our individual critical appraisals.
3. Look at areas of the website and begin to consider elements such as formatting and
word counts, using the SSC guide as a reference.
The next meeting will be on Tuesday 4th November in David Hume Tower.
04/11/14 – We went through the webpages as a group using google docs to ensure the
uniformity of writing style and double check grammar.
Tasks for next session:
1. Present our individual critical appraisals to Dr Bagot and the group in the next
meeting.
2. Finalise the webpage we were allocated and try to add more words if needed.
The next meeting will be on Tuesday 10th November in Royal Edinburgh hospital.
10/11/14 – We presented our individual critical appraisals to Dr. Bagot, and carried
out a group critical appraisal discussion following each presentation.
Tasks for the next session:
1. Attempt to finalise each of our individual sections.
2. Check accuracy of the references for each section.
3. Write a description for each of our chosen references.
The next meeting will be on Monday 17th November in David Hume Tower.
17/11/14 – We met up without our tutor to put together and introduction and
conclusion for the webpage. We also wrote the contributions page and cut words from
the group critical appraisal as it was slightly over the word limit.
Tasks for next session:
1. Tweak individual sections.
2. Get a screenshot of SCOPUS searches to put into the information search report.
3. Make sure everything is referenced and that references are correctly described.
The next meeting will be on the 19 of November in David Hume Tower,
19/11/14 – Our group met up to finalise the information search report. Each member
of the group had submitted screen shots on their method of searching for articles. We
identified the information gaps we encountered at the start, and any challenges we
faced while searching for relevant articles.
Tasks for next session:
1. Finalise conclusion and ensure our website looks how we want it to.
2. Ensure our website and appendices do not go over the word limit
3. Meet with our tutor to ensure our aims are met
Our next meeting will be on Wednesday, 26th November at the Royal Edinburgh
Hospital.
26/11/14 – Our group met up to finalise our website and group critical appraisal. We
ensured our word count was accurate and that our information read well. We have
finalised our conclusion and edited our website based on comments and critic from Dr
Bagot. This will be our last meeting and our project is ready for submission.
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