Tag Archives: ECT

ECT: Safe and Effective for Agitation and Aggression in Cases of Dementia?

On March 25 of this year, Psychiatric Times published an article titled Dementia, Agitation, and Aggression: The Role of Electroconvulsive Therapy.  The author is Manjola Ujkaj, MD PhD, and the article’s subtitle is “What role might electroconvulsive therapy play for short-term treatment of agitation and aggression in patients with dementia?”

According to their website Psychiatric Times is a medical trade publication that covers news, reports, and clinical content related to psychiatry “for psychiatrists and allied mental health professionals who treat mental disorders.”  The circulation of the monthly print publication is approximately 40,000.

Dr. Ujkaj is a psychiatry instructor at Harvard.

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Dr. Ujkaj begins by outlining the scope of the problem:

“Agitation and aggression are some of the most frequent and disruptive neuropsychiatric symptoms in patients with dementia. Approximately 45% to 80% of patients with dementia will exhibit agitation and aggression, depending on the clinical setting and dementia stage. Agitation and aggression have a major negative impact on disease burden, with higher incidence of functional decline and loss of independence, more frequent hospitalizations and premature institutionalization, higher rates of morbidity and mortality, and higher degree of caregiver stress and burnout.”


“Although agitation and aggression are among the most significant challenges in current dementia care, their treatment continues to be suboptimal. Currently there are no FDA-approved treatments for this indication.”

Dr. Ujkaj points out that behavioral interventions  “… are considered to be the first-line treatment approach”, but that  “… their use in everyday clinical practice is limited by multiple factors, most commonly lack of adequate training, time, and other resources.”

This is a routine claim in psychiatric literature, but the underlying question is seldom addressed:  if, in the care of our senior citizens, we can afford enormous sums of money for psychiatric consultations, expensive name brand drugs, and electric shock machines, why can’t we afford to hire some behavior analysts and trainers?

Dr. Ujkaj expresses concerns about the use of pharmacological agents to control aggression.

“Psychotropics should be considered only in cases in which agitation and aggression pose a serious acute threat to the safety of the individual or that of others. Nonetheless, in clinical practice, off-label use of psychopharmacological agents for agitation and aggression—including antidepressants (sertraline), antiepileptics (carbamazepine), cholinesterase inhibitors (donepezil), memantine, benzodiazepines (lorazepam), typical (haloperidol) and atypical (risperidone) antipsychotics (the antipsychotics are frequently used)—predominates over nonpharmacological interventions. However, most of these agents provide limited and short-lived efficacy, and there are serious concerns about adverse effects.”

All of which sets the stage for:

“ECT as a treatment option”

Dr. Ujkaj tells us that

“The use of electroconvulsive therapy (ECT) for short-term treatment of agitation and aggression has limited evidence consisting of 9 retrospective case reports and series and only 1 prospective study. Most of the case reports and series describe the successful use of ECT for treatment of agitation and aggression without previous mood or psychotic disorders.  In all of these cases, ECT was well tolerated, with no persistent cognitive impairment. Prolonged yet transitory postictal confusion developed in only 2 patients. ECT was found to be safe and efficacious for agitation and aggression comorbid with mood disorders in patients with dementia.

Findings from a recent open-label study indicate that acute ECT significantly decreased agitated and aggressive behavior by the third session. Moreover, most of the 23 participants showed a more significant reduction by the ninth session. Treatment was discontinued in 2 participants because of the lack of efficacy and in another 2 participants because of delirium. In a patient in whom atrial fibrillation developed, treatment was safely continued after transfer to a general medical hospital for ongoing cardiac monitoring.”

Which sounds pretty convincing.  But – skeptic that I am – I decided to take a closer look at the references that Dr. Ujkaj cites in support of this conclusion.  In her paper, these are references 9-18.

  1. Holmberg SK, Tariot PN, Challapalli R. Efficacy of ECT for agitation in dementia: a case report. Am J Geriatr Psychiatry. 1996;4:330-334. This paper is a case study on one individual.
  1. Roccaforte WH, Wengel SP, Burke WJ. ECT for screaming in dementia. Am J Geriatr Psychiatry. 2000;8:177. This is a letter to the editor, and describes a single case study.
  1. Aksay SS, Hausner L, Frölich L, Sartorius A. Severe agitation in severe early-onset Alzheimer’s disease resolves with ECT. Neuropsychiatr Dis Treat. 2014;10:2147-2151. This is a case report involving one 57-year-old client.
  1. Grant JE, Mohan SN. Treatment of agitation and aggression in four demented patients using ECT. J ECT. 2001;17:205-209. This paper describes four case studies.
  1. Bang J, Price D, Prentice G, Campbell J. ECT treatment for two cases of dementia-related pathological yelling. J Neuropsychiatry Clin Neurosci. 2008;20:379-380. This is a letter to the editor that describes two case studies.
  1. Wu Q, Prentice G, Campbell JJ. ECT treatment for two cases of dementia-related aggressive behavior. J Neuropsychiatry Clin Neurosci. 2010;22:E10-E11.  This is also a letter to the editor:  two case studies.
  1. Ujkaj M, Davidoff DA, Seiner SJ, et al. Safety and efficacy of electroconvulsive therapy for the treatment of agitation and aggression in patients with dementia. Am J Geriatr Psychiatry. 2012;20:61-72. This is a “retrospective systematic chart review” of 16 clients.
  1. McDonald WM, Thompson TR. Treatment of mania in dementia with electroconvulsive therapy. Psychopharmacol Bull. 2001;35:72-82. This paper presents case studies on 3 individuals.
  1. Sutor B, Rasmussen KG. Electroconvulsive therapy for agitation in Alzheimer disease: a case series. J ECT. 2008;24:239-241. This is a chart review study of 11 clients.
  1. Acharya D, Harper DG, Achtyes ED, et al. Safety and utility of acute electroconvulsive therapy for agitation and aggression in dementia. Int J Geriatr Psychiatry. 2014;30:265-273. This is an open-label study of 23 participants. I have done a detailed critique of this study in an earlier post.

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So to put matters in perspective, Dr. Ujkaj’s assertions that

“ECT was well tolerated with no persistent cognitive impairment”


“ECT was found to be safe and efficacious for agitation and aggression comorbid with mood disorders in patients with dementia”

are based on 18 published papers, most of which were case studies, none of which were randomized controlled trials, and together involved a grand total of 64 participants.

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I don’t have the time or the space to critique all of these papers, so I picked one at random.  It’s reference number 11 in the list above:  Severe agitation in severe early-onset Alzheimer’s disease resolves with ECT, by Aksay SS, et al.  Correspondence author is Alexander Sartorius, Professor in the Department of Psychiatry and Psychotherapy, Heidelberg University, Germany.

Below are some quotes from the paper interspersed with my comments.

“The patient was a 57-year-old, right-handed woman with a 4-year history of rapid progressive dementia of Alzheimer type…Her psychiatric history included two depressive episodes 26 and 18 years previous, following critical life events, which remitted in the course of months without specific therapy. She was admitted to our clinic for evaluation and treatment of severe behavior disturbances, including severe restlessness, yelling, crying, refusal to eat and drink, physical aggression, and resisting care, which made further caretaking of the patient at home by family members impossible.”

“Her medication on admission included the acetylcholinesterase inhibitor rivastigmine patch (9.5 mg/d) and antipsychotic agent quetiapine (50 mg/d).”

Rivastigmine is used to treat mild to moderate dementia, which is presumably why it was being prescribed in this case.  It has some potentially serious adverse effects.  These are listed below for the 9.5 mg patch with the percentages of people who experience each.  (Source: PDR)

These are fairly large percentages, and it is entirely possible that the individual was experiencing abdominal pain to which she was unable to alert her caregivers.  The authors tell us that verbal communication  “…was substantially hindered by impairment of language comprehension.”

There is no information in the paper as to why quetiapine (a second generation neuroleptic) was being used.  Perhaps this was a pre-admission attempt to “treat” the agitation.

“Her agitation symptoms proved unresponsive to combined behavioral therapy. Multiple trials of various psychopharmacologic agents were also ineffective: no improvement could be observed with quetiapine at increased doses (up to 175 mg/d), risperidone (up to 2.5 mg/d), melperone (up to 100 mg/d), and pipamperone (up to 80 mg/d). In due consideration of depressive episodes in her medical history, we started an antidepressive combination therapy with sertraline (200 mg/d) and mirtazapine (30 mg/d), which induced an improvement of sleep but no decrease in agitated behavior. Treatment with lorazepam (up to 4 mg/d) brought about a temporary affective loosening, which lasted only 4 days.”

The authors provide no details concerning the “combined behavioral therapy”.

It is noteworthy that so many psychiatric drugs were administered, all of which have potential side effects that involve pain/discomfort, including:  headaches, dizziness, nausea, vomiting, abdominal pain, constipation, diarrhea, blurred vision, etc…  In fact, most of the products mentioned can cause agitation!

“After 9 weeks in our hospital, ECT was initiated. At this time, the patient was receiving rivastigmine (9.5 mg/d), sertraline (200 mg/d), and mirtazapine (30 mg/d). Due to her inability to give informed consent, her daughters – who were also her legal guardians – agreed to the treatment, after detailed information and discussion.”

“A marked difference in the clinical presentation of the patient was noted after just two ECT treatments: the patient was noticeably less agitated, and crying occurred only for short episodes. Her improvement continued throughout the entire course of eight treatments given over 26 days. She stopped yelling and crying, showed no aggression, smiled spontaneously, and was more redirectable. The patient continued to pace, but she was able to sit and lay down for longer periods.”

Many individuals become more peaceful and apathetic after ECT.  This observation is presented, in psychiatric circles, as evidence that the “treatment” works.  But there is a growing recognition that it is more accurately characterized as post-concussional euphoria, a common, and usually short-lived, consequence of severe concussion.

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“The ECT treatment was tolerated well, with signs of headache after the first three sessions. In the third week of treatment, a single self-limiting, spontaneous generalized seizure was observed.”

“The patient was discharged 5 days after the last ECT treatment. The improvement in agitation symptoms was present on hospital discharge. The guardians refused maintenance ECT since the patient moved away from our clinic to be taken care of by other family members. Katamnestic [follow-up] data on clinical presentation and behavioral symptoms of the patient were collected, by caregiver interviews, every 2 weeks over a period of 4 months after hospital discharge. Based on this information, PAS [Pittsburgh Agitation Scale] scores were determined. The improvement of agitation symptoms initiated by ECT lasted for approximately 12 weeks without any additional therapy other than rivastigmine, sertraline, and mirtazapine (Figure 1). In the follow-up period, two further self-limiting, spontaneous generalized seizures were reported.”


Aksay et al Fig 1

Note that about four months after the electric shock treatment, the agitation and aggression had returned to pre-shock treatment levels.  It is also noteworthy that the family caregivers chose not to continue with the electric shock treatment.

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“The etiology of behavioral disturbances in dementia is poorly understood. Abnormalities of neurotransmission (eg, gamma aminobutyric acid [GABA]ergic and dopaminergic dysfunction, cholinergic and serotonergic deficiency, and noradrenergic hyperactivity) have been implicated to play a role in behavior modulation, promoting agitation and aggression. It has been previously postulated that ECT may mediate its beneficial effects through its known enhancement of GABAergic transmission and inhibition.”

Or it may be that the agitation stems from some discomfort or pain that the individual is unable to communicate – such as abdominal pain from ingesting rivastigmine, or akathisia from ingesting quetiapine, or any of the other adverse effects listed above (including withdrawal effects).  Or perhaps the critical factor was simple human frustration stemming from the fact that the woman was unable to communicate her concerns and needs!

“The occurrence of spontaneous seizures was considered to be a result of extensive neurodegeneration in the course of Alzheimer’s disease and not an adverse effect of the treatment since ECT is known to have considerable anticonvulsant effects and not to cause epilepsy.”

In support of the latter statement, the authors cite a paper by Ray AK:  Does electroconvulsive therapy cause epilepsy?  In this article, Dr. Ray describes a study completed at the Central Institute of Psychiatry, India.  The study was a retrospective chart review of 619 individuals, and the author reported:

“No case of tardive seizure or spontaneous seizure was found after ECT among the study group of patients during hospitalization and follow-up.”

But Dr. Ray also acknowledges that his study had some significant limitations:

“In the limitations, our study design being a retrospective chart review, technically, there remains some chance of information being not reported during follow-up.  Even the responses of postal communications were meager:  6.1%.” [Emphasis added]

So Dr. Ray has no information whatsoever on whether the other 93.9% of the study’s participants became epileptic.  It is truly telling that the only reference that Dr. Aksay et al could adduce to support the notion that ECT does not cause epilepsy is a study with such profound limitations.

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“The concern of greater long-term cognitive adverse effects of ECT in patients with severe dementia is not supported by any evidence so far, considering that in most of the reported cases, patients suffering from behavioral disturbances were in the last stage of dementia.”

What’s being said here, essentially, is that the cognitive ability of the individuals concerned is so poor that it would not be possible to discern any deterioration even if it had occurred.

This general theme is echoed in one of the other references in the Ujkaj paper.

  1. ECT for screaming in dementia, Roccaforte et al.

“Why ECT was effective is unknown.  Screaming may be a behavioral ‘equivalent’ of a psychiatric syndrome responsive to ECT, such as depression, mania, or catatonia.  Another possibility could be related to findings in patients with dementia that show a tendency for behavioral problems to spontaneously diminish in more advanced states.  ECT may temporarily ‘shift’ a patient to a ‘later stage,’ thus advancing them quickly past the point of behavioral dyscontrol.”

“Shifting” a patient to a “later stage” sounds awfully like causing damage, and accelerating the individual’s decline and, presumably, death.  Also note the truly perfect example of psychiatric “logic” in the first part of the above quote:  ECT “works” for depression, mania, and catatonia, so, since ECT suppresses screaming, maybe screaming is the “equivalent” of depression, mania, or catatonia.  Analogously:  hammers work well on nails; but they can also be used to crack walnuts;  therefore, walnuts are equivalent to nails!


Several of the papers provide a list of the drugs that the individuals were taking on admission.  For instance:  (psychiatric drugs are shown in red)

13.  Bang J et al:

Case 1:

“Two months prior to admission she was treated with risperidone and then quetiapine with no improvement. A trial of escitalopram was ineffective. Subsequent trials of olanzapine and divalproex were similarly ineffective.

Her medications on admission included those previously mentioned as well as spironolactone, ranitidine, oxycodone, lorazepam, memantine, and carbidopa/ L -dopa (sinemet).”

Case 2:

“Trials of haloperidol and thioridazine were ineffective. When her verbal agitation escalated to the point of disrupting the group home environment, she was referred for admission.”

“Her medications upon admission included ranitidine, levothyroxine, sertraline, and thioridazine.”

14.  Qun Wu, et al.

Case 1:

“Therapeutic trials of sertraline, risperidone, olanzapine, intramuscular haloperidol, and valproate at the nursing home were ineffective.

His medications on admission included satolol, metformin, acetaminophen, trazodone, oxycodone, memantine, levothyroxine, tamsulosin, donepezil, allopurinol, simvastatin, and lisinopril.”

Case 2.

“Trials of trazodone, quetiapine, sertraline, and topical lorazepam at his nursing home were ineffective or poorly tolerated.

His medications on admission included sertraline, pramipexole, thiamine, simvastatin, and acetaminophen. Memantine and donepezil were discontinued prior to admission due to poor tolerance.”

It seems clear that psychiatric drugs are used fairly liberally in these situations, and as mentioned earlier, it is entirely possible – given the adverse effects of these drugs – that this practice is exacerbating the agitation/aggression problem.

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All of the papers expressed a measure of optimism regarding the safety and efficacy of electric shocks in reducing agitation and aggression.  For instance:

#10.  “In conclusion, a small number of case reports indicate that ECT is a potentially helpful treatment for dementia patients with distressing screaming that does not respond to less invasive interventions.”

#11.  “Our case demonstrates that ECT can be safely and effectively used in treating pharmacotherapy-resistant severe agitation in early-onset Alzheimer’s disease in its last stage, without any recognizable worsening of cognitive functions.”

#12.  “We suggest that ECT is beneficial in these potentially life-threatening behavioral disturbances.”

#13.  “ECT is rarely considered as an intervention for severe, refractory behavioral dyscontrol in patients with dementia though its use is considered safe, with fewer potential side effects, and more cost-effective than psychopharmacology alone.”

#14.  “…a growing literature identifies ECT as an effective intervention for severe refractory agitation and aggression for patients with dementia.”

#15.  “These results suggest that ECT is an effective and safe treatment for agitation and aggression in dementia. Further prospective studies are warranted.”

#16.  “We conclude that a short course of ECT, followed by maintenance treatments every 2 weeks, can contribute significantly to the management of dementia patients whose behavioral agitation is associated with signs of mania.”

#17.  “Electroconvulsive therapy is a safe and effective treatment for agitation in AD patients.”

Several of the papers mention a need for further study, and two papers call for randomized controlled trials to assess safety and efficacy.  The two papers are references number 11 (2014) and 14 (2010).  As of this date, no RCT’s have been conducted.  Nevertheless, the “treatment ” is clearly being promoted as safe and effective, based on “growing evidence” of the sort set out here.

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Dr. Ujkaj recommends that ECT’s  “…availability as an off-label treatment option should be presented early during treatment planning.”

“Providing adequate, comprehensive, and timely information about possible risks and benefits associated with this specific ECT indication will allow the patient, family, and the authorized health care representative to achieve an optimal informed decision.”

But this is misleading, because adequate and comprehensive information about risks and benefits in this context is not available, and will not be available, until double-blinded randomized controlled trials have been undertaken.  It is not known, for instance, if routine ECT reduces life expectancy in this context.  And, if it does reduce life expectancy, it is not known by how much.

On the subject of informed consent, Dr. Ujkaj writes:

“A possible challenge is the continued refusal on the patient’s side to provide general assent despite ongoing efforts to identify and/or adequately address the reasons for refusal. In such a case, only a court order can allow ECT treatment to proceed.”

which has an ominous ring.


It is often not appreciated by the individuals receiving electrically induced convulsions that any gains they receive from the procedure will almost certainly be short-lived, and that the “treatment” will need to be repeated more or less indefinitely at intervals of about a month.  Dr. Ujkaj mentions maintenance ECT in her Psychiatric Times article, and most of the references also mention this requirement.  Interestingly, one of Dr. Ujkaj’s criticisms of the use of drugs in these situations is that they  “…provide limited and short-lived efficacy.”  [Emphasis added]  But she does not direct this criticism at ECT.


There is some prima facie evidence that some individuals with dementia who have been displaying agitation and aggression, and are subjected to electric shock “treatment” seven or eight times over a two week period, become more docile and compliant.  This docility lasts for about two or three weeks (sometimes a little longer), at which point they need more electric shocks, presumably for the rest of their lives.  The effect of this “treatment” on life expectancy for these individuals has not been formally studied.


Perhaps the biggest problem with Dr. Ujkaj’s paper, and the various studies that she cites, is that they convey the impression that the matter is being researched, when, in fact, it isn’t.  Case studies can be helpful and informative, but they tell us little or nothing on the general questions of safety and efficacy.  For instance, a case study that reports a successful outcome tells us nothing about other case studies that might have had unsuccessful – or even disastrous – outcomes.  In addition, little credibility can be attached to the assessments of practitioners who themselves administered the “treatment”, and who have a vested interest in the outcome.

It is for precisely these kinds of reasons that the double-blinded, randomized controlled trial has been developed.

And besides, there is a growing body of solid evidence that electrically induced convulsions cause brain damage.  It seems unlikely that elderly people with dementia would somehow be immune to these effects.

A second problem with Dr. Ujkaj’s paper is that it presents the matter as if it were a medical issue, when in fact it is an ethical/legal issue.  The fundamental point here is that electrically-induced convulsions do not treat agitation and aggression in the medical sense of the term.  Rather they suppress agitation and aggression, and probably inflict damage in the process.  And the fundamental question is whether or not this is an appropriate and proper thing to do.  But this is not a medical question.  It is an ethical/legal question on the use of restraints.  Medical research might throw some light on various facets of the matter, but ultimately the question needs to be shifted from the medical arena into the political/legal/civil rights arena.

People with dementia are still people, and they don’t surrender their human rights at the door of a mental hospital.  Throughout its modern history, psychiatry has abrogated these rights under the guise of providing necessary treatment for illness.  Restraints and confinement have been used with little more oversight than a psychiatrist’s signature.  When courts are involved, their contribution is usually a rubber-stamp endorsement of the psychiatrist’s decisions.

The critical need at this juncture is, I suggest, to recognize that the use of shock-induced convulsions to suppress agitation and aggression in people with dementia is not a medical treatment, but is rather a form of short-lived, and probably damaging, restraint.

Meanwhile, the “safe and efficacious” mantra which appears in almost all the papers mentioned earlier is a poor substitute for truthful and open dialogue, and is no substitute for appropriate protection of the civil rights of this, most vulnerable, group.

ECT for Agitation and Aggression in Dementia

On May 16, 2014, the International Journal of Geriatric Psychiatry published an article by Deepa Archarya, PhD, et al.  The article is titled Safety and utility of acute electroconvulsive therapy for agitation and aggression in dementia.  Here are the authors’ conclusions:

“Electroconvulsive therapy may be a safe treatment option to reduce symptoms of agitation and aggression in patients with dementia whose behaviors are refractory to medication management.”

In their Introduction section, the authors write:

“Despite the high prevalence of these agitated and aggressive behaviors, there are currently no treatment options approved by US Food and Drug Administration for this indication. Nonpharmacological interventions, including environmental and behavioral modification, are difficult to implement in nursing home settings because of low staff-to-resident ratios.”

“Atypical antipsychotics have been found to be only modestly helpful in addressing behavioral symptoms and unfortunately are associated with dangerous side effects including tardive dyskinesia, cerebrovascular adverse events, sedation, and increased risk of mortality;”

“A major concern for using ECT in older patients, especially those with dementia, is its adverse effect on cognitive functioning. Research has found that most neurocognitive effects of ECT in older patients without dementia are short term and tend to resolve within a 6-month period.”


Study participants were 23 individuals (mean age 73.8) who had been admitted to McLean Hospital, Belmont, Massachusetts, or Pine Christian Mental Health Services, Grand Rapids, Michigan, with a diagnosis of dementia, and who had been referred for electric shock treatment for agitation and/or aggression.  McLean Hospital is affiliated with Harvard Medical School, and Pine Rest with Michigan State University.

Patients were enrolled in the study after the authors  “…obtained written informed consent from the AHCR [authorized healthcare representative] and assent from the study participants.”  The term “assent” is widely used in the medical field to indicate that an individual, who is not legally competent to consent to a treatment, has indicated, verbally or non-verbally, a willingness to proceed.

Standardized agitation, neuropsychiatric, and depression inventories, as well as the Clinical Global Impression scale, were administered at approximately weekly intervals throughout the study period.  The inventories were completed by nursing staff, and the CGI by the treating psychiatrist.

In addition, a Mini Mental Status Exam (MMSE), Severe Impairment Battery (SIB), and an activities of daily living scale were administered at baseline (i.e. prior to the course of electric shocks) and at discharge.  Though, because of “…agitation and/or inability to sustain attention” only 10 participants completed the before and after MMSE, and only 6 completed the SIB.

Electric shocks were administered three times per week  “…or less frequently if clinically indicated.”


The mean number of electric shock sessions was 9.4, ranging from a low of 5 to a high of 14.

Participants’ scores improved significantly on the Cohen-Mansfield Agitation Inventory, and on the Neuropsychiatric Inventory.  “As needed” neuroleptic use declined from an average chlorpromazine equivalent dose of 7.8/week at the beginning of the study to 1.6/week at the end.  But there was no change in the use of standing neuroleptic drugs.  [“Standing” in this context means prescribed on a regular basis, through a standing order.]

Sixty-one percent of the participants (i.e. 14 of the 23) were using atypical antipsychotics on admission.  This increased to 65% (i.e. 15 out of 23) by the time the shock treatment began, and had reverted to 61% at discharge.

There was no significant change in scores on the activities of daily living scale.


The authors write:

“Overall, our results demonstrated ECT to effectively reduce symptoms of agitation and aggression in older patients with dementia who did not respond to  psychopharmacological intervention alone. This suggests that ECT may be a potential treatment option for patients with dementia who are refractory to medications for agitation and aggression. Importantly, there were significant reductions in behavioral disturbances by the third ECT session, and most participants showed a reduction in behavioral disturbances by the ninth ECT session. If borne out by subsequent trials, such rapid reduction in behavioral disturbances could have significant public health implications by improving the quality of life for patients with dementia, alleviating caregiver burden, and increasing residential placement options for patients.”


“In our study, ECT was discontinued for two participants (both with end-stage dementia) because of poor response, which was defined by recurrence of agitation and aggression that reached approximately baseline severity levels.  [Elsewhere in the report the authors state that one of these individuals died a month after his final ECT session, and that the treatment team determined that the cause of death was unrelated to the ECT.]   Three participants, despite improvement in agitation and aggression, had adverse events that resulted in discontinuation of ECT.”

The authors point out that the study design was naturalistic, and lacked a control group.


The authors acknowledge that the study had a number of limitations, including the fact that it was “open label”.  This means that the staff who rated the participants before and after the electric shocks were aware that the individuals had received these shocks.  In fact, as is made clear in the text, the raters were involved in the care of the participants, and were probably invested in the outcome of the study.  Under such circumstances, it’s very easy to see improvements and to ignore deteriorations in participants’ behavior.  This is particularly the case in that the kinds of ratings used in a study of this nature necessarily involve a good measure of subjective judgment and interpretation.

The authors were aware of this concern, and they state:

“As this was the first naturalistic, prospective study of the use of ECT to treat agitation and aggressive symptoms in patients with dementia, the goal was to collect preliminary data for the development of a randomized, double-blinded, controlled clinical investigation.”

Nevertheless, the authors express considerable optimism for this “treatment”:

“Despite these limitations, our results are encouraging and suggest that ECT may be a rapidly acting, safe, and effective treatment for certain patients with dementia and behavioral disturbances that do not respond to or tolerate standard behavioral interventions and pharmacotherapy.”

Despite the caveats in the earlier part of this sentence, the optimistic tone strikes me as unwarranted by the study’s results.

The phrase  “… patients with dementia and behavioral disturbances that do not respond to or tolerate standard behavioral interventions…” is also noteworthy, in that there is no mention in the study text that any kind of behavioral interventions had ever been attempted with the enrolled individuals, nor that a history of failure with these kinds of interventions was a pre-requisite for study enrollment.  This is a critically important matter because the use of psychiatric interventions to “treat” agitation and aggression in cases of dementia is often criticized on the grounds that behavioral interventions are safer, more effective and should always be tried first.  The authors’ implication that behavioral interventions had been tried without success seems misleading.

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In Table 1 of the article it states that 65.2% (15 out of 23) of the individuals enrolled were recommended for “continuation ECT”.  When we remember that five individuals were dropped from the study because of poor response or adverse events, it is clear that the effective percentage is 83% (15 out of 18).  This is important in that there is a perception among the general public that electric shocks to the brain are a one-time “treatment” that somehow fix aberrant neural mechanisms.  In reality, “continuation ECT” is very common.  It is also, I think, noteworthy, that apart from the line in Table 1, there is no mention of continuation ECT in the text.  It’s worth asking whether the medical proxies who signed the consent forms were aware that any gains from the “treatment” would be temporary, and that there was a high likelihood that electric shocks to the brain would become standard “treatment” for the individuals concerned.

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Many of the participants were taking psychoactive drugs on admission and on discharge.  The authors provide the following table:

Acharya et al Table 2

The admission percentages add up to 252, so it is clear that many of the participants were taking more than one of these drugs.

Several of these products have adverse effects that could readily contribute to agitation/aggression, and even to the dementia.  Atypical antipsychotics, more accurately known as neuroleptics, for instance, cause tardive dyskinesia and akathisia, both of which are extraordinarily impairing and unpleasant.  It is not difficult to accept that these drug-induced conditions could precipitate agitation and aggression, especially in people whose cognitive ability has declined.  In fact, extreme agitation is the primary feature of akathisia.

An additional consideration here is that although, in their opening remarks, the authors draw attention to the lack of efficacy and dangerous side effects of antipsychotics in these situations, they continued to prescribe them for participants during this study.

Here are some known adverse effects of the other classes of drugs mentioned in the article: 

Anticonvulsants:  These drugs are used to treat epilepsy but are also used in psychiatry for the condition known as bipolar disorder.  Lamictal (lamotrigine) is a member of this class.  PDR.net lists confusion as a frequent adverse reaction; and akathisia, dyskinesia, hostility, memory decrease, and paranoid reaction as infrequent adverse reactions.

Benzodiazepines:  These drugs are classed as sedatives/minor tranquilizers, and are widely used in geriatric populations.  Librium (chlordiazepoxide) is a member of this class.  PDR.net states that “Paradoxical reactions (e.g., excitement, stimulation, and acute rage) reported in psychiatric patients…” [Emphasis added]

Antidepressants:  Even in psychiatric circles it has been acknowledged that these drugs can cause manic-like episodes.  (DSM-IV:  “Manic-like episodes that are clearly caused by somatic antidepressant treatment (e.g., medication, electroconvulsive therapy, light therapy) should not count toward a diagnosis of Bipolar I Disorder”  p 332)

Cholinesterase inhibitors:  These are commonly used as a treatment for Alzheimer’s dementia.  Four cholinesterase inhibitors are approved by the FDA for this purpose:  Aricept, Exelon, Razadyne, and Cognex.  All four of these products (according to the NIH’s site MedlinePlus) have a wide range of unpleasant side effects, e.g., nausea, vomiting, incontinence, dizziness, blurred vision, muscle aches, headaches, extreme tiredness, stomach pain, uncontrollable shaking, etc., and it is certainly conceivable that individuals taking these drugs might become agitated or aggressive, especially individuals who, because of cognitive deficits, are unable to communicate their distress verbally.  It is also noteworthy that aggressive behavior is mentioned by the NIH as a specific adverse effect of one of these products (Exelon)

NMDA receptor antagonists:  This is a broad category of drugs, many of which induce a state known as dissociative anesthesia.  Examples include:  Ketamine, chloroform, alcohol.  Ketamine is sometimes used in psychiatry for depression.  Memantine, a member of this class, is approved by the FDA for the treatment of Alzheimer’s disease, and probably accounts for most, if not all, of the NMDA/RA’s reported in this study.  The NIH lists aggression as a specific side effect.

Given the extent to which these various drugs were being used by the study’s participants, it is certainly conceivable that the drugs were contributing to the agitation and aggression.  The authors don’t appear to have considered this possibility, and in fact, state:

“It may be possible that the reduction in agitation and aggression may have been due to a synergistic effect between ECT and pharmacological treatment.”

. . . . . . . . . . . . . . . .

Against all this, it could be argued that the incidence of these various adverse effects is generally low, and couldn’t account for the frequency of aggressive behavior in the study participants.  But the participants were not a random selection of people taking the drugs in question.  Rather, they were individuals selected because of aggressive behavior, most of whom had been taking some or all of these drugs on admission.  So it is a distinct possibility that the aggression was a drug effect for many, or even most, of the study participants.

In addition, it is noteworthy that the use of benzodiazepines, antidepressants, cholesterinase inhibitors and NMDA/RA’s was discontinued towards the end of the study period for many of the 23 participants.  From Table 2, reproduced above, we can calculate the number of individuals involved:

Acharya changes from table 2


Given that all of these drugs have the potential to induce aggression/agitation, it is surely possible that discontinuing these drugs for some individuals could lower the overall incidence of these kinds of reactions.

So when Dr. Acharya, et al, state that:  “It may be possible that the reduction in agitation and aggression may have been due to a synergistic effect between ECT and pharmacological treatment”, it is equally plausible that any reduction in the incidence of aggression is attributable to a combination of the state of docility often noted post-electric shock treatment plus the fact that aggression-inducing drugs were discontinued in many cases.

Unfortunately, what psychiatrists will likely take from the study is the self-serving conclusion that ECT is an acceptable way to manage agitation and aggression in people with dementia, and, unfortunately, this is also the message being given to the general public.  

Sue Thoms is a journalist who writes for MLive/The Grand Rapids Press.  On September 18, 2014, she wrote a piece for MLive.  The article was apparently based on an interview with Louis Nykamp, MD, one of the study’s authors.  Here are some quotes:

“Dementia patients who were severely agitated and aggressive benefitted from electroconvulsive therapy in a study conducted by researchers at Pine Rest Christian Mental Health Services and two other institutions.”

Note the unqualified assertion  “…benefitted from…”, even though such a conclusion is not warranted by the study.

“Doctors don’t know how the ECT treatments work, he [Dr. Nykamp] added.

‘It’s possible that we are treating underlying agitated depression,’ he said. ‘Or it’s possible we are simply working through another mechanism to help modify some of the brain circuitry that is leading to the substantial agitation and impulsivity.'”

There it is:  agitation may be caused by “underlying agitated depression”, the spurious superficiality of which notion is self-evident.  Or:  high voltage electric shocks delivered to the brain may fix aberrant brain circuits, a contingency which in any context other than psychiatric orthodoxy would be considered laughable.  Electric shock treatment causes brain damage, and any putative gains claimed by psychiatrists are attributable to a well-known transient effect called post-concussional euphoria.  Memory loss, in many cases, is more or less permanent.

It is, I suggest, a gross misuse of medical authority and medical credentials to subject older members of society to this kind of abuse.

A Macabre Celebration:  80 Years of Convulsive ‘Therapy’

There’s an interesting article in the June 2014 issue of the Journal of ECT.  It’s written by Max Fink, MD, and is titled Celebrating 80 Years of Inducing Brain Seizures as Psychiatric Treatment.  Dr. Fink is a psychiatrist and neurologist, and professor emeritus of psychiatry and neurology at the State University of New York, Stony Brook.

The article is short (approximately 400 words), and is essentially a tribute to Ladislas Meduna for his discovery  “…that induced seizures alleviated severe psychiatric disorders…”, which Dr. Fink describes as  “…a remarkable medical advance…”

Here are some quotes from the article, interspersed with my comments:

“When the Hungarian neuropathologist Ladislas Meduna found increased gliosis in the brains of epileptic patients and decreases in those with schizophrenia, he saw the illnesses as antagonistic and thought that inducing epileptic seizures might relieve psychosis.”

Glial cells are non-neuron brain cells.  In other words, they are not nerve cells.  Rather, they provide structure and support for the nerve cells.  Gliosis refers to a condition of the glial cells that occurs in response to damage.  The condition usually entails an increase in the number and size of the glial cells, and in extreme cases produces a scar.  Gliosis is associated with epilepsy, but it is unclear which is the cause and which is the effect.  What is clear, however, is that gliosis always has the potential to produce serious adverse effects.

In this context, there is an almost childlike naïveté to Dr. Meduna’s line of reasoning.  Essentially he has two groups of people:  those with epilepsy and those who have been “diagnosed with schizophrenia.”  On post-mortem examination, he finds relatively more scar tissue in the brains of the former group, and relatively less in the brains of the latter group.  He also had noticed that the incidence of epilepsy was low in people “diagnosed with schizophrenia.”  So, apparently, he reasons: the induction of grand mal seizures in the “schizophrenics” will have a therapeutic effect.  (Incidentally, given the low reliability of the label “schizophrenia,” the statement that the incidence of epilepsy was low in this group is fraught with problems.  But that’s another issue.)

The fact that epilepsy is a devastating illness and that grand mal seizures are clearly not benign occurrences doesn’t seem to have entered into Dr. Meduna’s reckoning.  He tried various chemicals to induce seizures in animals, and finally chose camphor.  Then, according to Wikipedia:

“For a population with severe schizophrenia, he moved from Budapest to the psychiatric hospital at Lipotmező, outside Budapest. He began his dose-finding experiments on January 2, 1934.” [Emphasis added]

Dr. Meduna later switched to pentylenetrazol (Metrazol), a stimulant drug which produces convulsions at high doses.

Incidentally, here’s a description of a Metrazol-induced seizure.  The quote is taken from Metrazol Therapy on the site fairfieldstatehospital.com.

“Metrazol produced an explosive seizure about a minute after the injection. Often these convulsions would result in fractured bones and torn muscles. For the therapy to be effective it would be given two or three times a week and a typical course of therapy would be thirty to forty injections. As the patient regained consciousness they would be confused and cooperative with staff which was seen as a marked improvement. Other times in this twilight state the patient would act in a more regressive manner, frightened and scared by the treatment. After a patient received one treatment they were resistant to subsequent treatment, resisting and pleading for it not to be done again and would have to be forcibly treated.”

And it is the inventor of this “treatment” that Dr. Fink wishes to honor!

. . . . . . . . . . . . . . . .

“In 1938, seizures using household electric currents replaced Metrazol, not for greater efficacy, but wholly for ease of use.  By the 1950s, grand mal seizures were being induced in thousands of patients in the main psychiatric treatment centers worldwide.”

ECT was first used by Ugo Cerletti, MD, in 1938, in Rome.  Here’s a description, written by Dr. Cerletti himself, of the first use of this “therapy”:

“A schizophrenic of about forty, whose condition was organically sound, was chosen for the first test. He expressed himself exclusively in an incomprehensible gibberish made up of odd neologisms, and since his arrival from Milan by train without a ticket, not a thing had been ascertainable about his identity.

Preparations for the experiment were carried out in an atmosphere of fearful silence bordering on disapproval in the presence of various assistants belonging to the clinic and some outside doctors.

As was our custom with dogs, Bini and I fixed the two electrodes, well wetted in salt solution, by an elastic band to the patient’s temples. As a precaution, for our first test, we used a reduced tension (seventy volts) with a duration of 0 2 second. Upon closing the circuit, there was a sudden jump of the patient on his bed with a very short tensing of all his muscles; then he immediately collapsed onto the bed without loss of consciousness. The patient presently started to sing at the top of his voice, then fell silent. It was evident from our long experience with dogs that the voltage had been held too low.

I, bearing in mind the observations with repeated applications of the day before upon pigs, made arrangements for a repetition of the test.

Someone got nervous and suggested whisperingly that the subject be allowed to rest; others advised a new application to be put off to the morrow. Our patient sat quietly in bed, looking about him. Then, of a sudden, hearing the low toned conversation around him, he exclaimed – no longer in his incomprehensible jargon, but in so many clear words and in a solemn tone – ‘Not a second. Deadly! ‘

The situation was such, weighted as it was with responsibility, that this warning, explicit and unequivocal, shook the persons present to the extent that some began to insist upon suspension of the proceedings, Anxiety lest something that amounted to superstition should interfere with my decision urged me on to action. I had the electrodes reapplied, and a 110-volt discharge was sent through for 0.5 second. The immediate, very brief cramping of all the muscles was again seen; after a slight pause, the most typical epileptic fit began to take place. True it is that all had their hearts in their mouths and were truly oppressed during the tonic phase with apnea, ashy paleness, and cadaverous facial cyanosis – an apnea which, if it be awe-inspiring in a spontaneous epileptic fit, now seemed painfully never-ending – until at the first deep, stertorous inhalation, and first clonic shudders, the blood ran more freely in the bystanders’ veins as well; and, lastly, to the immense relief of all concerned, was witnessed a characteristic, gradual awakening ‘by steps’. The patient sat up of his own accord, looked about him calmly with a vague smile, as though asking what was expected of him. I asked him: ‘What has been happening to you?’ He answered, with no more gibberish: ‘I don’t know; perhaps I have been asleep.'”

Note how Dr. Cerletti dismisses as “superstition” the notion that the victim’s prohibition (‘Not a second.  Deadly’) should be taken seriously.  And when Dr. Fink writes that electricity replaced Metrazol “…for ease of use,” he probably was not talking about the client’s ease.

The great tragedy of all this is that the “improvements” noted following electric shock convulsions are similar to, and essentially instances of, the transient state of euphoria and compliance that frequently follows severe head injury.

. . . . . . . . . . . . . . . .

“Widespread belief that electricity caused brain damage and persistent memory loss stigmatized the treatment.”

Note the word “belief” and the suggestion that these “beliefs” were unfounded.  In other writings, Dr. Fink has been more direct.  On October 1, 2006, for instance, he wrote an article for Psychiatric Times called The Camelford Hysteria: A Lesson for ECT?  In this piece, he states clearly:

“Complaints of persistent memory loss in otherwise well-functioning individuals after recovery from a psychiatric illness through ECT are best viewed as a conversion reaction or a somatoform disorder.”

In other words, if my readers will pardon the expression, the memory loss is all in their heads!  Psychiatry is a great disrespecter of people, but this statement of Dr. Fink’s must surely take the proverbial biscuit.

Back to the Celebrating 80 Years article.

“For more than half a century, our research interest focused on minimizing electricity’s hazards.  Electrode placement, electricity form and energy dosing were repeatedly tested, but no modification was without complaint.”

This strikes me as an interesting way to spend 50 years, if in fact the hazards were nothing more than the manifestations of victims’ neurotic imaginations.

. . . . . . . . . . . . . . . .

 “Meduna’s hypothesis that seizures, not the method of induction, were the basis for remission was repeatedly verified”

“An alternative to electricity using the inhalant anesthetic flurothyl is of renewed interest.”

And finally:

“Ladislas Meduna’s demonstration that induced seizures alleviated severe psychiatric disorders was a remarkable medical advance that developed despite universal fears of epilepsy and of electricity.  Although little heralded, the remissions of the illnesses of many hundreds of thousands of the severely ill justify the celebration of this remarkable discovery.”

In fact, however, electric shock “treatment” is no more effective than sham ECT, in which the client is prepared and anaesthetized, but not actually shocked (Bracken et al, 2012)

When one considers the pains to which real doctors go to protect their patients from seizures, I suggest that the deliberate induction of grand mal seizures, often involuntarily, constitutes neither “a remarkable discovery” nor a “remarkable medical advance,” but rather aggravated assault by a person in a position of trust.

In September 2005, Dr. Fink was interviewed by Arline Kaplan Long, and the interview was written up in Psychiatric Times.  Here’s a quote from the article:

“Asked what he wants psychiatrists and others to understand about ECT, Fink responded, ‘Over the 70-plus years that ECT has been around, we have learned to appreciate that something magical happens in the body when we produce an epileptic fit.'”

And here, dear readers, I have to confess that words fail me!

Transcranial Magnetic Stimulation

TMS is a psychiatric treatment that uses a rapidly alternating magnetic field to induce electric currents in the brain.  These currents stimulate neurons, causing them to “fire.” When used repetitively, TMS is said to alter the excitability of the brain area that has been stimulated.  In the psychiatric field, TMS is being used increasingly as a treatment for depression, particularly with so-called treatment-resistant clients.  I Googled the string “TMS + depression” and got 1.35 million hits.  So the idea is attracting attention.

One of the abstracts presented at the May 2013 APA annual conference in San Francisco was called A Multisite, Longitudinal, Naturalistic Observational Study of Transcranial Magnetic Stimulation (TMS) For Major Depression in Clinical Practice, by Mark Demitrack, MD, et al.

The abstract was a study of the efficacy of TMS involving 307 depressed participants who had failed to benefit from prior antidepressant treatment.  The authors’ conclusions were:

“These data support the view that TMS demonstrates a statistically and clinically meaningful durability of acute response over 52 weeks of follow up.  Maintenance of benefit was observed under a pragmatic regimen of continuation antidepressant medication and access to TMS reintroduction for symptom recurrence.”

The abstract also indicated that the study had been “supported by a grant from Neuronetics, Inc.”

The presentation generated some enthusiasm.  Medscape ran an article by Caroline Cassels on May 24, 2013, under the headline TMS for Resistant Depression: Long-Term Results Are In.  In this article Mark George, MD, a long-term advocate of TMS, is quoted:

“This is great news for our field and for the millions of patients who suffer from depression and do not respond well to medications…”

With regards to formal publication, the study is divided into three parts.

1.  L. Carpenter et al, 2012, focused on the effect of TMS on depressive symptoms.
2.  P. Janicak et al, 2013, focused on the effect of TMS on quality of life measures.
3.  Analysis of the 52-week follow-up, submitted for publication but not yet published.  Some of the data from the follow-up, however, was presented in the APA conference abstract.

The authors of the 2012 and 2013 articles are identical except for one person – Dafna Bonneh-Barkay, PhD – whose name appears on the 2013 article only.  Dr. Demitrack, listed as lead author on the APA conference abstract, is shown as an author on both the 2012 and 2013 papers.

The study, which started with 339 participants, was conducted on 42 sites which used TMS.  There was considerable participant attrition during the study.  By baseline the number was down to 307, and only 265 actually completed the acute treatment phase.  Reasons for drop-out were:

No post-baseline evaluation 17
Non-standard treatment protocol used 7
Did not meet diagnostic criteria 4
Prior TMS treatment 4
Failed to return 18
Unsatisfactory response efficacy 7
Satisfactory response efficiency 2
Adverse event (seizure) 1
Patient request 1
Other reason 13


Of the 265 individuals who completed the acute treatment phase, 257 entered the 12-month follow-up phase, and of those only 204 participants provided data across the entire study period.  Presumably the reasons for these follow-up phase attritions will be listed in the formal write-up, but at present this information is not available.

The 2012 paper begins by stating that

“…20-40% of patients do not benefit from, or cannot tolerate, adequate trials of antidepressant medications even after repeated attempts.”

The authors go on to describe TMS, and state that

“When used as an antidepressant, TMS produces clinical benefit without the systemic adverse effects associated with medications, and has no adverse cognitive effects.”

The authors state that although the efficacy of TMS has been established, there have been no multisite studies of its utility and effectiveness in routine clinical practice.  Their goal in the present study was

“…to summarize outcomes experienced by a large population of depressed patients treated with TMS therapy in various clinical settings.”


Clients were eligible for participation if

1.  Their primary “diagnosis” was a major depressive episode without psychotic features, using DSM-IV criteria
2.  They had no medical condition that precluded the use of TMS
3.  They had not received TMS previously
4.  They were pharmacoresistant as determined by the Antidepressant Treatment Record (ATR).  The ATR is a screening instrument developed by Neuronetics
5.  Their attending psychiatrists had determined that TMS was the most appropriate clinical option.


All treatments used the NeuroStar TMS system – a Neuronetics product.  The intensity of the magnetic field was set at 120% of motor threshold, which in turn was determined on an individual basis with the help of a computerized mathematical algorithm called MT Assist, which is also a Neuronetics product.  Each treatment session involved about 3,000 pulses (average 3,216), usually over the left dorsolateral prefrontal cortex.  The motor threshold, incidentally, is the minimum amount of power output that will cause the client’s thumb to twitch.  The actual treatment is administered at a point 5cm in front of the motor threshold determination point.

Participants who were taking antidepressant drugs at the time of enrollment were permitted to continue taking these at the discretion of the treating psychiatrist.  At study baseline, 300 of the 307 participants were taking one or more psychotropic drugs.

The average number of TMS treatments administered was 28.3 (range 2-94) across an average duration of 42 days (range 2-130).  The normal protocol was about five sessions per week.


Outcome measures of depressive “symptoms” were reported in the 2012 paper, (Carpenter et al, 2012).  The primary outcome measures were the changes from baseline to the end of the acute phase of treatment on:

  • the Clinical Global Impression – Severity Scale (CGI-S)
  • the Inventory of Depressive Symptoms, Self-Report version (IDS-SR)
  • the 9-Item Patient Health Questionnaire (PHR-9).  

The CGI-S is completed by the treating clinician; the other two scales are completed by the client.

The mean scores on all three scales declined (i.e., improved) during the treatment period.    Remission rates (as defined by a score of 2 or 1 on CGI-S, a score of less than 5 on the PHQ-9, or a 50% or greater drop in score on the IDS-SR) were 37.10%, 28.70%, and 26.50% respectively.

The actual duration of acute-phase treatment was determined by the treating psychiatrist’s estimate of the “point of maximum benefit.”  The authors report that 22% of the participants were treated beyond the 6 weeks duration.  The maximum duration was 130 days, or a little over 4 months.

The 2013 study focused on quality of life outcome measures.  These were assessed by:

  • Medical Outcomes Study-36-Item Short Form Health Survey (SF-36)
  • EuroQol 5 – Dimensions (EQ-5D) 

Each participant was assessed on these self-administered measures at baseline and again at the end of acute treatment.  As with the depressive “symptoms,” mean scores on these quality of life measures improved during the acute treatment period.


As mentioned earlier, the formal write-up of this phase of the study is not yet available, but the APA abstract provided the following information:

CGI-S, PHQ-9, and IDS-SR scores were obtained at the 3, 6, 9, and 12-month marks.  The reduction in mean scores, noted at the end of acute treatment, was sustained throughout the 52-week follow-up

End of Acute Treatment 52-weeks
CGI-S 3.2 3.0
PHQ-9 9.6 9.4
IDS-SR 27.4 27.3


Remission rates were also maintained.

End of Acute Treatment 52-weeks
CGI-S 37.10% 40.40%
PHQ-9 28.70% 33.60%
IDS-SR 26.50% 26.10%


[Note there is an erroneous transposition of PHQ-9 and IDS-SR scores in either the 2012 article or the APA Conference abstract.  I believe that the way I’ve presented the figures above is correct, but, as the numbers are fairly close anyway, it makes little difference to the overall result.]

The APA Conference abstract provides no information on quality-of-life scores during the follow-up period.


On the face of it, the two papers and the APA abstract suggest that TMS is an effective treatment for depression, and that its beneficial results are long-lasting.  But such an interpretation is misleading.

TMS is routinely presented as a safer alternative for the treatment of depression than ECT (e.g. TMS Center of Princeton).  It is well known that ECT provides, for some individuals at least, a temporary feeling of well-being, but that these effects are short-lived, and the treatment often needs to be repeated more or less indefinitely.  When Demitrack et al state (in the APA abstract) that TMS demonstrates

“…clinically meaningful durability of acute response over 52 weeks of follow up”

most people would, I suggest, interpret this to mean that the beneficial effects of the acute phase treatment lasted for 52 weeks.  In fact, both the TMS and the antidepressants were continued as needed to maintain therapeutic benefit for many of the participants for most of the year.  This is mentioned in the various documents.  For instance, in the APA Conference abstract it says:

“Maintenance of benefit was observed under a pragmatic regimen of continuation antidepressant medication and access to TMS reintroduction for symptom recurrence.” [Emphasis added]

In fact, 30.2% of participants required subsequent TMS after the 3 month assessment.

Earlier in the abstract, however, they had said that the participants who benefitted from “…acute TMS treatment were tapered from their TMS regimen, consented to long-term follow up over 52 weeks, and were evaluated for statistical analysis.”  [Emphasis added]

This, I suggest, implies that the TMS was discontinued after the acute treatment phase.  In my view, the fact that the TMS was reintroduced on an as-needed basis to combat “symptoms” might have been reported more prominently.

Further to this point, in Caroline Cassel’s Medscape article quoted earlier, there’s another quote from Mark George, MD:

“This is a very important and exciting study. Several prior studies have shown that prefrontal rTMS works to treat depression acutely. Until this study, we have had only limited information about how well these patients do a year after completing a course of TMS. Long-term data following remission produced by medications or electroconvulsive therapy [ECT] in these treatment-resistant patients have been disappointing, with only about 13% being still remitted a year later.”

“For example, over half of patients who remit with ECT are ill again 6 months later. Thus, having 45% in remission a full year later is very, very encouraging that rTMS is perhaps changing the underlying pathological circuitry associated with depression and producing a more stable remission than the other treatments.”

In this quote, Dr. George laments the fact that more than half the people who receive ECT are “ill” again 6 months later.

The transient nature of the ECT effect is a well-established fact, and these individuals are usually returned to the hospitals for further “treatment.”  By contrasting these individuals with the 45% still “in remission a full year…” after TMS , it appears that Dr. George is under the impression that these individuals did not receive further sessions.  Or at any rate, that is the impression he is giving, particularly with the phrase:  “…a more stable remission…”

Incidentally, I’m not sure where Dr. George got the 45% remission figure.  In the APA Conference  abstract, the highest remission rate was 40.4% (on CGI-S).  The others were 33.6% on PHQ-9 and 26.10% on IDS-SR.  Perhaps the 45% refers to individuals who remitted by any of the three measures – but there’s no mention of that in the paper.

Also incidentally, Dr. George is the director of the Brain Stimulation Lab in Charleston, South Carolina, which has received grant funding from Neuronetics.  (George et al, 2013, p 17).

After the conference PsychCongress ran an article highlighting the abstract.  Their headline read:  APA News:  Transcranial Magnetic Stimulation Shows Long-Term Benefit In Treating Depression, suggesting, here again, that the author of the article had been misled.


It is also of note that all of the authors of the 2012 and 2013 papers have significant conflicts of interest.

Scott Aaronson, MD:  speakers fee from Neuronetics.
Dafna Bonneh-Barkay, PhD:  Neuronetics, employee, with salary and stock options.
Terrence Boyadjis, MD:  Neuronetics research support contract.
David Brock, MD: Neuronetics employee, with salary and stock options.
Ian Cook, MD:  Neuronetics, speaker’s bureau, honoraria, research support, grant.
Linda Carpenter, MD: Neuronetics research support.
David Dunner, MD:  Neuronetics, grant support, research support, consultant fees.
Mark Demitrack, MD:  Neuronetics, employee (Chief Medical Officer) with salary and stock options.
Hugh Solvason, PhD, MD: Neuronetics research support.
Philip Janicak, MD:  Neuronetics, research support, advisor, consultant.
Karl Lanocha, MD:  Neuronetics, research support, speaker’s bureau.


On June 4, 2012, Shiv Gaglani posted an article on Medgadget.com.  The title was The Promise of TMS: Interview with Neuronetics Chief Medical Officer Mark Demitrack, M.DHere’s a quote:

“The makers of the NeuroStar TMS System, Neuronetics, contacted us to let us know about their new study released at the American Psychiatric Association meeting in May.” [Emphasis added]

This, incidentally, was not the same APA 2013 abstract mentioned earlier.  Dr. Demitrack had presented an earlier abstract – a preview of the Carpenter et al 2012 study – at the 2012 APA conference.  The Medgadget interview was based on the earlier abstract, and gave a brief summary of the study’s main findings, with quotes from an interview with Dr. Demitrack, but there is no mention of the concomitant use of the antidepressants, or of the continued use of TMS during the follow-up period.

An additional point of concern in this regard is Dr. Demitrack’s statement concerning safety.  Here’s the quote

Medgadget:  Were any side effects observed?”

Dr. Demitrack: The most common side effect directly related to the device is scalp pain or discomfort at the site of stimulation. Most patients find this to be mild to moderate in intensity, and it usually becomes unnoticeable after the first week.”

In fact, as the 2012 paper makes perfectly clear, one of the participants experienced a generalized tonic-clonic seizure (formerly known as grand mal seizure) during a TMS treatment session.

“There was one medical event considered probably or definitely related to the device and that was filed with the FDA as a Medical Device Report.  This event was a generalized tonic-clonic seizure that occurred in a female patient during her 10th TMS treatment session.  The patient had no prior history of seizure, however she had several clinical factors that may have contributed to altering her seizure threshold.  Specifically, the evening before her treatment she had completed a night shift of work, and was therefore sleep-deprived at the time of the TMS session.  In addition, she was also taking bupropion, sertraline, and dextroamphetamine/levoamphetamine at the time of her TMS acute-phase participation.  The patient recovered fully from the event without neurological sequelae.

Seizure is a known, but rare, medical risk associated with TMS.  In the entire postmarketing experience with this system, there have been six reports of seizure filed as MDRs to the FDA.  Based on this experience, the estimated risk of seizure is approximately 0.003% per treatment exposure, and <0.1% per acute treatment course.”

It seems obvious to me that this should have been mentioned in the interview and included in Medgadget’s article.  This is particularly important in that Medgadget is a credible and sophisticated website operated by a team of MDs and biomed engineers.  They have 11,700 Twitter followers, they have their own YouTube channel, and they have a large following on their Facebook site.  In addition, the article was picked up and hyperlinked by at least three other sites:  Regator, AllVoices, and Organized Wisdom.

At the end of the Medgadget article there’s a link to a 20-minute Neuronetics promotional video.  At about 18:28 minutes, the spokesperson says:

“Over 10,000 active treatments were performed across all NeuroStar clinical trials, demonstrating its safety.  During trials, no seizures or systemic side effects were seen.”

However, as mentioned earlier, the Carpenter et al study states that six seizures had occurred in the post-marketing experience, and one during the Carpenter et al study itself.  On this basis, the video statement seems deceptive, or at least misleading.

The authors of the 2012 paper estimate the seizure risk at 0.003% per treatment session.  This is about 1 in 33,000, and on the face of it seems like a very small risk.  But a treatment course typically consists of about 30 sessions (5 per week for 6 weeks), which brings the risk per treatment course up to 0.09%, or 1 in 1,100.  But, further, some individuals receive considerably more than 30 sessions.  The maximum in the present study was 94.  The risk for a person receiving 94 sessions is 0.28%, or 1 in 357.  And when we remember that many people receive repeat treatments, it is clear that the risk for these individuals becomes increasingly significant.  It is also clear that these risk estimates are based on very limited actuarial experience, and may have to be revised (upwards or downwards) as TMS use increases.


As mentioned earlier, TMS is getting a good deal of air-time in recent years.  In particular, it is being promoted as a “non-invasive” treatment.  I Googled the string “TMS + non-invasive” and got 317,000 hits, and the present authors use the term to describe the treatment (2012 paper, p 588).

This is misleading.  TMS involves sending multiple strong bursts of magnetic energy into the brain.  The pulses are increased in strength until they are actually causing neurons (brain cells) to fire, and are repeated at that intensity about 3,000 times in each session.  In the present study, the average number of sessions received by participants was 28.  Strictly speaking, a medical procedure is considered non-invasive if it doesn’t break the skin, but it seems a misnomer in the present context.  X-rays don’t break the skin, but would hardly be considered non-invasive.


George et al also note that “Mood regulating centers in the brain overlap significantly with the neural pathways involved in pain regulation…”  They also report that TMS, applied to the prefrontal cortex (the same general area that is used to treat depression), has an analgesic effect, from which they tentatively conclude that opiate receptors play a part in the effects of TMS.

The precise mechanism of action of TMS is not fully understood.  However, George et al suggest that depression results from neural “dysregulation” in the prefrontal and limbic regions.  They hypothesize that:

“…chronic, frequent, sub-convulsive stimulation of the prefrontal cortex might initiate a therapeutic cascade of events that rebalances and normalizes the dysregulated prefrontal and limbic circuitry.” [Emphasis added]

This sounds remarkably similar to the now discredited notion of antidepressants therapeutically correcting chemical imbalances.


TMS is being routinely presented as a safer alternative to ECT for “treatment-resistant” clients.  In some instances (e.g. the quote from Dr. George, mentioned earlier), it is being promoted as more effective than ECT.  And based on present information, TMS does not seem to be as immediately traumatic to the brain as ECT.  However, there is a fundamental similarity between these two interventions:  they both interfere with the normal electrical activity of the brain.  We know that in the case of ECT, the long-term results are catastrophic, and that it is only a matter of time before this procedure will be banned, though meanwhile psychiatry, to its shame, continues to tout it as safe and effective.

With TMS, the picture is less clear.  But as this technology becomes more widely used, and used more frequently for given individuals, we may see increasing evidence of cumulative neural damage, including even more pronounced anhedonia than the technology purports to address.  Certainly the already established risk of seizure suggests that TMS has more in common with ECT than its proponents might be willing to acknowledge.

There are already indications that TMS protocols may call for higher doses and more frequent treatments in the future, at least for some individuals.  Mark George, MD, et al wrote in January 2013:

“Another issue is determining the optimal dose over the optimal time period for alleviating depression.  Most studies have stimulated patients at or above motor threshold.  This is particularly important in elderly patients, in whom prefrontal atrophy may outpace motor cortex atrophy… There have never been dose-finding studies with rTMS.  Thus, some groups are studying whether higher doses of TMS might produce more rapid or more effective results …Also, there are a few case series suggesting that weekly or monthly rTMS can serve as maintenance therapy for acute responders…” [Emphases added]


A great deal of psychiatric research, including the present Neuronetics study, uses questionnaires and rating scale scores as outcome measures.  This is an inherent deficit in all research of this kind, in that there is inevitably some uncertainty as to whether positive responses on a questionnaire reflect positive changes in a person’s life.

An additional problem in this regard is that often the questionnaire items are ambiguous, or at the very least, difficult to unravel.


It is clear from material presented above that there are already close links between the TMS industry and psychiatric researchers.  As has become glaringly obvious in the pharma sphere, these kinds of links do not generally foster research objectivity and integrity.


The concept of “treatment-resistant depression” is an integral component of TMS promotion, and has become a hot topic in recent years (5.9 million hits on Google).  The idea is that there are some individuals whose feelings of depression are not alleviated by antidepressants to any appreciable degree despite multiple trials and high dosages.

Many of us on this side of the debate are of the opinion that this kind of chronic anhedonia is actually caused by long-term use of antidepressants, and this notion has been presented persuasively by Rif El-Mallakh et al, 2011.  Not surprisingly, this concept has garnered little support in psychiatric circles, where depression is assumed (groundlessly) to be an illness; antidepressants are promoted as the “cure;” and people for whom the cure is ineffective are labeled treatment-resistant.

Instead of recognizing and acknowledging the destructive effects of the drugs, psychiatry is salving its conscience by pretending that these individuals have some undefined (and hence unrefutable) quirk that prevents them from benefiting from psychiatric drugs, and is now busily developing and promoting TMS as a treatment for a problem that psychiatry very likely created in the first place.

The idea that people can find happiness or contentment or peace or mind by having their brains tweaked by chemicals or electromagnetism is a fundamentally dehumanizing and disempowering concept.  Feelings of loss and despondency are an integral part of the human condition, best resolved by dealing with the source of the problem, with the assistance and support of friends and loved ones.  The notion that we can banish these feelings with an effortless brain-altering intervention is precisely the same philosophy that underpins the marketing of street drugs.  It provides an increasingly short-lived sense of relief for some people, but always entails more problems than it solves.  Ask any member of Narcotics Anonymous.

Understanding Human Behavior

A couple of months ago I wrote an article concerning ECT which generated some controversy.  One of the issues that came up was the relationship between biological explanations of human activity and more global explanations, which, for want of a better term, I’ll call person-centered explanations.

Any human activity can be viewed from different levels of abstraction.  Suppose, for instance, that I am sitting in my living room reading a book.  Then I put the book down, stand up, and go outside.  If the question were to be asked:  why did he put the book down and go outside? A wide range of perspectives and answers are possible.  One could, for instance, focus on the fact that I am a biological organism, and one could develop a detailed and comprehensive flow sheet of every muscle movement, every heartbeat, every sensory input, neural impulse etc., that had occurred from the moment that I put the book down until I was standing outside.  Such an account might be more or less detailed.  There would, of course, be physical limitations on the amount of information of this sort that is attainable, but from a theoretical point of view, one could compile a detailed, complete, and accurate biological account of the actions in question.  And such an account would be a valid response to the question:  why did he put the book down and go outside.

But there are other perspectives.  One could, for instance, ask me why I had behaved in this way.  This would be a person-centered approach.  And suppose I reply:  I had been sitting inside for too long; I wanted some fresh air.  Assuming that I’m truthfully describing my motives and feelings, this is also a valid and accurate explanation.

Of particular note is that although the two explanations appear very different, they are entirely compatible.  In fact, if the biological account is thorough and complete, one would be able to identify the neural activities that corresponded to my feelings of restlessness, my decision to move, my muscular movements, and my relief on getting outdoors.  Again, I stress that I doubt if that level of precision is, or ever will be, possible in practice, but the concept is valid.  Every element of the person-centered explanation will have a corresponding element in the biological flow-sheets.

For this reason it makes no sense to argue about which explanation is correct.  They are both correct.  I – the subject of the person-centered perspective – am also the subject of the biological perspective.

The act of stepping outside for fresh air is trivial and unremarkable, but the same plurality of perspectives can be applied to all our actions, including dysfunctional or counterproductive behavior.  The activity can be viewed as biological and can be probed and catalogued by neurologists, physiologists, etc…  Or it can be seen from a person-centered perspective and explored and formulated from that point of view.  There are also other perspectives, e.g. economic, political, social, familial, occupational, etc…  From the economic perspective, for instance, I would be considered a consumer, and my restlessness and my desire for fresh air might identify me as a marketing target for outdoor wear, wilderness vacations, bird-watching magazines, etc…  From a familial perspective, I am a husband, father, father-in-law, and brother within a fairly extended network of supportive relationships.  From a political perspective, I am a voter.  And so on.  I can be observed and studied from all of these perspectives, and although the observations will look very different, they are entirely compatible provided they are accurate.

For every thought, feeling, and behavior there is a corresponding neural event.  Some people contend that the thought/feeling causes the neural event; others say that the neural event causes the thought/feeling.  Still others contend that the cognitive/emotional activity and the neural activity are the same thing, but viewed form different perspectives.  The relative merits of these contentions have been debated by philosophers for hundreds of years, but for our present purposes, it doesn’t matter which is correct.  The point here is that there are neural events and there are thoughts/feelings/actions, and there is a correspondence between the two.  A super-neurologist with super-equipment could probe my brain and identify and catalog various patterns and clusters of neural and chemical activity.  But I experience these neural activities as thoughts and feelings.  Each perspective is valid, and each has its proper place.

A neurosurgeon, for instance, would be primarily concerned with the biological perspective, while most of our day-to-day interactions with other people are approached from a person-centered perspective.  A person asking me, for instance, why I had stepped outside is not enquiring about neural activity, inside my skull.  He’s asking about my thoughts/feelings/actions.

It is often tacitly assumed in psychiatric circles that because every thought, feeling, and/or behavior has a corresponding neural underpinning, therefore counterproductive thoughts, feelings, and/or behaviors must be the result of faulty or malfunctioning neural equipment.  But this is an unwarranted assumption.

Let’s take the example of childhood temper tantrums – and let’s look at these from a person-centered perspective.

If a child throws a tantrum in a grocery store, demanding candy or a toy or whatever, and if the parent gives in to his demands, then other things being equal, the probability of a tantrum in future store visits is increased.  This is one of the ways that we learn:  if an action brings about a favorable result, we try it again.  This is an adaptive mechanism.  It is not an instance of something going wrong in the child’s brain.  Rather it is an instance of something going right.  The child’s learning “machinery” has worked perfectly.  And from a person-centered perspective, it is an instance of the child learning to navigate his way in social relationships.

In the example above, I’ve described the scenario and outcome in very simplistic terms and have included the qualifier “other things being equal.”  But in practice other things are never equal, and the precise outcome on any given occasion is impossible to predict.  But whenever we interact with our children, we are teaching them something, and they are teaching us something.  In the above example, the child has learned:  if I want candy, I throw a tantrum.  The parent has learned:  if I want to stop his tantrum, I give him candy.  Unless something significant changes, it is likely that two things will happen.  The child will start to throw tantrums in other situations besides grocery stores, and any attempt on the part of the parent to regain control of the situation will be met initially with escalation of the tantrums.  This is not an instance of something going wrong within the child.  Instead, and apparently paradoxically, it is something going right.  The child is expanding his behavioral repertoire in accordance with the normal principles of behavior acquisition.  What has gone wrong is that the parent is teaching a response that ultimately will be problematic and counterproductive.

From a person-centered perspective, even frequent and severe temper tantrums can be understood as normal responses to suboptimal situations.  Obviously, in this context, I do not mean statistically normal.  Severe and frequent temper tantrums are not normal in the statistical sense of the term, but in the circumstances outlined above, they are normal in that they can be understood if viewed from a person-centered perspective.  There is no a priori need to invoke explanations based on neural malfunctions or pathology in the absence of compelling indications that such factors are present and causally significant.

Obviously each tantrum has a specific neural underpinning, but it is fallacious to assume neural  pathology based purely on the presence of negative or counterproductive behaviors.  Neuronal circuits and neurotransmitters that are functioning perfectly can underpin and drive destructive behavior as readily as constructive behavior.

The distinction between a person-centered perspective and a bio-neurological perspective applies to almost every facet of human existence.  We are biological organisms, but we are also thinking, feeling and self-directed persons.  For instance, I carry within me memories of the home in which I grew up and of my family of origin.  These memories are complex and intertwined, but I can bring them to the forefront of consciousness more or less at will.  Now let’s say that my super-neurologist with his super-equipment can probe around inside my skull and locate the neurons in which all these memoires are stored.  And let’s make him (or her) even more super, and imagine that he can “read” these various neuronal engrams.  There is still a fundamental qualitative difference between his readings and my memories of my childhood.  A good analogy would be that he can read the book, but I’m living the part.  Another analogy:  a person could, in theory at least, analyze a movie on a DVD and identify every pixel and sound unit.  But this is not the same as watching the movie.  A chemist can analyze every molecule of paint and canvas in the Mona Lisa, and still know absolutely nothing about the picture as a work of art or the motivation of the artist.

Our super-neurologist could analyze and catalog perfectly every sensory input and neuronal impulse in the actions of a tennis player making a spectacular backhand return.  But this is not the same kind of experience as that of the tennis player or even of the exulting fans.  And so on.

It’s tempting in this context to say that psychiatry has lost sight of the forest for the trees.  But it’s worse than that.  They’ve lost sight of the tree for the minute fibers and biological processes that sustain the tree’s growth.

There’s a quality to human experience that transcends neurons.  One can know everything that there is to be known about neurons and neurochemicals and know nothing of human life.  People are living, sentient, motivated beings, and we each have our own perspective and point of view.  We can be studied at various levels of abstraction:  atomic, molecular, bio-molecular, physiological, neuromuscular, skeletal, psychological, social, economic, political, occupational, etc… But we can also be approached and understood simply as individual people, with our individual histories, contexts, hang-ups, and aspirations.  No one perspective has any legitimate claim to being the preferred point of view.  One’s perspective has to be chosen in the light of the context.  If a person is sick (with a real sickness), then a biological perspective is probably preferable.  If he is sad or anxious, then a person-centered perspective seems the most apt.  If he is lonely and isolated, a social perspective might be most fruitful.  And so on.

In my experience virtually all the problems listed in the various editions of the DSM can be best approached, understood, and ameliorated from a person-centered perspective.  If you want to know why someone is depressed, take the time to get to know him, and then ask him.  Most people can tell you why they’re depressed or worried or nervous or scared or whatever.  But if it’s clear that your only interest is a 15-minute med check, they will tell you nothing.

If there is neural pathology then this, of course, should be addressed and alleviated to the extent possible.  But tampering crudely with the brain in the absence of confirmed pathology is dangerous and destructive.  Drugs do create altered states of consciousness, but the notion that we can provide effective help to people with problems of thinking, feeling, and/or behaving by tweaking their neurons betrays a fundamentally flawed and condescending view of humanity.




Is Electroconvulsive Therapy (ECT) Effective?

ECT, or shock treatment as it’s sometimes called, is a controversial topic.  Adherents describe it as safe and effective; opponents condemn its use as damaging and ineffective.  But it is still widely used in the US and in other countries.

The treatment consists essentially of passing sufficient electricity across the brain to cause a seizure.  Clients are anesthetized during the process.  It is used primarily in cases of severe depression.  Typically, shock treatment is administered twice a week until the depression remits or until no further improvement is noted in two successive sessions.  Most courses of treatment involve about eight sessions.

After shock treatment, some clients do appear to be less depressed, but this phenomenon has been interpreted differently by ECT’s proponents and opponents.  Proponents claim that the ECT treatments have clearly alleviated the depression.  Opponents claim that the apparent improvement is an example of post-concussion euphoria, and that the effects are short-lived.

The subject is vast, and an enormous volume of material has been written on the topic.  I Googled “electroconvulsive therapy” and got just over one million hits.  There is a growing body of writing from survivors who state that they were harmed by the process, but one can also find occasional reports from people who say that ECT was helpful to them.  In former years the psychiatric community claimed that there were no significant adverse effects on memory associated with ECT, but today there appears to be a general acceptance that memory loss can and does occur.


Steven Novella, MD, is a neurologist, and works as an Assistant Professor at Yale.  He’s active and influential in the skepticism movement, and has his own blog as part of the New England Skeptical Society:  Neurological blog: Your Daily Fix of Neuroscience, Skepticism, and Critical Thinking.  On March 22, 2012, he posted How Electroconvulsive Therapy Works, and he opens the article by stating:

“There is no real controversy over whether or not ECT works for depression – it is highly effective.”

This statement is linked to the abstract of a study by Diercks BG et al:  Efficacy of electroconvulsive therapy in bipolar versus unipolar major depression: a meta-analysis which appeared in the journal Bipolar Disorder, 2012.

This meta-analysis combined the results of six earlier studies, and concluded:

“ECT appears to be equally effective for both bipolar and unipolar depression and the remission rates are encouraging, especially for bipolar depression.”

The first thing to note is that the Dierckx et al study was not designed to answer the question:  is ECT effective?  but rather to assess its effectiveness for bipolar depression versus unipolar depression.  This is a significant issue, because the only way that one can adequately assess the effectiveness of a procedure like ECT is to compare its use to a placebo.  None of the studies collated in the Dierckx et al meta-analysis were studying effectiveness as such.  But the authors did state that “…the remission rates are encouraging…,” and presumably that is the finding on which Dr. Novella is basing his claim.

I was able to find, and examine, all of the six base studies used by Dierckx et al:

  1. Medda P, et al, Response to ECT in bipolar I, bipolar II and unipolar depression. J Affect Disord 2009; 118: 55–59.
  2. Grunhaus L, et al, Response to ECT in major depression: are there differences between unipolar and bipolar depression? Bipolar Disord 2002; 4(Suppl. 1): 91–93.
  3. Sienaert P, et al, Ultra-brief pulse ECT in bipolar and unipolar depressive disorder: differences in speed of response. Bipolar Disord 2009; 11: 418–424.
  4. Bailine S, et al, Electroconvulsive therapy is equally effective in unipolar and bipolar depression. Acta Psychiatr Scand 2010; 121: 431–436.
  5. Daly JJ, et al, ECT in bipolar and unipolar depression: differences in speed of response. Bipolar Disord 2001; 3: 95–104.
  6. Sackeim, HA et al, Length of the ECT Course in Bipolar and Unipolar DepressionJ ECT 2005; 21 (3): 195-197

All six of the base studies used questionnaires and rating scales to assess depression.  The Hamilton Rating Scale for Depression was used in all cases.  Other scales used included Brief Psychiatric Rating Scale (BPRS); Clinical Global Improvement (CGI); Beck Depression Inventory (BDI); etc.

Follow-up periods after the end of treatment were:

  1. Medda P et al:             1 week
  2. Grunhaus L et al:        no follow-up
  3. Sienaert P et al:           1 week and 6 weeks
  4. Bailine S et al:             no follow-up
  5. Daly JJ et al:                1 week
  6. Sackeim et al:              no follow-up

Only study number 3 – Sienaert et al – assessed for cognitive side effects.  They administered the Mini Mental Status Exam before treatment and at one and six weeks post treatment.  The results show a small but consistent improvement in scores across time (i.e. from pre-treatment to post-treatment).  However, the Mini Mental Status Exam is not sensitive to the kind of cognitive deficits generally associated with ECT except in the period immediately following the ECT.  The Sackeim et al 2007 study The Cognitive Effects of Electroconvulsive Therapy in Community Settings,  for instance, found on average no persistent deficits in Mini Mental Status Exam scores associated with ECT, but did find significant and persistent deficits in “…memory for autobiographical events.”  This is precisely the area in which survivors of ECT have been reporting problems for decades.


I have written on the subject of ECT before, here, here, and here.  In my opinion, the evidence is clear:  ECT has no overall superiority to placebo in the treatment of depression, except in the period during and immediately after the treatment, and, in at least some cases, does a good deal of damage.

My purpose in this article is to examine the evidence that Dr. Novella adduced to support his claim that ECT “…is highly effective.”  This is important because Dr. Novella presents himself as a debunker of pseudoscience, and routinely characterizes those of us on this side of the psychiatry debate as unscientific “deniers” (e.g. Mental Illness Denial – Part IV)

People reading his sentence:  “There is no real controversy over whether or not ECT works for depression – it is highly effective,” with a link to  the Dierckx et al study would, I believe, assume that the Dierckx et al study provided some evidence for this conclusion.  In fact, this is simply not the case.  Neither the meta-analysis nor any of the base studies were designed to address the question of general efficacy.  In addition, only one of the studies (Sienaert et al) had follow-up assessment beyond one week, and none of the studies controlled for the placebo effect.  Only one of the studies (Sienaert et al) addressed the question of adverse effects, which, I suggest, must be considered in any assessment of general efficacy.

On the other hand, the evidence from randomized placebo-controlled trials is clear:  apart from some short-lived lifting of mood, ECT is not effective as a treatment for depression.  A comprehensive review of the efficacy evidence can be found in Read J. and Bentall R, The effectiveness of electroconvulsive therapy: A literature review, under the heading Comparison With Simulated-ECT For Depression (p 335).  Read and Bentall concluded:

“These placebo controlled studies show minimal support for effectiveness…during the course of treatment …and no evidence…of any benefits beyond the treatment period.” (p 333)

The authors also state:

“Since the 2004 review [Chapter on Electroconvulsive Therapy, in Models of Madness, by Read, Mosher, and Bentall, 2004] there have been no findings that ECT is effective, but significant new findings confirming that the brain damage, in the form of memory dysfunction, is common, persistent, and significant, and that it is related to ECT rather than to depression.

Few of those exposed to the risks of memory loss, and to the slight but significant risk of death, receive any benefit even in the short-term.  There is no evidence at all that the treatment has any benefit for anyone beyond the duration of treatment, or that it prevents suicide.  The very short-term benefit gained by a small minority cannot justify the significant risks to which all ECT recipients are exposed.”

And yet ECT continues – a tribute to psychiatry’s faith in its dogmas, and its enduring resistance to any evidence that challenges these beliefs.


On November 14, 2013, Dr. Novella, in an article titled Is There a Pseudoscience Event Horizon? provided a list of “typical behaviors” of pseudoscientists:

1 – Hostile to criticism, rather than embracing criticism as a mechanism of self-correction
2 – Works backward from desired results through motivated reasoning
3 – Cherry picks evidence
4 – Relies on low grade evidence when it supports their belief, but will dismiss rigorous evidence if it is inconvenient
5 – Core principles untested or unproven, often based on single case or anecdote
6 – Utilizes vague, imprecise, or ambiguous terminology, often to mimic technical jargon
7 – Has the trappings of science, but lacks the true methods of science
8 – Invokes conspiracy arguments to explain lack of mainstream acceptance (Galileo syndrome)
9 – Lacks caution and humility by making grandiose claims from flimsy evidence
10 – Practitioners often lack proper training and present that as a virtue as it makes them more ‘open’

With the possible exception of numbers 8 and 10, this list seems to me like a very accurate portrayal of psychiatry.

As mentioned earlier, Dr. Novella’s article of March 2012 opens with the claim that ECT is “…highly effective.”  The article then goes on to address the question: how does ECT work?  For this issue, Dr. Novella refers to another study, Electroconvulsive therapy reduces frontal cortical connectivity in severe depressive disorder, Perrin et al, 2012, which performed fMRI scans on nine individuals before and after ECT.  This study found that “…functional connectivity was considerably decreased after ECT…”

Given that ECT causes significant and persistent memory loss, which, incidentally, Dr. Novella acknowledges, it seems to me that the most parsimonious way to interpret the Perrin et al results is that the reduction in functional connectivity, which actually means the breaking of circuits, might be the cause of the memory loss.

Dr. Novella ignores this possibility, however, and, following the lead of the researchers, suggests instead that the individuals who received the ECT had:

“…overactive connectivity between that part of the brain that generates the emotion of depression and the part of the brain involved in cognition and concentration. In these patients, therefore, their depressed mood has a significant effect on their thoughts and ability to concentrate. ECT appears to reduce this hyperconnectivity, which should significantly reduce the symptoms of depression.” [Emphases added]

The “logic” here could be summarized as follows:  ECT alleviates depression; ECT breaks neural circuits; therefore it is these “overactive” neural circuits that caused the depression in the first place.  I suggest that this is an almost textbook example of the second item of Dr. Novella’s list of typical behaviors of pseudoscientists:

“Works backward from desired results through motivated reasoning.”

Despite the evidence of damage and ineffectiveness, psychiatry clings tenaciously to ECT.  For years, they denied that it caused memory loss, claiming instead that any such deficits were the result of the depression or, in at least one case (Fink M Psychosomatics, 2007), somatoform disorder!  (In other words, the memory loss was “all in their heads.”)

As the evidence mounted, they conceded that ECT entails some memory losses, but insisted that these were minor and/or transient.  Today they acknowledge that sometimes the memory problems are significant and persistent, but they claim that the impact of these problems is balanced by ECT’s “efficacy” as a treatment for depression.

How much longer can they continue this travesty?

ECT And Adolescents At The Mayo Clinic


At the APA annual convention in San Francisco in May of this year, Chad Puffer, DO, of the Mayo Clinic, presented a poster display titled ECT Use in Adolescents at the Mayo Clinic.  The poster was reported by Caroline Cassels of Medscape.com, a month later (ECT in Kids:  Safe, Effective, Robust and …Underutilized), and drew critical comment a week later (July 2) from Kelly Patricia O’Meara of CCHR International.

I didn’t spot any of this until last week, when it came up on the Twitter feed from DxRevision Watch and Peter Kinderman.

The research in question does not appear to have been written up in any journal – or if it has, I haven’t been able to find it.  All I’ve got to work with at this point is the APA ‘s abstract, which is reproduced below in full, and the Mayo Clinic’s poster, which was sent to me by Ms. Cassels.

APA Abstract NR7-34
Lead Author: Chad Puffer, D.O.
Co-Author(s): Christopher Wall, MD
Mark Frye, MD
Background: Electroconvulsive therapy (ECT ) remains a useful, yet infrequently employed treatment option in youth experiencing severe emotional illnesses. At Mayo Clinic, approximately 50 adolescents have been treated with ECT for a range of psychiatric illnesses over a 20-year span. Methods: This study reports a comprehensive practice and outcomes review of adolescents treated at Mayo Clinic with ECT. Treatment parameters including electrode localization, stimulus dosing, seizure duration and associated treatment complications are reported. Long-term follow-up clinical information regarding post-treatment outcomes as adults are also reported.
Conclusion: ECT use is a viable and appropriate treatment approach in youth experiencing severe, clinically debilitating illnesses that have been recalcitrant to other treatment options. Treatment parameters largely mirror the adult ECT practice, with some notable and important exceptions related to tolerability, seizure duration and variability of clinical outcomes.


1.  “Electroconvulsive therapy (ECT) remains a useful, yet infrequently employed treatment option in youth experiencing severe emotional illnesses.”

Firstly, note the word “illness.”  They continue to refer to depression as an illness despite the lack of any evidence to support this position.

Secondly, note the assertion that shock treatment is a “useful” treatment option for youth.

Thirdly, note the term “yet infrequently applied…”  I think the implication here is that if more psychiatrists were aware of how great this treatment is, it would be used more widely

Fourthly, note the term “severe emotional illnesses,” implying, I believe, that the shock “treatment” in the study was used to address only emotional problems.  In fact, in the poster text it states clearly that the electric shocks were used to “treat” affective, psychotic, and  other  disorders (including anorexia nervosa!)

2.  “This study reports a comprehensive practice and outcomes review of adolescents treated at Mayo Clinic with ECT.”

The study in question was a fairly rudimentary and retrospective chart review, and characterizing it as “comprehensive” is quite a stretch.  There were only 46 participants over 20 years.  Twelve-month follow-up data was available for only 29 of these, and there was no control group.

3.  “Long-term follow-up clinical information regarding post-treatment outcomes as adults are also reported.”

The only reference to follow-up into adulthood mentioned on the poster is:

4.  “Adolescents receiving ECT were eventually diagnosed with personality disorders approximately 13% of the time upon reaching adulthood.”

5.  “Conclusion:  ECT use is a viable and appropriate treatment approach in youth experiencing severe, clinically debilitating illnesses that have been recalcitrant to other treatment options.”

In my view, this rather strong conclusion is not warranted by the evidence presented in the Mayo Clinic poster.  (More on this below).


The poster opens with some general comments as to the effectiveness of ECT in adults and in adolescents, and laments the fact that there is still some reluctance to use this treatment with children “despite its recognized efficacy.”  In support of the latter claim, the authors refer to an earlier (1993) Mayo Clinic record review of 20 young patients aged 18 or younger.  This earlier review was conducted by Schneekloth et al, and found “…ECT to be safe and effective in adolescents with severe and medication-resistant mental illnesses.”  Interestingly, Dr. Puffer’s poster study draws almost identical conclusions:

“Despite controversy on ECT use in adolescents, these data suggest it is a safe, reasonably well-tolerated and effective treatment for the most severely ill adolescents resistant to pharmacotherapy and psychotherapy.”

The poster study records search identified 46 pediatric patients who had received ECT at the Mayo Clinic between 1993 and 2012.

“Each patient’s medical chart was reviewed to verify ECT administration during their care at Mayo Clinic. All available treatment settings, side effects, medications and diagnoses were recorded. Where possible, pre-ECT and post-ECT clinical data were recorded.”

Note the words “where possible,” which suggests that some of the pre and post assessments were missing.  Since these assessments are the essence of the matter, it is critical to know the extent of, and the reason for these omissions.  But the poster gives no other information.

“Most adolescents who received ECT were taking one less medication one year after ECT than they were at initiation of ECT, and the average change in number of medications prescribed pre- and one year post-ECT was -0.74.”

This is interesting, but hardly constitutes a great improvement, especially as one of the stated criteria for ECT was a lack of response to pharmacotherapy.

The most important item under the “results” heading was:

“ECT appeared to be effective in reducing symptoms of affective (major depressive disorder, bipolar affective disorder), psychotic (psychosis NOS, schizophrenia, steroid-induced psychosis), and other disorders (schizoaffective disorder, depression with psychotic features, catatonia, anorexia nervosa) as measured by Clinical Global Impression scales of Symptoms and Improvement upon independent retrospective analysis by a board-certified Child and Adolescent Psychiatrist and a PGY-2 Psychiatry resident.”

The words “appeared to be” seem noteworthy, and imply a good deal more caution than the conclusion given in the APA abstract.

The criterion for improvement is also noteworthy:

“…as measured by CGI scales…”

CGI stands for Clinical Global Impression.  This is a subjective assessment instrument used by psychiatrists to rate severity of a client’s problem immediately after a clinical interview.  It is widely used in clinical practice and in research.  It is subjective, but it does bring an element of uniformity to these kinds of assessments.  The CGI has been in use since 1976.

There are 3 CGI scales:

S – assesses the severity of the “mental illness.”
I – assesses any improvement since last assessment
E – assesses the therapeutic effect of the intervention and any side effects.

Back to the poster.  What Dr. Puffer and his colleagues seem to be saying is that ECT appeared to be effective with these various disorders, as measured by CGI-S and CGI-I scales – and this is where it gets murky – “…upon independent retrospective analysis by…” two qualified psychiatrists.

It’s the word “retrospective” that I’m having trouble with, and the poster does not make it clear what this means.  Under the heading “discussion,” it says:

“Retrospective CGI-S and CGI-I analysis showed significant improvement in ECT-treated adolescents.”

But again, the term retrospective is not clarified.  Two phone calls and an email to Dr. Puffer at the Mayo Clinic asking for clarification have gone unanswered.

It looks like this is what happened.  Between 1993 and 2012, 46 young people (ranging in age from 12 to 19, incidentally) received ECT.  The psychiatrist administering the shocks wrote up his notes in the clinical record in the normal way, but didn’t do a CGI assessment, either pre or post.  Then in 2012, the two expert psychiatrists retrospectively completed the CGI-S and the CGI-I pre and post- ECT based on the notes in the treatment record.  This is a very questionable research procedure, and it is with considerable hesitation that I even suggest it. But I can see no other interpretation.  If the CGI’s had been done at the time of the ECT, reading and transcribing the scores would have been a simple clerical task.  It certainly would not have required two independent psychiatrists.

If my interpretation is correct, then no safe conclusions can be drawn from the study.  A retrospective analysis of a psychiatrist’s record of his own work is fraught with possibilities for error.  This is why we have double-blinded, randomized, controlled trials!

Also of note is the fact that the third CGI scale – the efficacy index – was not used.  In fact, it says under “discussion” that “Systematic measurement of cognitive side-effects of ECT was not available.”  This presumably means:  not available in the record; which presumably means that no assessment of cognitive side effects was done either at the time of the ECT or at the one-year follow-up.  Or, I suppose it could mean that these assessments were done, but were so damaging that they were omitted from the write-up.

The lack of cognitive side effects assessment is particularly disturbing, in that the American Academy of Child and Adolescent Psychiatry in their 2002 Practice Parameter for Use of Electroconvulsive Therapy With Adolescents  state under the heading “cognitive assessment”:

“Every adolescent undergoing ECT must have a memory assessment before treatment, at treatment termination, and at an appropriate time after treatment (usually between 3 and 6 months post-treatment) [MS].”

MS means “minimal standard,” meaning that this is an absolute requirement.  The parameter was approved and published in 2002, so it was in place for the entire second half of the study (2002-2012).  In this light, an admission by the authors that measurements of side effects were not available is, in my opinion at least, a matter of grave concern.


Each adolescent received, on average, 10.4 shocks.  The range was 4 to 27.

The average seizure duration was 84.4 seconds.  The range is 16 seconds to 272 seconds (4 minutes and 32 seconds).  Sixteen participants had seizures lasting more than three minutes.


The Mayo Clinic is a prestigious medical center with a world-wide reputation for medical excellence.  I am truly surprised that they allowed this document to be displayed under their name and logo.

In my view, this is another flawed study in a long line of flawed studies that purport to demonstrate the efficacy of ECT.  If ECT proponents want to be taken seriously, they need to take on board Johnstone et al’s 1980 Northwick Park electroconvulsive therapy trial finding that sham ECT (where the patient is anesthetized but not shocked) is just as effective as real ECT.  Until then, it’s just more chaff in the wind.


Involuntary Shock Treatment To Be Banned in Ireland

Courtesy of Talla Trialogue on Twitter, I recently read an article in journal.ie on this topic.

Kathleen Lynch, Minister of State for Disability, Equality, Mental Health and Older People, has reportedly stated that “…the law will be changed so that unwilling patients will no longer be forced to receive ECT.”

At present, if an individual refuses ECT, his refusal can be overridden by the signatures of two psychiatrists.

However, not everyone is in favor of the ban on forced ECT.  There’s an article by Marie Feely, Proposed ban on Involuntary ECT criticized published in irishmedicalnews in January 2012.  The article reports on a survey of consultant psychiatrists published in December 2011.  Ms. Feely writes:

“The study found that for involuntary patients who have capacity to consent but are unwilling to do so, 32 per cent of respondents said they would prescribe the treatment.” (Emphasis added)

I have written on ECT before, here and here.  There are two aspects of ECT that in my opinion merit particular attention.

1.  There is no significant difference in outcome for real ECT vs. sham ECT (in which the individual is prepared, anesthetized, but not actually shocked).  For references and discussion see Bracken et al Psychiatry beyond the current paradigm.

2.  Loss of retrograde memory is a common and devastating side effect.  Linda Andre’s book Doctors of Deception is very informative reading on this matter.

Ireland’s move to ban forced shock “treatment” is a great step forward, with regards to civil rights and curbing the abusive, dehumanizing,  and destructive power of modern biological psychiatry.

I imagine that there has been a great deal of work done by survivors, activists, and others on this matter, and it is gratifying to see the dogmatic certainty of psychiatry being successfully challenged.

Psychiatry is founded on spurious premises and destructive practices.  It is like a sand castle, and the tide is coming in.

Psychiatry Has the Moral High Ground (According to Jeffrey Lieberman)


As I suppose everyone knows by now, psychiatry has been on the receiving end of some very serious criticism in recent years.  The criticism has come from many sources, including: survivors of psychiatric “treatment,” non-psychiatric mental health practitioners, journalists, the general public, and even from some psychiatrists themselves.

The content of the criticisms has been equally varied, and includes:  that the concept of mental illness is fundamentally spurious and devoid of explanatory significance; that psychiatric “treatment” (i.e. drugging people) is ineffective, physically damaging and disempowering; that psychiatry has forged and continues to maintain corrupt and corrupting relationships with the pharmaceutical industry with regards to the peddling of drugs and the hijacking of research for commercial ends; etc…

By any standard, these are very serious criticisms.  I cannot recall ever seeing another profession take such a hammering, but I believe that if a bona fide profession did receive such criticism, they would take it seriously, conduct investigations, and start cleaning house.  This kind of honest self-appraisal has been almost totally lacking in psychiatry’s case.  Instead, we’ve received spin, spin, and more spin.


Dr. Lieberman is the recently installed president of the APA.  On June 18, he posted an article on Psychiatric News, the online journal of the APA.  The article, What It Means to Be President, is a response to the recent criticism.  Or more accurately, it purports to be a response.  In fact, it addresses not one substantive issue.  The general tone is:  why won’t you bad people stop picking on us good psychiatrists?

My first inclination was to ignore the piece.  There are more important issues to write about.  But Dr. Lieberman is the president of the APA.  This is as close as it gets to psychiatry’s “official” response to its critics.  For this reason, I believe that Dr. Lieberman’s rhetoric should receive some scrutiny.


Dr. Lieberman begins by telling us that he was moved by a recent ceremony in San Francisco for swearing in the APA’s latest batch of distinguished fellows.  He attributes his emotionality on this occasion to the “current challenges” facing psychiatry.  He provides a list of these challenges:

1. undelivered healthcare reform
2.  continuing stigma
3.  wanton criticism of psychiatry and the APA, and
4.  an enormuous burden of illness caused by mental illness and unmet clinical need for treatment.

It’s not clear what Dr. Lieberman means by undelivered healthcare reform.  With regards to stigma, I presume that he’s talking about the stigma of clients.  He doesn’t seem to realize, however, that promoting the idea that “mental illnesses” are biological actually increases the degree of stigma (Angermeyer et al 2011).

My 2009 edition of Merriam-Webster’s dictionary, under the definition of “wanton,” includes the following:

wanton (adj) ….merciless, inhumane; having no just foundation or provocation, malicious …

By using the word “wanton” in this context, Dr. Lieberman is saying that our criticisms are unwarranted and malicious.  Isn’t this the way children argue with each other in the schoolyard?  Did so!  Did not!  You have cooties!  Do not!

Given his position and his history, I suppose it’s reasonable that Dr. Lieberman would challenge our criticisms, but by the same token (his position and his history), it would also have been reasonable to expect something along the lines of logical discourse and factual evidence.  Simply denouncing our criticisms as “wanton” seems, if anything, to add weight to our side of the argument.

I’m not sure what Dr. Lieberman means by the “enormous burden of illness caused by mental illness”.  The putative “unmet clinical need for treatment” is something we’ve heard before, and is difficult to square with the fact that at the present time in the US, antidepressants are the second most prescribed drugs, second only to antibiotics.  That hardly sounds like unmet needs.

Dr. Lieberman goes on to remind us that “we are living in a moment of unprecedented scientific progress and with an array of therapeutic interventions with extraordinary effectiveness.”

The holy grail of psychiatric research for the past three or four decades has been the neurobiological underpinning for its various “diagnoses.”  Literally billions of dollars and centuries of manpower have been poured into this endeavor, but the only way to honestly describe the outcome is:  a total failure.  Even Thomas Insel, MD, who is certainly not one of biopsychiatry’s wanton critics, has admitted this.

So if Dr. Lieberman is aware of some “unprecedented scientific progress” that lends support to psychiatry’s medicalization of virtually all human problems, this might have been a good time to unveil it.

Similarly, with regards to the “therapeutic interventions with extraordinary effectiveness,” it would have been nice to learn what these are.  Perhaps he means neuroleptic drugs that shrink brain volume and lead to poorer long-term outcomes?  Or perhaps he means antidepressants whose effectiveness is about on a par with placebos?  Or perhaps he means electric shock “treatment” that reportedly “works” by obliterating people’s memories?

Dr. Lieberman concedes that it is easy to lose sight of the positive aspects of psychiatry because of:

1.  the recession
2.  the mass shootings
3.  the criticism directed against DSM-5, which incidentally, was “aided and abetted” by the media.

Of course I would suggest that the reason that it is so easy to lose sight of the positive aspects of psychiatry is that they are so few and far between.  But undoubtedly that’s just another example of my wantonness!  And how in the world is the economic recession casting psychiatry in a bad light?

Incidentally, doesn’t the term “aided and abetted” contain a slight suggesting of nefariousness?  Those wicked journalists!

Dr. Lieberman tells us that neither he nor his colleagues could have foreseen any of these dreadful developments.  This strikes me as odd, because the general themes have been out there for decades.  Presumably his attention was elsewhere.  And then – in what I can only describe as a plaintive bleat – he says:  “…they [the criticisms] certainly were not what we signed up for when we decided to pursue a career in psychiatric medicine.”  Poor lamb.  And note the final word – “medicine.”  In other words:  we’re real doctors – really!  Why won’t anyone believe me?

Dr. Lieberman continues:  “…the stigma directed at mental illness and psychiatry continues to be perpetuated by the media disseminating exploitative and misleading information.”  The meaning here is a little veiled, but I guess the gist is that the wretched media have been spreading lies about psychiatrists.  Here again, he might have served his cause better if he’d actually refuted one or two of these “lies.”

At this point, Dr. Lieberman issues his rallying cry:  “…it is time for psychiatrists, and led by the APA, to stand up for our patients and our field.”  This sounds more like a cheerleader than the president of a professional association.

Psychiatry, Dr. Lieberman goes on to tell us, has – and I’m not making this up:

1.  scientific momentum
2.  public health imperative
3.  moral high ground

Momentum, of course, as any student of physics knows, is a directional variable.  It can be forward or backward.  So here I am actually in total agreement with Dr. Lieberman.  Psychiatry does indeed have enormous momentum – but it’s so far backwards that it could accurately be described as pre-scientific.

I’m not sure what public health imperative means.  Something to do with epidemics?

But I do understand the concept of moral high ground, and I find it difficult to reconcile Dr. Lieberman’s claim with the numerous reports of corrupt relationships between “eminent” psychiatrists and the pharmaceutical industry, and with the fact that the APA routinely endorses for continuing educational credit, pharmaceutical presentations that even psychiatrists acknowledge are nothing more than marketing sessions.

In this context, I think it is also noteworthy that Dr. Lieberman has, or has had, financial relationships with:  Allon; GlaxoSmithKline; Janssen Pharmaceutica Products, L.P. (US); Merck & Co., Inc; Novartis Pharmaceuticals Corporation; Pfizer Inc.; Sepracor Inc.; Targacept; Bioline; GlaxoSmithKline; Intra-Cellular Therapies, Inc.; Eli Lilly and Company; Pierre Fabre; Psychogenics; and Repligen Corporation.  According to ProPublica, in 2012, he received $43,204 from Eli Lilly alone.  But, of course, none of these relationships has ever influenced his professional judgment in the slightest.

If Dr. Lieberman genuinely wants to occupy the moral high ground (as opposed to just talking about it), he needs to introduce sweeping anti-corruption reforms in his own organization, and he needs to start now!

Then we have some more cheerleading.  Dr. Lieberman exhorts his constituents not to be defensive or even timid.  They must raise the awareness of the public and other physicians about – get this – “…the true nature and inherent value of psychiatric treatment and mental health care.”

Can you imagine the president of the kidney doctors association, or the lung doctors association, – or any bona fide medical specialty – spewing this kind of tripe?  People who have kidney failure or lung failure know the value of these treatments.  We don’t need speeches.  We don’t need to have our consciousness raised.  Psychiatry is the only medical specialty that needs spin.

And then it gets even worse:

“So while on one hand I have a healthy dose of frustration and outrage, on the other hand I am very optimistic and bullish on our profession.”

His profession is being criticized severely from several quarters on various issues, all of which have merit.  Dr. Lieberman tells us that this induces in him feelings of frustration and outrage.  These are strong terms.  Is it not almost the essence of maturity that one can listen to criticism with an open mind?  Not according to the president of the APA.  He assures us that his feelings of frustration and outrage are healthy.  In other words, it’s our fault that he’s feeling frustration and outrage.

The inmates I worked with back in the prison, used to call this “flip the script” (attributing the blame for one’s failings onto one’s accusers).

Finally, Dr. Lieberman recounts his goosebump moment as he administered the pledge to the distinguished fellows:

“I suddenly realized that the best strategy to respond to the challenges and criticisms that we faced was to rededicate ourselves to the principles and values that inspired our profession and that the pledge of Distinguished Fellowship beautifully articulated these precepts.”

Dr. Lieberman wraps up his article by quoting the pledge in full.  And it really is a wonderful pledge – replete with lofty goals and aspirations.  One might, however, have a little difficulty mapping it to current psychiatric practice, e.g. “I will faithfully dedicate myself above all to the welfare of my patients…” and “I further pledge to avoid commercialism in my professional life; …and to avoid any financial practice whatsoever that might debase my profession.”


The gist of Dr. Lieberman’s article is:  we psychiatrists are good guys because we have a really good pledge.  Those scoundrels who criticize us are cads and bounders.  And the reason I know they are cads and bounders is because they criticize us good guys.

So far, this is just funny in a pathetic sort of way.  But we need to remember that for Dr. Lieberman, rededicating himself and his psychiatric colleagues to this “beautifully articulated” pledge is: “…the best strategy to respond to the challenges and criticisms” that have been directed against psychiatry.

So, to other mental health practitioners like myself who criticize psychiatry as spurious in concepts and destructive in practice, Dr. Lieberman’s response is: we’re rededicating ourselves to our pledge!

And to those journalists who have seen through the self-serving lies and the facile “logic,” and repeatedly exposed the destructive and disempowering practices, Dr. Lieberman’s response is:  we’re rededicating ourselves to our pledge!

And to the survivors of psychiatric “treatment” who are coming out in increasing numbers and conscientiously cataloging the abuse and stigma and disempowerment they received at the hands of psychiatry, Dr. Lieberman’s response is:  we are rededicating ourselves to our pledge!

And to the heart-broken parents of children who have taken their own lives under the influence of psychiatrically prescribed drugs, Dr. Lieberman’s response is:  we are rededicating ourselves to our pledge!

And remember, dear readers, Dr. Lieberman is the president of the APA.

ECT – New and Improved?

I’ve just come across a strange article on Mad in America.  It’s called Researchers look at therapeutic benefits of ketamine.  You can see it here.  It doesn’t identify an author, but it’s from the University of Manchester.

The opening paragraph says:

“The largest trial into the use of Electroconvulsive Therapy (ECT) in the UK in more than 30 years will look into how the use of the Class C drug ketamine might reduce the side effects of ECT for those being treated for severe depression.”

The research team is to be led by Professor Ian Anderson, a psychiatrist, who is quoted as saying:

“It’s a great opportunity to really study ECT and see how we can improve it. ECT is the most effective treatment we have for severe and Treatment Resistant Depression – but it can cause cognitive and memory difficulties as a side-effect.”

It’s to be a randomized controlled study.  They’re planning to recruit 160 participants who have been referred for ECT, and then randomly assign them to ECT alone or ECT plus ketamine.


I was struck firstly by the comment that this is to be the largest trial into the use of shock “treatment” in 30 years in the UK.  There are to be 160 people in this study, which doesn’t seem all that large given the level of controversy surrounding this “treatment.”

Secondly I was struck by Dr. Anderson’s statement that shock “treatment” can cause cognitive and memory difficulties as a side effect.  The term “difficulties” seems like an understatement.  There is ample documentation in the literature that the memory losses are often massive and devastating.  It is also the case that several authorities on shock “treatment” have stated very clearly that memory loss is not a side-effect, but rather is the main effect.  The rationale that has been presented is that the electric current alleviates depression by obliterating painful memories!

It has also been well documented, incidentally, that shock “treatment” is no more effective at alleviating depression than sham shock treatment, where the person is anesthetized but not shocked.


But what surprised me most was the proposed use of ketamine as an adjunct to shock “treatment.”

Ketamine is a drug used as an anesthetic for animals, and in certain circumstances for humans.  Its effects in humans include anesthesia and hallucinations.  It is used recreationally as a psychedelic drug (street name: Special K), and is in the same drug class as phencyclidine (PCP), also known as Angel Dust.

Dr. Anderson expresses the hope:

“…that ketamine will reduce the longer-term loss of past memories, including autobiographical memory – which may include memories of childhood holidays, growing up and early life – that some people experience with ECT and which can be very distressing.”


I’m no neurologist, but it is my understanding that 450 volts of electricity coursing across the brain causes damage.  I find it hard to imagine how the concomitant injection of a hallucinatory anesthetic could have a mitigating effect on this damage.  I’m left with the suspicion that perhaps the researchers are hoping that the euphoric effects of the drug will reduce post-procedural complaints of headaches and feeling “wiped out.”

In other words, the drug might have some effect on what clients say about the treatment (i.e. fewer complaints), but it seems unlikely that it will reduce the amount of brain damage or memory loss.