Psychological Design

Neuroscience of mental illness in the city.

Introduction
The way the brain processes perceptions of the physical environment is of interest in the epidemiology of mental and behavioural health because of recent discoveries that have found that the city—the locus of human endeavours—is one of the most predictable factors of the development of schizophrenia and other psychotic and mood disorders [1, 2]. The ecological model of perception is an excellent model for understanding the relationship between the mental health and the physical environment, because it asserts that perception does not commence a cognitive process, but is part of the way the brain reacts to the demands for action that are intrinsic to objects and forms within the environment. Many studies show that the urban environment adversely affects mental health, with significant increases of incidence of severe anxiety, mood (depression and bipolar disorders), and the psychotic spectrum of disorders (paranoia through to schizophrenia), while other mental illnesses such as addictions don’t appear to change significantly [3]. The negative influence of city life has been previously subdivided into ‘direct’ effects, such as light, ambient temperature, nature, and exposure to pollutants or parasites; and ‘indirect’ effects, such as how the built environment moderates the psycho-social environment by forcing people together, isolating them, and by limiting their access to amenities or exposing them to illicit drugs, and so on [4, 5]. But the distinction between direct and indirect factors appears spurious in the light of the problem which is how the material world can so influence the mind that the brain is often permanently damaged, with no apparent causal pathways to factors such as air or noise pollution, or ambient temperature. In fact, on close analysis, it is the so-called ‘indirect’ factors that appear to have the strongest impact, and perhaps there is none so strong as the urban environment itself, which in the case of schizophrenia accounts for about 30% of incidence, assuming it is a causal factor [2]. This is greater than any single genetic factor, but may be confounded by other suspects, such as the developmental vitamin D deficiency hypothesis [6], which may in itself be a biomarker for the urban environment, because too little vitamin D usually means too little sunlight, and for most people that means too much time indoors [7, 8].1 One of the current hypotheses for the deleterious effect of city life is the Ecological Hypothesis for Schizophrenia, which details a vicious circle around an inability to cope in the face of the demands that the designed environment places of a person’s neural attentional system (see Figure 9.1)[9]. While this is far from obvious to designers who know little about the brain, it may in fact, be far more direct than the so-called ‘direct effects’ mentioned earlier that designers do feel are controllable [10]. Indeed, this hypothesis is based on a theory called ‘direct perception’, a key concept of both the Ecological Theory of

Perception [11] and Mirror Neuron Theory [12]. The strength of this hypothesis is that it links the external world to known neural mechanisms in the brain that are implicated in psychotic mental illness.

Extended brain theory and psychotic symptomatology

People tend to think of the brain as a knowledge-driven, probabilistic cognitive engine—as a mechanism to turn perceptual inputs (colors, sensations, sounds, etc.) into information by predicting and recognizing them as meaningful objects [13]. A hypothetical secondary process generates choice: objects are ordered and acted upon according to needs and preferences. This model of the hermetic, rational, cognitive brain was convenient for the development of functional anatomy for medicine (understanding the effects of stroke, lesions, etc.), but it fails to explain the profound impact of the environment on neural development or why people react so differently to concrete and real jungles; in short, knowledge-driven models of the brain have been very useful but fail to explain how the urban environment may be causal for psychotic mental illness. Over the years, challenges to the traditional brain model like these have led to ideas about a kind of extended mind. In 1979 James J. Gibson published a well- reasoned body of evidence called the Ecological Theory of Perception, which finds how animal behavior is an automatic and direct reaction to ‘affordances’, which are the opportunities for action that are structured into the environment, like shelters, pathways, and seats. Affordances are perceived directly (in other words, the actions that objects enable) and affordances are what stimulate behavior, not the recognition of the object itself [11]. As Gibson put it, ‘ask not what’s inside your head, but what head’s inside of!’ [14]. Remarkably, this affordance/behavior pathway precedes the consideration of raw sense data (qualia), such as colors, shapes, and so on [10], and, furthermore, it is estimated that more than 95% of adult actions and thoughts are not the end result of deliberate cognition and planning, but are precognitive, automatic responses [15].

The actions that are triggered (or are not, if sufficient inhibition occurs) are exactly what the object or setting suggests—a chair says ‘sit’, a path tells us to walk, and so on, but, more alarmingly, a knife instructs us to stab and cut, a cliff says ‘leap’, and a gun says ‘shoot’ [16]. The fact that this action precedes recognition of basic sense information suggests that the impulse to action is possibly even how we actually recognize objects and our own actions. It makes sense: greater awareness and understanding occurs only with greater inhibition [10]. Totally uninhibited actions go unregistered as amnesiac events, and may be identified as symptomatic—perhaps as ‘grossly disorganized behaviors’. If patients report an awareness of these very real ‘commands’ to act (‘the cliff told me to leap’), this may well be considered hallucinatory, especially if the command is misattributed (‘the TV told me to leap off the cliff ’), and any post-hoc justification for these bizarre, uninhibited behaviors could very well read as delusions (I tried to leap off the cliff because it was Lover’s Leap, and I’m a Lover . . . ), so it is a cogent hypothesis that the environment itself is an integral part of the psychotic symptomatology [17]. The initial research about direct perception looked at primal behaviors and animal-like instincts, but, in the human world, the ecological dynamic is more complex: we react not only to opportunities for action, but to learned actions and
even beyond these. We live in a world replete with meanings, which in themselves solicit or inhibit reactions, depending on the nature of meaning and the context. For humans, a symbolic reading of circumstances is every bit as potent in how a basic affordance mediates behavior. Symbolic meanings are not only in communication between people, they are embedded into the fabric of the built environment as ‘behavior settings’: these are environments that either inhibit or suggest affordance-stimulated behaviors—in the way a temple or church suggests quiet contemplation and inhibits the vulgar language that can be heard in places like a sports field [18]. (Note to President Trump: in contrast, people barely speak in a locker room, and thus ‘locker-room talk’ is highly inhibited.)
The extended mind concept has hitherto been understood in neuroscience through the perceptual apparatus [19] and mirror neuron theory—a concept very similar to the Ecological Theory of Perception, except limited to social
interactions. Like Mirror Neuron Theory, the Ecological Theory of Perception must take a step beyond the neurology of the perceptual apparatus (visual cortices, etc). Mirror Neuron Theory has identified harmonic neural networks that are stimulated in response to the actions of others, such as the premotor cortex and perigenual anterior caudal cortex (pACC) [20]. The critical neural structures that are involved in ecological perception have not been so clearly identified but must be similarly prefrontal. We know that the management of real, three dimensional representations in real time (what is called working memory) is handled by the right dorsolateral prefrontal cortex (rDLPFC) [21], although other structures may also be involved. The rDLPFC would not be
needed for well-known (learned of instinctive) representations (which will be managed subcortically—see later in this chapter), but is likely to be essential for all new or obscured ones, because prefrontal involvement is thought to be essential for all new (non-Hebbian) learning [22].

In the extended brain models, cognitive processes are not isolated, internal, and established by willful desires alone, rather they are mediated by the phenomenal context, often in advance of associated cognitive processes. In extended brain models, the brain does not cognize and act on choice, but it reads the contextual environment, and chooses only whether or not to inhibit (and thereby refuse) an experience or opportunity. And even this ability to choose is not always there. In fact, simple life forms have no choices at all, rather the inverse: simple animals like barnacles act on an affordance without any act of choice or cognition, much less the inhibition associated with frontal lobe function that humans have [10]. Even humans with frontal lobe damage show the bizarre symptoms of utilization behavior [23], and in more extreme cases, environmental dependency syndrome, conditions where patients lose personal autonomy and act only in ways that are prescribed by the environment [16]. In
short, the more complex and functional brains are, the less dependence there is on the physical and chemical world for behavioral cues and the more perception and cognition takes place. The extended brain models of perception are still neural, but acknowledge that the phenomenal world triggers event potentials in the brain, and therefore that there is an intrinsic relationship between the perceptual world and the function of the brain. Just as a foundation is to hold up a building, it cannot do so without the ground.
The city’s influence on the brain
This article is not a complete study of the regions involved in perception nor is it a detailed account of the entire extended brain concept. It is an introduction to the parts of the brain we currently recognize as implicated in the epidemiology of mental illness in the city. This means the neurotransmitter
that is most implicated in psychosis (dopamine) and the neural anatomy that
is statistically found to develop differently over a sample from an urban2 context compared with a rural and small-town milieus. It’s important to note that these data are correlational and statistical, which means they are not uniform, but bear out over an average, meaning these differences are not universal in all urban populations; however, they are likely to be more pronounced in some subgroups.

So far, the regions that have been identified have all shown significant grey matter deficits. These are the pACC and the connective tissue of the pACC in males; and the rDLPFC. In contrast, the amygdalae are prone to significantly increased activation in the same circumstances [24, 25]. Physically larger amygdalae have only been reported among bigger or more complex social groupings, which do not necessarily correlate with urban lifestyles [26].
The exploration of the functional roles of these organs goes back about 130 years to the birth of functional neuroscience, and yet findings remain in conclusive because they mostly rely on lesion studies, followed by observations of behavioural change and functional absences [27]. Most studies are of animals (usually caged laboratory rats and rhesus monkeys, but animals do not have the same cognitive functions, nor do they behave similarly to humans, especially in urban vs rural milieus) Lesion studies on humans rely on specific accidental or natural organic insults to the brains of otherwise healthy human subjects and these are rarely studied [27]. Other methodologies are easier, but weaker: currently most ‘in vivo’ studies rely on relevant photos being shown to participants while they pass through massive, scary, and loud magnetic resonance imaging scanners. This process provides images of ‘slices’ of the brain, which are analyzed to identify statistically significant patterns. It is not a perfect science, because all brains are unique at the outset. The result is that we still have to speculate about what various brain regions do, albeit with reasonable information to support our postulations.

One of the areas potentially affected by city life is the pACC. This is a medial gyrus of the anterior caudal cortex (ACC), adjacent to the corpus callosum; a mass of white matter (connective tissue) that carries signals between the two hemispheres of the brain [28]. Like other brain regions, the role of the pACC is not entirely certain, but we know that it is strongly associated with declarative awareness and creativity—it is the oldest part of the frontal lobe (in terms of evolution)—and that the pACC is highly connected to the limbic ‘emotional’ centre of the brain [29–31]. We also know that it appears to mediate an anxiety response in regard to social standing [32]. And, importantly for our purposes, we know that it and the tissue that connects it has a tendency to atrophy with urban life and also with poor self-image, especially in males [25, 32].
The pACC is thought to be a key organ in empathetic processes, possibly to bring (or generate) awareness to feelings of love and social connectedness, not-withstanding that these emotions are generated and observed by distributed and complex processes that are also endocrinal [30, 33]. This hypothesis is sup-
ported by the finding that pACC volumes are relatively diminished in severe psychotic illnesses, which are also associated with damaged social networks and poor emotional expression [34]. When deficient, the pACC fails to bring awareness to positive emotions as it should, possibly because of a dopaminergic process described elsewhere [35]. What this urban deficiency means is that people (especially males) who live in the city are likely to be less aware of a sense of love and connectedness than those in the country. Another area that is frequently found to be relatively small as a result of urban life is the rDLPFC. As mentioned earlier, an area that is thought to hold and manipulate spatial representations (drawn from both current circumstances and from recall) in the ‘working memory’. This is where information is considered, verified, and organized before it’s consciously acted upon [21].

That this area is frequently deficient in urban life is curious, because superficially it appears that city areas have much greater visual complexity than rural areas, and therefore the rDLPFC should be subject to greater growth. But this assumption may be incorrect: three-dimensional representations of space may, in fact, be far more important in rural areas where people often have to tell one tree from another as they change seasonally, or negotiate slopes and tangled organic paths just to find their way around, whereas many cities (including
Mannheim, where these data were gathered) are organized along a grid and are well sign-posted. And while negotiating traffic may well be one of those skills that will improve in the city, this skill will theoretically only really improve rDLPFC mass among chronic jaywalkers! But if the rDLPFC is the organ that processes new affordances, then this atrophy might speak of a failure to recognize new affordances in the ecological context—in other words, it suggests that there is a standardization of responses to a standard set of ecological cues, as
people get stuck in unchanging routines. In addition, the deficiency may speak of more time spent indoors in the city, perhaps in front of the TV, where the spatial information is that is provided is not complex, and affords the viewer no opportunities to act at all.

And although we cannot make strong assertions about why the rDLPFC atrophies with city life, the ability to maintain and assess spatial information is undeniably critical to normal activities of daily living. The atrophy may mean people find it hard to cope with the ‘real world’, and the increased responsibility that comes with adulthood once people step outside the spaces they know well. Bucking the trend of decreased activation and volumetric shrinkage, the amygdalae of city folk are subject to significantly increased activation [24]. There are two amygdalae: one in either hemisphere of the brain, where they are nestled into the hippocampi (again, there are two). A significant function of the hippocampi is to recognize emergent stories that are being presented by the environment, to identify both positive and negative scenarios before they even occur. The evolutionary advantage of this process compensates for the slowness of the frontal cortex, making sure a person is able to make the most of emergent circumstances or to pre-empt disaster and organize escape [36]. One of the speculative purposes of the amygdalae within these couplings are to identify an event’s relative importance to ‘me’ [37].3

When an event directly concerns ‘me’, one of the amygdalae will signal this to draw attention to the salient event, but if the event is of no concern, the amygdalae will not signal. Thus, rats with bilateral amygdala damage show no fear of cats [38], and humans fail to care about aversive imagery [39]. There are two hippocampi/amygdala couplings because where the left brain tends to be used for immediate concerns, the right is used for broader narratives [40]. This separation allows awareness that things which appear to be good may in fact be bad—like bait in a trap, for instance [36].

Excessive amygdala activity may then mean inappropriate or excessive attribution of self-involvement within a given context. And if there is no particular social context, this over-identification may be a symptom only too common in psychotic and anxiety illness spectrums: therapists know only too well the self-centred demands of patients. Even patients who have a severely reduced sense of self often identify relevance for themselves in stimuli that could not possibly concern them—such as the conversations of strangers or TV broadcasts [41]. This kind of inappropriate identification is a feature of paranoia [42]. For most people, the increased paranoia and excessive identification that we find in an urban context is unsurprising despite a paucity of knowledge about this connection. But what people do find surprising is just how significant this impact is, especially when the urban context is particularly loaded with the subtle negative messages that we read into the hustlers, traffic dangers, obnoxious people, fumes, and demands for payment that converge in the city. What is remarkable is that statistically high significance is noted on a battery of measures for anxiety, paranoia, and other psychiatric symptoms after very small doses (10 minutes) of urban exposure [43]. The Ecological Hypothesis for Schizophrenia (which relies on Extended Brain Theory) provides a compelling reason for these findings: all messages— whether symbolic, explicit (perhaps written), or ecological (such as traffic)—are triggers for affordance-stimulated behaviours, and in urban environments, these messages are ubiquitous, meaning that people effectively go about much of their business on autopilot. What is worse is they are often negative—and need constant inhibiting: demands to spend money they do not have, or leap in front of subway trains [9].The influence of affect—that is the positive or negative feelings about circumstances (be they architectural or social)—cannot be underplayed in this dynamic because feelings change the nature of reactions in a way that really separate those with mental disorders and those who do not. Reactions can be extreme at one end of the psychotic spectrum and of no consequence at the ‘healthy’ end, depending on the emotional quality of perceived circumstances and how much these impulses are inhibited. Whereas healthy controls are nonplussed by negative imagery (if it poses no real threat), matched cohorts of people with schizophrenia or bipolar disorder are extremely reactive—and the excessive neural excitation expresses as a range of psychiatric symptoms, including thought insertion and disorganized thought and behaviour. The in-verse is less extreme, but still highly significant; whereas the group with psychiatric diagnoses will overinhibit their reactions to positive imagery, the healthy controls will not, instead allowing a laugh or smile [44]. The amygdala/hippo campus couplings are pivotal to this process, because perspectives on what’s ‘good’ or ‘bad’ depend entirely on the narrative context and the perspective of the protagonist.
Beyond this ‘switching effect’, the amygdala/hippocampus couplings mediate the type of attention that is given to reactive actions by stimulating one of two dopamine pathways; the anterior pathway, which is rich with D1 dopamine receptors, is thought to draw declarative (highly aware) attention to deeply considered tasks (the attention used to ‘figure things out’). However, the D2 receptors that are more common in the striatum appear to trigger only latent awareness of a kind that is used for either instinctive tasks (like jumping out of the way of a car) or well-learned tasks (like driving a car) [35, 45]. In the ecological hypothesis for schizophrenia, excitation that is not inhibited turns to action, with the connections to the motor cortex, premotor cortex, and other regions determining the kind of action that eventually takes place.

Affect also determines the quality of attention that is given to these circumstances: if the stimulus is generally positive, actions will be guided, in part, by the latent awareness of the D2 receptors in the striatum and, in part, by the declaratively aware prefrontal areas of the brain, meaning that (in balance) some low level of declarative awareness is maintained. But if the stimulus is wholly negative, actions will be mostly striatal and therefore amnesiac [17, 44].
This is important because it explains why the psychiatric symptoms that are associated with unwanted actions are effectively treated by blocking the striatal D2 dopamine receptors—the central action of most effective antipsychotic medications [46].
Psychotic illness and city life

Recent findings that the urban environment correlates with an increased incidence of psychosis is echoed by further findings that the urban environment causes dose-dependent deficits in several neural regions, all of which are implicated in psychotic illness: the pACC, which is used to understand social interactions in a positive way; the amygdalae, which modulate the sense of our own involvement in circumstance; and in the organs we use to process complex spatial information and possibly even how we behave in relation to the affordances that the ecological environment offers us (rDLPFC). Taken together, these studies suggest the urban environment is causal for psychotic illness.
The correlation between psychotic illness and city life has been noted since the 1930s [5], but whereas it is usually thought that the city is a crucible for causal factors like social stress, poverty, and access to drugs, it seems the city (as a whole) has a more compelling relationship with psychosis than any of these individual factors when taken separately. All objects that have human purpose stimulate human action, but nowhere are these objects more ubiquitous than in cities. But whereas in rural areas these demands are possibly more varied and complex, in the city they may become more routine. This shift appears to be borne out in the neuroscience of the city—with the atrophy of the rDLPFC. In classical theory, the striatum is where learned routines and instincts are managed, while the prefrontal areas, including the rDLPFC, are used for processing novelty, and conscious consideration and meaning. Therefore, this atrophy may trace a difference in the quality of awareness of city dwellers versus those in rural areas—from a generalized alertness to the kind of dim awareness. The hypothetical actions of the deficient neural areas appear to correlate well with the very symptoms of psychosis and mood disorders, with the absences of the rDLPFC function easily explaining hallucinatory, delusional, and disorganized symptoms; the deficiencies of the pACC correlating well to diminished social networks, poor communication (disorganized speech), and low self-esteem; and the overactive amygdalae almost certainly relating to paranoid association and the distinctive ego-centric appearance of mania and some other presentations of depression.
Designing cities—and getting them right
That designers are generally unaware of the effects that their inventions have on the brain, and therefore take no responsibility of this role is deeply worrying. The world of design is like a highway, where each and every driver is asleep at the wheel [1]. Cities are designed by people for people. Every affordance is intended to trigger responses, and not always desirable ones—affordances that dangle, like bait, with expensive bills attached, affordances that come with barbs, caveats, and compromises. Designers should be very careful about how these action-triggers

Urbanization and processes

affect mental health. In contrast, most urban environments have a paucity of
positive, delightful affordances—ones with no strings attached, which are just
there to improve the environment and encourage a love of life. Designers also
should attempt to create new languages for urban design, just for variation, to
keep the humdrum away. These urban affordances should carefully consider
interpersonal relationships—perhaps putting strangers side by side for joyful
experiences. And the city should genuinely be about each and every individual;
in the spirit of human-centred design, to associate those amygdaloid signals
with joy, positivity, and companionship.
References
1. Golembiewski J. The designed environment and how it affects brain morphology and
mental health. HERD 2016; 9: 161–171.
2. Krabbendam L, van Os J. Schizophrenia and urbanicity: a major environmental
influence—conditional on genetic risk. Schizophrenia Bulletin 2005; 31: 795.
3. Peen J, Schoevers RA, Beekman AT, Dekker J. The current status of urban-rural
differences in psychiatric disorders. Acta Psychiatrica Scandinavica 2010; 121: 84–93.
4. Evans GW. The built environment and mental health. Journal of Urban Health 2003;
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Schizophrenia and Other Psychoses. Oxford: University of Chicago Press, 1939.
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Urbanization and processes

affect mental health. In contrast, most urban environments have a paucity of
positive, delightful affordances—ones with no strings attached, which are just
there to improve the environment and encourage a love of life. Designers also
should attempt to create new languages for urban design, just for variation, to
keep the humdrum away. These urban affordances should carefully consider
interpersonal relationships—perhaps putting strangers side by side for joyful
experiences. And the city should genuinely be about each and every individual;
in the spirit of human-centred design, to associate those amygdaloid signals
with joy, positivity, and companionship.
References
1. Golembiewski J. The designed environment and how it affects brain morphology and
mental health. HERD 2016; 9: 161–171.
2. Krabbendam L, van Os J. Schizophrenia and urbanicity: a major environmental
influence—conditional on genetic risk. Schizophrenia Bulletin 2005; 31: 795.
3. Peen J, Schoevers RA, Beekman AT, Dekker J. The current status of urban-rural
differences in psychiatric disorders. Acta Psychiatrica Scandinavica 2010; 121: 84–93.
4. Evans GW. The built environment and mental health. Journal of Urban Health 2003;
80: 536–555.
5. Faris REL, Dunham HW. Mental Disorders in Urban Areas: An Ecological Study of
Schizophrenia and Other Psychoses. Oxford: University of Chicago Press, 1939.
6. McGrath JJ, Eyles DW, Pedersen CB, Anderson C, Ko P, Burne TH, et al. Neonatal
vitamin D status and risk of schizophrenia: a population based case-control study.
Archives of General Psychiatry 2010; 67: 889–894.
7. Golembiewski J. Are diverse factors proxies for architectural influences? A case for
architecture in the aetiology of schizophrenia. Curēus 2013; 5: e106.
8. Eyles DW, Feron F, Cui X, Kesby JP, Harms LH, Ko P, et al. Developmental vitamin
D deficiency causes abnormal brain development. Psychoneuroendocrinology 2009;
34: S247–S257.
9. Golembiewski J. Architecture, the urban environment and severe psychosis. Part
I: aetiology. Journal of Urban Design and Mental Health 2017; 2: 1.
10. Bargh JA, Dijksterhuis A. The perception-behavior expressway: automatic effects of
social perception on social behavior. Advances in Experimental Social Psychology 2001;
33: 1–40.
11. Gibson JJ. The Ecological Approach to Visual Perception. Boston, MA: Houghton Mifflin
Company, 1979.
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science. The Behavioral and Brain Sciences 2013; 36: 181–204.
14. Mace W. James J. Gibson’s strategy for perceiving: ask not what’s inside your head,
but what your head’s inside of. In: RE Shaw, J Bransford (eds) Perceiving, Acting, and
Knowing. Mahwah, NJ: Earlbaum, 1977, pp. 43–66.

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