ECT Device Reclassification Draft Guidance – Moira Dolan MD to the FDA, 2016

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Moira Dolan MD

DATE  February 28, 2012

TO James M. Engles, M.S., M.B.A.                                                              

     Designated Federal Officer

     United States Food and Drug Administration

     Division of Dockets Management

     Food and Drug Administration

     5630 Fishers Lane, Room 1061

     Rockville, MD 20852

 FROM Moira Dolan, M.D.


FDA Executive Summary

Prepared for the January 27-28, 2011 meeting of the Neurological Devices Panel

Meeting to Discuss the Classification of Electroconvulsive Therapy Devices (ECT)

FDA’s selection of the medical literature regarding safety of ECT failed to obtain the objectives as mandated by the GAO.

ECT machines are “pre-amendment devices” that currently remain Class III. Until proven otherwise, it is presumed that insufficient information exists to assure the safety or effectiveness of the device through general or special controls. The current task of the FDA as demanded by the GAO is to determine 1.) if manufacturers of ECT machines should be required to submit pre marketing approval (PMA) for the devices, and 2.) if ECT machines should be reclassified as Class II devices.

The FDA stated that it set out to establish their answers to the above two questions for each of six diagnoses, including Depression (unipolar and bipolar), Bipolar manic (and mixed) states, Schizophrenia, Schizoaffective disorder, Schizophreniform disorder and Catatonia. However the literature often did not distinguish the types of depression or the types of schizophrenia, and there were no qualifying studies on catatonia. Thus of the seven intended categories to study, FDA only reviewed articles on three.

The FDA obtained comments through manufacturers and public dockets, Manufacturer and User Facility professional and/or governmental practice guidelines, Device Experience database (MAUDE), in addition to their own literature review. In order to satisfy the requirement of “well controlled investigations experiments”, FDA limited their literature interest to randomized controlled trials (RCT).

Studies were included if they examined the following comparator groups: ECT vs. sham ECT, ECT vs. placebo, ECT vs. active medication, ECT utilizing different waveforms (i.e., sine wave, brief pulse, ultrabrief pulse), ECT utilizing different electrode placement (i.e., bitemporal, bifrontal, unilateral dominant, unilateral non-dominant), ECT utilizing different energy dosages, ECT with different frequency of treatment administration, ECT + intervention to optimize safety/effectiveness vs. ECT without intervention, Post-ECT course maintenance ECT vs. continuation medication treatment.

The following 17 points will illustrate the failure of the selected literature to demonstrate ECT machine safety, and in fact will show that the ECT machine is not safe:

1. Four of the comparator groups only compare ECT to itself, the variations being in terms of wave forms, electrode placement, energy dose and frequency of administration. These studies are not designed to furnish information about the definite safety and absolute effectiveness of ECT, only the relative safety and effectiveness compared to ECT delivered in some other fashion.

2. Two of the comparator groups compare ECT with or without additional measures, but do not establish whether ECT is safe or effective, and thus do not serve to answer the safety and effectiveness questions as mandated by the GAO.

3. Only three of the nine types of comparator groups included by FDA are true comparisons of ECT versus no ECT. The remaining six types of studies have no role in determining the safety and effectiveness of ECT. These comparator groups strictly address mitigation of adverse events. These studies have no role in the determination as to the safety and effectiveness of ECT. Such reports should not be under consideration until after safety and effectiveness of ECT has been demonstrated, and then only to establish if it were possible to put mitigating factors into place.

4. Regarding safety, FDA stated that it only included studies that utilized established psychiatric rating scales. However, the lack of meaningful interpretation of such scales is admitted in this statement by FDA:

“Because ECT is used to treat psychiatric conditions, it is often difficult to distinguish between primary symptomatology and treatment-caused (or exacerbated) effects”. (ECT 515(i) Executive Summary Draft p.17, #5)

5. FDA admitted the obvious insufficiency of studies regarding the following serious, debilitating or deadly adverse effects:

b. Personality changes caused or worsened by the treatment. FDA concluded: “Because ECT is used to treat psychiatric conditions, it is often difficult to distinguish between primary symptomatology and treatment-caused (or exacerbated) effects.”

c. Mania, hypomania and manic switching caused or worsened by the treatment. FDA concluded: “Because ECT is used to treat psychiatric conditions, it is often difficult to distinguish between primary symptomatology and treatment-caused (or exacerbated) effects.”

d. Depression caused or worsened by the treatment. FDA concluded: “Because ECT is used to treat psychiatric conditions, it is often difficult to distinguish between primary symptomatology and treatment-caused (or exacerbated) effects.”

e. Anxiety, fear and panic caused or worsened by the treatment. FDA concluded: “Because ECT is used to treat psychiatric conditions, it is often difficult to distinguish between primary symptomatology and treatment-caused (or exacerbated) effects.”

f. Alterations in motivation caused or worsened by the treatment. FDA concluded: “Because ECT is used to treat psychiatric conditions, it is often difficult to distinguish between primary symptomatology and treatment-caused (or exacerbated) effects.”

g. Coma has been reported following ECT. FDA concluded: “No systematic studies have been conducted to examine the association of coma and ECT.”

h. Homicidality has been reported following ECT. FDA concluded:  “No case reports or studies have been published examining this association.”

i. Increased use of illicit drugs has been reported with ECT treatment. FDA concluded: “Given the increased co-morbidity of psychiatric illness and substance abuse, it is difficult to determine the cause of increased substance use associated with ECT. No systematic studies have been conducted to examine this association.”

6. FDA admitted the obvious insufficiency of studies regarding the following less severe adverse effects that can contribute to increased morbidity after ECT:

a. Nightmares and sleep disturbance have been reported with ECT treatment. FDA concluded: “…no systematic studies have been conducted to examine this association”.

b. Vision changes and eye trauma have been reported with ECT. FDA concluded: “…no systematic studies have been conducted to examine this association”.

c. Changes in hearing have been reported with ECT. FDA concluded: “No systematic studies have been conducted to examine this association.”

d. Urinary symptoms may be associated with ECT. FDA concluded: “No systematic studies have been conducted to examine the association of urinary symptoms and ECT.”

7. In addition, FDA admitted reports of neurological and motor problems associated with ECT, but failed to identify adequate studies addressing the frequency, extent, duration and severity or latent incidence of these adverse effects.

a. Neurological symptoms including include paresthesias, speech difficulty, loss of coordination, and gait or balance disturbance have been reported with ECT. FDA failed to identify adequate studies addressing the frequency, extent, duration, severity and incidence of late neurological symptoms with ECT.

b. General motor dysfunction including muscle weakness or paralysis, prolonged tremor, and residual muscle twitching/spasms have been reported with ECT. FDA failed to identify adequate studies addressing the frequency, extent, duration, severity and incidence of late motor dysfunction with ECT.

8. FDA found the literature to be sufficient to conclude that ECT is definitely associated with the following serious morbidities, yet failed to cite adequately controlled studies of sufficient duration to assess the long term consequences and to identify latent effects.

a. General functional disability. FDA found ECT-associated general debility to be relatively common and with significant effects, including:

i. Difficulties attending to activities of daily living.

ii. Loss of normal functioning.

iii. Difficulties with work.

iv. General decrease in quality of life.

b. Prolonged seizures have rarely been reported with ECT. However FDA fails to mention the more common occurrence of persistent seizure disorder, and omits the fact that there are no controlled studies of sufficient duration to assess the long term incidence of ECT-associated chronic seizure disorder.

c. Pain/discomfort. FDA found ECT-associated pain to be relatively common. Although FDA states pain is “time-limited”, this is contradicted by mention of the use of medication for “prolonged” pain. FDA fails to mention that there are no studies of sufficient duration to assess the long term incidence and impact of ECT-associated pain and discomfort, including:

                                           i. headaches

                                           ii. body pains

                                           iii. muscle pains

                                           iv. dizziness

9. FDA found the literature sufficient to conclude that pulmonary and cardiovascular complications of treatment are among the most frequent causes of significant morbidity and mortality associated with ECT. However FDA fails to identify any study of sufficient size and data integrity to assess the frequency of these serious and at times deadly complications, including:

              a. prolonged apnea

              b. aspiration

c. hypertension

d. hypotension

e. cardiac arrhythmias

f. cardiac ischemia

10. FDA admitted the occurrence of ECT-associated stroke, with increased risk in patients with intracranial lesions, cerebral aneurysm or recent unrelated stroke. However the primary study cited is Hsiao et al., (1987) which was simply a summary of various case reports. FDA fails to admit that there are no well designed studies of sufficient size and design to identify the incidence of acute stroke and sub acute ischemic vascular brain injury.

11. FDA states there is no increased suicidality associated with ECT treatment based on observational studies, but the specifically cited articles do not substantiate any such conclusion.

a. FDA says, “Results of these studies have reported no increased suicidality associated with ECT treatment (Royal College of Psychiatrists [RCP] 2004).” This refers to a report formally titled “The ECT Handbook”, subtitled “The Third Report of the Royal College of Psychiatrists’ Special Committee on ECT” authored by Royal College of Psychiatrists (2004) and edited by AIF Scott. There is nothing in this 243-page report addressing ECT-associated suicide. The chapter which covers adverse effects of treatment is only three pages long and makes no mention of treatment-associated suicidality.

b. Other observational studies cited by FDA include Kellner, et al (2005), which interviewed patients about suicidal contemplation during a three week course of ECT but did not include any post-treatment follow up to track actual suicide attempts or completed suicides.

c. FDA cited a study by O’Leary, et al (2001) which calculated suicide rates during different treatment eras. According to this report, suicides were 42% more likely in the ECT era than in the antidepressant era. Thus this actually demonstrates the opposite from what is concluded in the FDA summary.

Notwithstanding the contradictions between the actual studies and the faulty FDA conclusion about ECT associated suicidality, comment must be made about FDA reliance on observational studies on this topic. It is remarkable that the observational studies regarding suicide were cited as substantial evidence, while the observational studies demonstrating increased mortality were discounted.

12. Despite the limitations of the selected reports, there was no disagreement on the fact that ECT causes memory loss.  FDA concluded, “There is clear evidence that memory and cognitive impairment (i.e., orientation, retrograde memory, anterograde memory and global cognitive function) occur both immediately after administration of ECT and following a course of therapy.”

a. The evidence is insufficient to address the frequency, extent and duration of treatment-caused memory loss. FDA admits there are considerable problems in the medical literature regarding an accurate and reproducible assessment of memory loss. “Methodological issues such as lack of consistent definitions and use of nonstandardized cognitive instruments hamper assessment of cognition.”

b. The medical literature selected by FDA on ECT –induced memory loss consists of 7 reviews or meta-analyses conducted within a 6-year period, plus one more recent meta-analysis. Each one of these overlap considerably in the actual original studies they included. The use of 7 overlapping reviews (and one 2010 update) deceptively over-represents the adequacy of the original literature.

c. FDA cites the Semkovska and McLoughlin (2010) meta-analysis of memory loss after ECT and admits that the studies analyzed did not examine retrograde autobiographical memory. This is despite FDA’s acknowledgement that, “The primary type of retrograde memory affected is autobiographical memory.”  Retrograde autobiographical memory includes such essentials as knowledge of one’s own identity, childhood and family memories, learning experiences, and work and travel history.  It is not appropriate to include a study that omits addressing the single most commonly affected and most debilitating aspect of memory loss.

d. FDA indicates that the cited reviews and meta-analysis reports varied considerably in other aspects of memory loss, reflecting the lack of adequate studies in this field. For example:

i. FDA cites Rose, et al (2003) for estimating that memory loss ranges from 29% to 79%. Even this considerable variation ignores other reports (not included in the reviews) that show even greater variation ranging from 0 to 99%.

ii. FDA admits the evidence for determining the duration of memory loss is very limited. This crucial point which affects long term function has not been adequately studied.

iii. FDA admits that subjective reports of persistent memory loss are not adequately detected by some testing methods.

13. Cognitive losses after ECT are inadequately studied. FDA concludes: “There are no published prospective RCTs without crossover between treatment groups that examined cognitive outcomes at more than six months after ECT.”

a. FDA admits to “…lack of RCTs utilizing the appropriate standardized scale, the appropriate comparison groups within a comparable timeframe, and sufficient reporting of results.”

b. Due to the lack of adequate studies, FDA proceeded to draw conclusions from very small meta-analyses utilizing only two to four studies. The majority of the studies compared cognitive scores to the patients themselves and not to a control group, and the majority of studies compared types of ECT modalities (electrode placement, etc) rather than having a true control group for comparison.

c. Regarding long term executive function after ECT, FDA concedes, “There is limited long-term data on executive function. Therefore, no meaningful conclusions can be drawn.”

d. Regarding disorientation after ECT, FDA states,”There is no evidence that disorientation following ECT is long-term or persistent.”  The wording of this FDA statement is deceptive and appears to imply that studies have not found persistent disorientation. In fact as FDA admitted, long term studies have not been done.

e. Regarding global memory function immediately after ECT, in the sub acute period, in the medium term, and at 6 months, FDA notes that the evidence is “limited” or “equivocal”.

f. Regarding anterograde verbal memory, FDA notes that the data is “limited” and “equivocal”.

g. Regarding anterograde nonverbal memory, FDA cites there is data that ECT is associated with more decline immediately post-treatment than sham ECT, but then makes a contradictory statement that, “There does not appear to be any change from baseline.” This inconsistency is a reflection of the contradictions in the selected inadequate medical literature. Regarding sub acute and changes and changes 2 weeks post ECT, FDA states the data is “equivocal” and lacks conclusive evidence, respectively, again affirming the inadequacy of the existing studies.

h. Regarding retrograde impersonal memory, FDA states, “There are no studies reporting retrograde impersonal memory data from three to less than six months following ECT.” The selected studies that addresses retrograde impersonal memory 6 months post ECT include small subject populations utilizing different measurement instruments, and therefore are not legitimately combined.

i. Regarding retrograde personal (autobiographical) memory, FDA selected inadequate studies. Their summary of the studies of autobiographical memory loss at various post-treatment intervals is at times is exceedingly misleading, contradictory, and highly qualified (data is repeatedly characterized as “limited” or “equivocal”).

i. FDA considered analyses which largely consisted of comparing different ECT modalities. Only a minority of subjects were compared to actual non-ECT controls or to sham ECT. It is not legitimate to summarize the conclusions from this diverse treatment population.

ii. The largest single study cited in this section (Weiner et al, 1986) examined 74 subjects. The majority of the comparisons were among the differing ECT modalities. The majority of the memory tests were not for personal memory. There was a statistically significant decline in personal memory persisting at 6 months. This is grossly misrepresented in the executive summary report on page 30, where there is only mention of improvement from the 3-month memory deficits. Although clearly indicated in the appendix, FDA executive summary fails to identify the major outcome of this study, which was that significant personal (autobiographical) memory deficits persisted at 6 months.

iii. FDA conceded “the importance of ECT effect on autobiographical memory” and therefore they ran additional analyses. The selected studies did not meet FDA’s criteria of Randomized Controlled Studies (RCTs); instead they were nonrandomized and did not compare to control subjects. They were also very short term, with two studies measuring memory at 1-3 days post treatment, five studies reporting one-week post treatment memory, two studies reporting at one month and one study post-course. There was only one study which tested for personal memory at 6 months, and that was the aforementioned (Weiner, 1986) which documented statistically significant persistent personal memory loss. The selected studies are referred to in Table 7 of the appendix, which is falsely entitled “Autobiographical Memory – RCTs Reporting Change from Baseline Data”.

j. FDA largely dismisses subjective memory loss (self-reported complaints).

k. The FDA Executive Summary regarding cognitive adverse events is replete with a primary contradiction: The evidence for treatment-related deficits in various kinds of cognitive functions, especially memory, is summarized as limited, equivocal, or lacking, Yet, the evidence comparing adverse cognitive effects between various ECT modalities routinely describes greater or lesser deficits for one modality versus the other. FDA fails to explain the consistent finding of adverse effects when comparing ECT modalities but the relative lack of conclusive evidence for adverse effects when compared to a true control group not receiving ECT.

14. FDA only gives a cursory address to neuropathological and immunohistochemical evidence of brain damage. Two paragraphs simply highlight the contradictory evidence, from which no rational conclusion is valid.

a. FDA cites two papers from one researcher to conclude that there are not histopathological or cellular changes in brain tissue. Without acknowledging the contradiction, FDA admits to definite electroshock-induced neuroproliferative changes seen in other studies.

b. In the next paragraph FDA mentions the finding of no brain cell death associated with electroshock. However FDA admits definite brain cell loss due to electroshock in three other studies.

c. Furthermore, FDA endorses the idea that electroshock-induced neuroproliferation could be a therapeutic effect, without mentioning that this is not a widely held theory. In fact, studies omitted from review by FDA documented that electroshock-induced neuroproliferation is typical of the neuroproliferative response to other forms of brain injury. New brain cells do not integrate into existing brain structure in a normal pattern. After an electric shock, existing brain cells exhibit persistently abnormal conduction of electricity (Scott, et al, 2000; Gombos, et al, 1999). This is explained by the finding that synapses on such new brain cells have deranged structure, and are positioned along the nerve in atypical locations compared to normal brain cells (Chen, et al, 2009).

15. Neuroimaging evidence of brain changes are dismissed by citing Coffey et al. (1991) and Ende et al. (2000), both of which are misrepresented by the FDA summary.

a. The cited study by Coffey et al, looked at the MRI brain scans of patients before and after ECT. Out of 35 patients studied, 8 had new changes on MRI after shock.  22%, or greater than one in 5, sustained anatomic brain effects. Among those with the brain changes, one patient suffered a stroke and two had new abnormal neurologic signs on exam within 6 months of the ECT.

b. In the cited study by Ende, et al, brain scans demonstrated a 16% decrease in choline in the hippocampal region, attributed by the authors to” membrane turnover”. Membrane turnover is a direct indicator of cell wall damage.

16. The narrow literature selection by FDA could easily be considered as some evidence that ECT does not increase biomarkers of brain damage. However the selection inexplicably ignores the much larger body of literature that substantiates the opposite conclusion: there is abundant evidence that ECT does in fact lead to a brain inflammatory response, brain cell leakage, neuronal damage and BBB dysfunction.

a. Blood levels of S-100b are 2X to 8X higher after electroshock.  S-100b is a brain biochemical that is an irrefutable marker of brain damage when it is detected to rise in the bloodstream (Palmio, et al, 2010).

b. Gene expression of proteins relating to apoptosis is diminished after electroshock. This results in the blunting of normal programmed cell death in the brain; thus defective or aging cells do not undergo normal removal, but stay in place and continue to function in a faulty way (Jeon, et al, 2008).

c. Mitochondrial enzyme levels change with electroshock, particularly decreasing levels of one key regulating enzyme (Burigo, et al, 2006).

d. Biochemical damage of brain cells from electroshock has been demonstrated by the finding that brain genetic material is subsequently more accessible to chemotherapy toxins (Salford, et al, 2000).

17. Regarding mortality associated with ECT, FDA maintains a double standard for sufficiency of evidence.

a. FDA mentions “a number of observational and epidemiological studies [that] have examined the rate of mortality associated with ECT”. In fact, such studies identified a significantly higher mortality compared to depressed subjects not subjected to ECT. FDA concluded that there insufficient studies on the reduced life span associated with ECT.

b. FDA describes the death estimate of 1 in 10,000 mentioned in the 2001 APA practice guideline. The figure given in the practice guideline was never based on any study, and the source of the estimate remains a mystery. Thus this does not qualify as evidence.

c. FDA cites Watts, et al (2010) to indicate a death rate 800% lower than the APA estimate.  This was a Veteran’s Administration study based on in-hospital only deaths specifically reported as ECT related to the VA’s National Center for Patient Safety (NCPS) database. The NCPS has never been verified to be a statistically reliable repository of cause-of-death data. A review of medical charts to independently ascertain the precipitating causes of death was not undertaken.

d. FDA cites two studies by Kramer (1985; 1999) regarding extrapolated death rates associated with ECT in California. Like the VA study, the death registries in the Kramer studies were not verified by medical record review to independently ascertain the precipitating causes of death.

e. The significance of the lack of independent verification of ECT-related causes of death is suggested by the attempts to verify cause-of-death data in other types of registries. For example, incorrect assignment of cause of death has been responsible for large inaccuracies in databases for cardiovascular deaths (Harriss, 2011), pregnancy associated deaths (MacKay, et all, 2011), fetal deaths and stillbirths (Makelarski, et al, 2011), kidney disease (Pun, et al, 2011), AIDS (Trepka, 2011) and cancer (Polednak, 2011).

f. Studies excluded from consideration by FDA demonstrate increased mortality.

i. The largest study ever conducted of ECT recipients involved 3,288 patients in Monroe County, NY. ECT patients were found to have significantly increased death rates from all causes (Babigian, et al, 1984).

ii. A study of 37 patients who received in-hospital ECT had survival rates of 73.0% at one year, 54.1% at two years, and 51.4% at three years. In contrast, depressed patients who did not receive ECT had survival rates of 96.4%, 90.5% and 75.0% at 1, 2 and 3 years respectively (Kroessler and Fogel, 1993).

iii. The first three years of mandated recording of death within 14 days of ECT in the state of Texas yielded reports of 21 deaths. Eleven of these were cardiovascular, including massive heart attacks and strokes, three were respiratory deaths and six were suicides (Gilbert, 1996). Many of these were not sustained while the patient was in the hospital and would not be expected to be captured as ECT related in the absence of an independent review of the medical records.

Conclusions regarding review of the medical literature on SAFETY of ECT

The FDA Executive Summary (Draft) admits to inadequate medical literature, insufficient measuring tools, wide variability of results, lack of adequately populated randomized controlled trials, and virtually nonexistent long term studies.

FDA broadly discounts observational studies when the result support an ECT adverse effect (such as death and suicidality) but include observational studies in which ECT appears less treacherous.

FDA violates its own stated standards by including non randomized, uncontrolled studies, yet invoking its standards to eliminate from consideration hundreds of other studies.

FDA relies on review articles and meta-analyses that overlap, and include mostly small, short term, studies with incompatible measuring tools. The insufficient literature is then inappropriately combined in unsubstantiated conclusions. This includes several instances of misrepresentation of the original studies.


American Psychiatric Association. 2001. The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training and Privileging—A Task Force Report, 2nd ed., American Psychiatric Press, Washington, DC.

Babigian, et al Epidemiological considerations in ECT, Arch Gen Psych 1984;41:216-253.

Búrigo M, Roza CA, Bassani C, Fagundes DA, Rezin GT, Feier G, Dal-Pizzol F, Quevedo J, Streck EL. Effect of electroconvulsive shock on mitochondrial respiratory chain in rat brain. Neurochem Res. 2006 Nov;31(11):1375-9.

Chen F, Madsen TM, Wegener G, Nyengaard JR. Repeated electroconvulsive seizures increase the total number of synapses in adult male rat hippocampus. Eur Neuropsychopharmacol. 2009 May;19(5):329-38.

Coffey CE, Weiner RD, Djang WT et al. Brain anatomic effects of electroconvulsive therapy. A prospective magnetic resonance imaging study. Arch Gen Psychiatry 1991;48:1013-1021.

Ende G, Braus DF, Walter S, Weber-Fahr W, Henn FA. The hippocampus in patients treated with electroconvulsive therapy: a proton magnetic resonance spectroscopic imaging study. Arch Gen Psychiatry 2000;57:937-943.

Harriss LR, Ajani AE, Hunt D, Shaw J, Chambers B, Dewey H, Frayne J, Beauchamp A, Duvé K, Giles GG, Harrap S, Magliano DJ, Liew D, McNeil J, Peeters A, Stebbing M, Wolfe R, Tonkin A. Accuracy of national mortality codes in identifying adjudicated cardiovascular deaths. Aust N Z J Public Health. 2011 Oct;35(5):466-76.

Hellsten J, West MJ, Arvidsson A, Ekstrand J, Jansson L, Wennström M, Tingström A. Electroconvulsive seizures induce angiogenesis in adult rat hippocampus. Biol Psychiatry. 2005 Dec 1;58(11):871-8.

 Gilbert, D,  Commissioner, Texas Department of Mental Health and Mental Retardation, 1996.

Gombos Z, Spiller A, Cottrell GA, Racine RJ, McIntyre Burnham W. ‘Mossy fiber sprouting induced by repeated electroconvulsive shock seizures’ Brain Res. 1999 Oct 9;844(1-2):28-33.

Jeon WJ, Kim SH, Seo MS, Kim Y, Kang UG, Juhnn YS, Kim YS. Repeated electroconvulsive seizure induces c-Myc down-regulation and ‘Bad’ inactivation in the rat frontal cortex. Exp Mol Med. 2008 Aug 31;40(4):435-44.

Kellner CH, Fink M, Knapp R, Petrides G, Husain M, Rummans T, Mueller M, Bernstein H, Rasmussen K, O’connor K, Smith G, Rush AJ, Biggs M, McClintock S, Bailine S, Malur C.  Relief of expressed suicidal intent by ECT: a consortium for research in ECT study. Am J Psychiatry. 2005 May;162(5):977-82.

Kramer, B.A., Use of ECT in California, 1977-1983. Am J Psychiatry, 1985. 142(10): p.1190-2.

Kramer, B.A., Use of ECT in California, revisited: 1984-1994. J ECT, 1999. 15(4): p. 245-51.

Kroessler and Fogel, Electroconvulsive Therapy for Major Depression in the Oldest Old Am J of Geriatric Psychiatry 1993;1:1:30-37

MacKay AP, Berg CJ, Liu X, Duran C, Hoyert DL. Changes in pregnancy mortality ascertainment: United States, 1999-2005 Obstet Gynecol. 2011 Jul;118(1):104-10.

Makelarski JA, Romitti PA, Caspers KM, Puzhankara S, McDowell BD, Piper KN. Use of active surveillance methodologies to examine over-reporting of stillbirths on fetal death certificates. Birth Defects Res A Clin Mol Teratol. 2011 Dec;91(12):1004-10.

O’Leary D, Paykel E, Todd C, Vardulaki K (2001). Suicide in primary affective disorders revisited: a systematic review by treatment era. J Clin Psychiatr 62:10:804-811.

Palmio J, Huuhka M, Laine S, Huhtala H, Peltola J, Leinonen E, Suhonen J, Keränen T. Electroconvulsive therapy and biomarkers of neuronal injury and plasticity: Serum levels of neuron-specific enolase and S-100b protein. Psychiatry Res. 2010 May 15;177(1-2):97-100.

Polednak AP. US death rates from myeloproliferative neoplasms, and implications for cancer surveillance. J Registry Manag. 2011 Summer;38(2):87-92.

Pun PH, Herzog CA, Middleton JP. Improving Ascertainment of Sudden Cardiac Death in Patients with End Stage Renal Disease. Clin J Am Soc Nephrol. 2011 Nov 10.

Rose D, Wykes T, Leese M, Bindman J, Fleishmann P (2003). Patients’ perspectives on electroconvulsive therapy: systematic review. BMJ 325: 1363-1365.

Trepka MJ, Maddox LM, Lieb S, Niyonsenga T. Utility of the National Death Index in ascertaining mortality in acquired immunodeficiency syndrome surveillance. Am J Epidemiol. 2011 Jul 1;174(1):90-8.

Salford LG, Engström P, Persson BR.Treatment of rat glioma with electrochemotherapy. Methods Mol Med. 2000;37:313-7.

Scott BW, Wojtowicz JM, Burnham WM. ‘Neurogenesis in the dentate gyrus of the rat following electroconvulsive shock seizures’ Exp Neurol. 2000 Oct;165(2):231-6.

Semkovska M, McLoughlin DM (2010). Objective Cognitive Performance Associated with Electroconvulsive Therapy for Depression:A Systematic Review and Meta-Analysis. Biol Psychiatr 68:568-577.

Semkovska M, Keane D, Babalola, McLoughlin DM (in press). Unilateral brief-pulse electroconvulsive therapy and cognition: effects of electrode placement, stimulus dosage and time. J Psych Res.

Watts BV, Groft A, Bagian JP, Mills PD. An examination of mortality and other adverse events related to electroconvulsive therapy using a national adverse event report system. J ECT. 2011 Jun;27(2):105-8.

Weiner RD, Rogers HJ, Davidson JRT, Squire LR. Effects of stimulus parameters on cognitive side effects. Ann NY Acad Sci 1986;462:315-25.


ECT causes bleeding, with reports of fracturing of the micro-capillaries in the skin, to blood in the urine, to vaginal bleeding.


J ECT. 2009 Dec;25(4):287. Hematuria with electroconvulsive therapy: a case report. Blevins S, Greene G.

J Obstet Gynaecol Res. 2009 Jun;35(3):569-71. Association of vaginal bleeding and electroconvulsive therapy use in pregnancy. Ghanizadeh A, Ghanizadeh MJ, Moini R, Ekramzadeh S.

Dermatol Online J. 2008 Dec 15;14(12):7. Focal iatrogenic peticheae: An unusual post electroconvulsive therapy skin finding. McCallister MS, Athar A, Rashid RM.

Eye damage

ECT can cause vitreous detachment in the eye, eye inflammation, and dramatic increases in eye pressure.


Gen Hosp Psychiatry. 2009 Jul-Aug;31(4):385-7. Bilateral posterior vitreous detachment after electroconvulsive therapy.  Martínez-Amorós E, Real Barrero E, Fuste Fusares C, Hernández-Ribas R, Urretavizcaya Sarachaga M

Br J Pharmacol. 1997 Apr;120(8):1491-6.  Ocular inflammation induced by electroconvulsive treatment: contribution of nitric oxide and neuropeptides mobilized from C-fibres.  Wang ZY(1), Waldeck K, Grundemar L, Håkanson R.

Convuls Ther. 1990;6(3):209-213.  Intraocular Pressure Changes in Nonglaucomatous Patients Undergoing Electroconvulsive Therapy.  Edwards RM, Stoudemire A, Vela MA, Morris R.