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This website has not been peer reviewed.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]

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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.

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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.

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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.