Abstract
The McNaughton rules for determining whether a person can be successfully defended on the grounds of mental incompetence were determined by a committee of the House of Lords in 1843. They arose as a consequence of the trial of Daniel McNaughton for the killing of Prime Minister Sir Robert Peel's secretary. In retrospect it is clear that McNaughton suffered from schizophrenia. The successful defence of McNaughton on the grounds of mental incompetence by his advocate Sir Alexander Cockburn involved a profound shift in the criteria for such a defence, and was largely based on the then recently published ‘scientific’ thesis of the great US psychiatrist Isaac Ray, entitled ‘A treatise on the medical jurisprudence of insanity’. Subsequent discussion of this defence in the House of Lords led to the McNaughton rules, still the basis of the defence of mental incompetence in the courts of much of the English-speaking world. This essay argues that the rules need to be reconsidered in the light of the discoveries of cognitive neuroscience made during the 160 years since Ray's treatise. It is shown, for instance, how the conflation of ‘the power of self-control’ with ‘irresistible impulse’ by Cockburn is not supported by cognitive neuroscience because these are separate capacities requiring normal activity in distinct brain structures for their expression. In this way cognitive neuroscience assists in distinguishing between different capacities. It is further shown that failure of appropriate restraint in the expression of a capacity can be related to failure of synapses in particular parts of the brain. This raises the question as to what level of synaptic loss will the legislature and the courts rule as sufficient for a subject to be no longer held responsible for their lack of restraint.
Keywords
McNaughton rules and cognitive neuroscience
McNaughton rules
In 1843 Daniel McNaughton shot the secretary of the Prime Minister of England, Sir Robert Peel. In retrospect there is no doubt that McNaughton suffered from schizophrenia [1]. The trial was held before Lord Justice Nicholas Tindal (1776–1846) and the advocate briefed on behalf of the assassin was Sir Alexander Cockburn (1802–1880), later Lord Chief Justice of England [1]. Cockburn made effective and extensive use of the recently published (1838) work A treatise on the medical jurisprudence of insanity by the celebrated US psychiatrist and founder of mental health institutions, Isaac Ray [2]. Cockburn was then able to shift the plea of insanity made on the basis of the defendant being unable to tell right from wrong to other considerations given in Ray's treatise. The treatise is based on the thought that [2]:
In all of this, however, there is nothing different from what occurs in many, if not the greater proportion of chronic diseases. That the intermissions of mania are ever so complete that the mind is restored to its original integrity, would seem scarcely probable, from the fact, that the very seat of the pathological changes is the material organ on which the manifestations of the mental phenomena depend. For if the mind be rendered as sound as before the attack, it necessarily follows that the brain is equally restored, since in point of health they stand to each other in the relation of cause and effect [p. 321].
It was now placed beyond doubt that madness was a disease of the body, the result of morbid organization, and that its nature was to be precisely and accurately ascertained by those only who had made this disease and its pathology the object of long reflection and diligent investigation. The discoveries of modern science had thrown much light upon this subject, and many of the positions laid down by Lord Hale and the other authorities of former times were left to very great objection and doubt [p. 2].
was the creature of delusion and uncontrollable impulse, which took away from him the character of a responsible being [p. 2].
After McNaughton was found not guilty on the grounds of insanity the House of Lords began an enquiry into considerations of murder evidence in insanity. In particular the Lords put a series of questions to a panel of judges headed by Lord Tindal concerning the course to take when a defendant claimed to have committed the crimes while insane. Lord Tindal's report, the foundation of the law of insanity throughout the English common law world, is indebted to Isaac Ray, as is a later addition that received the enthusiastic support of Lord Cockburn.
The report states (the designations in square brackets are mine) [4]:
it must be clearly proved that, at the time of the committing of the act, the party accused was labouring under such a defect of reason, from disease of the mind, [T1] as not to know the nature and quality of the act he was doing; [T2] or, if he did know it, that he did not know he was doing what was wrong. [T3] that he labours under such partial delusion only, and is not in other respects insane, we think he must be considered in the same situation as to responsibility as if the facts with respect to which the delusion exists were real. [C] there are forms of mental disease in which, though the patient is aware he is about to do wrong, the will becomes overpowered by the force of irresistible impulse, the power of self-control, when destroyed or suspended by mental disease, becomes (I think) an essential element of responsibility.
Isaac Ray's ideas form part of the foundation on which the Tindal/Cockburn rules were later formulated. In relation to [T1], Ray had suggested that [2]:
Intellectual mania is characterized by certain hallucinations in which the patient is impressed with the reality of facts or events that have never occurred, and acts more or less in accordance with such beliefs; or having adopted some notion not all together unfounded, carries it to an extravagant and absurd extent. It may be general, involving all or the most of the operations of the understanding; or partial, being confined to a particular idea, or train of ideas [p. 152]. (for) the senses have no share; the imagination alone is exalted; the brain is exclusively the seat of the disturbance; the patient mistaking creations of his imagination, for objects actually present to his senses [p. 154].
In relation to the issue raised in [T3], Ray had previously commented that [2]:
When a man suffers under a partial derangement of intellect, and on one point only, it would be unjust to invalidate acts which were totally distinct from, and uninfluenced by this so-limited insanity; but if the act done bears a strict and evident reference to the existing mental delusion, we cannot see why the law should not also interpose a limited protection, and still less why courts of equity, which in their ordinary jurisdiction relieve against mistake, should deny their aid in such cases [p. 245].
And in relation to [C] Ray had made the point that [2]:
The various forms of homicidal insanity have thus been illustrated, by selecting a few cases only, from a mass that would fill a considerable volume. Now, however these cases may differ from one another; whether the individual has succumbed to the propensity to kill, after a long struggle with his better nature, or has yielded to it at once and instantaneously; whether harassed by previous disease of body or despondency of mind, or apparently in sound health and with a cheerful disposition; whether his passions have been tamed by the discipline of a good education, or allowed to seek their gratification without restraint; they all possess one feature in common, the irresistible, motiveless impulse to destroy life [p. 229].
The Tindal/Cockburn guide to the law of insanity has been adopted and extended to different degrees in the USA and Australia in more recent times, but with very little if any reference to the progress made in our understanding of the workings of the human brain since Ray's thesis that so influenced the formulation of the guide.
Consideration of one of the McNaughton rules in the light of cognitive neuroscience
The lack of understanding of what one is doing [T1], arises under the condition of a delusion or of a hallucination, which I have recently discussed in relation to the associated neural mechanisms [5]. This is not considered further here. The lack of capacity to know that what one is doing is wrong [T2] and the extent of criminality under a delusion [T3], are not considered here either. It is to [C], understood as ‘the lack of capacity to control one's actions’ [6], that this essay is principally addressed. To this end consideration is given as to how lesions in particular regions of the brain, detected for example with magnetic resonance imaging (MRI), restrict our capacity to inhibit an ongoing act. More subtle changes in these brain regions, detected as abnormal synaptic activity due to a low complement of functioning synapses, can be detected, which lead to difficulties in switching from one act to another. Consideration is also given to how lesions in other parts of the brain lead to a failure of restraint as in impulsivity and delay aversion. Again, detected differences in the complement of synapses without an overt lesion are correlated with failure to control impulsivity and delay aversion. These sections indicate that Cockburn in [C] was incorrect in conflating ‘irresistible impulse’ with ‘the power of self-control’ because neuroscience shows that two different areas of the brain are involved in supporting these actions and so they should not be conflated. Neuroscience can help us clarify our terms as well as establish the important principle that abnormal behaviour is very likely due to failure of restraint as a consequence of an incapacity that arises from loss of synapses in a particular part of the brain. Where the legislature and the courts draw the line as to when loss of synaptic connections is of such an extent as to excuse a defendant is a key issue for further deliberation. In the final section the concept of ‘will power’ or ‘the will’ in Cockburn [C] is considered. It is argued that willpower, as exemplified in an act requiring great effort, can fail to be realized due to restrictions on the range of behaviours consequent on a loss of synapses.
Thinking about a future act but unable to inhibit an ongoing act and so initiate the new act
Apparent lack of self-control and the pre-supplementary motor area of the brain
Patients with lesions located by non-invasive MRI in the pre-supplementary motor area (pSMA) of the brain, may display behaviour in which they have great difficulty in resisting picking up and using the nearest object to them, showing an apparent lack of self-control in these instances [7], a condition called utilization behaviour (for a review see [8]). Such behaviour is manifest when, for instance, the patient who is already wearing glasses picks up another pair of glasses nearest to them on a table and proceeds to put these on over the existing pair. The absurdity of the situation is apparent to the patient; nevertheless they find it very difficult to resist utilizing the second pair of glasses.
A related phenomenon is anarchic limb, which occurs in patients with lesions encompassing pSMA as determined by MRI (for a review see [8]). In this case, with a lesion on one side of the brain, the patient will tend to firmly grasp objects and even people with the opposite hand, experiencing great difficulty in releasing them [9]. Again the patient generally realizes the inappropriateness of the act but is unable to resist carrying it out, feeling ‘magnetically drawn’ to the object or person.
Thus the propensity of some subjects to fail in restraining themselves from inappropriate acts and to initiate appropriate acts, even though recognizing what is appropriate and attempting to act on such thoughts, can be correlated with brain lesions, particularly those that involve the pSMA. This brain area has therefore been singled out for detailed investigations, which we now turn to before considering further effects of lesions in pSMA and loss of synaptic connections in pSMA consequent on a disease such as schizophrenia.
In normal subjects the pre-supplementary area functions during preparation to carry out an act
A normal subject is instructed, on hearing one of two tones (each at a different frequency), to either extend or not to extend their middle finger on hearing a further tone some 2 s later (at a third frequency). In the intervening 2 s, at approximately 0.1 s immediately following the instruction, considerable electrical activity is recorded in the pSMA, peaking at approximately 0.6 s. There is, however, very little activity in the adjacent cortical area [10]. Electrical activity is not evident at all if the experiment is reversed and the initial tone warns the subject that 2 s later they will be presented with one of two tones indicating that they should move or not move their middle finger. These observations suggest that pSMA is concerned with supporting our capacity to select an appropriate action set, that is, a set of neurons that are necessary to carry out an action during the preparatory period before the act is implemented [10].
Such an interpretation is supported by functional magnetic resonance imaging (fMRI) studies of pSMA in normal subjects executing finger movements. The subject is asked to either execute a finger movement at 0 s or to think of executing the movement without doing so while counting down from 10 to 0 s and then up to 5 s. The fMRI shows greatly increased activity in the pSMA during the 10 s before executing the act, but only a relatively small or no increase in the adjacent cortex; similar results are obtained when the act is not executed, but simply imagined [11].
Taken together, these observations indicate that pSMA is involved during the preparatory phase of carrying out an act, that is, in engaging the appropriate neurons required in order for the act to be subsequently implemented.
In normal subjects pre-supplementary area functions during switching from one act to another.
Giving a normal subject the task of moving, on instruction, their eyes in a particular direction (a saccade), and then subsequently instructing them to reverse the direction of the saccade before it has occurred, gives rise to heightened activity in pSMA, closest to the front of the brain as determined using fMRI [12] Such heightened activity does not occur unless the original instruction is reversed [13]. It seems then that rostral pSMA is active when a subject is involved in resolving a conflict of actions.
Electrical observations support the conclusion that pSMA is involved in inhibiting one act and establishing another. Nerve cells can be recorded in the pSMA that fire impulses at high frequency when instructions require a sudden switch from one kind of activity to another [14]. For example, a screen might be viewed with two different coloured squares on it, one to the left and the other to the right of a central fixation point, the instruction being to make a saccade to one or other of the colour squares, depending on a matching colour to one of them presented at the fixation point. Following a series of trials during which the requested colour matching occurs at random to the left or right of the fixation point, a sudden switch is made in the colour at the fixation point so requiring that the other colour should be matched. Nerve cells in the pSMA begin heightened firing approximately 0.015 s later, reaching a maximum at 0.25 s and falling to low levels at 4 s, which is approximately 0.1 s before the correct saccade commences [14]. If a mistake in the directions of the saccade is made, the pSMA neurons show only a low and delayed increase in activity before the saccade commences, with no increase in firing occurring at all during trials when no switch to a new colour to be matched occurs [14]. Clearly, the activity of these neurons reflects a successful switch in the saccade before this commences as well as the failure of a correct saccade at switching. It is therefore consistent with attributing to pSMA a function related to a subject being able to quickly and successfully resolve changes in required action.
Subjects with lesions in pre-supplementary area have significantly decreased ability to inhibit one act and switch to another
A small injury to the pSMA leads to an incapacity to carry out an appropriate action. This area of the brain must function normally in order for a set of nerve cells (the action set) to be chosen over that of another action set in order to efficaciously fulfil a particular act at a subsequent time (see [15] for a short review). This is seen in patients with highly localized lesions to their pSMA. If such patients are given instructions to carry out an action, such as pushing a button with the left hand, and then told to countermand this and to push it with the right hand, they have difficulty in doing so and although eventually successful, the act is clearly slow and somewhat laborious [12].
Injury to pSMA leads to a high probability of failure to change direction in a saccade when instructed to do so shortly after the original saccade is begun [16]. If transcranial magnetic stimulation, in which the field from the magnetic coils is used to interrupt electrical activity in the cortex, is applied over the pSMA, then switching is disturbed between cued right- and left-handed responses but does not interfere with ongoing responses that do not require switching, nor does it affect switching when the field is applied elsewhere over the frontal cortex [15].
Subjects with decreased grey matter (synapses) in pre-supplementary area have significantly decreased capacity for switching to another act
It is not necessary for a small lesion to disturb the normal functioning of pSMA because a decrease in grey matter from the normal can also lead to errors in switching, The relative lack of self-control in subjects with different schizophrenia-related personality disorders and the volume of grey matter in the pSMA as determined by MRI are negatively correlated [17]. The extent of disorganized behaviour in chronic schizophrenia patients is also negatively correlated with grey matter volume in areas next to pSMA [18]. Given the substantial evidence now available that changes in grey matter volume during development are most likely due to changes in numbers of synaptic connections (reviewed in [19]), it is very likely that the aforementioned observations indicate that loss of synapses in pSMA leads to an inability of the subjects to easily switch between motor acts and avoid socially unacceptable behaviour.
We have considered in this section a spectrum of behaviours ranging from overtly bizarre acts as in utilization behaviour through to difficulties in switching hand and eye movements, associated with lesions of different sizes in pSMA, to conditions in which there are no lesions but a likely loss of synaptic connections with resulting behavioural difficulties. These various observations indicate a need to determine the normal extent of synaptic connections in pSMA so as to be able to evaluate the capacity of an individual to control their actions. Most importantly, these considerations lead to more subtle observations of behaviour, often only seen under experimental conditions in which both behaviour and non-invasive brain imaging occur, so as to be able to assess the extent to which the subject is able to express normal psychological capacities related to self-control.
Failure to think about a future act and therefore acting only to satiate an immediate desire
Impulsivity, delay aversion and the orbitofrontal cortex of the brain
Impulsive behaviour is that characterized by acting without thought, that is, on the impulse. Such behaviours are inappropriate for the context, premature, poorly planned with often adverse consequences. The Barratt Impulsiveness Scale is the self-report method that is most often used to assess the extent of impulsivity and includes items for measuring attention, and perseverance. Very interestingly, healthy subjects show a negative correlation between their degree of impulsivity and the volume of grey matter in their orbitofrontal cortex (OFC) [20], a part of the brain that is involved in satisfying appetites concerned with olfaction, sexual arousal, as well as the ingestion of food (for a full description, see [21]). Indeed, fMRI shows a positive correlation between the capacity to successfully maintain restraint and activity in the OFC [22].
Delay aversion behaviour refers to the inability to weigh short-term minor rewards against long-term major rewards, so that decreased delay aversion indicates an increased inability to postpone the reward. Delay aversion then gives a measure of the extent of acting to immediately satiate a desire and so is measured in trials for which a choice is offered between a small immediate reward and a large delay reward. Delay aversion behaviour is also dependent on the functioning of the OFC [23].
Thus impulsivity and failure of delay aversion, acting without prior thought as to the consequences of one's actions, are associated with abnormal activity in the OFC. This part of the brain, together with adjacent cortical and subcortical areas, forms part of the neural circuits that are thought to be involved in cravings to satisfy appetites and in addiction (for a review see [24]). The importance of the OFC is highlighted in the following sections because of its role in impulsivity and delay aversion, and the changes in the OFC that accompany drug addiction, particularly those due to the loss of synaptic connections.
Impulsivity arises after lesions to the orbitofrontal cortex
Lesions and neurodegeneration in the OFC give rise to disinhibition and so impulsive and socially inappropriate behaviour [25–28].
Impulsivity is characteristic of a number of psychiatric conditions that involve decreases of activity in orbitofrontal cortex
Impulsivity is a major characteristic of borderline personality disorder in which a subject also has paranoid ideas, difficulties with relationships, outbursts of anger as well as violent behaviour that often leads to criminality. The risk of suicide is very high, up to 5000-fold that of the general population. Non-invasive brain imaging with positron emission tomography shows that subjects with this disorder have decreased activity in their OFC compared with normal subjects [29], an observation confirmed on fMRI [30].
Delay aversion is dependent on the functioning of orbitofrontal cortex
The ability to weigh short-term minor rewards against long-term major rewards, that is, delay aversion, is critically dependent on the normal functioning of the OFC [31, 32]. Use of the Iowa Gambling Task as a measure of appropriate decision-making in reward-related behaviour shows that the appropriateness decreases with a decrease in activity in the OFC [32].
Changes in impulsivity and delay aversion in drug addicts correlates with changes in the orbitofrontal cortex
Drugs of addiction that lead to increased impulsivity and decreases in delay aversion, such as methamphetamine and cocaine [33–36], are associated in drug-addicted subjects with decreases in activity of the OFC as measured using non-invasive brain imaging techniques [35–37] (for a review see [38]).
Decreases in grey matter (synapses) of orbitofrontal cortex in schizophrenia and drug addiction
Addictive drugs not only modulate transmission in the OFC, but also lead to a loss of synapses, exacerbating the abnormal behavioural state characterized by impulsivity and failure of delay aversion. Cocaine users show a 5–11% decrease in the grey matter of OFC [39] and there is a loss of synaptic connections in OFC following amphetamine use [40].
Early studies of structural changes in the OFC of those suffering from schizophrenia, using MRI, could not find any loss of grey matter [41–43], although more recent studies do [44, 45]. The most recent research on this topic has identified the technical basis for these differences and shows a correlation between the extent of loss of OFC grey matter and the extent of expression of core components of the schizophrenia syndrome [46]. This decrease of grey matter is most likely due to a decrease in the loss of synaptic connections, because there are no changes in the density of nerve cells in the OFC of patients with schizophrenia [47].
Voluntary, involuntary and not voluntary acts
An act may be not voluntary although it could have been performed voluntarily but was not, as in smiling and blinking. Utilization and anarchic limb behaviour, as when one puts on a second pair of glasses or grasps nearby objects, falls in this not-voluntary behaviour category. Acts that are not voluntary may be so because they are neither voluntary nor involuntary, as when one unknowingly or unintentionally acts – for example, unknowingly treads on a snail. It may be argued that impulsivity and the failure of delayed aversion falls into this category of not-voluntary behaviour. An act may be not voluntary because it was done under duress or required to be performed, such as students directed to take an exam. The question of whether acts are voluntary, intentional and involve exercise of free will often arise when considering mental incompetence, and so are now considered (for a review see 49).
Intentional, unintentional and not intentional acts
Voluntary acts may be intentional, unintentional or not intentional. Intentional acts are voluntary unless they are performed under duress or one is obliged in the circumstances to perform them, and so such acts as eating, walking, talking are voluntary and intentional. Voluntary acts need not be intentional, as in grimacing. Clearly, utilization and anarchic behaviour cannot be said to be intentional because they are not voluntary.
Voluntary acts typically involve making physical movements, but of course making a movement does not mean it was done so voluntarily. Marks of a voluntary act are of a kind that one can try to perform, decide or intend to perform; can perform on request or to order; and one can learn to perform them – none of which applies to utilization or anarchic behaviour. For when one acts voluntarily, one exercises a two-way power to do or refrain from doing, knowing that it is in one's choice. But the patient with utilization or anarchic behaviour is very disturbed by the behaviour, does not want to do it, is surprised by it, disowns the action but feels there is no choice – so these behaviours are not voluntary. It may also be argued that because little thought is given prior to the act in the case of impulsivity and failed delayed aversion then the two-way power to do or refrain is greatly impaired, so that the act is not voluntary.
One proves that one can do something voluntarily by doing it, but one does not know one has done it voluntarily by a special feeling. In the case of an anarchic arm it does not feel the same when it is raised as compared with when it is raised voluntarily, but one does not know one has raised one's arm voluntarily by any special feeling. If this were so, then one might forget which feeling was the right feeling to indicate voluntariness, and therefore make a mistake as to whether one had acted voluntarily or not – which is absurd in non-pathological cases.
A fully voluntary movement is the exercise of a two-way power, to do or to refrain from doing; it is behaviour that is under one's control. This clearly does not apply to utilization or anarchic behaviour that are therefore not voluntary. Impulsive behaviour, participating in acts that should normally require prior thought and consideration as to whether they are appropriate but which do not, may be considered then to be not voluntary, because the exercise of a two-way power is not present. Subjects may recognize the acts as inappropriate but continually fail to exercise restraint.
Note that impulsivity and delay aversion have a dimension to them associated with feelings, which is not the case with utilization and anarchic behaviour. This follows because the OFC, which is involved in impulsivity and delay aversion, is also involved with the appetites such as in sexual arousal and feeding, whereas the pre-supplementary cortex involved in utilization and anarchic limb behaviour is not.
Acts of will, willpower, and free will
Voluntary movement is not movement caused by a volition or act of will. An act of will is an act performed with great effort to overcome one's reluctance or difficulties in acting, typically in adverse circumstances. In the case of anarchic limb, the patient unsuccessfully attempts to overcome the involuntary movement of the anarchic limb, to exert their will. In the case of delay aversion the subject puts little effort into overcoming the need to act in the short-term in relation to their reward (perhaps an amphetamine high) rather than reject this reward in favour of the long-term benefits of a drug-free lifestyle.
Voluntary and attentional actions are not bodily movements caused by antecedent acts of willing to move. There are no mental acts called ‘willing’ that cause bodily movements. Willpower is not a mental equivalent of muscle power, but rather a determination and persistence in pursuit of one's goals in the face of difficulties. The patient with anarchic limb may exert considerable willpower, that is, be both determined and persistent in attempting to prevent the limb grasping a nearby object but fail to do so. This willpower is to no avail in overcoming the restriction in this range of behaviours imposed on them by lesions or neuronal degeneration in their pSMA, or malfunctioning of neural networks in these centres as a consequence of polymorphisms in their genes controlling key molecules (proteins) in the networks.
There are logical reasons for rejecting the idea (‘the picture’) that voluntary acts are caused by acts of will.
What could an act of will be? They cannot be inner acts, as we have seen, or indeed feelings. If willing were a feeling then it would simply be something that happens when it happens and its causal consequences would not be voluntary actions, but movements. How does one identify an act of willing? Because without this we could not say whether an act was voluntary or not. But we can. These unidentified acts of will arise from a false picture of what free, voluntary action must be. It is patently absurd to claim that before each voluntary act there is a separate act of willing. When we ascribe responsibility for an action to another person, we do not do so on the basis of identifying an act of will that they have performed and which has caused their bodily movement. In contrast, in the case of utilization or anarchic behaviour, we identify the patient/subject as attempting to exert willpower, as described here, to overcome the inappropriate bodily movement – which is certainly not caused by an act of will.
Wanting, intending and deciding are not causes of actions or movements. We commonly act because we want to. But this ‘because’ is not causal. If it were, then once the want has occurred, the intention been formed, or the decision taken, then we could remain passive, sit back, and let nature take its course. If I want (have decided, intend) to put my glasses on at 6 o'clock, then when I hear the clock chime 6.00, I should not have to put my glasses on to fulfil my purpose. I could just let the want (intention, or decision) cause my arms to rise and put the glasses on. In utilization and anarchic behaviour, the glasses may be put on but this act is not preceded by any intention.
Cognitive neuroscience theories of voluntary movement
Electrical activity begins in the brain before one makes a physical movement; in particular, while pyramidal neurons in the motor cortex are active during the contraction of muscles that are responsible for physical movement. This is preceded for some second(s) by activity in the pSMA, and perhaps some second(s) before that by activity in the most rostral portions of the brain (Brodmann areas 9, 10, 11). pSMA is involved in exciting the appropriate action set of pyramidal neurons in the motor cortex recruited to allow the particular physical movement. pSMA is not involved in repetition of the movement once such repetition has been set in train, but it is if a switch is suddenly required to a different physical movement.
Interestingly, cognitive neuroscientists have used these phenomena to inquire into the role of intention and will in the performing of voluntary acts, adhering to the false picture of voluntary movement requiring an act of will. In this research subjects are asked, before carrying out a particular physical movement, when were they ‘consciously aware of wanting to move’, believing this to indicate the ‘role for conscious free choice or will’ [48]. But it has been argued that it is neither necessary nor sufficient for an act to be voluntary that it be preceded by a feeling or desiring, wishing, wanting or intending to perform it or by an urge to do it. The fact that neurons in SMA are active for a fraction of a second (approx. 350 ms) before the ‘feeling of wanting to move’ is allegedly apprehended merely shows that the neuronal process that lead to muscle activation and movement began before the time at which the subject reported a ‘feeling of desire’ or ‘feeling an urge to move’ to have occurred. Voluntary movement is not a movement caused by a felt urge, any more than to refrain voluntarily from moving is to feel an urge not to move that prevents one from moving.
Movements caused by a felt urge are not voluntary
Delay aversion, in which there is feeling of an urge to do something and being aware of the desire, is not a voluntary act. That is, movements to assuage the desire are caused by the urge and are therefore not voluntary. One may feel an intense desire to take a drug in delay aversion or move one's hands and, other things being equal, one will go on to take the drug and move one's hands. But the desire is not the cause of one's doing so. Rather, one takes the drug to assuage one's craving, moves one's hands on purpose, for example, to cease touching something repulsive (not as in utilization behaviour when the hands move independent of one's purpose). So one may feel an urge to do something, as in delay aversion, and then act because one feels the urge, but this ‘because’ is not causal. The urge one feels to take more of a drug does not make one's hand move irresistibility towards the drug packet, any more than feeling inclined to go to the cinema tonight will, by 7 pm, cause one's legs to move.
Need for reconsideration of the McNaughton rules
Definition of ‘mental illness’
There have been recent attempts in Australia to bring some clarity to the plea of ‘mental illness’ under the McNaughton rules. Shea suggests replacing ‘imprecise phrases such as ‘mental illness’ and ‘mental defect’ (and associated terms such as ‘abnormality of mind’, ‘mental disturbance’, ‘mental dysfunction’ and ‘mental disorder’)’ [49] with a few symptoms that need only consideration in the defence of mental illness, namely ‘delusions, hallucinations, severe mood disturbances (depression or elevation) and severe impairment of intellect’ [49]. More recently The Victorian Law Reform Commission has drawn up its own ‘categories of mental illness/impairment’ namely psychotic illness, depression or depression-related illness, IQ-related illness, personality disorder and alcohol/drug abuse [50]. The first three of these are allied to the Shea list of symptoms, namely delusions/hallucination, severe mood disorder and severe impairment of intellect. The statutory definition covering impaired mental functioning in the Australian Capital Territory is especially interesting, stating that such an impairment amounts to ‘[A] disturbance or defect to a substantially disabling degree, of perceptual interpretation, comprehension, reasoning, learning, judgment, memory, motivation or emotion’ [51]. A number of these psychological categories are open to investigation by both behavioural and neuroscientific means [52] so that contributions of both psychology and neuroscience might be illuminating. Indeed the ACT definition could be paraphrased as ‘A disturbance of psychological capacities’ because these capacities include perceiving, thinking, remembering and feeling. It has been argued that the word ‘mind’ is merely a convenient façon de parler, a way of speaking about, human capacities and their exercise [53]. If this is so then the paraphrase becomes ‘A disturbance of the mind’, without any imprecision of the kind that Shea alludes to. These considerations need to be developed much more fully, perhaps by the NSW Law Reform Commission that is at present reviewing the criminal law relating to people with cognitive and mental health impairments.
Conclusion: a McNaughton rule and cognitive neuroscience
To what extent do the considerations of this short essay on normal and abnormal activity in pSMA and OFC impact on Cockburn's suggestion that:
[C] there are forms of mental disease in which, although the patient is aware he is about to do wrong, the will becomes overpowered by the force of irresistible impulse, the power of self-control, when destroyed or suspended by mental disease, becomes (I think) an essential element of responsibility.
We humans, like other animals, can act in the world only by contracting muscles, and therefore initiating limb movements and vocalization, or excreting sweat, tears and saliva. I have focused on a small group of these behaviours that require normal working of the pSMA or the OFC in order for us to be able to execute the behaviour appropriately. It is very likely that the disruption of synaptic connections between nerve cells in these areas of the brain restricts our capacity for appropriate behaviour within the activities considered here, and that the more extensive the synapse loss the greater is the incapacity. So large lesions in pSMA, due for example to benign tumour growths or localized failure of the vasculature, are associated with utilization behaviour and anarchic limbs; small lesions, requiring fMRI to be detected, may be associated with difficulties in switching behaviour from one pattern to another; and other changes in synaptic connectivity, again requiring fMRI for detection, may be associated with some core symptoms of behaviour manifest in certain psychiatric diseases. Cockburn would probably have regarded this class of behaviours as indicating ‘the power of self-control’. Neurodegeneration in the OFC, which leads to loss of synaptic connections in this brain structure, gives rise to actions made without prior thought – and so poorly planned, premature, inappropriate for the context and therefore often with adverse consequences. This impulsivity is greater the larger the decrease in grey matter, of synaptic connections, in the OFC. It can be a particularly dangerous condition, often leading to criminality and suicide. Another consequence of the failure of synaptic connections in the OFC is incapacity to restrain a drive to satiate appetites. A principal means of destroying the synaptic connections in the OFC is chronic use of methamphetamine or cocaine, which, because of the breakdown in the capacity to delay aversion, of being able to weigh the short-term minor reward of the drug-induced high against the long-term major reward of a healthy life, reinforces the addiction. All of these examples indicate that failure in appropriate behaviour very likely arises as a consequence of a failure in restraint consequent on loss of synapses in appropriate parts of the brain and that there is at least a qualitative relation between the lack of restraint and the number of synapses that have been lost or fail to function. This leads to the important question as to what level of synaptic failure the legislature and the courts will consider as indicating that one is no longer responsible for an inappropriate, indeed criminal, act.
Although Cockburn conflated ‘irresistible impulse’ with ‘the power of self-control’, cognitive neuroscience distinguishes between them and shows that different brain regions support them. Neuroscience has in this way clarified distinctions in behaviour as a consequence of their dependence on normal functioning of different brain regions. One might anticipate that more fine-grained distinctions in our behavioural repertoire will be identified through this kind of research. I hope this essay makes obvious that much work needs to be done concerning the extent to which contemporary cognitive neuroscience bears on issues in the ‘medical jurisprudence of insanity’. For as Ray comments in his great work of that name 170 years ago [2]:
It would seem, therefore, an almost self-evident proposition, that a certain knowledge of the mind in its healthy state is an essential preliminary, to the attainment of correct ideas concerning its diseased manifestations. If, in addition to this, it is considered, that opinions on the nature of insanity, viewed solely in the light of a disease – of a derangement of the physical structure, – have been constantly changing for better, it follows of course, that its legal relations, which should be determined in some measure by our views of its nature, ought to be modified by the progress of our knowledge. That much of jurisprudence of insanity, in times past, should bear marks of the crude and imperfect notions, that have been entertained of its pathological character, is not to be wondered at; but, it is a matter of surprise, that it should be adhered to, as if consecrated by age, long after it has ceased to be supported by the results of more extensive and better conducted inquiries. It is to be feared, that principles, laid down on this subject by legal authorities, have received too much of that reverence, which is naturally felt for the opinions and practices of our ancestors; and that innovations have been too much regarded, rather as the offspring of new fangled theories, than of the steady advancement of medical science.