Notes on RD Laing "The Divided Self"

 

The schizophrenia spectrum encompasses both schizotypal or schizoid personality disorder and schizophrenia and related psychoses. These schizophrenia psychosis are distinguished from schizotypal/ schizoid personality disorder by the presence of notable and persistent psychotic symptoms (Laing, 1965: 17). The schizotypy concept – a distinct behavioural phenotype associated with increased risk for psychotic symptoms with empirical evidence supporting it (Linscott & Van Os, 2010) – is regarded as co-existent with the schizophrenia spectrum. This part will discuss RD Laing's model for disorders of self associated with the schizophrenia spectrum in particular. It will not focus on how these states develop or theoretical models of how psychotic symptoms develop from them.

Laing described ontological insecurity of loss of individual identity as an important feature of the schizophrenia spectrum which he refers to as the schizoid state (Laing, 1965: 39-46) where people have fear of engulfment (of identity by other individuals during interpersonal interactions), implosion (where the individual feels empty and reality threatens to invade and destroy them) and petrification (whereby someone’s autonomy is negated and they become objectified by another person).

This ontological insecurity leads to schizoid individuals protecting themselves by creating a ‘false self’ that interacts with the world. In most individuals a vital embodied self has real perceptions of or meaningful actions on the ‘other’ (such as other individuals or the external world). By contrast, schizoid individuals have an inner true self interacts with the world via a false self that has a generalised deadness and results in unreal perceptions of or futile actions on the ‘other’ (Laing, 1965: 78-82).

The inner self aims to protect itself from destruction by others but only results in this self losing any firm attachment to reality and becomes like a tenuous gas occupying this self, it “becomes unreal”, “empty, dead and split” and experiences strong negative angry emotions as result (Laing, 1965: 139-140). The split in the sense of self leads to problems distinguishing what is self and not-self including one’s own body, “disembodying  the sense of ‘I’” (Laing, 1965: 175). 

References

 

Laing, R.D., 1965. The divided self: An existential study in sanity and madness. Penguin: Middlesex, UK.

Linscott, R.J. and van Os, J., 2010. Systematic reviews of categorical versus continuum models in psychosis: evidence for discontinuous subpopulations underlying a psychometric continuum. Implications for DSM-V, DSM-VI, and DSM-VII. Annual review of clinical psychology, 6, pp.391-419.

 

Answering evolution’s challenge to Davidson’s anomalous monism may create opportunity for neuroscience in mental health

0.    Abstract

Neuroscience aims to explain mental health problems as well as provide other useful clinical information such as measuring severity and predicting treatment response using nomothetic techniques which rely on type identity. Davidson’s anomalous monism states that there is token identity but not type identity for mental events. I will argue that evolution favours type identity for at least some mental functions in hominids (including those likely to of interest to clinical neuroscience such as anxiety) because natural selection can only work through genetics replicating physical structures and processes. I will discuss several possible defences of anomalous monism. Rejecting evolution entirely as a theory creates too many problems and trying to argue evolution has not influenced the development of the mind is unlikely to be true. The concept of multiple realisation does not apply to minds belonging to evolution of members of the same species. It may be that some aspects of mental functioning have anomalous monism properties but others have been influenced by evolution and have type identity properties and are accessible to neuroscience allowing potential clinical utility for these techniques.

1.1   Anomalous monism’s challenge to the neuroscience of mental health

Applied neuroscience has several goals  in mental health. The first is explanation – how do the mental states and events of clinical interest arise i.e. their mechanisms which can lead onto methods of how to prevent undesirable mental states and promote more desirable mental states and how to alter undesirable mental states into more desirable ones (leaving aside whose values determine desirability). Furthermore, if we have a better idea of the explanation of mental states of clinical interest then we can change diagnostic criteria of psychiatric disorders from mostly descriptive constructs to those based on explanation.

A further goal of neuroscience in mental health is to identify biomarkers which can have several clinical functions: assess risk of developing a condition, in order to confirm a diagnosis or measure a trait, to measure severity of a clinical state (which can also be used as a proxy marker of treatment response), to identify the stage of someone’s illness , as a predictor of treatment response and to help estimate prognosis (Davis et al, 2015 and Steele & Paulus, 2019).

Are these goals of neuroscience possible according to philosophy of mind? One influential position by Davidson outlines three principles which all operate: “at least some mental events interact causally with physical events” , that where causality exists it “will fall under strict deterministic laws” and “there are no strict deterministic laws on the basis of which mental events can be predicted and explained” (Davidson, 1970: 208). In anomalous monism there is token identity of mental events/ states that is the mental event/ state is also a physical event/ state (the physical state/event is the token of the mental state/event in the physical realm).  So, the mental event/ state supervenes on the physical event/ state but it cannot be reduced to a physical state and any examination of the physical event/ state will not allow a prediction of the mental event/ state. Type identity of mental events/ states with physical events/states means that you can predict the mental event/state from knowing the physical event/state and that the equivalent mental event/state in different individuals would be accompanied by the same physical event/ same in them (as discussed in Heil, (2013A:128-130) but Davidson objects to “psychophysical laws” applying between mental events/ states, as this would lead to physical events/states having causal deterministic interactions with each other and this would eliminate mental events/ states forming “reasons” for behaviour such as thinking it is going to rain and taking an umbrella outside as they are just the mental event/ state marker of the real deterministic interactions at the physical level (Heil, 2013: 130-132) hence token identity but no type identity.

Neuroscience especially in its application in mental health clinical practice relies on nomothetic research methods. In other words for a group of participants whose common principle is that they have a mental event/ state x (for instance depression, hallucinations or responding to a treatment) at least some of them must have sufficient similarities in brain structure and/ or processes which allows this similarity to be detected and demonstrated in research participants and then extrapolated to patients in clinical practice. There are formidable methodological difficulties for this type of clinical neuroscience research (Steele & Paulus, 2019) even if type identity exists but anomalous monism would a priori mean such research is impossible. There is no type identity i.e. mental events/ states are not “reducible” to physical events/states.

1.2   Is evolution involved in the development of the human mind?

Davidson presents an ontological description of mind’s relationship to the brain but how did the mind come about in humans - the ultimate subject of interest of neuroscience in mental health? Evolution is the most widely accepted theory explaining the development of physical human attributes such as the eyes, the structure of cells or the functioning of the cardiovascular system. Has evolution shaped the brain’s development and what are the implications for the mind and anomalous monism?

Evolution is a process involving selection pressures that preferentially favours certain attributes to be passed down to the next generation in organisms if they allow them to produce more viable offspring. This might be because this attribute (which may be discontinuous/ categorical or a particular point on a spectrum such as increased length or a particular colour) increases the lifespan of the organism (increasing the opportunity to produce offspring) or increased fertility increasing the numbers of viable offspring. Conversely certain attributes may be selected against because they reduce the likelihood of viable offspring. This natural selection is a dynamic process as the attributes’ advantage depends on its fit with the environment which fluctuates through time.

A classic example are moths with a darker coloured variant – this variant was more thought to be more easily spotted whilst resting on tree barks by predators so tended to have shorter lifespans with subsequently less offspring and was a rare variant. When the industrial revolution produced pollution darkening tree barks which favoured the darker variant surviving by being harder to spot against the dark bark then this dark variant became more common.

Some attributes are selected for despite some disadvantages because they offer some selection advantages such as sickle cell trait in humans which can result in sickle cell disease but in the milder sickle cell trait offers increased resistance to malaria a common dangerous endemic illness in regions where sickle cell trait is commonly found.

A “Whiggish progress” view of evolution as continual improvement ignores that fluctuating variation in attributes in response to changing environments occurs through time. Whilst being aware of this tendency there does appear to be a dramatic increase in brain size through time in hominids. This bigger brain has survival costs – it requires a large proportion of the body’s nutritional intake as energy to power its neural activity; it’s lengthy maturation time requires many years of parenting and protection and the large head combined with a bipedal gait tilting the pelvis increases reproductive casualties dramatically for both mother and child in the form of death and disease and associated impairment.

Given all these costs of the large brain through hominid evolution what could be the gain in survival advantage or increased viable offspring that justifies the selection of increasing brain size by evolutionary forces? I will start by eliminating some brain functions as possibilities.

The brain has regulatory input into the cardiovascular and respiratory systems but in humans there does not appear to be any impressive additional abilities from the brain that would be favoured by evolution. Control of the endocrine system resides in the hypothalamic-pituitary areas but again there does not appear to be any human-specific evolutionary advantages. None of these areas described above seem particularly enlarged in size.

The human cerebral cortex is dramatically enlarged. It is involved in initiation and control of movement along with the basal ganglia and cerebellum. Yet there is nothing particularly amazing about human movement such as speed or agility compared to other species, the bipedal gait tends to make us slower on the ground but it does free up our hands. Yes the hands are capable of precision and manipulation but in the natural environment this does not add up to much in terms of enhanced survival or increased viable offspring by itself – the advantages come when the hands can be used to manipulate objects created by people using the advantages created by the another function which we shall discuss in the next paragraph. The cerebral cortex is also involved in processing sensory perception but human senses are again not outstanding compared to many other species to justify such an enlarged brain.

The final major brain function is to incorporate a variety of data – external sensory perceptions, interoceptive information (such as hunger), relevant past data such as memories, possible scenario planning/ anticipation of events and subsequent action and evaluation / responses (such as emotions) . This evaluation of data (which may come from a variety of locations in the brain) and then initiation of action takes place in the cerebral cortex and involves the cerebellum and deeper ganglia such as the amygdala. Given that the cerebral cortex is the part of the hominid brain that has been greatly enlarged through evolution it seems likely that this function is the evolutionary advantage that has been selected for – it has allowed us to make tools, form complex societies and perform more advanced hunting, practice agriculture and herding all of which increased our foodstuff availability increasing survival and numbers of viable offspring. These brain functions may be taken to be mind functions in many cases. A mind is “guided by representations” (Heil 2013B, 138) – the various data the brain receives is converted into representations and these guide actions. This is compatible with anomalous monism (and also with type identity theories of mind states with brain states). The rest of this section will proceed with the assumption of anomalous monism or type identity.

Dennet classified several times of minds developed through evolutionary processes as discussed by Heil (2013B: 138-40)  - Darwinian minds react in predictable ways to stable environments, next are Skinnerian minds learn through trial and error to act in the most optimal ways in their environment, then there are Popperian minds which create mental representations of their environment to test internally to decide the optimal actions and finally Gregorian minds are capable of self-conscious representation i.e. they are conscious of themselves carrying out the representation. Animals with the more advanced types of mind also contain in themselves the earlier types of minds. So far only humans can be shown to have Gregorian minds but for example can have their behaviour altered by operant conditioning as Skinnerian minds are. In this case the evolutionary selection pressure seems to be increasing adaptive capability of the organism whilst in their environment at least until the Popperian to Gregorian transition.

One can ask though will evolution be involved in the mind? Using  Maslow’s hierarchy of needs with “physiological needs” as an essential base of needs such as food and water and then safety and security (I quibble with the order but that can be set aside for now) then an organism that ignores these essential needs, for example does not recognise when it needs to prioritise seeking food or water or does not avoid danger is clearly at a risk of premature death reducing survival. An organism that does not seek to create opportunities to reproduce is similarly less likely to create viable offspring. Hence there will be selection pressures to create brains that monitor interoceptive signals triggering scanning the external environments for opportunities to seek to meet these physiological needs or to monitor the environment for threats and respond appropriately.

So evolutionary processes exert selection pressures to create brains and hence minds that can meet these needs. As a simple example it is advantageous for organisms to have mental events such as “I am hungry therefore I should seek food” which can also be understood as reasons for behaviour.  If higher levels of Maslow’s needs (such as self-actualisation) can be shown to exert evolutionary positive selection pressure then evolution will favour the development of brains and hence minds that seek to meet that meet these minds. It is not necessary to show all levels of need have an evolutionary input from an applied neuroscience point of view just that evolution influences at least some brain/ mind functions of clinical interest such as anxiety. I am not deploying an expansionist evolutionary theory that all mind activity is influenced by evolution – that the ability to write plays or fill out spreadsheets is all down to natural selection – just that the neuroscience of mental health only requires type identity for brain and mind states that have clinical usefulness as discussed in 1.1.

1.3   The mechanism of evolution affecting the mind and the challenge for anomalous monism

An example relevant to clinical neuroscience that has been influenced by natural selection due to its usefulness increasing survival by promoting avoidance of threatening situations is anxiety, the subject of a recent set of editorials in the American Journal of Psychiatry (Cisler (2020), Kalin (2020), Kessler (2020) and Smoller (2020)). They discussed how high degrees of anxiety are common across many psychiatric disorders, it is an evolutionary conserved mechanism, many different aspects of anxiety share common genetic factors, that several neurological circuits that seem to perform cross-species equivalent roles have been discovered in rodents, other primates and humans and that neuroscience techniques can also be used for several roles such as identifying common neural signatures of clinical problems or investigating correlates of effective behaviour therapy. It does seem plausible that anxiety would be influenced by natural selection.

If an organism lacked an anxiety response to threats it is more vulnerable to shorter lifespan if it has no anxiety to drive avoidance of predation or other dangers. Conversely too much anxiety will lead to excessive inhibition of behaviour and passing up opportunities to seek food or seek mates thus reducing lifespan or numbers of offspring. Thus, evolution is likely to lead a variety of degrees of anxiety responses in a population with the environment determining the appropriate level. Some anxiety disorders such as phobias are clearly influenced by evolution – we tend to develop phobias to dangerous situations that are part of our evolutionary inheritance (such as snakes, spiders or situations where we can be pounced upon such as busy spaces) rather than contemporary dangerousness (such as guns). Other mental disorders often generate anxiety (for example persecutory delusions) which will then involve anxiety mechanisms influenced by evolution.

For natural selection to have a positive selection pressure for attributes it relies on the organism with the advantageous attribute to pass it on to their offspring -fidelity of replication. (A negative selection pressure will be where the trait is disadvantageous for survival or having less viable offspring and so there is less offspring carrying this trait). The attributes or traits are passed on by genetic transmission. For genetic transmission though to act as the mechanism by which natural selection is carried out then it requires the advantageous trait or attribute to be largely replicated in the offspring from the parent organism. If the alteration in kidney structure or the modification in the clotting process enhances an organism’s survival, then this is what needs to be passed on to its offspring. So genetic material must produce a similar copy in offspring. If there is no similarity then natural selection cannot work – if an attribute is advantageous but is not passed on by producing similar structure and or process in the offspring then it is only advantageous in the generation of organism it arose in and stops there. This would mean evolution would not occur as there is no mechanism through which advantages could be passed on.

Genetics works primarily through DNA sequences being translated into amino acid sequences and hence proteins. These proteins then lead to structural and/ or process changes directly or indirectly. Proteins are biological and hence physical in nature and so are any results of their influence and thus potentially accessible to scientific measurement.  There is no evidence of genetic transmission of non-physical material. This means that if a mental function is affected by evolution – and it seems likely that at least some mental functions (discussed in 1.2 and anxiety earlier in this section) will be affected by evolution – then genetic transmission will be expected to create a close similarity in structure and/ or processes between parent and offspring such as an organised neurological circuit or altered levels of neurotransmitter activity. This close similarity for inherited structure and process has to lead to similarities in mental function (i.e. type identity) which is the attribute being selected for. If the structure/ process being inherited does not lead to similarity in mental function then natural selection will not be able to take place and in 1.2 there is strong evidence to suggest natural selection in hominids has favoured the development of mental functions such that are found in current humans.  Natural selection therefore means type identity for at least the mental functions influenced by natural selection thus opening the door to neuroscientific investigations for them.

It may be that some mental functions are replicated as a capability and other factors then build upon a common underlying structure (such as a distributed circuit) to produce final mental end-products (perhaps between individuals they have very different connections between neurones and consequent activity). For mental functions though that are more basic to survival and evolutionarily conserved in species that there is greater fidelity of replication as natural selection is unlikely to rely on a more haphazard arrangement or indeed that this haphazard arrangement to be conserved.

Clinical neuroscience does not need to be able to explain the production of all mental contents of mental health problems to be useful, for example they can used as a diagnostic marker or to measure illness severity (see 1.1). Depression can affect mental functions likely to be influenced by natural selection such as appetite, sleep regulation and ability to concentrate – neuroscience could be used to measure severity of the impact of depression on these functions. Anxiety disorders are often maintained by operant conditioning and this Skinnerian mind function has been developed through natural selection Heil (2013B: 138-40) then clinical neuroscience has the possibility of demonstrating the neural signature of these processes. Hallucinations are a perception without an appropriate stimulus and are found in several types of mental health problems – these to some degree involve mental functions involving perception to some extent which will have been influenced by natural selection which gain implies type identity for these processes again opening the door to clinical neuroscience.

2.1 Defending anomalous monism against evolution’s challenge

Several counter arguments can be deployed to fend off this challenge. Firstly, one can assert that that evolution is only a theory and reject it out of hand. This causes multiple difficulties – why are so many biologists wrong about a theory that seems to have much usefulness it leaves the problem of how did species come about and their similarities and differences? If we resort to creationist theories we could equally be opening the door to occasionalism and anomalous monism is lost by the back door.

Secondly, evolution may be accepted but it may be argued that it does not apply to the mind.  The mental functions that we may regard as comprising the mind (such as consciousness in the broad sense, abstract thought,  emotions, memories) may be an accidental by-product of evolution: a spandrel - “by-products of the development of other traits, but they themselves have never possessed any adaptive function”   (Murphy & Woolfolk, 200: p.243). Yet as discussed in 1.2. this argument it has several difficulties. What are these other traits that the mind got a free ride on? What else could explain the investment in increasing brain size in hominids as other possibilities seem unlikely? How did the mind develop in humans if not through evolutionary processes?

The third argument is that multiple realisation for analogous structures/ functions occurs due to evolution (such as eyes in insects, cephalopods and vertebrates) means no type identity is required for mental functions but multiple realisation applies to different species or even alien species or different types of entities such as computers with artificial intelligence having similar functions to mental functions of human minds. This however does not apply to members of the same species and at least some mental functions such as pain are likely to be based on “uniform physical processes” in humans (Papineau 2010: 189-190).  Clinical neuroscience is ultimately interested in the human species not aliens or Robbie the Robot.

The argument can be further developed for example that some higher mental functions such as  problem solving and learning capabilities may be “variably realized at the physical level across different individuals” even if these capabilities are selected for by evolution (Papineau, 2010: 186-187). The division between mind functions with evolutionary input and type identity (such as anxiety) and those with evolutionary input but only for a “variably realised” capability (such as a problem solving capability) or mental functions with no evolutionary input (such as the ability to write a novel) may appear conceptually “reasonably clear-cut, but on reflection it is by no means obvious where it lies” (Papineau, 2010: 191). This analysis is compatible with Heil’s analysis of Davidson’s position – that the “mental events” Davidson is referring to are only a subset of particular activities of the mind such as sentences involving propositional attitudes (Heil 2013A: 133-137). So a capability for certain mental functions may show type identity to a certain degree but the final realisation – altered by culture or experience – may be more “variably realised” (see discussion in 1.3 about common circuits between individuals but different connections between neurones within these circuits).

To use dreaded computer analogies acknowledging this is a metaphorical not exact comparison it may be that evolution could be thought of as creating the hardware and operating system (though the system settings may be influenced by the particular environment the organism is in) and this operating system allows a form of self-created programs to be made or the programs to be created by external inputs (the metaphorical programmer of the mind would be experience and meaning or extra-individual factors such as sociological factors): these programs in themselves are not influenced by evolution, but the capacity for these to be created were influenced by evolution. Since the operating system and hardware is influenced by evolution this allows type identity and a possible target of investigation by neuroscience using nomothetic techniques. The programs running on the operating system on the other hand, whilst using the operating system, can follow Davidson’s anomalous monism principles and are not able to investigated by neuroscience using nomothetic techniques. These programs may be regarded as operating on a “different level” and be investigated and described using other techniques such as qualitative research and schools of knowledge such as non-reductive psychology or sociology (Thornton, 2015). So whilst the higher level of thought triggering anxiety (“people are going to laugh at me because I look vulnerable”) may have a token identity and be inaccessible to neuroscience but the associated threat response is realised through anxiety neurological circuits which show type identity and are accessible to neuroscience.

3.1 Conclusion

Davidson’s anomalous monism involves token identity and no psychophysical laws for mental events but not type identity which would make neuroscience for mental health problems using nomothetic techniques impossible. Evolution is likely to have favoured the development of increased brains in hominids and these are likely to be for mental functions. Evolution requires the replication of structures and processes in the next generation which necessitates type identity for at least some mental functions. A metaphorical model of the computer hardware and operating system being influenced by evolution and hence having type identity for some mental functions and accessible to neuroscience using nomothetic techniques and programs whose outputs may have token identity but not type identity which would be the equivalent of Davidson’s mental events and better investigated with other methods.

References

Cisler, J.M., 2020. Semantic Networks and Mechanisms of Exposure Therapy: Implications for the Treatment of Panic Disorder. American Journal of Psychiatry, 177(3), p.197-199

Davidson, D., 1970. “Mental Events”. I L. Foster & JW Swanson (ed.), Experience and Theory. University of Massachusetts Press (s. 207-224).

Davis, J., Maes, M., Andreazza, A., McGrath, J.J., Tye, S.J. and Berk, M., 2015. “Towards a classification of biomarkers of neuropsychiatric disease: from encompass to compass.” Molecular psychiatry, 20(2), pp.152-153.

Heil, J., 2013A “Causation”. LePore, E. and Ludwig, K. eds., 2013. “A companion to Donald Davidson.” Wiley-Blackwell.(p.126-40)

Heil, J., 2013B. “Philosophy of mind: A contemporary introduction.” (Third edition) Routledge.

Kalin, N.H., 2020. Novel Insights Into Pathological Anxiety and Anxiety-Related Disorders. American Journal of Psychiatry, 177(3), p.187-189

Ressler, K.J., 2020. Translating Across Circuits and Genetics Toward Progress in Fear-and Anxiety-Related Disorders.  American Journal of Psychiatry, 177(3), p.214-222

Murphy, D. and Woolfolk, R.L., 2000. The harmful dysfunction analysis of mental disorder. Philosophy, Psychiatry, & Psychology, 7(4), pp.241-252

Papineau, D., 2010. Can any sciences be special.”  Chapter 12. Macdonald, G. and Macdonald, C.( eds.), 2010. Emergence in mind. Oxford University pp.179-197

Rosenberg, A., 2001. On multiple realization and the special sciences. The Journal of Philosophy, 98(7), pp.365-373.

Smoller, J.W., 2020. Anxiety Genetics Goes Genomic. The American Journal of Psychiatry, 177(3), p.190-194

Steele, J.D. and Paulus, M.P., 2019. Pragmatic neuroscience for clinical psychiatry. The British Journal of Psychiatry, 215(1), pp.404-408.

Thornton, T., 2015. Against explanatory minimalism in psychiatry. Frontiers in psychiatry, 6, p.171.

Should psychological formulation replace diagnosis for psychiatrists?

Should psychological formulation replace diagnosis for psychiatrists?

Summary

Psychological formulation has been promoted as a replacement for diagnosis in mental health. This does not take into account the time pressures facing psychiatrists and their needs in clinical practice. Using an example of a published psychological formulation for psychosis it can be demonstrated that psychological formulation is inferior to psychiatric diagnosis for clinical functions (prognosis and choosing treatments). It is also inferior for research (classifying participants) and social roles (including access to welfare and administrative integration with the rest of healthcare). For psychiatrists, diagnosis is still superior but should be supplemented by diagnostic formulation which can incorporate psychological mechanisms.

Declaration of Interest

The author has written a book awaiting publication which has large sections focussed on the value of diagnosis in mental health.

Introduction

Psychological formulation – sometimes called case formulation - has been promoted to replace diagnosis in clinical practice ^1,2 particularly to increase understanding of the patient and choosing appropriate interventions ².

Psychological formulation involves the organising of relevant clinical material to map out and summarise a patient’s problems – in collaboration with the patient over the course of clinical work - using psychological theories and knowledge to understand the patterns of difficulties and suggest ways forward to resolve these problems ^2,3,4.

Statements on the superiority of psychological formulation compared to diagnosis tend to be made on the assumption that the clinician works in a particular way – that they can spend a long time with relatively few patients, will see these patients many times with short intervals between sessions (for example weekly), often in non-urgent situations at civilised hours and that psychosocial interventions are the main therapeutic activity.

For their outpatient practice psychiatrists average 60 minutes for first appointments and 18 minutes for follow-up appointments⁵ (usually separated by weeks or months between appointments) carrying caseloads up to ten times of their colleagues⁶. Emergencies/ overnight and inpatient assessments are often similarly brief and patients may only be seen once or twice by the same doctor. This makes providing psychosocial interventions difficult and where effective medications are available these tend to be used as these are usually taken outside of the assessments thus making effective therapeutic interventions possible.  

This paper briefly discusses the usefulness of psychological formulation for psychiatrists in clinical, research and social functions.

Usefulness of psychological formulation for clinical practice

To evaluate the usefulness of psychological formulation for clinical functions an example of psychological formulation will be used to illustrate the points; the formulation used to understand ‘Dan’ and his psychosis in Section 7 of ‘Understanding Psychosis and Schizophrenia’⁷. This example is chosen for two reasons. Firstly, it is given as a good example of psychological formulation to enable understanding of psychosis by the Division of Clinical Psychology so has been given a stamp of approval by professionals whose core professional skills include psychological formulation⁴. Secondly, it is used for a case of psychosis and my main clinical work is with patients with schizophrenia and other related conditions, so this is an example I can relate to my clinical practice.

The ‘medical model’ relies on advising on and helping deliver interventions that improve health based on the best possible evidence⁸. For clinical practice, classification systems (such as diagnosis or psychological formulation) utility is judged on whether they allow communication of useful information between clinicians/patients/carers, accurate conceptions of the nature of the problem, provide information on prognosis (such as rates of relapse), aetiology/ causation, complications and which interventions to use and their chances of success^9,10,11,12. This utility is context-sensitive (such as limitations imposed on the way the professional works by resource demands including limited time)⁹. This information is probabilistic in nature rather than giving absolute certainty. Psychological formulation also aims to allow understanding of the patient and their situation^1,2,3,4.

Looking at the formulation of ‘Dan’⁷ it is about 150 words in boxes connected by of arrows linking past experiences, current events, thoughts, beliefs, responses and feelings. It certainly communicates information such as how these different aspects may be connected and lists important aetiological factors for psychosis such as adverse childhood experiences and substances.

The formulation plausibly links hypervigilance to childhood bullying (but ignoring that this hypervigilance would presumably be directed towards others and not his own body); somatic hypervigilance may lead to a belief that there is a lump in the neck but does not explain why the patient believes that this lump is transmitting thoughts. The lacunae in this formulation reflects the gaps in the evidence for purely psychological mechanisms linking adverse childhood experiences and psychotic symptoms content and nature¹³. It is possible the substance misuse is more closely linked to the generation of psychotic symptoms and the other factors such as childhood bullying are linked to the substance misuse rather than as depicted in the formulation.

The formulation provides some prognostic information such as substance use, childhood bullying and criminal activity being linked to worse outcomes such as higher relapse rates or aggression. The formulation provides useful pointers for psychotherapy such as addressing substance misuse or the links between past experiences, current life difficulties and thoughts and feelings.

On the other hand, this formulation has important information gaps. It is not clear how severe the psychotic symptoms are and whether they persist when substances are not being abused (such as psychosis related to substance intoxication or relatively brief psychotic episodes triggered by substance misuse) or whether the psychosis is caused by mood problems caused by adverse childhood experiences and/or current life difficulties – all these distinctions have clinical relevance not just for prognosis but for appropriate interventions and treatment¹⁴. For example, if the psychotic symptoms are only present during substance intoxication or for short periods afterwards then prolonged antipsychotic treatment is unlikely to be indicated.

In the text before the formulation of ‘Dan’ the diagnosis of schizophrenia is mentioned. This diagnosis is associated with a great deal of information such as factors associated with increased risk, associated differences in biological or psychological factors and the effectiveness of interventions¹⁵. Diagnostic constructs are associated with information that is learned by the clinician that allows easier recall and use of this information under time/ fatigue/ workload and other pressures in the context of brief appointments or emergency/ overnight working practices of most psychiatrists.

Schizophrenia as a diagnostic construct is defined by the absence of known organic factors explaining the clinical picture, nevertheless it is associated with multiple factors known to increase the risk of meeting the diagnostic criteria such as childhood adverse experiences and cannabis^16,17. Like many general medical conditions there is no single fixed outcome but we have evidence for a range of probable outcomes including recovery and their likelihood¹⁸. We also have evidence for the likely effectiveness of interventions in people meeting schizophrenia criteria such as antipsychotics¹⁹ and cognitive behavioural therapy for psychosis²⁰ to guide choice of therapeutic interventions.

An additional diagnosis – such as substance harmful use- will need to be used to indicate the important role of substance use affecting prognosis and to influence clinical management to include providing information on the effect of substances to the patient and referring for a psychosocial intervention to address the substance misuse. Two diagnostic constructs may thus need to be used but the total word count is still far less than that of the formulation. Although the diagnostic construct schizophrenia does not explicitly state the causative factors of this case many general medical diagnostic constructs - such as type 2 diabetes - do not state the causative factors in their title and even when a necessary cause is included in the title – such as tuberculosis – other important factors in the aetiology are not included in the title (for instance the role of overcrowded housing in tuberculosis)²¹. Psychosis is a very broad concept that some extend to unusual experiences that cause little harm or dysfunction to more severe states that can meet diagnostic criteria for schizophrenia or bipolar disorder²². It is therefore useful to identify a more specific classification than psychosis alone¹⁴ to provide more useful information to guide clinical decision making for the individual patient.

Research and Social Functions

Psychological formulation – except psychodynamic formulation - has disappointing reliability²³ impairing its usefulness in classifying participants in research. Conceptually as a classification system for research, psychological formulation would have to be reduce the emphasis on the individual-specific factors as they will vary a lot between individuals – they will need to focus on a few common elements otherwise the number of participants in each group would be too small and underpowered to detect statistically significant differences between groups. Although not suitable as a classification system for research, psychological formulation can be used as part of an intervention in studies evaluating their effectiveness.

There are many social functions of a health classification such as diagnosis – administrative (activity measurement and billing), organisational (services organised according to diagnosis or group of conditions), statistical (incidence/ prevalence and planning healthcare provision on basis of need) and access to benefits or special educational support²⁴. Given the high word count of psychological formulation, it’s highly individualised nature and the lack of horizontal integration with general medical diagnostic systems it is not very suitable as system for administrative, organisational, statistical or access to benefits or special educational support. Most health activity involves payment from third parties such as health insurance or government and providers are required to provide activity data to justify their expenditure – psychological formulation would not satisfy the requirements of third party funders as it would differ greatly between individuals making counting categories difficult. Similar problems apply for statistical and organisational purposes. Psychiatric diagnosis for all its faults is the most convenient system to fulfil administrative/statistical social functions²⁵.

To gain access to benefits for example, a diagnosis – with empirical evidence of association with impaired functioning and a recognised classified entity in ICD10 for instance – with additional description of impaired functioning in the individual is more likely to convince welfare agencies of eligibility for benefits – it relies on empirical evidence (lacking for psychological formulation in comparison to psychiatric diagnosis²)  and a standardised recognised classification not just expert assertion and is compatible with existing systems for general medical conditions.

Discussion

Psychological formulation is unable to replace psychiatric diagnosis for psychiatrists’ clinical work for the contexts in which they work – such as brief appointments or emergency/ night work – and requirements for empirical-based advice and decision-making⁸ as much of the evidence base is based on diagnostic classifications². This statement carries caveats. For those – including some psychiatrists – whose clinical work uses primarily psychosocial interventions in the context of long appointments with relatively few patients during routine hours may find psychological formulation more useful.  For some ‘organic’ conditions such as dementia or general medical conditions with psychological problems then psychological formulation will be used to address specific problems rather than overall management of the primary condition. Conversely for conditions where medication has little benefit – such as where people meet borderline personality disorder diagnostic criteria – then management plans would preferably be based on psychological formulation rather than diagnosis. This difference in clinical utility of psychological formulation depending on presenting condition illustrates the usefulness of psychiatric diagnosis – different conditions have different implications such as range of likely outcomes, treatment responses and usefulness of psychological formulation.

For the social functions of classification – such as administrative, statistical or access to benefits – diagnosis is superior to psychological formulation. Psychological formulation would not easily used as a classification system for participants in research making it harder to close the evidence gap with diagnostic based research. Diagnostic formulations – although disagreement exists as to what they should contain ^26,27 and can exclude or include psychological theories³ including incorporating psychological formulations from other professionals or their own work – can incorporate both the diagnosis (and differential diagnosis) as well as individual predisposing, precipitating, perpetuating and protective factors in the patient³.

For general medical conditions it is common practice to use additional information apart from the diagnosis to help with estimating prognosis and guiding clinical decision-making such as the use of staging for cancers, Glasgow Coma Scale for acute brain injury, DAS28 for rheumatoid arthritis and Modified Blatchford Score in acute upper gastrointestinal haemorrhage²¹.

Diagnostic formulation – beginning with a diagnosis then expanding with further relevant individual information and can include psychological theorising – is the best complex classification system for most psychiatrists in the context of the way they work and their need to provide evidence-based advice to the patient and to guide decision-making. It can build on the empirical information attached to a diagnosis with further individual and contextual factors (which may provide additional empirical evidence affecting prognosis or clinical management or aid further understanding of the patient and their predicament³). Diagnosis can also be combined with psychological formulation as they provide supplementary information.

References

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