Abstract
This paper reviews the ways in which memory disorders and memory distortions arise in the criminal courts. Amnesia for offences is considered in terms of automatisms, alcohol, and crimes of passion. False memories arise in false confessions, allegations of false memory for child sexual abuse, and, just occasionally, with respect to delusional memories. More generally, memory and neuropsychiatric disorders may have implications at each stage of the legal process (fitness to plead, the insanity defence, cases of automatism, diminished responsibility, and at sentencing). However, patients with memory and neuropsychiatric disorders remain very vulnerable within legal and court processes.
Introduction
I come to this topic from an interest in neurological amnesia, as in the amnesic syndrome. So that, for example, Wilson et al (2008) described a man who had herpes encephalitis – he was a musician – and he had a severe amnesic syndrome because his left temporal lobe was virtually entirely knocked out and his right medial temporal lobe also.
I also have an interest in psychological forms of amnesia. For example, the so-called “Piano man” received publicity all round the world. Psychological forms of amnesia can occur as either global amnesia, as in a fugue state, or as situation-specific, gaps in your memory, such as you see in post-traumatic stress disorder, the victims of crime (for example, rape), or the perpetrators of crime. There are actually now neurophysiological imaging studies which show the brain correlates of what goes on during memory suppression or inhibition. These show activation in the frontal lobes and also deactivation in the medial temporal lobes (Anderson et al 2004; Kikuchi et al 2009).
I also have an interest in confabulation in neurological disease, when patients report entirely false memories or memories jumbled in temporal sequence and retrieved inappropriately. In “spontaneous confabulation”, they produce a persistent unprovoked outpouring of these false memories. We now have some knowledge of the brain areas where damage gives rise to this (e.g. Schnider 2003; Gilboa et al 2006; Toosy et al 2008).
I am going to be talking about three issues in medico-legal cases today:
Amnesia for offences, which just occasionally can be neurological, but is more usually a form of psychogenic amnesia. False memories in the law courts: I am going to be talking about false confessions, which have been described as a form of confabulation. Then towards the end I am going to talk more generally about courts and brain disease. Various neuroscientific explanations of crime have been postulated, and I would argue that those who have definite brain disease are very vulnerable in the legal process.
Amnesia for offences
Let me begin by talking about amnesia for offences. As many of you will know, this is commonly reported in about 25–45% of people charged with homicide (Pyszora et al 2003; Kopelman 2002), and it occurs in four different sorts of circumstances.
There are the medically-based disorders, including automatisms, which we will talk about in a minute. They are legally important, but in fact rather rare. Much more common are young men, or older men, getting severely intoxicated and then they cannot remember what they have done at the time of the offence. Just occasionally you see people who are so psychotic that they give a completely deluded account of their offence, and then: There are the group that I call “crimes of passion”, and I will come on to those in a moment.
Automatism
Automatism, considering its importance, is remarkably badly defined. There is no agreement. Peter Fenwick (1990) described it as: “An involuntary piece of behaviour in which the individual has no control. The behaviour itself is usually inappropriate for the circumstances, and may be out of character for the individual. It can be complex, coordinated, and apparently purposeful and directed, though lacking in judgment. Afterwards, the individual may have no recollection or only partial and confused memory for his actions.” In other words, there were a lot of ifs, maybes, and buts. Jonathan Bird et al (2009) has a definition which is essentially circular: “An automatism is a behaviour that lacks voluntariness.” I myself have a definition which is philosophically totally unsound, but I put it forward as pragmatically useful: “An abrupt change of behaviour, in the absence of conscious awareness or memory formation, associated with certain specific clinical disorders”, and I have listed them: epilepsy, parasomnia, hypoglycaemia, and head injury (Kopelman 2013).
Now, as many of you will know, English law distinguishes between “sane” and “insane” automatisms. So-called “sane” or “non-insane” automatisms result from something external, such as a blow to the head or taking too much insulin in diabetes, and lead to acquittal. An insane automatism results from an intrinsic factor, such as disease of the brain, and that used to lead to secure hospitalisation, but there is more flexibility now. The trouble is that this distinction between extrinsic factors, which were thought to happen once and then would not happen again, and intrinsic factors which might well happen again, does not work: we all know that people on insulin may well be at risk of having another hypoglycaemic attack, and that, by contrast, epilepsy can be treated and well controlled. So, this apparent legal clarity is complete medical and psychological nonsense.
An example would be a man killing an acquaintance shortly after taking his insulin, and then displaying classical hypoglycaemic symptoms when the police arrived. Another example would be a man who viciously assaulted his girlfriend during a parasomnic episode two hours after going to bed: he was roused by the partner going to the toilet.
Neuropsychologists have put proposed “models” of voluntary experience and action (Haggard 2008). These are derived from experiments in healthy participants which differ greatly from what happens in an automatism; but it is thought that the medial frontal regions are involved in the physiological preparation for action, and the frontal poles in the deliberation and forming of a prior intention. If these “functions” are lesioned or “knocked out”, a person may still be able to perform an action in an “automatic” fashion, i.e. without the sense of self as agent or the sense of voluntary control. But these experiments are based on procedures very distant from clinical “automatism”. Moreover, there have been very few studies of automatism itself, important though it is, because (a) it is very difficult to study, (b) it is short-lived and transient, and (c) of course, you may put yourself at risk in doing such studies!
Alcohol
Alcohol can obviously give rise to amnesia in a so-called alcoholic blackout, which is related to the dose of alcohol imbibed, and is a common phenomenon in heavy drinkers. But alcohol, as you probably know, is not in itself a defence, because it was your fault that you took the first drink of the day; you had the will or volition to do so, the mens rea. There are rare circumstances in which it constitutes a defence, which boil down to the so-called “Tandy defence” in homicide, where the law talks about the “disease of alcoholism”, in which, because of withdrawal symptoms from the moment you awakened, it is postulated that you had no choice but to take the first drink of the day. So, under the old rules (pre-2009), this was grounds for diminished responsibility or manslaughter in homicide cases, because the drinker's mens rea was compromised.
For example, Person A had a full house of alcohol dependence syndrome symptoms. By 10 am on the day of the offence, he had consumed a bottle of vodka and several strong lagers. He was observed by many witnesses to be severely intoxicated. He killed his drinking partner with a knife, and he had an amnesic gap of several hours, with a few islands of memory and some confabulation. His blood alcohol was estimated at over four times the driving limit. His lawyers successfully argued for diminished responsibility on the grounds of the Tandy defence that he had the alcohol dependence syndrome with no choice but to consume the first drink of the day.
Crimes of passion
The cases I find particularly interesting are the so-called “crimes of passion”. These offences occur in what amounts to a psychogenic or dissociative state, and the victim is almost invariably wife, lover, or partner. The offence is unpremeditated and unplanned, usually homicide, and often takes place in a state of extreme emotional arousal. Such offences are often associated with a history of clinical depression, and the person may have been expressing suicidal ideas or become suicidal afterwards. The amnesic gap (memory loss) usually covers a period of a few minutes to an hour.
Gisli Gudjonsson and Jim MacKeith (Gudjonsson and MacKeith 1983) described a 67-year-old man who battered his wife to death without any apparent motive. Subsequently he telephoned the police and gave himself up. At the time he claimed to have no memory of the actual attack, but recalled standing over the body realising that he had been responsible for his wife's death. Pamela Taylor and I (Taylor and Kopelman 1984) described a 40-year-old Egyptian married to an English woman, who had two children. He discovered his wife was having an affair with a musician, and he became depressed and was treated with antidepressant. One afternoon the man had a furious row with his wife, during which he threatened to kill the musician. Later he could recall going to kiss his daughter goodnight, but he could not recall anything after that until the police arrived. In the meantime, he had telephoned the police; and he was subsequently charged with the murder of his wife by stabbing.
In such cases, many people, including university-based psychologists, assume that “They are putting it on”, as does the Crown Prosecution Service. Christianson and Merckelbach (2004) argued that (i) offenders' amnesia does not resemble neurological – Well, it does and it doesn't. (ii) Some offenders have been shown to fake – That does not mean they all do. (iii) Alcoholics do not necessarily experience alcoholic blackouts – So what? (iv) Victims and eyewitnesses do not claim amnesia – Well, that is not actually true. (v) They argue for forms of symptom validity testing, which, although good in principle, are often very difficult to conduct in practice because of the circumstances of these types of crime as well as the context of an interview in prison.
Tolstoy also adopted this view. In ‘The Kreutzer Sonata’ (1889) he makes his protagonist say:
“When people say they don't remember what they did in a fit of fury, it is rubbish, falsehood. I remember everything and did not for a moment lose my memory. … I felt, and remember, the momentary resistance of her corset and of something else, and then the plunging of the dagger into something soft. … I remembered that for an instant, before the action, I had a terrible consciousness that I was killing, had killed a defenceless woman, my wife! I … even dimly remember that, having plunged the dagger in I pulled it out immediately, trying to remedy what had been done.”
The case against these amnesias being always faked is that a rather consistent account is reported by many offenders, who presumably have not read the literature. Moreover, their subjective account is rather like that of other people with psychogenic amnesia; they talk about the memories being there, locked away but they just cannot get access to them. Moreover, as in the Gudjonsson and MacKeith (1983) case, these offenders often give themselves up and report their own crime, or at least make no attempt to avoid capture. The victims and eyewitnesses of offences can also show impaired recall of the offence, but their motives are unquestioned. Furthermore, except in automatisms, there is not actually any legal advantage to claiming amnesia, and it may in fact be damaging to mounting a defence.
Natalie Pyszora and I looked at everybody given a life sentence in 1994 (Pyszora et al 2003). We looked at Home Office files, and it is interesting to note that, although these were high profile offenders, 11% of the files were missing. 29% had claimed amnesia, 31% of the homicide cases. At three-year follow-up, 2% said they had feigned amnesia, 2% were suspected of having feigned it. Of the rest, approximately a third had recovered their memory, a third had had partial recovery, and a third had no return of their memory.
False memory
I am now going to say a few words about the opposite: false memories in the law courts. First, I want to contrast false confession, which gets you into trouble, with false memory for child sexual abuse, which I am not actually going to talk about, but which gets someone else into trouble.
Gudjonsson and MacKeith (1988) argued that false confessions occur (i) to protect a real criminal; (ii) to relieve guilt for some real or imagined previous transgression; (iii) out of a morbid desire for publicity or notoriety; (iv) as a consequence of the inability of some individuals to distinguish reality from fantasy; and (v) or as a result of (a variable degree of) coercion. Gudjonsson's (2003) model suggests that false confessions arise (i) when someone has low self-esteem and/or may be depressed; (ii) there may be a degree of coercion; and (iii) the person often scores highly on his scales of “compliance” or “suggestibility”. In these circumstances, people start to distrust their memories: i.e. they do not know if what they are remembering is a real memory, or if it is something that they have read in the newspaper or read in the legal documentation. They distrust their memories and are uncertain from where they have arisen, in what psychologists call “source amnesia”. In such circumstances, an accused person may make a “confession”, and this may be internalised to varying degrees. If strongly “internalised” and believed in, Gudjonsson calls this a “confabulation”.
Person B was aged only 17, when a 14-year-old girl was killed in his home town, while she was out riding her bicycle, many years ago (Gudjonsson et al 1999). B had recently been dismissed from the military because of an illness. He had low self-esteem and was being treated by his GP for depression. The police interviewed everybody who had been in a particular barracks at that time and, because of a misunderstanding about when precisely he had left the military, he was interviewed twice. He became very excited and, following the interview, he became very agitated, and that night, he said that he had “visions” of the victim. The next day, he took himself to the police station to see if his ‘visions’ would match a photograph of the victim. From the police's own detailed record of his interviews during the next 72 hours, he became extremely agitated and talked himself into a confession. This was before the PACE Act of 1984 and no doctor or lawyer was present – he kept asking for both, but his requests were turned down. From the transcripts, he went from being uncertain whether he had committed the crime (“I don't know if I killed her”) to an apparently unequivocal confession (“I am sure I killed her; I know I did it”). It was this confession which was the main evidence on which he was convicted. He did not change his mind for a few years, and it took 25 years before his conviction was overturned as unsafe.
In another case, the accused man actually had an alibi. At the time that two ladies were killed, while walking their dogs, he was in a bank several miles away cashing a cheque. However, because he had kept telephoning the police in an intoxicated state, encouraging them to interview him, he talked himself into being charged with the offence and then found guilty. It took 17 years for his conviction to be overturned and, rather unusually, the Court of Appeal actually said in their judgment that, not only was the conviction unsafe, but that the accused could not have committed the offence.
It is also possible that false memories can occur in witnesses as well as defendants, especially in cases given wide publicity.
Neuroscience, memory disorders, and brain disease
In the final section of the talk I am going to talk a bit more generally about the courts and brain disease. This is a hot topic, it appears, at the moment. A lot of neuroscientists have recently discovered and written about the law, just as the lawyers have discovered neuroscience. In December 2011, the Royal Society (2011) produced a report on the topic entitled Neuroscience and the Law. As brain imaging, neurological pathophysiology, and brain science advance, increasingly issues are going to be posed for the courts. I will talk briefly about that, but I also want to make the point that those with definite neuropsychiatric disorder are often very vulnerable to legal and court processes.
There is a man called Adrian Raine, a British psychologist practising in California, who has written on what he calls The Psychopathology of Crime: Criminal Behavior as a Clinical Disorder (1993). He has argued, from genetics, neurochemistry, neuropsychology, psychophysiology, medical, and neuroimaging studies, that there is a biological precursor to crime, and that this has implications for criminal responsibility. A problem is that these investigations have consisted of group studies, whereas in legal matters, predictions have to be made about the individual, as Raine himself acknowledges.
Various others have conducted similar studies trying to show brain changes associated with antisocial personality disorder, psychopathy or other traits predisposing to criminality. Chris Frith and colleagues have pulled this evidence together, and have stated that: “New studies on the criminal brain are likely to shape moral views on responsibility and free will with possible impacts on how legal systems punish and treat criminals” (Mobbs et al 2007). But they have added some appropriate words of caution. They say that brain imaging is not mindreading, which it is not. Brain imaging is not a pure science. Many other factors – social, economic, and otherwise – are important as determinants of or contributors to offending. Moreover, there is, of course, a danger that the courts will be over-impressed by brain imaging.
There have been other relevant reviews published recently. For example, Brown and Murphy (2010) wrote a paper called “Through a Scanner Darkly”, in which they said that the probative value of functional MRI to a defendant's mens rea is “extraordinarily low”. Stephen Morse (2011), in a paper called “Lost in Translation: an essay on law and neuroscience”, said that the law is ultimately concerned with mental states, rather than with the neuroscientific causes of mental states. We respond to reasons, including legal rules and standards. The law treats people as “intentional creatures”, not as “mechanical forces of nature”.
But, of course, neuropsychiatry and neuropsychology are already involved in criminal trials at various different stages: fitness to plead, the insanity defence, cases of automatism, which I have already mentioned, diminished responsibility (manslaughter cases), and at sentencing. For example, arguments for “unfit to plead” in a case of brain injury can be corroborated not only by witness statements pertinent to whether the individual can fulfil the Prichard criteria, but also by neuropsychological, neuroimaging (CT, MRI), or neurophysiological (EEG) evidence of the nature and severity of the brain injury.
However, I want also to make the point that those with brain disease and memory impairment can be very vulnerable in court processes. For example, patients with low IQ, poor memory, or poor executive function may be (just about) fit to plead, but very vulnerable to legal and court processes – talking themselves into getting arrested in the first place; vulnerable in the witness box, or having “adverse inferences” drawn if they decline to appear; and/or behaving strangely or inappropriately in court. Patients with absence status epilepticus can be especially vulnerable to having their difficulties underestimated. Patients in absence status epilepticus have been described by Dreifuss (1995) as acting in “a stuporous, confused, dazed manner with little spontaneity and marked perseverations”. Other patients with absence status epilepticus say things like: “My mind slows down … I am able to understand, but it takes me longer to formulate answers.” “I become slow, but can communicate with others.” “I slow down in my behaviour … muddling my words.” “I feel confused, like in a trance, missing bits of information.” “I could hear what the other people were saying, but had to struggle … to find the meaning” (Koutroumanidis 2008).
Conclusions
To sum up, I have said that amnesia for offences arises in cases of automatism, alcohol misuse, and so-called “crimes of passion”. There remains a question about how we define and delineate automatisms; and the only thing to be said, in my view, about the sane/insane distinction is that it is not sane. Amnesia for crimes of passion arises in characteristic circumstances, but this form of amnesia still gives rise to a lot of controversy. False memory in the criminal courts can arise in false confessions, also in child sexual abuse, and just occasionally delusional memory, which I have not discussed. Gisli Gudjonsson (2003) has suggested that false confessions can be analogous to “confabulation” in brain disease. What these false confessions certainly show is that “intention” or “will” can be complex.
What I have said about the courts and brain disease, more generally, is that definite brain disease and cognitive impairment produce vulnerability in court, and that there is a real question about when responsibility is affected. There is still a huge gap between our understanding about the neuropsychology of action and explaining, for example, automatisms. Moreover, many of us would agree that someone with a frontal glioma, or a patient with bilateral frontal resections, might have their criminal responsibility affected. But how much damage do you need to have? What about a small degree of frontal grey matter thinning? This is where future studies involving functional MRI (fMRI) are going to pose a lot of questions. In my view, there is a slippery slope in arguing that all serious offenders have subtle or not-so-subtle brain disease, as Raine (1993) implies. But, as science and brain imaging advance, this issue will increasingly be raised in the courts, i.e. that subtle brain changes affect responsibility and culpability. Neuroscience already exists in the courts, and these issues arise, but they are going to become more prominent. To me, however, a much more important and major issue at the moment is how we get existing clinical science properly represented in the courts – not the clinical science of the future, but already established clinical science. Everything that is happening to Legal Aid, in the NHS, and in our Universities, is going to make this increasingly problematical.
Finally, Ian McEwan (1997) wrote in one of his novels:
“No one could agree on anything. We lived in a mist of half-shared, unreliable perception, and our sense data came warped by a prism of desire and belief, which tilted our memories too. We saw and remembered in our own favour and we persuaded ourselves along the way. Pitiless objectivity, especially about ourselves, was always a doomed social strategy.”
Nowhere is that truer than the law courts.
