Professor Jonathan Green Hello,  I’m Jonathan Green. I’m a Professor   of Child and Adolescent Psychiatry at the  University of Manchester and a Clinician,   a Child and Adolescent Psychiatrist at  Manchester Royal Children’s Hospital.   And I’m pleased to talk to you today about  neurodiversity, autism and healthcare [pause]. Yes, well, neurodiversity, at the first  level, is really what its name implies,   which is that it implies the range of  neurological function, of brain development,   of functioning of mind that we all have.  So, it’s neurodiversity, and in that sense,   it is part of a regular, if you could say,  biological variation across the population,   a distributed trait, if you like, and similar  to many other distributed traits that we have   in our physical being and our characters  and personalities. Within that, autism is,   as it were, a subset of neurodiversity. So,  neurodiversity is a broader category than   autism and within that, autism is a clinically  defined condition, from a Clinician’s perspective,   and has a history of shifting definitions, as  time has proceeded, based on clinical perception   and the evolving clinical science that has  happened around this – around the topic. So, that’s a first level. Of course, we all know  that the neurodiversity movement is something   slightly different, although allied to that.  And this is a social movement, in some sense,   also, for some people, a political movement, which  wishes to celebrate and certainly, raise awareness   of neurological differences, have recognition  for that, representation for diverse voices,   within a model of social equity.  So, the neurodiversity movement,   which has been gathering pace for certainly  30 years and is very prominent now, really   speaks for the legitimacy rights of neurodiverse  people, and wishes to, as they see it, certainly   de-pathologize the notion of autism as a, sort  of, biological trait or a clinical disorder. So,   we have the social element of the neurodiversity  movement and then, the third level, or component,   if you like, is the healthcare component. For us, as Clinicians, we are wishing to   diagnose, and we’re charged with diagnosing  autism and looking after autistic people,   children and adults, as they come to our  services. So, we have these three different   levels and at the moment, sometimes the language  around this is contested. And for this audience,   certainly, I think it’s a useful thing to try  and develop a conceptualisation of autism and   neurodiversity, starting at a biological  level and then, move forward from that. So, this slide, which comes from a recent paper  from Mike Owen’s group in Cardiff, genetics,   looks at the modern, current understanding of the  genomic architecture behind neurodiversity and   autism. And I think this is instructive and useful  for us in thinking about what neurodiversity is   and how it relates to autism and other conditions.  So, what this paper does rather elegantly is   to show that there are two separate kinds of  genetic, genomic architecture behind autism. Firstly, there is the range of common variants,  so-called SNPs, multiple genes of small effect,   which influence biological development,  brain development and these underpin the   variations that we call neurodiversity. And  these are represented in the slide here,   along the X axis, as the burden of common autistic  risk alleles. But in the range of neurodiversity,   we also have a more extreme end, which  is a number of rarer genetic variations   that are more disruptive to brain and biological  development, either comp – copy number variations   or single gene mutations, and these are rarer,  but are shown up the Y axis in this graph. So,   the common risk alleles along the bottom really  underpin what is often called neurodiversity   and here, characterised as the broater aud –  broader autism phenotype in the yellow figures   here. And this is a – what would be considered  within a lot of the neurodiversity literature,   a non-pathologized notion of biological  variation, an individual difference. Up here we have the effect of these rarer,  but more disruptive, gene variants that you   also find in autism, and these are associated  with a number of other expressions. Firstly,   intellectual disability, developmental delay  and other kinds of developmental disability   which are highly associated with these gene  variants, and then we have autistic disorder,   which is associated with intellectual disability.  And here you have a combination of these common   risk alleles and a degree of these  rarer neurodevelopmental mutations,   as they’re characterised here. And  this is the more, as it were, severe,   developmentally disabled and complex needs  version autism that we often see in the clinic. And then, in this group here, with the green  figures, we have what’s typically characterised   and diagnosed as familial autism. And here  you’ll see that there are lee – less likely   to have these rare gene mutations and more likely  to have – be a combination of these risk alleles,   these familial inherited variants, on hundreds  or even thousands of genes of small effect   combining together. And this is what we call  common or familial autism in its expression. And I think in this diagram, what you can see  encapsulated, in a way, is the relationship   between an individual difference view of  neurodiversity, on the one hand, and the more,   if you want, medical model or extreme version  of disability and complex needs associated   with autism, associated with other genetic  conditions. And in this group, the two aspect,   risk alleles and these common genetic mutations,  are additive, in fact. And you’ll see that often,   people who speak, Clinicians and autistic  advocates, are often speaking at somewhat   cross-purposes here, because talking  about slightly different realities. But this encapsulates at least the genetic  architecture behind autism and neurodiversity,   and in a clinic, from a clinical sense, I think we  commonly see a mixture in our clinics of children,   adults, with common variant familial autism,  who have also been stressed with life events   and other adversity, whether it’s from social  circumstance or from intrinsic variations in   their biology. We see a combination of those  in our clinics for – who need help, with   these children with the rarer conditions, with  neurodevelopmental problems, roughly speaking,   about 5% with single gene conditions and up to 10%  with what we call copy number variants. So, round   about 15% or so of autistic expression from this  group. And it’s a combination of those two things   that we see in the clinics, and what we don’t tend  to see, and don’t come to us for help, indeed,   is this range of neurodiversity as a population –  individual difference in the population [pause]. So, this model that I published in the  ACAMH journal recently and then previously   in other journals, really follows on from the  genomic architecture that I’ve just described,   because it’s really concerned with thinking  about how that genomic architecture which   expresses itself in differences in early brain  development, how that then translate into the   life of children and adults as they experience the  world after birth, in the early years and then,   later on in development. And so, the model that I  have in mind here begins with the idea that we’ve   already talked about, that neurodiversity can  be understood as a neutral and in other words,   non-pathological notion, autistic and other  individual difference, within the population. So, this is like a trait variation, like  temperament or other – a variation of ability   and perception and characteristic, amongst us  all as humans. And then, as I’ve indicated,   there is this degree of neurodiversity where –  which is a difference that really makes quite   a difference, which is gene variants that  cause more significant neurodevelopmental   disruption in brain development.  So, you’ve got these two aspects,   common individual difference and more just  neurodevelopmental disruption, to the early   child experience, as they come into the  world. And then, what we’re talking about   is the role of environment, because of course,  brains only express themselves and as it were,   inform the growth of mind and self as  they interact with the environment. And it’s this environmental interaction,  what I call here a ‘transactional process’,   at the level of brain, body and mind, which  we then study in relation to how this alters,   consequent on the neurodiversity, the individual  difference in brain development. And we can   understand these early transactional  processes and what environments work   well for neurodiverse people and what don’t, and  particularly in early childhood, which has been   my main focus. And we can see the autism as a  behavioural phenotype, as what we characterise,   recognise, as an autistic expression in the  world, emerging in the first years of life   out of this transactional development. And the  reason I emphasise it like this is because of   the work that we’ve done in altering those early  environments using structured interventions and   then clinical trials testing the results of  those interventions on downstream development. And what we find is that as we alter the  environment around the early neurodiverse child,   then actually, that impacts on the later  trajectory, their later autistic and other   adaptive trajectory, and we see a difference from  that alteration of the early environmental change.   While we have applied that in early parent –  what we call parent mediated intervention, to   alter this environment around the child in early  life, the same principle actually occurs later   in school, in adolescence and adulthood. When we  talk about modifying, adapting and optimising the   environment to relate well to neurodiversity in  the school, workplace and other social settings.   So, it’s the same kind of idea, but we’re doing  this early on in early interpersonal development. And what we’ve found from these studies is  that the environment makes a difference,   so that this is not – autism is not just an  emergent property dependent on brain difference   and genetic structure. There is not a one-to-one  correlation like that. That sets the scene,   but actually, autism as an emergent property, as  I call it, actually results from the interaction,   the transaction between those early brain  differences, neurodiversity and environmental   conditions. And this is important to understand  ‘cause it makes autism a more human dynamic   ac – presentation than we might otherwise think.  And it relates a lot to how we may want to see   autism presenting with disability and clinical  need on the one hand, and on the other hand,   not needing any healthcare at all.  And this speaks to this issue of,   how does the notion of neurodiversity and  autism really relate to healthcare needs? So, this developmental model can be put  forward because of our developmental science   and intervention science, and this is an example  of some of the studies that I’ve personally done,   although other people have done similar  kinds of studies, which have shown an   intervention process having a long-term effect  on autistic trajectories in later childhood. So,   this is our infancy intervention, called iBASIS,  and this is our PACT intervention for preschool   children. And what we see here is that we  get an effect of modifying the environment as   we’re doing the intervention, which then sustains  itself right through until middle childhood. So,   these are early environmental effects that have  long-term consequences. And that’s how I can   characterise the developmental model of autism as  what I call transactional and emergent [pause].  The notion of phenomenology is essentially,  the study of consciousness and subjective   experience and there is a tradition of clinical  phenomenology, whereby professionals use a   phenomenological understanding to try and  understand their patients’ experience. So,   phenomenology can be used in both ways, so  individual – examining one’s own consciousness   and using empathic understanding to understand the  consciousness of someone else to the extent that   one can. And interestingly, phenom – autism  is one of the very few conditions, really,   where we don’t have a systematic phenomenology  and unlike many other conditions that we deal with   in mental health, we don’t have that aspect to  understand the condition in our patients/clients. Autism is diagnosed, characterised by what we  call the behavioural phenotype, which really is   about observed behaviour in children and indeed,  in adults. And there are historical reasons why   that came to be the case, but I feel that now,  it is a good time for us to reconsider subjective   experience, and this is certainly something that  the autistic community themselves are very keen to   do. They wish to have their experiences recognised  and are challenging us, really, to think about   that in relation to how we see autism as a  condition that we might deal with in healthcare. So, there is now the beginning of phenomenological  investigation of autism, and I just want to   take a little time to tell you a little bit  about the – some of the results of this. So,   here is a very small study that I took part  in with three autistic adult colleagues,   and me as a neurotypical person. And really,  this was an immersive and a collegiate activity   where I wasn’t a – the Researcher, I was a  participant, along with them, and we really   came together to share our experiences across the  autistic/non-autistic divide, if you like, to see   what was seen to be associated with autism, what  – and what might not be. It’s a small sample, but   the importance of it is that it – for the first  time, we did something that was participatory   and also, at considerable depth. A number of themes arise – arose out of this  exercise and we published it in a number of papers   now, and this is a summary of the themes that  came out of our investigations together. You’ll   see here in the colour coding that there are two  aspects that were particularly different between   autistic and non-autistic experience, as we  explored it. There were a number of aspects that   were pretty similar and there was one that was  a bit similar and a bit different. The ones that   were really different was what we’ve called here  the ‘sensorium’, and these – this is, basically,   the fundamental experience of consciousness,  of the experience of space, time, sensation,   sensory experience and along with that,  interpersonal experience at a very basic   sensory level. This, as we explored it, was really  very different in the autistic participants to the   non-autistic participant and from very early on.  And this notion of the sensorium then became a   real focus for how – what we might identify  as a core feature of the autistic phenotype. Another aspect that was really different  was what we called ‘social joining’,   which was an experience from very early on that  the autistic participants had of not being able to   link in to the ordinary flow of social activity.  And of course, people vary hugely in how well   they are able to integrate socially, generally. I  mean, that’s part of the normal human variation,   but this was very striking in its – in how  extreme it was and how difficult it was from   a very early stage. And it often was first  manifest in the sense that autistic people   had about their relationships with close family,  parents, others, siblings, etc., as well as school   friends. Social joining became very difficult.  They started to feel socially disconnected,   alienated, sometimes scapegoated, in  a very painful way, from very early. On the other hand, there are a number of things  very similar. So, we’ve got trust here and what   this really refers to is that the impulse, the  need of autistic people for trust, relationships,   intimacy, acceptance, understanding, was no  different, either qualitatively or quantitatively,   in these people, in the participants that we had,   between autism and non-autism.  There was the same need. Similarly, different kinds of states of mind, from  pleasure to pain, to difficulty, to distress and   the capacity for empathy and interest in other  people, all these fundamentally looked and   felt very similar between autism and non-autism.  Similarly, with the ups and downs of emotionality.   What was different in the empathic response and  the emotionality response was that autistic people   found themselves more liable to difficulty in  those areas, but the quality of their responses   was fundamentally similar. The other area where  there was some – quite a lot of difference between   autism and non-autism was in what we call  interest and attention, the quality of how   au – the autistic people use their attention,  the so-called monotropism or focused attention. So, these are interesting findings. Of course,  they would need to be looked at across a much   broader representative sample and indeed,  there’s a – quite a big literature on this.   But there seems to be consistency across  the literature, as it is at the moment,   that these findings are broadly representative,  particularly of verbal and non-intellectually   impaired individuals, which – who were the  people that we were working with or together   with in this context. That, as I said,  trust is common, sensorium very different,   interest and attention somewhat different,  empathic states of mind similar and social   joining challenged. And right from the start,  then, this kind of phenomenological exercise   challenges some of the notions that we have  had in the standard behavioural phenotype. For instance, that social avoidance is a primary  feature of autism and social impairment and that   the lack of capacity for understanding someone  else’s mind and empathy. The phenomenological   evidence challenges these ideas, and it makes  us think that actually, these difficulties may   be actually secondary to primary neurodiversity  differences, secondary based on social experience,   rather than the primary difficulty, and we are  focused much more on fundamentals of sensorium.   And these ideas, also, are consistent with  what I’ve already talked about in terms of   intervention science, because what we find when  we change the early environment and make it more,   as it were, neurodiverse, sensitive and  adapted, what we find is that the children   under those circumstances become spontaneously  more socially initiating and socially engaging,   in a spontaneous sense. In other words, they’re  socially motivated when the environment is right,   and that turns out to be a core finding that  we replicate in a number of different trials,   that you change the environment and the  social functioning changes as a consequence. This, I think, presages a new phase in autistic  science, healthcare and clinical observations,   and what we hope is that we can move towards  a situation where autistic diagnosis,   as well as relating to autistic  people within a healthcare setting,   is much more focused around phenomenology than  just behavioural observation. We want to do   both. The behavioural observation has been  definitely useful, don’t want to discard it,   but we want to add in the subjective  and the phenomenological [pause]. So, this is a – it’s certainly  an extraordinary phenomenon, that   now coming onto health services and how we respond  to neurodiversity in autism, it is, in – true,   that the first thing to consider is this huge  increase in awareness and referrals to health   services. To the extent that within Child and  Adolescent Mental Health Services at the moment,   around the country, up to around 80% of new  referrals are related to neurodiversity in   one way and another, and often autism.  So, this is a really striking phenomenon. What’s it due to? Well, I think that it  certainly relates to increased awareness.   People are much more aware of soci –  of neurodiversity and autism now than   there has been in the past. And I think in the  community generally, the neurodiverse community,   as well as the general community, it is  recognised that an understanding or a labelling   of neurodiversity or autism is actually a useful  way of understanding and accepting difference,   conceptualising the struggles that there  have been. And people find this kind of   label and identification very helpful. And  we know that the idea of an autistic identity   is a strongly held and often felt to be very  valuable phenomenon in people’s development. From a medical point of view, also, we know  that the neurodiversity differences across   the population do increase the liability for  many mental health outcomes and conditions,   and so, it’s more likely that people with  neurodiversity will be presenting to health   services. What needs to be understood is  that neurodiversity per se does not have   to be pathologized and is not necessarily  in need of care. But it does have its own   developmental needs and vulnerabilities  for needing support and healthcare [pause]. In this situation now, where we have a plethora  of referrals and need, we have services that   are often quite overwhelmed with the need  for responding to referrals of this kind,   we need a way that is organised, efficient  and evidence-based within healthcare services,   to manage the situation and do best by  neurodiverse and autistic people. And   this is my proposal for an integrated  early care pathway based on that,   which is based on evidence accumulated  over the years for enduring healthcare   conditions of various kinds, the evidence from  intervention trials for neurodiversity and autism,   and also, new detection methods for  identifying neurodiversity and autism. And it’s a pre-emptive pathway, above all.  This starts early and its basic idea is to   start pre-diagnosis with a stepwise  monitoring, identification and care,   support for early neurodiversity in  autism pre-diagnosis, so that people   aren’t stuck on waiting lists waiting for a  diagnosis, to then give them access to care.   And this is much better for families, but it  also, arguably, we think, would be better for   health services and for efficiency because  it is pre-emptive and we know we have the   interventions that will improve the adaptation  of families and the autistic young people,   going forward downstream. And this is a good  way of organising a health service, rather than,   kind of, reactive care, where you wait for  problems to reach a crisis period and then,   try and firefight them, which is commonly how  things are presented and done at the moment,   in a very – fairly ad hoc and reactive way  that is rather too late in development. So, this is the basic pathway, which is a  developmental pathway, starting with this   detection early pre-diagnostic care.  So, this is what we call pre-emptive,   and we have now good surveillance instruments  that we can use in the community to pick up   likely autism trajectories from the early  years of life. So, from about a year of age,   these instruments, particularly this instrument,  the SACS, is – it’s very good at picking this up,   particularly if it’s used over time. And then,  we triage into – for children who show positive,   as it were, on this surveillance,  we triage into early parent-mediated   support and that is the so-called iBASIS,  which we’ve trialled in randomised trials. Then leading into and after diagnosis, we can  then put in place a primary family-focused   parent-mediated intervention which – of a kind  that can be shown to have long-term impact on   development. And this is the kind of intervention  that is recommended by NICE at the moment,   a parent-mediated social communication  intervention, and an example is the PACT   programme, that I’ve been involved in testing.  There are other examples, such as JASPER from the   US. And we put this in place as a family focus  from early on preschool or early school years,   and this really has its main focus in skilling  and empowering parents to be able to parent their   child effectively, understand, respond to them and  feel confident and empowered in their roles as a   parent. And we also know that this improves the  child’s longer-term development in ways that are   measurable in terms of communication, adaptation  and some aspects of autistic behaviours. Then, later on, we – after this pri – that primary  family-focused care, then we need longer-term   support for other kinds of mental health  difficulties that may arise later in development,   and we hope that some of these will be headed  off by that early support. But if it does arise,   the anxiety, depression, behavioural difficulties,  etc., then we need step-up specialist care and   this needs to be organised at a specialty team  regional level. And it’s step-up, step-down,   so that we have good interventions organised  for autistic people, which do their job and then   the family go back into the  longer-term support with co-workers. This is the pathway that is pre-emptive, it’s  evidence-based, it’s focused on family resilience,   child development and wellbeing and the  best adaptation. And we’ve shown that   this – in clinical trials, that this  is going to have long-term positive   effects in development and then later,  step-up care is needed. And it’s work   that is now under implementation in  the UK, in Australia and South Asia. One final component of this is the possible future  use of digital technologies, and here we hope,   though this hasn’t been incorporated yet, that  in the future we’ll be able to use digital   applications, electronic health records,  digital navigators, within this pathway,   to make the care process more seamless  and effective for families, so they feel   hooked into support, even if it’s online, as  they go through development with their child. So,   this is an ideal longer-term use of  digital technologies within healthcare   to support a healthcare service  of this kind for autistic people.