For many years it was believed that psychotic symptoms were discontinuous from `normal’ psychological functioning. This position is becoming increasingly untenable in the light of research evidence that positive psychotic symptoms can be understood with reference to normal psychological processes. This paper will outline the evidence from current psychological conceptualizations that psychotic symptoms are closely related to a person’s psychological functioning and that they are therefore amenable to psychological intervention (Yusupoff et al., 1996). Current psychological conceptualizations of hallucinations and delusions hold that the content of these symptoms contain material which is personally relevant to the individual. Indeed, this personal relevance is critical to the understanding of, and cognitive interventions with psychotic symptoms.
(From An Interacting Cognitive Subsystems Model of Relapse and the Course of Psychosis by Andrew Gumley, Craig A. White and Kevin Power – page 262)
In the previous post I began to outline a picture of the kind of traumatic life experiences which can give rise to psychosis.
There’s more to add to the list of factors.
Many who experience psychosis also, for example, according to Murphy at al (Modelling the co-occurrence of psychosis-like experiences and childhood sexual abuse), have experienced heightened levels of social deprivation, discrimination and isolation even beyond the age of 16. Additionally, members of the group with no history of Childhood Sexual Abuse were more likely to have experienced Childhood Physical Abuse, PTSD, social isolation and neurotic disorder. Interestingly, members of this class were also more likely to be male.
This profile seemed to indicate that, in the absence of Childhood Sexual Abuse, individuals who experienced psychosis were likely to endure a wide range of other traumatic experiences. It seemed that the composition of this class, particularly in terms of sex, suggested that, while psychosis may be a phenomenon highly associated with traumatic experience and adversity, the precise nature of this trauma and adversity may be dependent upon the sex of the individual. The Child Sexual Abuse-only class was more likely to be female and was characterised by elevated probabilities of childhood physical abuse and adult sexual trauma, neurotic disorder and cannabis consumption.
It may be worth spending sometime teasing out the exact level of risk of psychosis represented by trauma.
Longden and Read (The Role of Social Adversity in the Etiology of Psychosis – page 7) focus on two substantial meta-analyses (ie collated data from a number of well validated studies). The first screened 736 articles, retaining 41 of the best designed. When results were pooled, individuals with a history of childhood trauma (child sexual abuse, physical abuse, emotional abuse, neglect, bullying, parental death) were shown to be 2.8 times more likely to develop psychotic symptoms than those who had not. The second meta-analysis retained 25 studies from a search result of 1104, and found that rates of childhood adversity (including child sexual abuse, physical abuse, emotional abuse, neglect, witnessing domestic violence, and loss events) were 3.6 times greater in people diagnosed with schizophrenia relative to “healthy controls.”
It is important that we make sure we are not being misled into attributing cause when we have only correlation. By this I mean that just because, when I am holding my key to either open or lock my front door, the light goes on, I should not jump to the conclusion that my door key is switching the light on. I need to understand that my mere presence with no key is enough to trigger the motion sensor. The key is a confounding variable that needs to be eliminated, for example by leaving the house without locking the door one night. I’d be wise not to go further than strictly necessary to prove the point though.
Longden and Read (pages 7-8) deal extensively with this problem:
Large-scale population studies have shown that associations between adversity and psychotic experience remain significant when controlling for possible confounders, including: family history of psychosis and other mental health problems (which negates the notion that psychosis only occurs in those genetically predisposed), age, sex, ethnicity, marital status, exposure to discrimination, other psychiatric diagnoses, education level, neuroticism, and substance use. Furthermore, the association has repeatedly demonstrated a dose-response relationship; that is, the likelihood of psychosis increases relative to the extent of adversity exposure.
Even this does not end the list of factors (ibid.):
Despite much emphasis on childhood abuse, this is by no means the only environmental adversity associated with psychosis. Other cited factors (Larkin & Morrison, 2006; Read, 2013a; Scott, Chant, Andrews, Martin, & McGrath, 2007) include discrimination, witnessing domestic violence, prenatal stress, war trauma, torture, adulthood rape and physical assault, excessive marijuana use in adolescence (in some instances this may represent attempts to self-medicate posttraumatic symptoms . . . ), and disturbed attachment relationships with one’s caregivers, including abandonment, being the result of an unwanted pregnancy, being raised in institutional care, dysfunctional parenting (often intergenerational), and parental death or separation. Another factor receiving significant attention is poverty and inequality . . .
Longden and Read feel (page 9): ‘that erroneous reports of sexual victimization are no different between patients diagnosed with schizophrenia and the general population,’ so we have as much reason to believe a patient diagnosed with schizophrenia as anyone else, and we have already established in the first post of this sequence that this level of credibility is basically compelling.
Now is the time to return to a closer examination of the role of the brain in all this.
Longden and Read describe what they intimidatingly label (page 12) ‘the traumagenic neurodevelopmental (TN) model of psychosis’ by which they mean how, during our formative years, trauma can affect the brain in ways that make psychosis more likely. They argue that there are similarities between abnormalities in the brains of abused children and those of adult patients with psychosis.
A key point is this: ‘A major premise of the TN model is that the heightened stress sensitivity consistently found in patients with psychosis is not necessarily inherited, but caused by formative exposure to abuse and neglect.’ This is key because it moves the debate away from genes to life experience.
They give various examples of the research including (pages 20-21):
A . . . study with 45 individuals considered at clinical high risk for psychosis found significant positive associations between trauma exposure (psychological and/or physical bullying, emotional neglect, emotional abuse, physical abuse, Childhood Sexual Abuse) and feelings of being watched or followed, as well as false beliefs about power or status. . .
An equally important finding is the relationship between psychotic content and precipitating trauma (ibid.):
Comparable work with 41 patients experiencing a first episode of psychosis found that attributes of stressful events in the year preceding psychosis onset were significantly associated with core themes of both delusions and hallucinations.
Implications for Therapy
How might this realisation help?
Murphy et al (Modelling the co-occurrence of psychosis-like experiences and childhood sexual abuse) feel that:
. . . . identifying and evaluating trauma specificity in the onset and maintenance of psychological distress may aid clinicians and service users alike, in
(1) clarifying sources of distress and
(2) understanding symptom content and expression, while enhancing treatment design and efficacy also.
They emphasise that point that ‘symptoms of psychosis are often characterised by content that can be meaningfully attributed to past personally significant experiences.’
Longden and Read (page 22) feel that their evidence points in this same direction and ‘reinforces a standpoint formed in the earliest days of psychiatry and that has gathered a striking momentum in the past two decades; that it is no longer a scientifically or morally tenable position to view psychosis as a purely biogenetic disease.’
This has clear implications for the approach we should adopt. They remind us that the British Psychological Society ([BPS] Division of Clinical Psychology) recently published a report emphasizing the utility of psychotherapeutic approaches to psychosis. The executive summary opens with the observation that “Hearing voices or feeling paranoid are common experiences which can often be a reaction to trauma, abuse or deprivation. Calling them symptoms of . . . psychosis or schizophrenia is only one way of thinking about them, with advantages and disadvantages” (BPS, 2014, p. 6)
Unfortunately the evidence I find in what I read now suggests that the situation that confronted someone I worked with in the 1990s may not have changed much. She wrote me as follows, after she moved to another city:
Today I saw my new CPN. He’s called D, and I’m feeling very upset as a result of our meeting. I’d be able to give you a ten foot long list of insensitive things he said, if I wanted to! His main objection was that I’m not out there working, earning money and contributing to the country. He said he’s going to phone the DRO tomorrow and get her to come out and see me to assess me for a job. . . . D was also very heavy-handed in his approach to “disability”. He said there’s people much worse off than I am and they’re using their abilities to the benefit of other people. I think one of the worst things that anyone can say to someone who’s got my kind of disability is that there are people worse off than they are. It has to come from the individuals themselves to say that sort of thing. I’ve applied to do a BA at the Open University — D wasn’t even satisfied with that, because it won’t lead to a “practical skill.” He questioned the intensity of my voices, the fact that I’m not sleeping . . . and he also physically tried to stop me rocking. I’m feeling really upset by it all.
[Later] My new CPN is . . . . refreshingly gentle and unassertive, but he’s only here for another couple of weeks. It’s very unsettling all this changing around, because I can’t work consistently with them, and by the time I feel ready to talk in confidence it’s time for them to move on to another post. I think it will be like this for the next six months until the permanent CPN comes back from maternity leave.
Layard and others certainly do not think things have changed for the better. It is an indictment of our society’s approach to mental health that effective treatment for many forms of mental problem is not sufficiently available to meet the need. Writing in 2014, Layard and Clark’s in their book – Thrive – draw this forcefully to our attention. The data the authors use to prove their case include the fact that (page 381):
. . . while over 90% of diabetes sufferers receive treatment for their condition, under a third of adults with diagnosable mental illness do so. This is largely because good evidence-based psychological therapy is not readily available.
If anything things have got worse in the intervening period. The value of talking therapy for psychosis is clearly not sufficiently well recognised to guarantee that it will be funded and, if funded, that it will be safeguarded and prioritised. In the few areas seeking to provide some form of psychological support, Health Care Commissioners, even while knowing that CBT for psychosis should be available in 12 session packages, in itself a minimum requirement, frequently fund only six sessions or less. If this policy were followed for the prescription of antibiotics or the provision of cancer treatment there would be a national outcry.
Part of the reason for this blindness is the still prevailing implicit conviction that psychosis is basically a biological problem and is best treated with drugs not psychotherapy. Hopefully this sequence of posts will go some way to adding momentum to the increasingly powerful wave of dissent from this conveniently short-term cost-saving point of view.
In fact, it doesn’t save any costs at all in the long-term. With even the minimum basic intervention of CBT mounted early enough, sufficient benefits would accrue for enough patients to save the costs of relapse and readmission further down the road.
Beyond this though, in my view, we need more widely effective forms of ‘talking cures’ before we will see really major benefits long-term. But better half a loaf than none at this point.
So, having dealt at some length with the relatively straightforward issue of trauma and psychosis I plan to embark in the next sequence of posts on the trickier issue of thresholds of consciousness and psychosis. Wish me luck!