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ECT_AutismCatatonia_p1.pdf

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OVERVIEW

Electroconvulsive therapy (ECT) is well known to psychiatrists as a highly effective and safe treatment for severe neuropsychiatric conditions. ECT’s reputation in the lay public suffers from stigma based partially on historically accurate accounts of its use, especially pre-anesthesia, and partially on widely-propagated falsehoods, including that it causes brain damage. Based on this stigma, ECT has been the subject of laws limiting its use, particularly in children. Autism is a debilitating neurodevelopmental condition. Parents of children with autism are sometimes known to pursue non-traditional treatments and many things purported to treat autism have little scientific evidence to back them up. In this module, learners will read and critique a 2016 article from The Atlantic on the use of ECT in children with autism.

PART 1: READ / WATCH / LISTEN TO MEDIA

The Atlantic: How ‘Shock Therapy’ Is Saving Some Children With Autism. https://www.theatlantic.com/health/ archive/2016/10/how-shock-therapy-is-saving-some-children-with-autism/505448/

PART 2: CRITIQUE OF MEDIA COVERAGE

NEUROSCIENCE IN THE MEDIA:

Electroconvulsive Therapy, Autism, and Catatonia Joseph J. Cooper, MD and Stephanie Lichtor, MD

1. What is the central claim / “take home point” of this media piece? ECT is a more benign treatment than its reputation with the lay public suggests. Autism with severe self-injury may be a manifestation of catatonia, which is a syndrome effectively treated by ECT.

2. What is the author’s agenda? What (if any) biases are present? (“what’s the angle?” how/why will they get people to care about it?) The term “Shock Therapy” is used in the title, which is a term used to grab attention. It is used in quotes, implying some degree of disagreement with the use of this term to describe ECT. The author is looking to challenge the public’s conception of ECT.

3. What is the face validity of the article’s central claim? (True/False/Maybe). Maybe/Probably True – While Kyle and Doug’s stories in isolation may provoke skepticism (as many treatments of “autism” that worked for n=2 should), this story appears to be well referenced with physicians from major academic medical centers. It also seems more plausible once they clarify the ECT treats catatonia rather than ECT for autism, per se.

4. What questions do you imagine a patient or family member might ask you about it? Is this real? Are the doctors cited

mainstream or quacks? What is catatonia? How effective is ECT as a treatment? How does ECT work? What are the risks?

5. What other follow-up questions did you have that were raised by the media piece? Is catatonia a common feature of autism? Is there any shared neurobiology between the two? So is there a difference between the “repeti- tive behaviors” which are a diagnostic feature of autism and “catatonic repetitive behaviors”? Or does all autism have some catatonic features? Is there data on ECT (or benzodiazepines) for catatonia in autism? Does ECT treat catatonia regardless of underlying condition driving the catatonia? How often is ECT a lifelong treatment? Are there considerations (such as comorbidities, age) that might make ECT less effective? Is ECT covered by insur- ance for this indication?

6. Where might you look for additional data / information? Pubmed – searching for “catatonia AND autism” to learn more about the relationship. Search for “ECT AND autism” to learn about safety and efficacy in this specific popula- tion. Search for “ECT AND catatonia” to learn more about ECT for catatonia due to any cause.

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PART 3: READ SUPPLEMENTAL MATERIALS AND ANSWER THE FOLLOWING QUESTIONS:

For this part, we will have the learners break into 3 groups, and each gets one article to summarize.

Group 1: Catatonia and autism: a historical review, with implications for electroconvulsive therapy [1]

i. What is the central finding of the scientific article? Catatonia is increasingly recognized as a common comorbid syndrome in autism. Catatonia and related symptoms including compulsions, tics, and self-injury in individuals with autism have been effectively treated with ECT. Barriers to treatment are related to stigma and negative public perception of this treatment, particularly in children and those with a developmental disorder, as well as restrictions that prevent access to ECT for these patients in many states.

ii. What additional background info and data in the paper are relevant to the media portrayal of the work and could help answer the questions above? (e.g. How valid is the central claim of the media article? Are there other data that speak to the broader questions you imagine a patient or family member might ask?)

• Of adolescents and young adults with autism, prevalence of catatonia was 12-17%. • Indications for ECT in patients with autism include catatonia, compulsions, stereotypies, self-injury, tics, and Gilles de la

Tourette syndrome. • ECT effectively and safety treated patients with catatonia and autism, though this response was slower when catatonia

had remained undiagnosed or untreated for long periods of time. • There has been limited study of ECT in patients with autism and catatonia related to limited public acceptance of ECT

as well as lack of recognition of autism as a diagnosis until the 1940s.

Group 2: Etiopathogenesis of catatonia: generalizations and working hypotheses [2] i. What is the central finding of the scientific article? The current understanding of the neurobiology of catatonia is informed

by clinical treatments and a small amount of direct investigation. Some evidence supports a role for impaired orbitofrontal-striatal circuits. These circuits’ connections to the hypothalamus are especially important in malignant forms of catatonia. Altered GABA function has been demonstrated in catatonia as well as hypo-dopaminergic func- tion. Other hypotheses that warrant further investigation follow from the known conditions with at high rates with catatonia: neuroleptic malignant syndrome (NMS), which is most commonly accepted as a drug-induced form of catatonia; Prader-Willi Syndrome, caused by lack of expression of genes in a portion of chromosome 15 which contains a cluster of genes for GABA receptor sub-units; Klein-Levin Syndrome, with altered diencephalic function; and anti- NMDA-receptor encephalitis, with NMDA-receptor hypofunction in the hippocampus. Additionally, ECT’s efficacy at treating catatonia helps support hypotheses including altered HPA-axis function and the need for neurogenesis in the hippocampus.

ii. What additional background info and data in the paper are relevant to the media portrayal of the work and could help answer

the questions above? (e.g. How valid is the central claim of the media article? Are there other data that speak to the broader questions you imagine a patient or family member might ask?)

• Catatonia occurs in children and responds to the same treatments as adults. • Catatonia can occur in autism and in patients with Prader-Willi Syndrome, who have behavioral symptoms that

include repetitive and self-injurious behavior. • ECT is an effective treatment for catatonia regardless of the associated conditions (e.g., autism).

Group 3: READ Searching for the mechanism(s) of ECT’s therapeutic effect [3] and watch 0:00 – 1:37 of https://vimeo. com/148422000. (The full video of Dr. Sarah H. Lisanby on Electroconvulsive Therapy and Neuromodulation can be found at: http://www.nncionline.org/course/dr-sarah-h-lisanby)

i. What is the central finding of the scientific article? Long disproven theories including the induction of brain damage, psychoanalytic notions of punishment-seeking, and an amnesia-centric notion of “forgetting ones troubles” are briefly reviewed. Several modern hypotheses exist to connect ECT-induced brain changes to therapeutic effects, however which one(s) of these is(are) more essential remains unproven. ECT induces a potentiation of serotonergic,

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noradrenergic and dopaminergic circuits, potentially contributing to antidepressant and antiparkinsonian effects of ECT. ECT is a powerful inducer of neurogenesis and synaptogenesis in the hippocampus, which is an important aspect of other antidepressants therapeutic effects. The authors conclude with a reflection on why ECT is criticized for lacking precise knowledge of mechanism where as other treatments, such as vagal nerve stimulation for epilepsy, are not.

• Understanding of ECT’s mechanism has progressed significantly in recent decades but remains incomplete. • No evidence of brain damage. Some evidence to the opposite, neurogenesis and dose-dependent favorable neurohis-

tological changes. • “Ultrabrief pulse ECT has led to a form of efficacious treatment with nearly invisible cognitive adverse effects in most

patients.”

Large Group Discussion: What additional questions are raised by the scientific articles? • What is the success rate of ECT in patients with autism and catatonia? • What percentage of patients achieve response and remission? • What are the risks of ECT, particularly in patients with autism and catatonia? • Why has so little been investigated regarding catatonia? • Why has this condition been “rediscovered” over the last 20 years if it was described in 1874?

PART 4: ROLE PLAY EXERCISE: WITH A PEER, PRACTICE COMMUNICATING ABOUT THIS MEDIA TO SOMEONE WITH NO TECHNICAL KNOWLEDGE OF PSYCHIATRY OR NEUROSCIENCE.

Following a review of the scientific literature, trainees are instructed to practice communicating about the media coverage of the use of ECT in children and adolescents with autism and catatonia with someone who has no technical knowledge of neuroscience. For this exercise, a trainee might say, “Electroconvulsive therapy (ECT) might sound scary or bring to mind images of Jack Nicholson in One Flew Over the Cuckoos Nest. However, ECT is neither torturous nor dramatic as depicted in the media. False ideas, including that it causes permanent brain damage, have reinforced the stigma around ECT. ECT is not controversial in the medical and scientific literature; it is safe and the most effective treatment for several psychiatric conditions. When someone receives ECT, he/she is monitored and given anesthetics and a muscle relaxant so is not awake or aware and not in any pain or distress while a controlled seizure is induced. The patient may mildly quiver and clench jaw muscles and then relax, typically lasting less than a minute. One of the conditions for which ECT is best studied and most highly indicated is for catatonia. Catatonia is a syn- drome that may manifest along with neurologic or psychiatric disorders and presents as a person who is slow-moving, motionless, not speaking, not eating or caring for him/herself or engaging in repetitive, purposeless movements such as repeatedly injuring oneself. Catatonia in children with autism is often unrecognized and untreated – it may include repetitive, uncontrolled behaviors that severely impact a child’s ability to function. Recurrent ECT treatments can de- crease of catatonic symptoms, improving quality of life. Studies of the potential side effects of ECT include memory loss that is often mild and resolves within weeks of stopping treatment. In comparison to the significantly limited functioning of a child with autism and catatonia, the side effects of ECT are relatively minor. The stigma around this treatment, false assumptions about its potential dangers, and ill-informed laws in several states have limited its availability and use, especially in children, which leads to cases of prolonged suffering for patients and families.”

PART V: GENERAL DISCUSSION / Q & A / FUTURE DIRECTIONS FOR CURIOUS LEARNERS

An alternative learning goal might be to have learners role play discussing the mechanism of ECT to a patient for whom ECT has been recommended. The trainee might say “A lot has been learned recently about how ECT works. What has been known for a much longer time is that ECT does work and is the most efficacious treatment for severe depression and several other psychiatric conditions. There has been a lot of work to uncover the mechanism of these improvements. One limiting factor is that the neurobiology of depression is not as well known as other medical diseases, making it

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complex to describe how treatments work. We know that several chemicals in the brain important in depression like serotonin, norepinephrine and dopamine are dysfunctional in depression and ECT has a profound effect on these sys- tems, resulting in a normalization of their function. These are the same chemical targets as antidepressant medications. Also ECT has been shown to stimulate new brain cell growth in a part of our brain important for mood and memory, the hippocampus. Antidepressant medications may also share this mechanism, but it is clear the ECT is a safe and effective treatment for severe depression that is not improved by medications.”

A clinical review of the treatment of catatonia [4] The evidence for treatments of catatonia is reviewed including clinical factors which may influence treatment selection or response rates. The evidence for using ECT to treat catatonia across a range of conditions, including mention of autism, is reviewed.

Bearing Witness: Personal and Poetic Descriptions of Seizure Therapy [5] Personal descriptions of the experience of ECT, including those who have had positive results counterbalanced against more stigmatizing and negative descriptions depicted in the media.

Catatonia: a syndrome appears, disappears, and is rediscovered [6] A historical account of the reasons for the “disappearance” of catatonia. These include the rise of psychoanalytic models and the fall of physical examination of psychiatric patients.

REFERENCES:

1. Dhossche DM, Reti IM, Wachtel LE. Catatonia and autism: a historical review, with implications for electroconvulsive therapy. J ECT. 2009 Mar; 25(1):19-22.

2. Dhossche DM, Stoppelbein L, Rout UK. Etiopathogenesis of catatonia: generalizations and working hypotheses. J ECT. 2010 Dec;26(4):253-8. doi: 10.1097/YCT.0b013e3181fbf96d. Review.

3. McCall WV, Andrade C, Sienaert P. Searching for the mechanism(s) of ECT’s therapeutic effect. J ECT. 2014 Jun;30(2):87-9. 4. Sienaert P, Dhossche DM, Vancampfort D, De Hert M, Gazdag G. A clinical review of the treatment of catatonia. Front

Psychiatry. 2014 Dec 9;5:181. doi: 10.3389/fpsyt.2014.00181. Review. 5. Dr. Sarah H. Lisanby on Electroconvulsive Therapy and Neuromodulation. National Neuroscience Curriculum Initiative,

Expert Video. http://www.nncionline.org/course/dr-sarah-h-lisanby 6. Fink M. Bearing Witness: Personal and Poetic Descriptions of Seizure Therapy. J ECT. 2016 Mar; 32(1):13-6. 7. Fink M. Catatonia: a syndrome appears, disappears, and is rediscovered. Can J Psychiatry. 2009 Jul;54(7):437-45. Review.

PubMed PMID: 19660165.