“He whose eyes happens to look down into the yawning abyss becomes dizzy.”

–Kierkegaard.

This essay will briefly examine the genetic, evolutionary, cognitive (and behavioural), and psychodynamic approaches to the aetiology of panic disorder (PD). Throughout, this essay will attempt to orient the reader to the centrality of bodily experience to any consideration of PD, and will utilise this as a means to sketch a philosophical as well as psychiatric understanding of the disorder. In order to approach this, the body’s relationship to death will be considered, an approach that will be mediated by introducing existential themes from both philosophic and psychological literature. This essay will provide a modest overview of the ground, and serve as the beginning of an attempt to place existing aetiological theory of PD within an understanding of the human being as ontologically vulnerable to the world.

This is not a disinterested essay, and I will not apologise for excluding certain worthwhile and important dimensions of the rise of the experience of and psychiatric responses to panic. To be complete, I would need a more thorough account of technological, social, economic and political upheavals. I think these have been covered pretty thoroughly elsewhere and so for now (but not indefinitely) they won’t be broached at length. Furthermore, this is not a disinterested essay- although it is more academically styled than most of my writing- because I was once in the throes of an undiagnosed panic disorder (my GP providing me with breathing exercises and a few quips about Sartre). When I entered my training in psychiatric nursing, I went in with this experience and a sense that the psychopathology of panic was on the rise. Experiencing panic acutely, I could see manifestations of it and more chronic anxiety all about me in others and in the social fabric itself- nowhere was this more obvious than in the changing architecture and policing of London in the earliest post-9/11 period. Aspects of this essay may be familiar to readers of my other online work. I tend to agree with EM Cioran’s observation that thought is the product of sensation but I disagree that it is a “descent” or a “failure”: rather, thought is so often the obsessive retrieval and retracing of experiences, often archaeological, always a kind of dangerous play or magical ritual. In this way, this essay itself form part of my own therapeutic work: the attempt to articulate the inarticulate.

PD is classified in the DSM-IV-TR (APA 2000) as an anxiety disorder. According to DSM-IV-TR a person can only be diagnosed with panic disorder if she has experienced repeated and unexpected episodes of panic, and that this be accompanied by a period of worry regarding having more panic attacks, possible negative consequences of such attacks, and/or with a marked change to their lifestyle or behaviours related to such attacks (APA 2000). Added to this, the person’s attacks must not be explainable by substance-misuse or physical morbidity (APA 2000). Panic itself is defined through a symptom cluster; the individual must experience four of the following to meet criteria for the experience of panic: shortness of breath, feeling faint, an elevated heart rate or an awareness of a pounding heart, trembling or ‘the shakes’, choking sensations, sweating, nausea or gastric discomfort, numbness or tingling sensations, derealisation, hot flushes or the chills, chest tightness or pain, and finally an intense fear of going insane or imminent death (APA 2000).  The average panic attack is estimated to last somewhere between 10-20 minutes (Rachman and Silva 1996, p.2) and is considered to be a disabling condition that operates both physiologically, cognitively, and, commonly, behaviourally (Bruce and Sanderson 2010, p. 106). Panic attacks themselves may be ‘unexpected, situationally predisposed, or situationally bound’ (Barlow 2002, p. 137); that is, they may have no recognisable trigger or more or less strongly triggered by recognisable cues. PD has a prevalence rate of approximately one in one hundred people across the UK (NHS 2012).

In a seminal study of twins with PD, Torgersen (1983) discovered concordance rates of 31% in monozygotic twins (MZ) as compared to zero concordance in dizygotic (DZ) pairs, whilst Kendler et al. (1993) discovered a concordance rate of 24% in female MZ twins but only 11% in DZ pairs. Findings such as these, corroborated by other twin and family studies (Crowe et al. 1983; Goldstein et al. 1994 and 1997; Maier et al. 1993; Hettema et al. 2001) indicate that any aetiology of PD would be incomplete without addressing the role of genetics and inheritability. Twin studies such as these aid in demarcating genetic components of pathology from environmental ones as MZ twins share 100% of their genetic material, whereas DZ twins share the 50% of genes that any siblings would have inherited (Finn and Smoller 2001, p.131). Concordance is defined as the percentage of twins that both meet given criteria for a disorder (Finn and Smoller 2001, p.131). As such these finding strongly suggest the existence of a genetic component to the development of PD, with Kendler et al. (2001) reporting an estimated ‘liability to panic disorder’ (p.404) of between 30-40%. Despite these findings genes responsible for inherited susceptibility and/or panicogenesis remain ‘undiscovered’ (Maron, Hettema, Shlik 2010, p.695). What these studies establish is that genetics play some role in the development of PD.

Yet genetic psychiatry is not without its critics, and even the genetic evidence that is currently at hand demonstrates only that genes play a role in having a susceptibility to PD. For instance, Torgersen’s seminal 1983 study reporting such high concordance rates reported that concordance via the probandwise method, which many of the other cited studies have used. Probandwise concordance rates involve calculating the proportion of twins affected by a given pathology  by accounting for each twin independently of the other, as opposed to the pairwise concordance measure which merely accounts for the twin-pair singularly (Bentall 2010, p124). As such, Torgersen’s results are inflated by counting some twins more than once; the 30% reported rate thus appears artificially large, even as other genetic researchers regard such a figure as merely suggestive of moderate heritability (Finn and Smoller 2001, p.132). Among the genetic researchers into PD, Kendler (2005) has considered the notion that locating singular or multiple pathogenic genes for psychiatric disorders is a misguided effort, considering the role of genes on the risk of developing psychiatric disorders ‘small, nonspecific, and embedded’ (p.1250) in complex gene-environment interactions. Notably, these considerations do not exclude genetics from the aetiology of PD but merely indicates their modest, but nevertheless valuable, contribution to building such a project.

If PD is to some degree inheritable the natural question is to ask why this would be. Neese (1987; 2002) situates PD within an evolutionary perspective. This perspective views the physical and behavioural symptoms of panic as adaptations designed to promote retreat from life-threatening danger but which is triggered in PD in the absence of such a danger (Neese 1987, p.77S). However, the adaptive advantage that panic confers in the absence of a true threat-situation is absent in Nesse’s argument, and it remains possible that the genes mediating PD also play a strong role in some other more adaptive function that evolution has selected for and as a consequence has been unable to eliminate those mediating irrational panic (McNally 1994, p.204-205).

The evolutionary argument stems from the common flight-or-fight characterisation of PD (Barlow, Brown, and Craske, 1994; American Psychiatric Association, 2000).The panic response, adaptive or otherwise, features intense levels of physiological arousal, currently thought to be triggered by hypothalamic activity and driven by the neurotransmitter norepinephrine and, it is suspected, by low levels of fear-regulating neurotransmitter GABA with the possible support of serotonin, although the latter’s role remains under-theorised (Bennet 2006, p. 186). Gorman et al. (1989; 2000) first put forward a neuroanatomical hypothesis of PD based on reports of the benefits of cognitive-behavioural therapies and pharmacological anxiolytic agents. In this model, which also included considerations of anticipatory anxiety and agoraphobia- a common comorbidity of PD (Barlow 2002; Noyes, et. al. 1986; Craske and Barlow 2008)- panic was identified as mediated by the brainstem. The brainstem sits atop the spinal cord and beneath the limbic system and its functions include regulation of autonomic functions (such as those that produce panic symptoms), as well as attention and alertness, and is the most primordial part of the brain (Rajamanickam 2008, p.141). In Gorman’s (1989; 2000) model of PD it is a miscommunication from more developed brain regions to this primordial system that produces the physiological and behavioural symptoms of the pathology. As Dresler et al (2012) argue in an extensive review of the neuroanatomical and psychological literature since Gorman’s revised 2000 hypothesis, the notion of a ‘fear network’ (p.?) based on that model remains cogent and well evidenced, although that model would require further revision in the light of new findings. In this model PD is caused by the sensitisation of the fear network in response to bodily sensation and environmental stimuli that would not ordinarily be perceived as threatening (Taylor, Cox, and Asmudson 2009, p.137). A dysregulation in the communicative pathways between the brainstem and other brain regions in the network produces an over-activity of the panic response. Interestingly, this neuroanatomical model is profoundly similar to, even giving some biological grounding to, earlier cognitive accounts of PD (Taylor, Cox, and Asmudson 2009, p.138).

The cognitive model of PD was first presented by Clark (1985) as being based on experimental procedures he and colleagues had used to induce panic attacks in those with PD and in non-PD control subjects. In previous studies it was found that hyperventilation (Clark and Hemsley, 1982) and CO2 inhalation (van den Hout and Griez, 1982) could induce panic but that this was dependent on the expectations of the subjects. Clark (1985) proposed a somatic heuristic in which normal anxiety symptoms were subject to ‘catastrophic misinterpretation’ (p.462) by healthy subjects. Clark (1985) provides the example of palpitations being misrecognised as signs of an imminent heart attack (p.463). In Clark’s elegant theory a neutral stimuli (a phobic object or a somatic sensation) is wrongly ascribed as threatening and the resulting apprehension is catastrophically interpreted and thereby accelerated, the process continuing until the experience and extinction of panic (p.462-463). Among the strengths of this theory is its symmetry with the neuroanatomical model, misinterpretation being the result of miscommunication in the fear network, and its sense of embodied cognition (Valera, Thompson, Rouch, 1992; Lakoff and Johnson, 1999; Kaschak et al., 2009) – a mind that is not separable from the body.

Bandura (1988) argued that in contrast to this distorted learning, panic attacks could better be described as problems with self-efficacy. Bandura’s contention was that it was not a learned threat that lies at the heart of panic but people’s own conceptions of their own ability to cope with anxiety, and the pallet of skills they hold to that end, that determines the movement from apprehension to panic (Fava and Morton 2009, p.627). For Bandura, I might perceive an external threat and, based on by assessment of my ability to deal with that threat- which is in turn based on the ways I have handled such threat in the past- I may conclude I am incapable. This model is remarkably similar to that of Beck, Emery, and Greenburg (1985), in which self-efficacy- the individual’s rating of their own coping-performance- is replaced by ‘vulnerability’ and is mediated not just by a perceived threat or ability to cope but also by the individual’s perception of the likelihood of danger and the presence/absence of rescue factors (Casey, Oei, Newcombe 2004, p.532). Casey, Oei, and Newcombe (2004) present a detailed review of evidence for these cognitive models and conclude that each of them are well grounded in empirical testing and clinical treatment, but finds that an approach that combines each of the three aids in plugging theoretical gaps in the other (p,550-551). There is no discussion of genetic-evolutionary inheritance in these theories, although it has already been demonstrated that inevitably plays some part in the development of PD.

At this point it is worth recapping that the aetiology of PD thus far sketched is one that is genetically influenced, mediated by neuroanatomy and neurotransmission in the fear network, a network which is both activated by and accelerates the perception of a threat to the body from the body or the environment which the individual, who is that body, is unable to cope with, rescue themselves from, and which thereby reveals that individual’s vulnerability.

The idea that panic is a response to an awareness of vulnerability has its origins in Freudian psychoanalytic theory (Busch, Milrod, Singer 1999, p.237; Klein, 1981). Freud (1926) identified two modes of anxiety that he labelled signal and traumatic anxiety. Signal anxiety is the means by which the individual is able to observe a potential threat that might result in ‘helplessness’ and which might impair her capacity for ‘self-preservation’ (p.166). In Freud’s understanding panic is the experience of traumatic anxiety conceived of as an ‘excitation…which cannot be dealt with’ (p.81). For Freud psychology is never a matter of abstractions, the ego being ‘first and foremost a body-ego’ (1962, p. 18). More recent psychodynamic theories have tended to emphasise the presence of intra-psychic conflicts (Sweeney and Pine 2004; Shear et al. 1993;), the experience of trauma (Bandelow et al. 2002), and the notion that insecure childhood parental attachment produces a sense of radical insecurity in children at adulthood (Bowlby 1973). What is crucial in Freud’s early conception of PD is that he explicitly links it to the fear of death. Vulnerability in this case is thus rendered ontological, existential; I am constitutionally vulnerable to death and I know that I will die.  While psychoanalysis has been regarded as a pseudo-science (Popper, 1968) Freud was always a scientist first, having trained as a neuroanatomist, and believed that all psychopathology has a genetic as well as environmental component (Kandel 2012, p.621) and the validity of psychoanalytic insights is now being echoed by neuroscientists (Damasio 2012). Yet it is specifically the existential dimension that is most fruitful. Freud and Bowlby share this explicitly, whereas other psychodynamic theorists merely gesture at the figure of vulnerability that Beck highlighted.

In the looming vulnerability theory of anxiety disorders (Riskin 1997) the notion that anxiety has an evolutionary component in threat-avoidance is taken as a physical reality. Riskin (1997, p.687) states that a fear-anxiety response is dependent on spatio-temporal movement, and cites examples of stinging insects, deadlines, illnesses and social failures. These threats loom because they are seen as approaching in time and/or space and are referred to as bodies in motion (Riskin 1997, p.688). In the panic driven individual anxiety becomes a schema, an underlying cognitive system through which the world is viewed (Beck and Emery 1985). This ‘looming cognitive style’ (Riskin, Williams, Joiner 2006, p.785) biases predisposed individuals to heightened vigilance and attention biasing that actively seeks out sources of threat, even in the absence of a clear and present threat. In PD this sense of looming threat is internalised to bodily sensations; palpitations are evidence of a body in motion towards death (Riskin, Williams, Joiner 2006, p.787).

This idea that anxiety is generated by the human consciousness of death is central to the terror management theory (TMT) school of psychology (Greenberg, Pyszczynski, and Solomon 1986). The core of TMT is an awareness of the contingent nature of living and its inevitable (but never domesticated) end in death, and that the same cognitive powers responsible for this grim awareness are marshalled into avoiding a confrontation with mortality (Greenburg et al. 2000; 1986). TMT provides a structure by which we can understand how a cognitive style that emphasises threat, specifically the threat of death, could result in PD. In order to domesticate death-anxiety, which TMT sees as the root of all anxieties, humans construct vast systems of meaning which they call cultures or world-views, and invest heavily in sources of self-esteem (Greenberg et al. 2000, p.207). The individual who develops anxiety is that person who has failed to maintain these identifications. Of particular concern here is the failure of individuals to maintain those meaning systems that ‘help us deny our creatureliness’- for instance, when sex is conceived of as romantic-loving rather than physical-pleasuring activity (Greenburg et al. 2000, p.209). While TMT sounds like another existential philosophy it is a rigorously, empirically validated social psychology (Rosenblatt et al. 1989; Greenberg et al. 1990). This reading of TMT is limited in scope since no literature currently exists from a TMT perspective that deals specifically with TMT. However, studies have shown that people with PD or who experience panic attacks have a higher than average rate of death-anxiety (Furer and Walker 2008; Starcevic et al. 1993; Randall 2001). Death-anxiety and threats to meaningfulness are also at the heart of the work of established clinicians (May 1977; Yalom 1980) and has a rich history in philosophical literature (Kant 1970; Kierkegaard 2008; Heidegger 1962; Sartre 1969; Becker 1975).

That much of the foregoing has focussed on the threat-detection in non-threatening external stimuli as well as bodily stimuli might also be accountable within this nascent perspective. It has already been established that evolutionarily primal brain systems mediate attention and panic via the fear network. This is important because attention, and the information-processing abilities that accompany it, are limited resources (Slagter et al. 2007; Martens et. al. 2006; Marois and Ivanov 2005). This is important as these abilities were evolved to cope with a limited amount of stimuli but the social environment has experienced a ‘semiotic inflation’ (Berardi 2009a, p.159) in which too many signs, symbols, events, in the physical, media, and digital realms scramble for our limited attentional and processing power. For Berardi (2009a, p.180) this results in exhaustion and an over extension of what we consider meaningful that results in the collapse of meaning. At the same time, the body is hyperstimulated in its semiotically rich environment and cannot help but panic in response (Berardi 2009b, p.113). Essentially, overproduction is the new repression; there is only so much stimulation a body can take before the social environment itself becomes panicogenic.

There is no definitive aetiology of PD, and it is a psychopathology that remains caught up in the tiresome nature versus nurture dichotomy that in various guises of a Cartesian dualism that still haunts psychiatry. Instead, this essay presents itself as a modest gesture towards a theory of PD that is not caught up in such ontological dualism but which sees the body and the mind as being non-dichotomous. Such an embodied realist interpretation of PD would have no need to claim either biomedical, psychodynamic, or existential aetiological theories as the definitive theories. That embodiment, death-consciousness and failures of meaning-systems form the crucial nexus of this essay does not detract or seek to compete with existing aetiological theories but wishes to place them into contact with the reality of carnal existence. It is for this reason that a brief consideration of the current social milieu of the human species is used to reveal the overstimulated state that the body finds itself in today. That death is central to my story of PD might be considered a speculative moment, yet it is also a consideration that allows for a plasticity to individual manifestations of panic that does not depart from the scientific contributions to models of PD. If there is a central concept in this sketch of an aetiological theory, it is that PD is first and foremost a disorder of an intensely experienced corporeal vulnerability to the world itself.

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