mind over matter? ii: implications for psychiatry

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It is a sign of weakness to combine empirical and logi- cal arguments, for the latter, if valid, make the former superfluous. ––Bertrand Russell [1] The preceding paper [2] offered the following two propositions: 1. The faculty of mind is contingent upon the function- ing human brain; in this sense mind and brain constitute two aspects of a unity. At a fundamental level there appears to be an ‘identity’ between specific mental states and specific brain states upon which they are contingent. 2. Any attempt to explain the subjective essence of a mental state or process in terms of a brain state or process must inevitably fail as it leaves out the ‘mind’ that we seek to explain. Discourse about mental states is not reducible to discourse about brain states, and there- fore brain states and mind states are not identical. (If x is identical to y then any property of x is also a property of y, and vice versa. Subjective mental events and objective brain events have distinct and differing properties.) The preceding paper suggested that there are good grounds for accepting both of these propositions: (1) on the basis that it is the hypothesis that best fits the cur- rently available scientific data; (2) on the basis that it is a self-evident truth. It also acknowledged the logical dif- ficulty in entertaining both propositions simultaneously. Strictly speaking they do not constitute a solution to the mind–brain problem, which as a metaphysical problem may be insoluble. They are proposed as the most satis- factory formulation of the problem possible given the limitations of our knowledge and/or understanding. This second paper argues that, if these paradoxical propositions are accepted, they carry important theor- etical and practical implications for concepts of causal explanation and aetiology as they are applied to the mind and psychiatric disorders. Causality and a unity theory If we accept proposition one, that mental states and brain states constitute ‘double aspects’ of a unity, this suggests that in some fundamental way they are the same thing, or they arise as different manifestations of a unitary phenomenon (double aspect theory). If they con- stitute such a fundamental unity then one cannot simply be said to cause the other. We may say that the existence Mind over matter? II: implications for psychiatry Paul Schimmel Objective: To explore concepts of causality within the mind and aetiology of psychiatric disorders in the light of the proposed formulation of the mind–brain problem. Method: Taking the two propositions of this formulation as ‘first principles’ a logical analy- sis is attempted. Results and conclusions: Neural activity cannot in principle be regarded as causing mental activity, or vice versa. Causal processes are most coherently conceptualised in terms of the ‘mind–brain’ system. Determination of causal and aetiological effects will always necessitate consideration of contextual evidence. Because of the ‘explanatory gap’ between explanation in neurophysiological terms and ‘mentalistic’ terms, whenever formu- lation in mentalistic terms is possible this will carry greater explanatory power; that is, it will carry meaning in the way a neural formulation cannot. Key words: causality, mind–body problem, mind–brain problem, philosophy Australian and New Zealand Journal of Psychiatry 2001; 35:488–494 Paul Schimmel, Consultant Psychiatrist P.O. Box 37, Roseville, New South Wales 2069, Australia Received 27 September 2000; revised 21 February 2001; accepted 2 May 2001.

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Page 1: Mind over matter? II: implications for psychiatry

It is a sign of weakness to combine empirical and logi-cal arguments, for the latter, if valid, make the formersuperfluous.

––Bertrand Russell [1]

The preceding paper [2] offered the following twopropositions:

1. The faculty of mind is contingent upon the function-ing human brain; in this sense mind and brain constitutetwo aspects of a unity. At a fundamental level thereappears to be an ‘identity’ between specific mental statesand specific brain states upon which they are contingent.

2. Any attempt to explain the subjective essence of a mental state or process in terms of a brain state orprocess must inevitably fail as it leaves out the ‘mind’that we seek to explain. Discourse about mental states isnot reducible to discourse about brain states, and there-fore brain states and mind states are not identical. (If x isidentical to y then any property of x is also a property ofy, and vice versa. Subjective mental events and objectivebrain events have distinct and differing properties.)

The preceding paper suggested that there are goodgrounds for accepting both of these propositions: (1) onthe basis that it is the hypothesis that best fits the cur-rently available scientific data; (2) on the basis that it isa self-evident truth. It also acknowledged the logical dif-ficulty in entertaining both propositions simultaneously.Strictly speaking they do not constitute a solution to themind–brain problem, which as a metaphysical problemmay be insoluble. They are proposed as the most satis-factory formulation of the problem possible given thelimitations of our knowledge and/or understanding.

This second paper argues that, if these paradoxicalpropositions are accepted, they carry important theor-etical and practical implications for concepts of causalexplanation and aetiology as they are applied to the mindand psychiatric disorders.

Causality and a unity theory

If we accept proposition one, that mental states andbrain states constitute ‘double aspects’ of a unity, thissuggests that in some fundamental way they are thesame thing, or they arise as different manifestations of aunitary phenomenon (double aspect theory). If they con-stitute such a fundamental unity then one cannot simplybe said to cause the other. We may say that the existence

Mind over matter? II: implications for psychiatry

Paul Schimmel

Objective: To explore concepts of causality within the mind and aetiology of psychiatricdisorders in the light of the proposed formulation of the mind–brain problem.Method: Taking the two propositions of this formulation as ‘first principles’ a logical analy-sis is attempted.Results and conclusions: Neural activity cannot in principle be regarded as causingmental activity, or vice versa. Causal processes are most coherently conceptualised interms of the ‘mind–brain’ system. Determination of causal and aetiological effects willalways necessitate consideration of contextual evidence. Because of the ‘explanatory gap’between explanation in neurophysiological terms and ‘mentalistic’ terms, whenever formu-lation in mentalistic terms is possible this will carry greater explanatory power; that is, it willcarry meaning in the way a neural formulation cannot.Key words: causality, mind–body problem, mind–brain problem, philosophy

Australian and New Zealand Journal of Psychiatry 2001; 35:488–494

Paul Schimmel, Consultant Psychiatrist

P.O. Box 37, Roseville, New South Wales 2069, Australia

Received 27 September 2000; revised 21 February 2001; accepted 2 May2001.

Page 2: Mind over matter? II: implications for psychiatry

of mind is contingent upon the existence of certain statesof the brain, but it seems doubtful that it can be mean-ingfully said that brain states cause the mind states thatthey ‘coexist’ with, or for that matter, that mind statescause the brain states that they ‘coexist’ with. Rather wemight say mind states are the brain states that they‘coexist’ with.

Despite apparent widespread acceptance of some formof identity or unity theory within science in generaland psychiatry in particular, its potential incompatibilitywith the idea that, at a given moment in time, mentalactivity is caused by brain activity (rather than simplycontingent upon it) is apparently not often appreciated.Discourse and practice in psychiatry often carry an imp-licit assumption of brain activity causing mental activity;sometimes to the extent of relegating mind to the posi-tion of an epiphenomenon. Consider, for example, a clin-ician who tells a depressed patient (in whom there are nospecific primary organic factors), that the depression iscaused by a ‘biochemical imbalance’ in the brain. Thisstatement recognizes the existence of something of themind (the experience of depression), while relegatingthis to a secondary, or ‘epiphenomenal’, role to brainbiochemistry. It suggests that the patient’s mental expe-rience of depression (the same argument holds for anymental experience), is caused by a set of other (whetherobserved or presumed) physical events taking place withinthe brain. However, it would make just as much, or justas little, sense to say that the experience of depressionwas causing the biochemistry or physiology of the brainto become disturbed. Within the framework of a unity,identity, or double aspect theory, neither of these propo-sitions is logically defensible as it stands.

To the extent that a theory of mind is epiphenomenal itattributes causality to the brain, and excludes the attribu-tion of causality to the mind, but if we are serious aboutsome form of unity theory, it follows that in the unfold-ing sequence of brain/mind events, mental events have,in principle, the same causal status as brain events. Asstated mental events cannot simply be regarded as causedby the activity of the brain, because mental events are theactivity of the brain.

If it is incoherent to speak of brain activity causingmental activity (at least in cross-sectional time), how thenare we to speak about causality, and by implication aeti-ology, in relation to brain and mind, and to psychiatricdisorder? I suggest causality is most usefully consideredin relation to the mind–brain system as a whole, and ifformulations of psychiatric causality are proposed, theymust be consistent with concepts of causality employedin science generally. Within a dynamic system, evidencefor causality is found in the identification of a set of reli-able antecedent conditions/events that would seem to, or

can be utilized to, predict subsequent conditions/events.The concept of causality carries the idea of somethingover and above this temporal juxtaposition of events, anda theory of cause is a formulation as to what this some-thing is. Implicit in the concept of cause in a dynamicsystem is the passage of a period of time, however, briefor infinitesimal.

To say that the brain events cannot be considered tocause mental events is not to say that identified eventsthat cause change or disturbance in the brain do not causechange or disturbance in the mind; it is obvious that theydo. Equally, identified events which cause change or dis-turbance in the mind cause a corresponding change ordisturbance in the brain. The situation might be repre-sented symbolically as follows, where Me stands for a‘mental event’ and Be stands for the ‘brain event’ uponwhich that mental event is contingent:

If a cause can be conceptualized as operating upon themind to produce Me1 it simultaneously produces Be1. Ifa cause can be conceptualized as operating upon thebrain to produce Be1 it simultaneously produces Me1.Me1/Be1 may then act causally to produce a secondevent in the mind–brain system, Me2/Be2. [Of course,while all mental events will be contingent upon brainevents, not all brain events need be linked with contin-gent mental events. For example, the following sequenceis possible: Be(n) → Be(n + 1)/Me(n + 1).]

To consider an example of the construction of asimple, but valid, causal model: a patient sustains a headinjury with subsequent emotional disturbance and memoryloss. There is a case for supposing that the immediateand determinate cause of the mental disorder is the phys-ical injury. This conclusion is suggested by the fact thatan unusual physical event, the head injury, was followedby, and seemed linked with, a disturbance of mentalfunction. The cause is conceptualized as acting in longti-tudinal time. That the head injury was the cause of thedisturbance would seem a reasonable working hypothe-sis, and for practical purposes might be regarded as con-firmed on the basis of supporting evidence, for example:(i) evidence of physical damage to the brain resultingfrom the injury; and (ii) the fact that similar mental dis-turbance has been observed in the past to be associatedwith the sort of injury to the brain sustained by thepatient. That events of apparent cause and effect havepreviously conformed to a similar pattern supports theassumption of cause and effect on this occasion. Such apattern may justify the formation of an inductive theoryof causes and effects of this type.

P. SCHIMMEL 489

Me1 Me2time →

Be1 Be2

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If the brain injury was a random event outside thepatient’s control, then we have an example of an unin-tentional and physical brain-impinging event causing adisturbance in the ‘mind-brain system’. In this instance acommonsense understanding of causality would notemphasize the mind, but rather emphasize that there wasan identified physical cause. It would make commonsense to say that the cause operated via its impact uponthe brain, leading to a disturbance of the mind–brainfunction.

Consider, in a similar way, an event impacting uponthe mind–brain system that would usually be describedas operating via the mind. A person, following news of abereavement, is precipitated over a period of weeks intoa melancholic depression. In this situation support forthe hypothesis that the bereavement was the proximateand determinate causal factor might be gained from: (i)evidence from the patient’s description of his/her experi-ence of a link between the bereavement and the depres-sion; and (ii) the fact that similar mental disturbance haspreviously been observed associated with the experienceof bereavement.

The identified causal factor, the bereavement, is apiece of knowledge or something given to awareness. Itsimpact derives from its meaning for the patient in termsof his or her mental life and social matrix of relationship.It is an essentially mind-impinging event causing a dis-turbance of the mind–brain system. Although our mind–brain theory entails that there will be a neural ‘substrate’of this meaningful impact, a commonsense understand-ing of causality would not emphasize the brain, but ratheremphasize that there was an identified mental cause. Itwould make common sense to say that the cause oper-ated via its impact upon the mind, leading to a distur-bance of the mind–brain function.

There is both meaning and economy in saying that theeffect of the head injury is via the brain, and the effect ofthe bereavement is via the mind. It would make littlesense to say that the effect of the head injury was via themind and the effect of the bereavement was via the brain.

The bereavement example is more complex than thehead injury because bereavements are a less reliablecause of depression than head injuries are of impairedmental function. So in the bereavement example theremust also be important vulnerability factor(s) within thepatient. Assuming there are no specific organic factorscontributing to vulnerability, then because the cause canbe conceptualized as operating via the mind, it followsthat the vulnerability factor(s) must also be able to beconceptualized as existing within the mind; logically itcannot be otherwise. This is simply to recognize that abereavement can only impact upon a mind if it is experi-enced as meaningful. It is implicit in our mind–brain

identity theory that the vulnerability factor(s) must alsobe represented in the brain, but if we wish to conceptu-alize the aetiology of the depression in this particularsituation we can only meaningfully do so in terms of theinteraction of the news of the bereavement and the vul-nerability within the patient’s mind. The logical implica-tion of this is that an aetiological formulation based onidentified neural processes, although possible in theory,will lack meaning.

If causality is to be considered in the genesis of psy-chiatric conditions then, as argued, this can only be donethrough the exploration of putative antecedent conditionsor forces that lead to apparent alterations in the mind–brain system. Given that aetiology represents the sum ofcausal factors the same argument applies to the consid-eration of aetiology.

Aetiology and a unitary theory

Related to the tendency within psychiatry to relegatemind to an epiphenomenal position rather than to acceptthe implications of a unitary theory, is the assumptionthat evidence of physical brain disturbance is sufficientto establish a physical aetiology for a mental illness.

In principle a unitary theory predicts that any mental‘disturbance’ is accompanied by a corresponding ‘distur-bance’ of that part of the brain that underlies mentation,and vice versa. It follows that, in principle, neither thepresence of brain disturbance nor the presence of mentaldisturbance would, in itself, be sufficient to establisheither a physical or mental aetiology. Some other evi-dence will always be necessary.

The presence of physical brain disturbance alone canconstitute reasonable and sufficient evidence of a physi-cal aetiology only if that physical disturbance is in someway characteristic (pathognomonic) of a proven physicalaetiology. For example, the presence of the characteristicmorphological changes of Alzheimer’s disease in a patientwith clinical dementia would seem a reasonable basisupon which to make this diagnosis, and to assume theoperation of the physical aetiological factors (known orunknown) associated with this disorder.

Obviously the presence of apparently irreversible struc-tural changes influencing brain function is suggestive ofpossible physical aetiology, however, factors operatingvia the mind cannot be dismissed without further evi-dence. If we consider schizophrenia, it is often assumedthat because apparently pathological changes can reli-ably be detected in the brains of patients with this clini-cal diagnosis, then the aetiology of the disorder must be‘physical’ in the first instance, even if the specific natureof the purported physical cause(s) is not known. If thestructural changes detected in the brain have an irreversible

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aspect, then in a commonsense way we might say thatthese changes are the immediate cause of the disturbedmind–brain function, but this does not establish aetiol-ogy. Unless the changes can be recognized to be a con-sequence of a proven physical aetiology, the possibilitycannot be excluded that they represent the manifesta-tions of the impingement of some ‘psychosocial’ factors,such as the developmental matrix of relationships. Atpresent it would seem that the supporting evidence thatwould establish schizophrenia as a disorder of provenphysical aetiology in all, or even many, cases is lacking.

If the logical constraints upon establishing grounds forcausal and aetiological theories within the mind–brainsystem that have been put forward here are valid, theyare not widely recognized within the psychiatric litera-ture. Journals frequently publish papers where inferencethat aetiology is ‘biological’ is made on the grounds thatsome biological, brain feature of a mental disorder hasbeen (apparently) reliably identified. Mental illnesses arefrequently reduced to ‘neural’ illnesses: consider the fol-lowing opening sentence of a paper on brain imaging inpsychiatry, and published in Science [3]. ‘Psychiatristshave known for at least 100 years that mental illnessesmust be fundamentally due to perturbations of normalneural activity in the brain’. While this statement mayat first glance seem plausible this is appearance ratherthan reality. ‘Fundamentally due to’ suggests a cause,and as already argued there is logical difficulty in thedescription of brain events as causing mental eventsper se.

Even if we gloss over this ‘in principle’ logical diffi-culty, there is still no apparent reason why brain eventsare always more ‘fundamental’ than mental events. Inthis quotation the mental events in question are mentalillnesses, and the brain events are ‘perturbations ofnormal neural activity’. As has been argued, if somekind of irreversible neural disturbance were present, itmight make sense to speak of a mental illness being‘fundamentally due to’ this neural disturbance in cross-sectional time. However this would not, in itself, estab-lish that the mental illness was ‘fundamentally due to’some physical/neural causal aetiological factor. Further-more if no such irreversible change in brain structureor function is present in a particular mental illness, noprima facie case exists to support the claim that theneural events must be more fundamental than the men-tal events. There is greater explanatory economy to say,of at least some mental illnesses, that they are funda-mentally due to perturbations of ‘normal’ psychologicalactivity. Whether a description using neural terms ormentalistic terms has the greatest utility in formulatinga ‘fundamental’ explanation depends on the nature ofthe mental illness.

The proper study of the mind

Turning now to proposition two, as stated at the begin-ning of the paper; if we accept that neuroscientific dataand the data of mental experience are two differentwindows upon the unity referred to as the mind–brainsystem, we are left with the mystery that they appear to constitute ontologically distinct points of view. Itfollows that discourse in terms of one cannot be reducedto the other, and the two are not simply interchangeable, areality which often seems to be lost sight of. It may be thatthe best we can hope to achieve is a descriptive correlationbetween the two. Neuroscience can, at least in theory, tellus a great deal about the neural correlates of a consciousexperience, but it cannot tell us, at least not directly, any-thing about the inherent nature of that experience.

Despite those such as Kendell [4] who reject the term‘mental illness’ in favour of ‘psychiatric illness’ (Kendellrejects the concept of ‘mental’ in favour of the descrip-tion ‘psychiatric’), mental illnesses are called mentalillnesses for a good commonsense reason; namely thatthey are, for the most part at least, experienced in themind. The construct ‘mental illness’ reflects this fact,and from the patient’s viewpoint the existence of such an‘illness’ state is established through his or her awarenessof parameters that reflect mental activity, either directly(‘psychological symptoms’) or indirectly (‘behaviouralsigns’).

Causal and aetiological theories in psychiatry are con-structed in terms of mental processes, brain processes orboth together (attempts to establish behavioural or socio-logical aetiological theories are usually instances of the-ories framed in terms of subjective meaning, that is interms of the mind). In practice, the patient usually expe-riences, and the psychiatrist often judges, the presence ofmental disturbance in terms of subjectively meaningful‘mental’ phenomena. In these situations only aetiologicalformulations in terms of mental processes will be of thesame ontological order as the primary phenomena underconsideration.

In a patient where an aetiological formulation in termsof mental process is possible, this will inevitably bemore meaningful (so long as the formulation is a correctone), and therefore offer greater coherence in the par-ticular case, than an aetiological formulation in terms ofbrain process. A formulation in terms of the mind avoidsfalling into the ontological ‘explanatory gap’. In otherpatients, aetiological formulation in terms of mentalprocesses is either not possible or insufficient. Suchcases require aetiological theories formulated in part orwhole in terms of primary brain processes. To the extentthat it is not possible to formulate a sufficient explanationin mentalistic terms (that is in terms of meaning, or the

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‘dynamics’ of the mind), then further explanation mustbe sought in terms of neurophysiological processes inthe brain that have an independent aspect. A factor(s)extraneous to the inherently integrated mind–brainsystem must be exerting an effect via the brain. That is, a physical/organic factor is added to the sequenceMe1/Be1 →Me2/Be2, and is exerting its effect via ‘B’.For example, in a state of alcohol intoxication, a factoroperating independently of the normal integration of themind–brain system, introduces an element of random-ness into the system. It might be predicted that thisrandomness would be detected as an interference withmental process, and experience confirms that mentalcapacities are diminished in alcohol intoxication. Simi-larly, the symbolic richness and meaningfulness of theworld of a patient with Alzheimer’s disease graduallydiminishes with the progression of the disease.

In the hypothetical case of the patient who becamedepressed following news of a bereavement, it is in theorypossible to describe the development of the depressivestate of the mind–brain system in neural terms. Thiswould involve documenting the sequence of neuro-physiological events, presumably involving many mil-lions of neurones, over time. Such a task would hardly bepractical, but an alternative would be to formulate a sim-plified model documenting the general patterns of brainactivity. If such processes can be documented in thebrain, then could the vulnerability to depression beconceptualized as residing in the brain? While it must in theory be possible to conceptualize the vulnerabilityof the mind–brain system to depression in neural terms,as already suggested, such conceptualization will lackmeaning.

Neural processes that underlie the presentation of appar-ent mental disturbance or disorder must presumably eitherbe part of an ongoing sequence of integrated mind–brainactivity, or represent a primary organic pathology. Oldage, for example, is a specific organic factor that, beinglinked with a general impairment of cerebral function,may contribute to the vulnerability to depression. If weassume, in our patient, the absence of significant organicaetiological factors requiring description primarily inneural terms, then as has been argued, because bereave-ment is an experience that impacts upon the mind, thepatient’s vulnerability to the experience must be able to beconceptualized in mentalistic terms (presumably in termsof the nature of the patient’s attachments). The premorbidstate of cerebral functioning that confers vulnerability to depression is presumably therefore the neurophysio-logical correlate of the premorbid state of mental func-tioning that confers the vulnerability to depression.

It is evident that, in this hypothetical case, only expla-nation in terms of psychological processes, including the

psychological vulnerability factors within the patient’smind, will lead to an aetiological formulation which isinherently meaningful (in the sense of offering under-standing rather than a ‘mechanistic’ material explanation),and also potentially meaningful to the patient (whether infact such a correct formulation is meaningful to a patientwill depend upon his or her capacity to understand it).However accurate any model of the process of thepatient’s altered brain function over time might be, anyattempt to employ it in a comprehensive explanatory sensewill inevitably take on an arbitrary and reductive quality.It will not be inherently obvious how the documentedbrain phenomena ‘explain’ the mind phenomena (thepatient’s experience), because the relationship betweenthem is one of correlation established by observation,rather than one established on the basis of the apprehen-sion of inherently meaningful links.

To restate, because of the ontological ‘explanatorygap’ between formulations in mentalistic terms andformulations in neural terms, a formulation in terms ofmind will, if correct, introduce or elucidate the meaningof the patient’s experience and behaviour in a way that‘explanation’ in terms of constitution or neurophysiologycannot do. I emphasize, ‘if correct’, because: (i) an aeti-ological formulation in terms of mental processes maybe more or less correct or incorrect. An incorrect formu-lation will not, of course, elucidate the meaning of thepatient’s experience and behaviour, and may obscure thatmeaning; and (ii) I am not suggesting that aetiologicalformulation in terms of mental process is possible forall mental illness, but in any instance where such formu-lation is possible it will inevitably offer a level of under-standing which formulation in terms of neural processescannot.

Perhaps our hypothetical depressed patient consults theclinician who formulates the cause of his depression as a‘a biochemical imbalance in the brain’. It may not beunreasonable to postulate that there is a state of bio-chemical ‘imbalance’ in the patient’s brain, but can this inany sense logically constitute the ‘cause’ of the disorder?

The fact that what initiated the ‘disorder’ (bereave-ment) is meaningfully conceptualized in mentalistic terms(the dynamics of the mind), would suggest seekingunderstanding of the developing state, at least in the firstinstance, in terms of processes that can be characterizedin mentalistic terms. This would mean adopting a work-ing hypothesis that the ‘biochemical imbalance’ is thebrain representation in cross-sectional time of a distur-bance within an integrated mind–brain system. So longas a sufficient explanation of the patient’s clinical pre-sentation can be formulated in mentalistic terms, thenfrom a logical viewpoint an aetiological formulation interms of neurophysiology, however accurate, remains

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P. SCHIMMEL 493

redundant to meaningful explanation. It may be a validexplanation but it will not be a meaningful one. Onemight say therefore that it would lack explanatory power.

A principle of explanatory economy could be postu-lated as follows: it is only when formulation in terms ofthe dynamics of the mind falls short of providing ade-quate explanation that it becomes necessary to postulatea neurophysiological causal factor acting independentlyof an integrated mind–brain system. It would contradictthis principle to postulate an explanation primarily inneurophysiological terms in the absence of evidence thatsome primary and therefore independent pathophysio-logical process has supervened.

The presence of biochemical disturbance alone in thebrains of depressed patients is not sufficient to justifythe assumption of a physical/neural aetiology. Supportingevidence will always be required. Where a ‘biochemicalimbalance’ idea is employed as a kind of a priori aetio-logical ‘theory’, such reasoning is inimical to the processof inquiry and analysis, in other words the process ofthinking about, that is necessary to elucidate meaning.In practice the acceptance of this kind of ‘biochemical’thinking about, for example, depression is often associ-ated with a closure that fails to recognize the possibilityof other, potentially more coherent, and clinically morefruitful, avenues of investigation.

The invocation of any aetiological theory withoutspecific and sufficient supporting evidence contributesto premature closure. The ‘concrete’ and measurableaspect of brain events in comparison with mental eventsmay make neural formulations appear attractive, perhapsbecause they seem easier to grasp than psychologicalformulations, but as our theory of mind and brain assumesthat neural disturbance and mental disturbance accom-pany one another, we should be aware of the fallacy ofinvoking physical/organic aetiological theories on thebasis of identified neural disturbance without supportingevidence.

I have referred to the possibility of formulating distur-bances in the mind–brain system either in terms of neuro-physiological processes or in terms of mental processes,the ‘dynamics of the mind’. The nature of the empiricalmethods employed in order to characterize neurophysio-logical processes are well known and their conceptualvalidity apprehended relatively easily. In contrast theempirical methods employed in order to characterizedynamic mental processes are less well known, and theirconceptual validity apprehended with greater difficulty.They are essentially the elements of an analytic approachto mental phenomena which seeks to establish meaning,whether employed in psychoanalysis, in analytic psycho-therapy or in an observational context. This paper hasassumed the validity of such ‘psycho-analytic’ methods,

but there remains contention within psychiatry as to thevalidly of knowledge attained by interpretive methods.Yet it is self-evident that meaning is only conferred uponhuman experience through interpretation. Pataki [5] pointsto the ‘explanatory work’ done in ordinary narrative ‘bycommonsense “mentalistic” concepts like love, hatred,fear, belief, feelings of weakness and dependence, and soon. These are the concepts we commonly use to makesense of ourselves and others. They are immensely richconcepts’, and they are ‘basic, in (roughly) this sense: itis impossible to see how any description of human action(or of society) can be made without them and their kindin a way which will preserve its subject.’

It is beyond the scope of the paper to enter further intothe question of how the validity of knowledge attainedthrough interpretive methods may be established. Thiswould lead inevitably to consideration of the validity ofthe concept of ‘unconscious’ mental processes.

Mind over matter?

I believe that there is a bias within psychiatry againstthe investigation of the patient’s mind. Without any con-ceptualization of the dynamic processes occurring withinthe disordered mind, it is difficult to formulate any aeti-ological theory that takes factors operating via the mindinto account, and difficult to approach treatment via themind. This results in an explanatory vacuum which neuralmodels are often invoked to fill. Wherever it is possibleto formulate a correct aetiology in terms of mental pro-cesses, and if a clinician is able to do so, then, for thereasons outlined, this will possess a maximum explana-tory economy. It will certainly be meaningful in a waythat a ‘neural’ formulation cannot be.

This does not amount to suggesting that mind is moreimportant in psychiatry than brain. A psychiatrist needsto understand about brains and about minds, and thereare different forms of psychiatric practice. It is an argu-ment for the utility of giving consideration to the pro-cesses taking place within the patient’s mind. I haveattempted to base this argument upon (i) what seems areasonable formulation of the mind–brain problem givencurrent knowledge; and (ii) drawing out the implicationsof this formulation in clinical situations. The main con-clusions reached are: (i) that neural brain activity cannotin principle be regarded as causing mental activity (orvice versa), and therefore more evidence or informationwill need to be considered if the causal relationshipsbetween ‘mind’ factors and ‘brain’ factors are to be eluci-dated in a particular case, or in a particular psychiatriccondition; and (ii) that because of the ‘explanatory gap’between descriptions in mentalistic terms and descriptionsin neurophysiological terms, wherever an explanatory

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MIND OVER MATTER: IMPLICATIONS494

formulation of a mental illness in mentalistic terms ispossible, this will carry greater explanatory power (mean-ing) than a formulation in terms of disturbed neural func-tion. If an explanatory formulation in terms of mentalprocesses does not seem possible, or is insufficient, thena formulation in terms of some other primary neuralprocess is necessary.

We have two windows to view the mind–brain system,observation of the brain and observation of the mind.The observation of mental contents and processes, eitherthrough introspection or second-person observation, offersa privileged and readily available point of access. It isboth the obvious and the logical point to begin investiga-tion into the nature of mental disturbance. Despite thispsychiatry appears increasingly preoccupied with theidea of getting at some ‘essence’ of mental disorderthrough brain research. While we must have an under-standing of the manifestations of primary disturbances ofthe brain in order to understand many psychiatric ill-nesses, and while we must have an understanding of thepathophysiology of the brain that supervenes in somepsychiatric illnesses, this does not mean that a brain focuswill serve well to gain understanding of all psychiatric

illnesses. Because of the ‘explanatory gap’ we are facedwith when we try and understand mind in terms of brain,a ‘mind’ focus will better serve understanding in theabsence of specific independent or irreversible patho-physiological disturbances.

Acknowledgement

I am grateful to the Melbourne philosopher TamasPataki for his helpful critique of this paper.

References

1. Russell B. Berkeley. In: A history of Western philosophy.London: Counterpoint, 1984:623–633.

2. Schimmel P. Mind over matter? I: philosophical aspects of themind–brain problem. Australian and New Zealand Journal ofPsychiatry 2001; 35:481–487.

3. Andreasen NC. Brain imaging: applications in psychiatry.Science 1988; 239:1381–1388.

4. Kendell RE. The nature of psychiatric disorders. In: Kendell RE,Zealley AK, eds. Companion to psychiatric studies. 5th edn.Edinburgh: Churchill Livingston, 1993:1–7.

5. Pataki T. Psychoanalysis, psychiatry, philosophy. Quadrant1996; April:52–63.