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Psychotherapy is one of the oldest items in the clinical toolkit. Yet, despite its familiarity, it remains somewhat mysterious. How does it actually work? What are the neural mechanisms by which psychotherapies (

 [CBT], psychodynamic therapy, and others) create lasting changes in patients’ mental health?

For several years, I have worked with other researchers in pursuing the answers to these questions into the frontiers of memory neuroscience. Our goal is to capitalize on major advances in our understanding of the neural basis of memory, emotion, and emotion-memory interactions. If we could start to explain the basic mechanism of action behind 

, then maybe we could understand how to conduct psychotherapy more effectively, with the ultimate goal of working with our patients to produce transformational and durable change.

Recent studies have made important discoveries about the neural mechanisms underlying memory, and 4 are of particular interest (

Drawing upon these observations, my colleagues and I hypothesized that there were 3 key ingredients to lasting change in psychotherapy:

1. activating problematic memories and the associated painful affect;

2. concurrently engaging new emotional experiences that change old memories through reconsolidation;

3. reinforcing the strength of new memories and their semantic structures by practicing new ways of behaving and experiencing the world in a variety of contexts.

We briefly discussed the application of this model to 4 different psychotherapy modalities including behavioral, cognitive behavioral (CBT), emotion focused (EFT), and psychodynamic psychotherapies in a previous article.

Realizing that there was much more to say about this new way of understanding change in psychotherapy, I coauthored a book that expands upon our previous research in 3 sections.

 The basic science section includes chapters on emotion, memory, emotion-memory interactions, the 

 in shaping emotion and memory, and the role of sleep in memory consolidation and reconsolidation. The clinical section includes chapters from leading experts in psychodynamic psychotherapy, CBT, EFT, coherence therapy, and integrative approaches. Each author considers the role of memory reconsolidation in both psychotherapy and achieving lasting personal change. The final section includes chapters on recurrent maladaptive patterns, a computational neuroscience perspective on the proposed model, and a discussion of a proposed preclinical and clinical research agenda. Considerable effort was made within and across chapters to promote cross-fertilization between basic science and clinical application.

If one takes this model seriously it could influence psychiatric practice in several ways. For example, it is useful to consider how interventions might be adjusted in therapies that have stalled or failed. Rather than talking about feelings with the goal of promoting 

, it is also important to experience feelings, especially the old painful feelings, from which individuals have protected themselves for years, and to juxtapose these feelings with corrective emotional experiences.

Another clinical implication emerges from the observation that consolidation of emotional memories occurs primarily during REM sleep. Because reconsolidation may work in the same way, medications that inhibit REM sleep may be counterproductive to enduring change in psychotherapy. It is, therefore, important to know that selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclics, and 

 inhibit REM sleep, whereas trazodone, bupropion, and mirtazapine do not.

 The book describes these and other implications, and provides a fresh perspective on how psychotherapy practice may be optimized and integrated in psychiatric care.

Exploring the Backstory: What Led to My Interest

My interest in this topic emerged over the course of my 35-year career as an academic psychiatrist. I was initially trained as a clinical psychiatrist and psychodynamic psychotherapist and have continued to practice and supervise residents ever since. I was also fortunate enough to receive research training (resulting in a PhD in experimental psychology) that focused on cognitive neuroscience and functional neuroimaging of emotion. I have found the dialogue between the basic science of psychiatry and its clinical application to be particularly enriching and informative.

In my role as educator, I have become well acquainted with the challenges (eg, significant differences in the theoretical backgrounds, mindset, and clinical interventions required by these different approaches) psychiatry residents face in developing competence in CBT, psychodynamic psychotherapy, and supportive psychotherapy. Because there is a strong interest in finding common factors and common mechanisms across psychotherapy modalities, it occurred to me that a systems neuroscience perspective could provide an integrative mechanistic framework that would highlight commonalities instead of divergences. Moreover, the goal of integrating 

 and psychotherapy is likely to be advanced by explaining how each works in brain-based terms.

It is important to emphasize that we have not yet established that change in psychotherapy occurs through memory reconsolidation. One of the conclusions of our book is that a focus of intervention is recurrent maladaptive patterns, which can be understood as an expression of schemas. Schematic memory is a type of semantic memory and, as an area of neuroscientific investigation, it is relatively new. It remains to be demonstrated empirically that schematic memories can be updated with emotional information. If so, it must then be determined whether this applies to psychotherapy. Although research of this type is still underway, it might be argued that it is important to consider the clinical implications of this model if it were true.

 is a professor of psychiatry, psychology, and neuroscience at the University of Arizona. Along with Lynn Nadel, PhD, Lane is the author of

Neuroscience of Enduring Change: Implications for Psychotherapy

Memory editing from science fiction to clinical practice.

2. Ryan L, Hoscheidt S, Nadel L. Perspectives on episodic and semantic memory retrieval. In: Dere E, Easton A, Huston J, Nadel L, eds. 

Beyond arousal: prediction error related to aversive events promotes episodic memory formation.

4. Lane RD, Ryan L, Nadel L, Greenberg L. 

Memory reconsolidation, emotional arousal, and the process of change in psychotherapy: new insights from brain science.

Client emotional productivity-optimal client in-session emotional processing in experiential therapy.

Adverse effects of psychotropic medications on sleep.

8. Borbély AA, Mattmann P, Loepfe M, et al. 

Effect of benzodiazepine hypnotics on all-night sleep EEG spectra.

A Brain-Based Approach to Psychotherapy

FROM THE ACADEMY OF CONSULTATION-LIAISON PSYCHIATRY

This article is the second of a 3-part series that aims to highlight and review the prevalence, risk factors, clinical manifestations, diagnostic recommendations, proposed mechanisms of disease, and current treatment recommendations of folate, B

As reviewed in the previous article, key nutrients—or what Casimir Funk, PhD, termed vital amines—are essential to maintaining good health. Deficiencies in these key nutrients lead to certain pathognomonic disease states, as Funk initially observed when he fed birds a diet of only polished rice and they developed a diffuse polyneuritis (beriberi). Afterwards, the same birds were fed a diet of brown rice, and their “nervous symptoms rapidly disappeared.”

 What did this experiment establish? The importance of vital amines, or as we know them, 

Vitamins can be broadly delineated into 2 categories: water-soluble and fat-soluble. Water-soluble vitamins are absorbed rapidly via the gastrointestinal tract and distributed widely in various body tissues; however, as these vitamins are water-soluble, they are not efficiently stored in tissues. Therefore, these vitamins require regular consumption (either through diet or supplementation) to avoid deficiency states. Fat-soluble vitamins, on the other hand, are more easily stored, typically in adipose tissue, and require less frequent intake.

 Examples of water-soluble and fat-soluble vitamins can be found in 

 (cobalamin) is a water-soluble vitamin that is found in certain foods and is required for DNA synthesis and the formation of several hematologic elements, such as red blood cells (RBCs), white blood cells, and platelets.

 Individuals who have low levels of vitamin B

, due to either increased demand or poor absorption, are labeled vitamin B

 deficiency can lead to the formation of abnormal hematopoietic precursor cells such as megaloblastic RBCs, as seen in 

 deficiency is not only problematic for hematopoiesis; it also has severe neuropsychiatric consequences, including cognitive impairment, depression, 

, peripheral sensory deficits, and weakness. Lhermitte sign (

 can be tested by flexing the neck and assessing for shock-like sensations radiating to the feet. The mechanism is better understood for neuropathies (primarily dorsolateral myelopathy) associated with this deficiency as opposed to neuropsychiatric conditions. Most theories suggest that elevated methylmalonic acid (MMA) levels found in vitamin B

 deficiency may lead to demyelination of the peripheral nervous system and central nervous system.

 MMA accumulates in cells due to lack of vitamin B

 as a cofactor in the conversion of MMA to succinyl Co-A in cell metabolism.

There are several potential causes of vitamin B

 deficiency. Autoimmune pernicious anemia is the most common cause of vitamin B

 deficiency. Intrinsic factor (IF) and gastric parietal cells are attacked by gastric autoantibodies. IF is a glycoprotein that binds cobalamin and aids in the absorption of vitamin B

 in the terminal ileum. The depletion or lack of IF in pernicious anemia causes cobalamin deficiency.

 Other causes such as poor absorption related to pancreatic insufficiency, gastrectomy, intestinal surgeries, and inflammatory bowel disorders can also contribute to poor vitamin B

 absorption. Intestinal infections competing for vitamin B

 absorption such as small intestinal bacterial overgrowth or a parasitic infection should also be considered. 

 affecting absorption and transport of vitamin B

, such as transcobalamin deficiency, are currently being studied. Several medications can also lead to vitamin B

 deficiency via impaired absorption, metabolism, and utilization; these are listed in 

 Pure nutritional deficiency is usually only seen in strict vegans and is extremely rare.

Who Is at Highest Risk for This Disorder?

Some people are at more of an increased risk of vitamin B

 deficiency than others. Older adults are at increased risk of vitamin B

 deficiency due to gastric malabsorption secondary to gastric atrophy, chronic H. pylori infection, increased probability of gastric surgery history, and chronic use of medications like metformin and proton pump inhibitors.

 In patients with alcoholic liver disease, cobalamin levels may remain falsely elevated or normal despite low concentrations of liver tissue cobalamin and its active metabolites. This leads to a functional cobalamin deficiency. Proposed mechanisms of action include impaired uptake of serum cobalamin by the damaged liver, impaired storage of cobalamin in the liver that causes it to leak out, and reduced hepatic ability to synthesize transcobalamin. Vitamin B

 treatment has proven beneficial to some alcohol-dependent patients with megaloblastic anemia.

 Older adults, individuals taking the medications listed in 

 those with alcohol use disorders, pure vegans, and individuals with poor access to adequate nutrition (either through economic limitations or malabsorptive limitations) are at highest risk.

In 2008, the World Health Organization recommended vitamin B

 fortification standards in order to prevent deficiency in high-risk populations. Since then, some nations have implemented these strategies and are working to improve dosing standards. The United States has yet to implement mandatory vitamin B

 fortification, but certain foods, such as cereals, can be found to be fortified voluntarily.

When Should Screening and Prevention Be Done?

Screening and testing should occur in the following groups: those at high risk; individuals who have evidence of a macrocytosis or hyper-segmented neutrophils on peripheral blood smear; those with unexplained neurological conditions (eg, cognitive decline, weakness, ataxia, paresthesia); and those with unexplained psychosis and mood disturbances. Serum cobalamin levels are not always reliable in detecting vitamin B

 deficiency. If an asymptomatic high-risk patient presents with low to normal serum vitamin B

 levels, obtain serum homocysteine and MMA levels as a confirmatory test.

 If pernicious anemia is suspected, confirm the diagnosis by obtaining anti-IF antibody levels and serum gastrin/pepsinogen levels.

Those aged 50 years or older and strict vegetarians may benefit from vitamin B

 supplements or food fortified with vitamin B

, as the crystalline formulation is better absorbed than natural dietary cobalamin. Following gastric bypass surgery, patients should supplement with vitamin B

In the United States, older adults have the highest prevalence of vitamin B

 deficiency. In the United States and the United Kingdom, the prevalence of vitamin B

 deficiency was found to be 6% in adults 60 years of age or younger. In adults 60 years of age or older, the prevalence increases to 20%.

Patients exhibiting macrocytic anemia on initial complete blood count and peripheral blood smear should be evaluated for both folate and vitamin B

 deficiency, as these 2 conditions often present simultaneously. This can be done by assessing serum folate and B

 deficiency is usually made when serum levels are less than 111 pmol/L (150 pg/mL).

 Measurement of serum homocysteine and MMA can also aid in differentiating between folate and vitamin B

 deficiency, both homocysteine and MMA levels can be elevated.

 is the standard treatment. The cause of the deficiency will dictate how one administers the medication and how much to dose. Those with poor absorption, altered anatomy, and/or neurological/neuropsychiatric manifestations would likely benefit more from parenteral than from oral administration. Typical dosing for adults is 1000 mcg parenterally several times per week until the deficiency is corrected, then once per month.

 are both effective treatments for vitamin B

 is a key nutrient that is essential for our hematologic and neuropsychiatric functioning. With the prevalence of vitamin B

 deficiency reaching 20% in certain populations, it is crucial to recognize patients who are at risk and/or require treatment. Vitamin B

 replacement is relatively inexpensive and can be lifesaving when administered via the appropriate route and at the appropriate dosage.

 is an associate clinical professor in the Department of Psychiatry at the University of North Texas Health Science Center in Fort Worth, Texas.

is a research coordinator in the Department of Behavioral Health Research at John Peter Smith Health Network in Fort Worth, TX. 

is a resident physician in the Department of Psychiatry at John Peter Smith Hospital. 

 is a pre-med Neuroscience student at the University of Texas at Austin. Drs DeMoss, Elbasheer, Kunnel, and Mahi Raju report no conflicts of interest concerning the subject matter of this article.

1. Piro A, Tagarelli G, Lagonia P, et al. 

Casimir Funk: his discovery of the vitamins and their deficiency disorders.

3. National Center for Biotechnology Information. PubChem Compound Summary for CID 46853873, Cobalamin. Accessed August 26, 2021. 

https://pubchem.ncbi.nlm.nih.gov/compound/Cobalamin

5. Leishear K, Boudreau RM, Studenski SA, et al. 

 and sensory and motor peripheral nerve function in older adults.

6. Rodriguez NM, Shackelford K. Pernicious anemia. In: 

7. Busti AJ. Medications known to decrease vitamin B

 levels. Evidence-Based Medicine Consult. October 2015. Accessed August 26, 2021. 

https://www.ebmconsult.com/articles/vitamin-b12-medication-interactions-lower-levels

Herb, Nutrient, and Drug Interactions: Clinical Implications and Therapeutic Strategies

9. US Department of Agriculture, Agricultural Research Service. USDA National Nutrient Database for Standard Reference. Accessed August 26, 2021. 

https://www.ars.usda.gov/ARSUserFiles/80400535/DATA/sr21/sr21_doc.pdf

10. Andrès E, Loukili NH, Noel E, et al. 

 (cobalamin) deficiency in elderly patients. 

11. Fragasso A, Mannarella C, Ciancio A, Sacco A. 

 deficiency in alcoholics: an intriguing finding in a retrospective study of megaloblastic anemic patients

Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline

Key nutrients are essential to maintaining health. Here's an overview of B12. 

Exploring Vital Amines: The Who, What, When, Where, Why, and How of B12 Deficiency

 was honored and delighted to present Sheldon H. Preskorn, MD, as Educator of the Year at this year’s 

. An academic psychiatrist, a researcher, an educator, and a mentor—Preskorn is, as John J. Miller, MD, described “a pioneer in the field of psychopharmacology.”

Preskorn shared with attendees the unexpected beginning of his more than 40-years-and-running career in psychiatry. On his TV, he watched a video of Jose Delgado being able to stop a ball, “charging in his tracks.” To Preskorn, that meant that the brain was related to behavior—and he wanted to learn more.

Amongst his many honors and awards, Preskorn is known for spending the 1980s establishing the value of the therapeutic drug monitoring of tricyclic antidepressants and understanding toxicity. Additionally, in the 1990s, he helped explain the liver cytochrome P450 enzyme system.

“My personal goal has been, and remains, bringing science to the practice of psychiatry,” Preskorn shared.

During the session, he pointed out the overlap between diagnoses and science in signs and symptoms of borderline personality, bipolar disorder, major depression. He claimed it is not the symptoms that distinguish these disorders, but rather the 

“Psychiatry has been mainly stuck at the level of syndromic diagnoses, but we are making inroads and have over the last 50 years into pathophysiology and etiology,” he stated.

Additionally, Preskorn thinks of his therapeutic drug monitoring focus as toxicity-centric rather than efficacy-centric. The reason? “We've had a better signal to noise ratio in trying to understand toxicity of the drugs and the avoidance of that than we did with antidepressant efficacy. “As a matter of fact, in another article that I published, I showed that it's really almost impossible given the signal to noise problem in clinical trials of antidepressants to show any relationship between our blood levels and clinical benefit.”

Preskorn also shared an equation of his creation. According to him, 

 determine clinical response: sites of action (affinity, intrinsic activity); drug concentration and its site(s) of action (absorption, distribution, metabolism, elimination); and underlying biology of the patient (genetics, age, disease, environment).

“We are born different,” said Preskorn. “Age, how we vary over our lifespan, disease (which is acquired through pathophysiological processes), and then the environment here referring to the internal environment. That is what underlies drug-drug interactions, where a drug enters the environment of the body and interacts with another drug, either pharmacodynamically, which is the first variable, or pharmacokinetically, which is the second variable in this equation.”

Preskorn closed his speech, smiling, with a promise for the future: “It’s been a great pleasure for me to have shared these few minutes with you and to talk about the developments over the last 40 years. But as I would say: You ain’t seen nothing yet.”

1. Preskorn SH, Baker B. The overlap of DSM-IV syndromes: potential implications for the practice of polypsychopharmacology, psychiatric drug development and the human genome project. 

Clinical Pharmacology of Selective Serotonin Reuptake Inhibitors

. Professional Communications, Inc; 1996.

Bringing science to the practice of psychiatry has been the personal goal of Sheldon H. Preskorn, MD—the Educator of the Year. 

Pioneering Psychopharmacology: Educator of the Year Award

The US Food and Drug Administration approved atogepant (Qulipta) for the preventive treatment of episodic migraine in adult patients, making it the first oral calcitonin gene-related peptide (CGRP) receptor antagonist—known colloquially as 

The decision to approve AbbVie’s medication was made based on data from a clinical program evaluating the efficacy, safety, and tolerability of atogepant in almost 2000 patients with episodic migraine, which was defined as 4 to 14 migraine days per month. One of the studies, the pivotal phase 3 ADVANCE study, included 873 patients with episodic migraine who were randomized 1:1:1:1 to receive a once-daily dose of oral atogepant (10 mg, 30 mg, or 60 mg) or placebo for 12 weeks.

"Millions of people living with migraine often lose days of productivity each month because attacks can be debilitating. Qulipta can help by reducing monthly migraine days with a once-daily, oral dose that works quickly and continuously," Michael Severino, MD, vice chairman and president, AbbVie, said in a press statement.

 "We are proud that AbbVie is now the only pharmaceutical company to offer three products across the full spectrum of migraine treatment, which include preventive therapies for chronic and episodic migraine and an acute treatment for migraine attacks."

Atogepant demonstrated an ability to improve several prespecified, multiplicity-controlled secondary end points across the 12-week period of the ADVANCE study. Those patients in the atogepant 10-, 30-, and 60-mg dose groups experienced decreases in mean monthly headache days of 3.9 (baseline, 8.4), 4.0 (baseline, 8.8), and 4.2 (baseline, 9.0) days versus a 2.5-day (baseline, 8.4) decline in the placebo arm (P <.0001 for all doses).

 These translated to 56%, 59%, and 61% of patients in the 10-mg, 30-mg, 60-mg dose groups, respectively, compared with 29% of patients in the placebo arm.

Additional results showed that treatment with the medication met primary end point, with decreases in mean monthly headache days of 3.7, 3.9, and 4.2 days, respectively, in the 10 mg (n = 214), 30 mg (n = 223), and 60 mg (n = 222) atogepant groups compared with a 2.5-day decline in the placebo arm.

The study also revealed a change of –3.7, –3.7, and –3.9 in the mean number of days of use of medication to treat migraine attacks per month from baseline that was reported across all 3 treatment groups, compared with –2.4 for placebo (P <.001 for all comparisons with placebo). A reduction of 50% or more in the 3-month average of migraine days was reported by 55.6% of participants in the 10-mg atogepant group, 58.7% of those in the 30-mg group, 60.8% of those in the 60-mg atogepant group, and 29% for those in the placebo group (P <.001 for all comparisons with placebo).

For both the 30-mg and 60-mg dose groups, investigators observed significantly greater score improvements of –2.5 points (P = .0005) and –3.3 points (P <.0001) in the mean monthly AIM-D Performance of Daily Activities domain. Similarly, patients in these dose groups also showed statistically greater improvement in the Physical Impairment domain in the AIM-D score (30-mg atogepant, –2.0 [P = .0021]; 60-mg atogepant, –2.5 [P = .0002]). On the other hand, those in the 10-mg atogepant group did not have significant differences on the Performances of Daily Activities domain of the AIM-D (difference, –1.2 [95% CI, –2.6 to 0.2]) and the score on the Physical Impairment domain of the AIM-D (difference, –1.1 [95% CI, –2.3 to 0.1).

"This approval reflects a broader shift in the treatment and management paradigm for the migraine community. Qulipta provides a simple oral treatment option specifically developed to prevent migraine attacks and target CGRP, which is believed to be crucially involved in migraine in many patients," Peter J. Goadsby, MD, PhD, DSc, neurologist and professor, University of California–Los Angeles, and King's College, London, and co-author of the ADVANCE study, said in a statement.

 "I'm particularly encouraged by the convenience of the oral daily use of QULIPTA, its rapid onset of significant efficacy, and its safety and tolerability as well as its high patient response rates. This is a milestone in preventive migraine treatment that I hope will help many patients for years to come.”

(A version of this article originally appeared with 

1. FDA Approves QULIPTA™ (atogepant), the First and Only Oral CGRP Receptor Antagonist Specifically Developed for the Preventive Treatment of Migraine. News release. AbbVie. September 28, 2021. Accessed September 28, 2021. 

https://news.abbvie.com/news/press-releases/fda-approves-qulipta-atogepant-first-and-only-oral-cgrp-receptor-antagonist-specifically-developed-for-preventive-treatment-migraine.htm?view_id=1531

2. Ailani J, Lipton RB, Goadsby PJ, et al. Atogepant for the preventive treatment of migraine. NEJM. 2021; 385:695-706. 

3. AbbVie Announces Positive Phase 3 Data for Atogepant in Migraine Prevention. News release. AbbVie. July 29, 2020. Accessed August 23, 2021. 

news.abbvie.com/news/press-releases/abbvie-announces-positive-phase-3-data-for-atogepant-in-migraine-prevention.htm

The US Food and Drug Administration approves first of its kind medication for migraine prevention. 

FDA Approves New Medication for Migraine Prevention

Conversations in Critical Psychiatry is an interview series that explores critical and philosophical perspectives in psychiatry and engages with prominent commentators within and outside the profession who have made meaningful criticisms of the status quo.

Robert Chapman, PhD (they/them or he/him) is a philosopher in the United Kingdom (UK). They are an associate of the department of philosophy at the University of Bristol, UK, focusing on the philosophy of neurodiversity. They have published widely on issues in philosophy of disability, the ethics of autism, and critical neurodiversity studies, and are currently writing their first book on the philosophy of neurodiversity. Their Shirley Foundation-funded doctoral research was carried out at the University of Essex between 2013 and 2018 and focused on the ethics of autism. They have taught at the University of Essex, King’s College London and the University of Bristol. They are proudly neurodivergent and disabled. They also blog for 

Dr Chapman’s work on the intersection of neurodiversity and psychiatry has had a substantial impact on my own thinking, and their writings have consistently forced me, and many others, to rethink long-standing assumptions related to pathology and medical care. Among Dr Chapman’s writings, of particular note are: “Neurodiversity Theory and its Discontents: Autism, Schizophrenia, and the Social Model of Disability,”

 “The Reality of Autism: On the Metaphysics of Disorder and Diversity,”

 and “Neurodiversity and the Social Ecology of Mental Functions.”

 In recent years, the neurodiversity perspective has not only emerged as a vital player in our philosophical understanding of health and disease, but also has also had begun to shape how societies relate to disabled individuals. Furthermore, the neurodiversity perspective and sister movements such as Mad Pride center the voices of mad and neurodivergent individuals, transforming what has so far been, in the words of Michel Foucault, PhD, “a monologue of reason about madness,” to a dialogue enabling collective self-reflection on the relational nature of dysfunction and disability.

: Let’s start by an introduction to the neurodiversity movement and the neurodiversity paradigm. What is neurodiversity and where does it clash with mainstream medical thinking?

: The neurodiversity movement is a social justice movement pushing for a shift away from the default pathologizing of mental, developmental, and cognitive disability, and towards what I have called a 

 approach to understanding disablement. It all started when autistic individuals began meeting and raising consciousness online in the 1990s. Many realized they were tired of being represented as tragic deviations from supposedly normal functioning, and they were also often traumatized by ensuing attempts to treat or cure their autism. Eventually, as a new way to challenge how we think about normality, they began to talk about whether the principle that increased biodiversity is necessary for a robust ecosystem also applied to neuro-cognitive diversity within species. Just as we value, see beauty in, and try to conserve biodiversity, why not think about neuro-cognitive diversity in the same way? Based on this, Judy Singer, a member of these communities and, at the time, a sociology student, coined the term 

 and called for a “politics of neurological diversity” in her 1998 thesis. Singer circulated her thesis, which was grounded in the theories of disability studies, among other autistic activists before publishing a revised version as a book chapter in 1999.

 This became a founding text of the movement, which rallied around both Singer’s concept as well as existing themes from disability studies.

 was proposed a bit later, in 2012, by autistic scholar Nick Walker, PhD (she/her),

 who was also a graduate student at the time. By then the ideas initially developed by Singer were increasingly being adopted by individuals with other diagnoses such as bipolar, dyspraxia, and attention-deficit/hyperactivity disorder (ADHD). Walker was interested in the philosophical implications of this broader application and how it challenged theoretical assumptions and cultural and scientific practices. Walker proposed a distinction between the 

, which she took to be dominant and to rest on a relatively restricted conception of neurological, cognitive, and developmental normality, and the emerging 

, which begins from the acknowledgement that neurological diversity is natural and beneficial for the cognitive and cultural richness of the species. On this paradigm, instead of being labelled medically 

, those who are more enabled in a given society are considered more 

, while those who diverge further from functional norms are more 

. Walker argued that developing and cultivating such a paradigm shift, to then be adopted for research, policy, and practice, would be necessary for the long-term emancipation and well-being of neurodivergent individuals. Although Walker's chapter was relatively brief, it became highly influential within the movement, and I count it as another of the seminal texts of neurodiversity theory.

: You have talked about neurodiversity as a sociopolitical idea, centered around social models of disability, as well as neurodiversity as a scientific concept, offering a new way of thinking about function and dysfunction. Can you elaborate on these strands of neurodiversity (among other strands) and the shape they have taken in your own work?

: I see the cultural paradigm shift as quite similar to the change we have been seeing regarding the LGBT community, away from pathologization and towards pride, acceptance, and inclusion. The neurodiversity movement is also part of the broader disability rights and justice movement. With neurodiversity, while there is a long way to go, we are already seeing, for instance, neurodiversity paradigm vocabularies being used in newspapers and magazines, and a shift to disability rights-based practices for neurodivergent individuals in schools and workplaces.

Among other things, researchers increasingly recognize neurodivergent strengths alongside limitations.

Accompanying this, a scientific paradigm has also been emerging, albeit in a somewhat piecemeal way. More neurodivergent individuals have become involved in research, and more neurotypical researchers have begun to listen to neurodivergent perspectives. This is beginning to change how researchers formulate hypotheses and produce knowledge. Among other things, researchers increasingly recognize neurodivergent strengths alongside limitations, study cognitive problems as relational rather than as arising from individual deficits, and view neurodivergent disablement and distress based on a social model of disability rather than a medical model.

In my own work, I developed the ecological model of functioning to help clarify and formalize the theoretical basis of the emerging shift in the scientific paradigm, and to challenge the default pathologization of neurodivergence. I became interested in developing a new model of mental functioning partly because neurodiversity proponents had long been (successfully) using the social model of disability, and yet many researchers were still dismissing the idea that things like autism were not pathological. I realized that this was, at least in part, because the social model of disability leaves the dominant notion of individual dysfunction or impairment relatively intact, which is important because individual dysfunction is a core part of the definition of mental disorder (or of somatic disorder for that matter). As such, even the most successful application of the social model, while vital in other ways, is insufficient for undermining the ascription of neurological or mental illness, disorder, or pathology. After all, we can and do use social model interventions for things everyone agrees are genuine pathologies, such as dementia. Thus, I realized we needed an alternative model of functioning to augment alternative models of disablement and to help shift the paradigm.

Traditionally mental functions and dysfunctions have been determined through what I call “individualist comparativist” models, which compare all individuals to an aggregated norm and then rank them in levels of functioning. These models—which I date back to Darwin’s half-cousin, the eugenicist Francis Galton—seek to be continuous with the kind of evolutionary biology that focuses on individual fitness or adaption, and they thus rank fitness levels from highest to lowest in members of a population. If we accept these models, then it seems like an objective fact that members of low-ranked groups such as autistics and dyspraxics are naturally dysfunctional, and hence pathological, in comparison to neurotypicals—even if the social model can be helpful for alleviating disablement. The continued use of these models reifies neurodivergent disablement as natural fact and also lends scientific authority to the normalization of neurodivergence.

By contrast, the ecological model, as the name indicates, is more influenced by how ecologists talk about functioning. Ecologists tend to be less interested in ranking individual fitness levels, and more interested in how broader systems function as a whole, how functions emerge from the relations between organisms, and how the dominance of some forms of organisms can be harmful for the functioning of others. Bearing this in mind, in 

 I drew on theoretical and empirical research to argue that many neurodivergent functions, or relational functions that emerge from group neurodiversity, are overlooked on the traditional models.

 To avoid these problems, I then combined the arguments of neurodiversity proponents with ecological functional models to propose a preliminary ecological model in line with Walker’s call for a paradigm shift. To the extent this proves to be useful for researchers, I hope it will help with the scientific paradigm shift by orientating researchers towards asking different questions, formulating different hypotheses, and ultimately producing knowledge that helps us move beyond the default pathologizing of neurodivergent disability, and which supports a broadly conservationist approach to neurodiversity.

: How does your ecological model of mental functions play out within psychiatry and in the context of existing philosophical debates about neuropsychiatric dysfunction?

: It may be helpful to look at this historically. The modern debate could be dated to the 1960s, when the antipsychiatrist Thomas Szasz, MD, argued that mental illness was a myth and that psychiatry was a pseudoscience. Szasz was happy to acknowledge that neurological illnesses exist. But he nonetheless held that there could be no mental illnesses, since for him, an illness must be biological (including neurological) by definition. The Szaszian position, while challenging the pathologization of emotional distress, is entirely continuous with the Galtonian project of ranking neurocognitive functions in relation to an assumed norm. This challenged the psychoanalytic psychiatry of the time, which was not based on biological research, and pushed psychiatry towards the more biocentric and cognitivist models that are still used today. While this argument still has some influence, contemporary psychiatry has largely neutralized Szasz’s critique not just by analyzing the conceptual flaws of his arguments, but also by finding ample evidence that biological processes in some form or another, though they may not take the form of discrete dysfunctions, are part of the story for many conditions listed as mental disorders. In many ways contemporary psychiatry has thus become more Szaszian, although nobody likes to admit that.

By contrast, while they have some surface overlap with Szasz in that they challenge pathologization, the neurodiversity perspective and my ecological model present a novel philosophical position that is equally at odds with mainstream psychiatry and the Szaszian tradition (including its various offshoots within critical psychiatry). At base, the ecological model rejects the assumption that humans have enough neurocognitive uniformity across the species that legitimizes the notions of normal neurological functioning. Instead, my model begins with the acknowledgement that we are a neurologically diverse species, and the insight that neurocognitive functions and dysfunctions are (at least in significant part) relationally produced and upheld, both between different minds, and between mind and environment. It is not just that cognitive niche construction enables or disables different forms of functioning, it is also that a trait associated with individual disability may contribute to functioning at the group level, while a trait associated with individual ability may contribute to maladaptive group functioning. So things are a lot more complex than being normal or abnormal.

Part of the significance of adopting this model is that we recognize more neurodivergent mental functions, and that many dysfunctions are relational, often stemming in part from the neurotypical side, rather than being intrinsic to neurodivergent individuals. Simultaneously, by incorporating a social model analysis of cognitive niche construction, this also allows us to shift to viewing neurodivergent abilities as forms of marginalized functioning rather than inherent dysfunction. This model challenges the idea that many neurodivergent individuals necessarily have neurological or cognitive pathologies, as well as the idea that neurotypicals are necessarily superior, while fully acknowledging the fact of neurodivergent disablement. Moreover, unlike the Szaszian critique of psychiatric pathologization, this model is compatible with disability justice more broadly, because it applies equally to learning and cognitive disabilities and neurodevelopmental disabilities, instead of reinforcing their pathologization. More concretely, I thus hope the model will help reorientate the surrounding biopolitics, away from the normalizing tendencies developed by 19th-century eugenicists, and towards a conservationist approach to studying and supporting human neurodiversity.

: A common objection that is raised against neurodiversity is that the framework applies poorly to severely disabled individuals who have high support needs, and may live in specialized settings. Given that this may be on the minds of many readers as well, I think it is worth bringing up here.

: This is a very important question on a complex topic. I will restrict myself to a pair of key points. First, the form of neurodiversity that I, and I believe most proponents, endorse does not deny that there are different forms of disability, and that in some cases much more direct support is needed (even if we have critiqued the utility of terms like 

). In fact, the clear implication of adopting social models of disability (not to mention my ecological model of functioning) would be that individuals with more complex disabilities should get more support, not less.

A key point of contention, of course, regards whether we prefer to see complex disabilities more as mental pathologies to be treated, or marginalized minorities to be supported. This brings me to my second point. Because my approach to neurodiversity is based on a disability justice perspective, it relies more on standpoint epistemology, centering the lived experience of marginalized individuals or groups. My own view, then, is that we need to do more to center the voices of those with intersecting disabilities and high support needs when talking about those who sit at the same intersections (as I wrote about 

 At the moment, we have no data on the views of those considered severe on such topics. Interestingly, though, just looking through texts written by nonverbal autistics with intersecting disabilities and high support needs, it is quite easy to find many who hold views consistent with the neurodiversity perspective, as I have 

 Indeed, some of the most influential neurodiversity proponents, notably the late Mel Baggs, were labelled severe and had high support needs. So, we cannot assume that everyone with higher support needs would reject the neurodiversity perspective. My hope is that empirical researchers will, where possible, survey the preferences of those with high support needs in a more systematic way. As a philosopher I do not have the right resources to do that kind of research, but I can say I do think that should be the starting point of any conversation on this.

: A related issue is that of whether the neurodiversity movement rejects medical care per se. My understanding is that the proponents of neurodiversity movements are not against the use of medical interventions, but these medical interventions need to be offered on terms that are acceptable to and desired by neurodivergent individuals. Is that an accurate characterization? What do you think medical care would look like within a neurodiversity paradigm?

: Views differ among neurodiversity proponents, but for the most part, I think you are right. The key thing most are against is the default assumption that neurodivergent individuals should be normalized, and, in turn, most are against the invariably harmful attempts to cure us or to prevent neurodivergence from existing. What we want is support so neurodivergent individuals of all abilities can thrive. In certain respects, medical care would not change all that much. For instance, when it comes to depression, the neurodiversity paradigm, although it is certainly not committed to these, may be compatible with a range of existing approaches found in many forms of psychotherapy. And, for that matter, it is equally consistent with alternative approaches from beyond the Western medical tradition.

But there are certain things most neurodiversity proponents are very against. An example of this is Applied Behavior Analysis (ABA), which was initially used as gay conversion therapy and is still used on autistics. Traditional ABA uses a system of punishments and rewards to alter behaviors, although more recently punishments have become less popular. Today it is often touted as the gold standard of autism interventions, despite the protests of many autistic individuals who are clear that their experience of ABA was dehumanizing, focused on normalization, and traumatized them. Myself and my co-author Virginia Bovell recently reviewed the evidence and ethical arguments for or against ABA for a forthcoming book chapter. We found the evidence stacked up against the moral permissibility of ABA. I have uploaded a 

 and I invite anyone who is skeptical of worries regarding ABA and normalization to read through and assess the reasoning and evidence we present.

Is neurodivergence to be cured or is it a healthy part of our social ecology?

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