Discuss at least two new things you learned from completing the lab activity. Discuss at least one way you will apply this knowledge to your future PMHNP practice.ECT_AutismC

page 1

www.nncionline.org

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.

page 2

www.nncionline.org

NEUROSCIENCE IN THE MEDIA:ELECTROCONVULSIVE THERAPY, AUTISM, AND CATATONIA

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,

page 3

www.nncionline.org

NEUROSCIENCE IN THE MEDIA:ELECTROCONVULSIVE THERAPY, AUTISM, AND CATATONIA

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.

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?)

• 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

page 4

www.nncionline.org

NEUROSCIENCE IN THE MEDIA:ELECTROCONVULSIVE THERAPY, AUTISM, AND CATATONIA

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.

page 1

www.nncionline.org

PROGRESSIVE CASE CONFERENCE: PART 1

Catatonia: Introduction Joseph L. Kugler and Joseph J. Cooper

OVERVIEW

Catatonia is an incredibly common psychiatric syn- drome. Yet it is misperceived by many clinicians as either rare or as a historic syndrome which has disappeared. Modern studies show about 10% of inpatient psychiatric patients suffer from catatonia1. In truth, the only thing which has disappeared is clinicians’ ability to properly identify catatonia’s signs and symptoms2,3. In this series of modules, we will introduce learners to the syndrome of catatonia through an example in the inpatient psychiatric hospital, identify common symptoms of catatonia, and review techniques necessary for identify- ing signs on motor and cognitive exams. We then review the normal motor regulatory systems in the brain and finally review what is known about dysfunction in these systems in catatonia.

MODULE A — RECOGNIZING THE CLINICAL SYNDROME

LEARNING OBJECTIVES At the completion of this session, participants will be able to: 1. Name and define core symptoms of catatonia 2. Recognize catatonic symptoms in a clinical case 3. Use the Bush-Francis Catatonia Rating Scale 4. Perform motor exams on patients, when indicated 5. List the most common causes of catatonia and be

able to generate a differential diagnosis

PROGRESSIVE CASE CONFERENCE (45-60 mins) This session is designed to be conducted using a real- time, interactive, web document. We recommend using google drive to create a new “google doc.” If you’re running the session with a small group of people, you can send them each invites. Alternatively, you can click “share” in the top right corner to make the document public and then go to tinyurl.com to create an easy to remember link that you distribute to the group. 1. Print paper copies of the student version of the case

in advance or post it for them progressively. 2. Ask students to work in groups of two or three to

answer the questions.

3. Give them the link to your shared google doc and ad- vise them that you will be posting links to additional resources as you go.

4. Note: for the rest of the Facilitator’s Guide we will use: • Black text indicating the materials that students

are given; • Red text to indicating “stage directions” for the

instructor; • Blue text indicating the correct answers in a ready

to post format; For most sections, you will ask students to work on their own to answer questions and then discuss them as a group. Keep this document and your running google doc open simultaneously. To share the correct answers with the group, you should cut & paste the blue text directly from this document into the google doc.

page 2

www.nncionline.org

PROGRESSIVE CASE CONFERENCE: PART 2

Catatonia: Module A Joseph L. Kugler and Joseph J. Cooper

[Break the class into groups of two or three and ask them to read the vignette and start answering the questions be- low. Share the link to the google doc and advise them that the main portion of this session is an “open book”, “open internet” experience – they should be looking up what they don’t know and you will post helpful links that they can use to find answers along the way.]

CLINICAL VIGNETTE:

Part 1

You’re on call overnight covering the emergency depart- ment (ED). At 2AM, you get a call from the ED doc alerting you to a 34-year-old man, brought in by police, who just got medicated and they want you to see. His friends called 911 after he locked himself in his room for several days. Police had to taze him due to agitation in his apartment. In the ED he was agitated, yelling, and mostly incoherent. He is now quiet after getting haloperidol 5mg and diphenhydr- amine 25mg intramuscularly.

Questions: 1. What’s your differential diagnosis as you walk over to

see the patient? 2. What other things do you have in mind?

Answers: 1. Decompensation of chronic psychotic disorder; drug-

induced psychosis; mania; delirium 2. SAFETY!!!; ensuring he is robed and has had belongings

taken away; ensure interviewing space is safe and secu- rity is in place if needed

Part 2

You gather more history from police notes and chart, and then attempt to interview the patient: He is a musician, on arrival of EMS, he rapidly became more agitated, intrusive, and was screaming continuously. Police forced entry, he was not answering coherently. He was repetitively yelling, “Is everything OK, Mr. Rothstein?”

“Here we are! Here we are!” and “let me in! let me in! let me in!”. He was covered in feces and urine. When the

police attempted to talk to him, he threw a soiled shirt at an officer and was tazed. Initially in ED he was awake, but uncooperative. Without provocation, Mr. R became agitated, pacing, and gesticulating wildly around the room. He refused to allow staff to clean him of feces. He was medicated, as above. On exam, the patient is malodorous. At times he looks excited and at times withdrawn, barely moving. He stands stiffly and motionless for several minutes at a time, not making any eye-contact, nor answering any questions. He then becomes spontaneously verbal and, though dif- ficult to understand, makes grandiose statements as to his wealth and power to help others through his music. At times, mid-sentence, his speech unravels into perse- verative, but logically-disconnected phrases. He doesn’t respond to gentle interruption. After several minutes he suddenly stands, and walks over to the corner, turning his back to you for 2-3 minutes. He then turns three times to the left and three times to the right and tiptoes out of the room. As you follow him out into the hall, he grabs a tech by the arm and will not let go, staring ahead blankly. A code is called. After receiving 5mg haloperidol IM, and 50mg diphenhydramine he is put transiently in restraints.

Questions: 1. What is your differential diagnosis now? 2. What are your next steps?

Answers: 1. Decompensation of chronic psychotic disorder; drug-

induced psychosis; mania; delirium; catatonia 2. Physical exam, cognitive exam

Part 3

You notice now his head is raised off the pillow. He appears to be in a fetal position but with his arms in the same position as they were in the chair. He repetitively taps his fingers. He continues to stare straight ahead without blinking. On motor exam, he displays initial resistance to any attempts to move his arms. On being asked to relax he ultimately does somewhat but keeps his arms fixed in the position you leave them. His speech continues to be sig- nificantly decreased and impoverished with the exception of a few repetitive utterances, “bothering you, bothering

page 3

www.nncionline.org

you.” After significant latency, he does demonstrate orien- tation to month, year, place, and city. He won’t engage in further cognitive assessment or history gathering.

Questions 3. What is the initial approach for systematically evaluat-

ing this patient? 4. Describe the exam findings in our patient.

After 1-2 minutes, post the following resources to help learners answer the questions: • Oldham MA and Lee HB. Catatonia vis-à-vis de-

lirium: the significance of recognizing catatonia in altered mental status. General Hospital Psychiatry. 37 (2015) 554-559.

• Bush G, Fink M, Petrides G et al. Catatonia I: rat- ing scale and standardized examination. Acta Psychiatr Scand (93): 129-136.

After a couple more minutes, review as a group—again, please note: the sections below are designed so that you can discuss the question from the exercise and then cut and paste the answer key from below directly into their google doc]

3) What is the initial approach for systematically evaluat- ing this patient? Initial clinical evaluation of the patient with suspected catatonia: • Perform a bedside neuropsychiatric assessment

including, at least, observation of arousal level and awareness. Attempt specific assessment of attention, orientation, memory, language, executive function, and visuospatial-constructional ability.

•. Formally evaluate catatonic symptoms: conduct psy- chomotor examination and document findings in a Bush-Francis Catatonia Rating Scale. (Includes review of nursing notes, vital sign trends, dietary and fluid input/output metrics, discuss staff’s observations of patient).

•. Obtain a clear and detailed psychiatric history includ- ing natural history of catatonic presentation. This will very likely include interviewing reliable informants and thoroughly reviewing medical records.

•. Thoroughly review medications and consider possible toxin exposures (illicit substances, environmental expo- sures, and potential iatrogenic precipitants).

•. Appraise likelihood of other conditions in which cata- tonic features for catatonia are commonly expressed.

•. Consider further medical work-up.

4) Describe the exam findings in our patient. • Let’s review some definitions and videos of catatonic

symptoms.

ADDITIONAL RESOURCES

For more on catatonia assessment, Josh Wortzel, MD and Mark Oldham, MD at the University of Rochester, collaborated with Andy Francis, MD, PhD to create a comprehensive suite of catatonia assessment resources using the Bush-Francis Catatonia Rating Scale (BFCRS; freely available at https://bfcrs.urmc.edu/). Some of the highlights include:

1. BFCRS Training Manual and Coding Guide, which describes how to use the BFCRS and explains each item in detail. 2. Educational modules on using the BFCRS, which includes standardized patient videos, test questions with explanations, and answer keys. 3. Videos on scoring individual BFCRS items; also ac- cessible on the hyperlinked PDF version of the BFCRS.

REFERENCES

1. Fink M, Taylor MA: Catatonia: A Clinician's Guide to Diagnosis and Treatment. Cambridge, UK, Cambridge University Press, 2003

2. van der Heijden FM, Tuinier S, Arts NJ, et al: Catatonia: disappeared or under-diagnosed? Psychopathology 38(1):3–8, 2005

3. Cooper JJ, Roig Llesuy J. Catatonia Education: Needs Assessment and Brief Online Intervention. Acad Psychiatry. 2017 Jun;41(3):360-363.

4. Oldham MA and Lee  HB. Catatonia vis-à-vis delirium: the significance of recognizing catatonia in altered mental status. General Hospital Psychiatry. 37 (2015) 554-559.

5. Bush G, Fink M, Petrides G et al. Catatonia I: rating scale and standardized examination. Acta Psychiatr Scand (93): 129-136.

6. Taylor MA. Clinical Examination in Catatonia: From Psychopathology to Neurobiology, American Psychiatric Publishing, 2004, p. 45–52.

7. Fink M and Taylor MA. Signs of Catatonia are Identifiable in Catatonia: a Clinician's Guide to Diagnosis and Treatment, by Max Fink and Michael Alan Taylor, Cambridge University Press, 2003, pp. 19-32

8. Psychiatry Teacher. Catatonia. New Castle University. YouTube, 16 Feb. 2011, [Waxy_Flexibility.mp4, Gegenhalten.mp4, Negativism-Aversion.mp4] https:// www.youtube.com/watch?v=_s1lzxHRO4U

9. Lehmann, Heinz E. Schizophrenia: Catatonic Type. [Catalepsy and Posturing 2.mp4, Posturing_and_ Catalepsy.mp4] Ottawa, Canada: National Film Board of Canada, 1951.

10. Lehmann, Heinz E. Schizophrenia: Hebephrenic Type. [Mannerisms_historic.mp4, Grimacing.mp4] Ottawa: National Film Board of Canada, 1952.

</

Collepals.com Plagiarism Free Papers

Are you looking for custom essay writing service or even dissertation writing services? Just request for our write my paper service, and we'll match you with the best essay writer in your subject! With an exceptional team of professional academic experts in a wide range of subjects, we can guarantee you an unrivaled quality of custom-written papers.

Get ZERO PLAGIARISM, HUMAN WRITTEN ESSAYS

Why Hire Collepals.com writers to do your paper?

Quality- We are experienced and have access to ample research materials.

We write plagiarism Free Content

Confidential- We never share or sell your personal information to third parties.

Support-Chat with us today! We are always waiting to answer all your questions.