Explaining Psychosis

We—meaning doctors, scientists, clinicians, et al.—pride ourselves in knowing about psychosis:

We know its symptomology, which is parsed into positive and negative categories.

We know that antipsychotic medications work fairly well for positive symptoms, but less so for negative symptoms.

We know that each one of these medications interacts with its own specific array of dopamine receptors that crowd the somatic and synaptic membranes of our neurons.

We know that chemical or electrical synapses link individual neurons in order to consolidate their electrical activity.

We know that consciousness emerges from the interplay of diverse functional ensembles of neural activity, which themselves rely on the precarious balance between excitatory and inhibitory neural connections within and among distinct brain locations.

We know that emergent functional network properties rely on physiological processes like neuroplasticity or neurogenesis, which themselves are partly dictated by our genes, and partly dictated by our environment.

We know that a stressful environment, paired with certain vulnerability-enhancing gene variants, will give rise to psychosis.

And yet we have trouble explaining all this to our clients, who, for the purposes of this discussion, are defined as those who—even if they don’t know as we do—are nevertheless prone to experiencing a different type of consciousness, one that may require some explanation.

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The question I’d like to address in this essay is:

Do our clients need to know as we do?

At the risk of ruining any suspense I may have engendered, I’m going to provide the answer up front, which is:

Surely not, because even if they did, they would still need help.

That said, anyone seeking help because they are in the throes of a psychotic episode will hopefully find their way to a specialized service that can provide it. Luckily these services exist, and are flourishing in various locales worldwide. In Montréal, where I live, there are many such services, and one of these, the Prevention and Early Intervention Program for Psychoses (PEPP) has been gracious enough to employ me as a symptom evaluator.

Needless to say, I am writing this essay on the basis of my time with PEPP, where I learnt that a huge part of the help we—and again, I mean doctors, scientists, clinicians, et al.—provide our clients is to enable them to make sense of their experiences, an effort typically referred to as psychoeducation.

As originally conceived in Germany in the 1980s, psychoeducation is meant to provide information that can enable people to better cope with mental illness. The information that’s provided can be anything really, so long as it’s useful; it should impart meaning to experience, and thus bolster our clients’ ability to monitor their thoughts and behaviours.

In other words, psychoeducation should enable insight, which as we know, is almost always vital for recovery from mental illness.

A recent meta-analysis (Schizophrenia Research (2007) 96:232-45) suggests that standard approaches to psychoeducation are only partially effective with respect to psychosis. The study in question yields a twofold conclusion: (i) current psychoeducation methodologies need improvement, and (ii) novel approaches could also be useful.

In line with the latter response, I would like to suggest that we employ a relatively new description of psychosis—that of aberrant salience.

Before continuing however, I am best to address a longstanding criticism of all psychoeducation, and ask whether it’s ethical (or alternatively, useful) to impose a ‘scientific’ framework of experiential mastery on someone who lacks scientific knowledge. Or, simply put, do we—who know so well—have the right to do so?

An obvious answer, which is founded on a Liberal conception of basic human rights, is no, of course not, people should be free to inform themselves about any topic in any way they please.

However, as with all sticky ethical questions, an obvious answer does not and cannot suffice. For example, if an individual’s beliefs (whether delusional or not) enable sociopathic behaviours, then it would be in their best interest (not to mention, society’s) to change them.

But, just who or what will effectuate this change? And, what is the optimum framework to guide this change? The first question is addressed by the various societal institutions that promote law and/or health, which themselves arise from various democratic processes. The second question is a true conundrum, and as such, is best addressed by the full breadth of our intellectual resources.

This essay is meant to promote a framework for psychoeducation that’s rooted in the neuroscientific concept of salience. In line with the above statements, it’s important to qualify this approach as one among many, each with its own merits. To be sure, deciding which approach is the optimum for any given client requires a thorough examination of their psychosocial background, which may or may not accommodate (or rather, embrace) the salience paradigm.

And so, what does it mean to be “salient”? A good place to start, as always, is the Oxford English Dictionary, which tells us that to be salient is to be:

Most noticeable or important; Prominent; Conspicuous.

Within consciousness, the salience of sensory stimuli (sights, sounds, smells, tastes, or textures) emerges from the dynamic interplay of functionally relevant brain loci as they respond to these stimuli in real time. Even though our senses are always active, our attention cannot be split evenly between all five modalities, all of the time. Accordingly, as our senses detect the various stimuli that surround us, the analytic parts of our brain have to determine which of these deserve salience. The implication here is that our brains are constantly and automatically making value judgements about what we should be paying attention to, a mechanism that actually works to our advantage, at least given the vast array of different stimuli we routinely encounter, and their varying levels of utility…

Thus, in the context of psychology, salience refers to our center of attention. In the context of neuroscience, it refers to the neurological processes that focus and/or maintain our attention on one stimulus versus another. In either case, salience is absolutely required to maintain a coherent and adaptive worldview. Accordingly, aberrant salience is now considered a phenomenological hallmark of psychosis, which, after all, involves a profound departure from the “normal” consciousness experienced by most, and more often than not, hinders day-to-day functioning.

Of particular interest to this discussion, recent work in neuroscience has uncovered two complementary and temporally sequential facets of salience that can be aberrant for those who suffer psychosis.

The first facet is proximal salience, which describes the process whereby a stimulus is accorded a place within (or rather, proximal to) your center of attention. In the context of consciousness, proximal salience refers to the here and now of what you experience. For example, when you attend an NHL hockey game, you are bombarded by stimuli, things like: the crowd noise, the aroma of arena food, the lights and text of the flashing screens around you, or the game in front of you. Just which stimuli occupy your center of attention is the result of a very complex and never-ending internal calculus that incorporates many different thought processes. These compete with one another to divert your attention in a normal way, which in the example given above, would mean that your centre of attention typically matches that of others in the crowd. The result: you behave similarly to these others; you cheer when your team triumphs, you go to the concession between periods, or you look around during a stoppage of play. In other words, you experience what it is to be like-minded, which is the criterion of normality, and, generally speaking, engenders the most adaptive behaviours.

Aberrant proximal salience, on the other hand, would likely deflect your attention from these shared experiences in a way that you cannot control. You might end up detecting relatively arbitrary stimuli, or stimuli that falsely derive from your mind. For example, you might end up hearing one voice within the crowd (or, one that’s not within the crowd), you might detect strange patterns in the behaviours of the crowd, or, you might see that the roof of the arena is on fire (or is it?), and miss the goal that was just tallied…

The second facet is motivational salience, which describes the process whereby a proximally salient stimulus is deemed worthy (or not) of goal-directed behaviour. In the context of consciousness, motivational salience refers to the micro-decisions you unconsciously make every instant of every waking hour about which stimuli should occupy your attention. In other words, it’s the instant-to-instant answer to the question: Should I continue paying attention to this stimulus, or should I move on to the next one? For example, if you’re riding the city bus and you notice that a stranger is looking in your direction, and this impression becomes proximal to your attention, it then demands a motivational response. Normally you would take that impression and link it to the simplest explanation based on your previous similar experiences and their affiliated emotional states. For example: That stranger is looking at me… but I always see people looking in my direction, and nothing ever happens, so it probably doesn’t matter. Of course this line of reasoning—being the result of a bewilderingly complex yet stunningly efficient algorithm—is more or less instantaneous, well outside your attention, and, in the example given above, would end with your attention being diverted to another stimulus.

Aberrant motivational salience, on the other hand, would mean the same impression could linger within your centre of attention, which could give your mind the opportunity to link it with ever more idiosyncratic explanations that may or may not be exacerbated by your previous emotions and memories. For example: That stranger is looking at me…could it be that they know me? …if they know me, how do they know me? …are they spying on me? …maybe there’s a conspiracy that’s working against me? …are all these people who are always looking at me part of the illuminati? …if so, does that mean they want to kill me? …should I be afraid of them? This particular stream of motivational reasoning would surely strengthen your attention with respect to the stranger looking at you. After all, if you think someone is out to get you, it’s in your best interest to maintain your awareness of them…

The two facets of salience are thus coupled temporally, where only certain stimuli are selected to enter your center of attention, and are subsequently deemed worthy of maintaining their illustrious position. Normally, a benign stimulus experienced within a benign context serves to rescind motivation and shift your attention. Sometimes however, even “normal” salience can lead to disastrous results (like, for example, if that stranger on the bus is looking at you because they do mean you harm). Such is the unpredictability of life, and the reason why we’ve evolved the capacity for cognition, memory, and emotion, which, in a very general way, can be seen as mutually reinforcing processes that serve to guide salience, and thus engender normal adaptive motivations and/or behaviours.

For we who know, the salience paradigm is reassuring because it aligns itself with phenomenological accounts of psychosis. That’s all well and good, but what about our clients? Is it reassuring to them? Unfortunately, there is a dearth of evidence to answer this question, where no large-scale peer-reviewed study has yet been orchestrated that gauges the efficacy of salience-based psychoeducation.

This lack of evidence is hardly surprising however. The salience paradigm of psychosis is still in its infancy, and has yet to achieve widespread notoriety within scientific circles, let alone the world at large. Hence this essay, whose main goal is to demonstrate that the salience paradigm can be explained using non-technical language, and can thus enable our clients to understand their experiences in a universal (rather than idiosyncratic) way.

And so, how can salience dysregulation come to explain psychosis? A useful model can be derived from analyzing the links between cognition, memory, and emotion, which combine to guide salience. According to this model, which is admittedly quite rudimentary, stimuli are processed in a stepwise process that begins before they become salient, as follows:

  1. Your environmental context spurs your brain to predict which stimuli are likely to follow, given what it already knows about that context.
  2. A stimulus is detected by your senses, i.e. it enters your center of attention, i.e. it becomes salient.
  3. This stimulus is compared to the closest pre-conceived version from step (i), and a “decision” is made as to whether it fits your expectation.
  4. Based on this “decision”, the stimulus is deemed worthy (or not) of continued attention and thus, some form of behaviour.
  5. Because it coincides with your body’s endocrine state, the stimulus will be accorded an emotional valence (which can be negligible).
  6. Because it drives behaviour (or lack thereof), the stimulus updates your memory, which may in turn affect your expectations toward the next stimulus, and thus brings the entire process back to step (i).

Of particular importance to the concept of salience are steps (ii) and (iv), which represent proximal and motivational salience, respectively. Basally, these steps only involve the switch from one stimulus to another, which is precisely what the neuroscientific concept of salience covers. Steps (iii), (v), and (vi) represent cognition, emotion, and memory, respectively. These steps are grossly generalized, seeing as each of them can be subdivided into many overlapping sub processes, but they work for the purposes of this discussion. Step (i), which is not really a step, but rather a pre-step, can be regarded as the mind’s default state, the perpetual starting point for the cyclic process subsequently described.

An even more condensed summary of the above process entails that if a stimulus becomes salient, it should invoke the cognitive analysis that can drive behaviour, whereupon it’s likely to be incorporated into your memory (or rather, the myriad schemas that constitute your memory); if this occurs, the schematized version of the stimulus is also coded with a certain emotional valence, which is also memorized. By this process, any given stimulus can influence a future salience loop derived from a similar stimulus. Accordingly, every turn of the salience cycle has the potential to strengthen memories and thus, reinforce beliefs. If aberrant, these loops can serve to memorize hallucinations (or, misperceptions) and thus, reinforce delusions. After many iterations, this process can lead to a fundamental shift in your way of paying attention, which, it would seem, is a fair description of psychosis.

Accordingly, entering into a psychotic episode reduces your ability to detect this shift in your way of paying attention. While psychotic, you continue to think that everything you experience is actual, and so you rarely question the direction that your thoughts are taking you. In fact, the odds of your being able to achieve this insight are against you, because psychosis also imposes certain cognitive deficits that impinge on your ability to do so. In other words, if you are susceptible to psychosis, it’s very likely that your brain is configured in such a way that makes it difficult for you to notice your susceptibility.

And so, depending on the specific stimuli encountered in any given environment and the way these are processed by your mind, your day-to-day functioning may become compromised, which is especially true if you find yourself in the midst of a psychotic episode. By virtue of this mental illness, you may begin to lose your relationships, your job, your values, your priorities, etc., in favour of more arbitrary, less adaptive versions of these same things. Indeed, if you end up seeking help from a mental health professional this is almost certain to have occurred, because a drop in functioning usually precedes help-seeking behaviour.

This brings us back to our main topic, because an important part of any mental health clinic is the provision of some form of psychoeducation, which, as mentioned above, is meant to facilitate insight, and thus, promote recovery.

Within the clinic, psychoeducation is often geared toward explaining how antipsychotic medications work. This is to be expected because as we know, adherence to these meds is often vital for effective recovery. However, it should also be noted that placing too much emphasis on antipsychotic medications can detract from psychoeducation’s ultimate goal, which is to help people understand their limits, their strengths, or their weaknesses, and how these relate to the here and now of their daily life.

To its immense credit, the salience paradigm of psychoeducation—which attempts to explain certain dopaminergic processes within the brain—facilitates both ends simultaneously. That is to say, just as the salience paradigm can be used to great effect when explaining psychosis, it can also open the door for a meaningful discussion regarding the effects of antipsychotic medications, which target the dopamine systems of the brain.

And so, just how do these medications work within the salience paradigm? As we know, the neurotransmitter dopamine mediates important interactions within and between functionally distinct brain loci, including the basal ganglia/thalamus, the hippocampus/amygdala, and the medial prefrontal cortex, which, very loosely speaking, mediate sensory perception, memory/emotion, and rational cognitive analysis, respectively.

There is an abundance of evidence suggesting that one of dopamine’s more important roles is to help establish an optimum connective balance among these brain loci and their affiliated aspects of the holistic mind, and thus, to mediate salience. Antipsychotic medications are thought to help restore that optimum connective balance, or at least do so in an approximate way, which is why these medications have side effects.

In fact, various studies have implicated dopamine signalling in all six steps of the rudimentary model outlined above, a fact that underscores the very blunt nature of current antipsychotic medications.

Obviously there are many questions of detail that have yet to be resolved, but overall, this picture holds true.

The bottom line: antipsychotic drugs do help people who are recovering from psychotic mental illness. In some cases they can make all the difference, especially when they serve to modify the saliency of false, maladaptive, or irrelevant stimuli, and thus provide the mental space needed to achieve insight.

Understandably, many clients are tempted to dismiss this explanation, especially as it would typically come from someone who has never experienced a psychotic episode nor received antipsychotic medications.

That is the challenge of providing psychoeducation.

However, from my humble perspective, having offered some of the above explanations to people who recently lived their first psychotic episode and who were subsequently treated for it with antipsychotic meds, I can report that they listened to what I had to say, and appeared interested. Certain of these people even acknowledged that our conversations helped them better understand their lived experiences.

It’s clear that my paltry few interactions are a far cry from robust quantitative evidence confirming the same result, but then again, given the insufficiency of current methods, perhaps now is the time to start gathering that data.

After all, just because the salience paradigm of psychoeducation is still too recent to know how well it works, it doesn’t mean we shouldn’t try it.

For any client—or doctor, or scientist, or clinician, etc.—who is open to exploring a robust scientific model that attempts to describe the experience of psychosis, I would say it’s a conspicuous choice.