A (Attach. Arch. Disr.)

Bowlby considered care-eliciting, care-giving, competitive power-seeking and cooperating as derivatives and developmental expressions of the affiliation & bonding archetype. Neurotic illness may occur due to deficient parental care frustrating archetypal anticipations, as maturation proceeds through a sequence of innate expectations which the environment either fulfils or fails to meet.

1.1A (Mod. Malf. Dis. / Attach. Arch. Disr.)

Schore (2002) argues that the predisposition for arousal dysregulation under stress in those with anxiety disorders, results from dysregulation of both central and autonomic nervous system circuits as a result of failure of the attachment & affiliation archetype causing maldevelopment of the right frontal cortex.

B (Rank. Arch. Disr.)

Stevens & Price (2000) suggest "Agonistic Anxiety" may occur when an exaggeration of the normal inner sanction against inappropriately assertive behaviour causes excessive fear that one will suffer defeat in an agonistic encounter.

C (Mating Arch. Disr.)

Stevens & Price (2000) suggest "Hedonistic Anxiety" may be due to an exaggeration of the normal inner sanction against making oneself unattractive.

1.2D (Integ. Malf. Dis. / Threat-Resp. Arch. Disr.)

Stevens & Price (2000) propose the following "neuro-evolutionary" model to explain where treatment modalities are acting within the triune brain (MacLean 1985). Furthermore, they argue that this model may assist clinicians to determine what modality to use in different patients based on the specific aetiology of their anxiety disorder (assuming an "integrative malfunction" is explanatory).

1.1D (Mod. Malf. Dis. / Threat-Resp. Arch. Disr.)

LeDoux (1996) conceptualises the arousal dysregulation that occurs in anxiety disorders to result from dysfunction of the fear module, leading to "phobias, panic attacks & PTSD emerging out of the depths of the unconscious workings of the fear system".

LeDoux suggests that the introduction of an active coping response may reroute processing from the pathway inducing dysfunctional passivity to one controlling successful engagement with the environment. Rather than going to the central nucleus and engaging the passive fear response, the information is sent from the lateral nucleus to the basal nucleus of the amygdala, which does not project to the brainstem but instead to motor circuits in the ventral striatum. By engaging these alternative pathways, passive fear responding is replaced with an active coping strategy. This diversion of information flow away from the central nucleus to the basal nucleus, and the learning that takes place, does not occur if the rat remains passive. It requires that the rat take action. It is "learning by doing," a process in which the success in terminating the conditioned stimulus reinforces the action taken. When the rat shifts from passive to active coping, it is performing the neurological equivalent of "getting on with life" (LeDoux 2001).

LeDoux speculates, in his book The Emotional Brain, that "the struggle between thought and emotion nay ultimately be resolved, not simply by the dominance of neocortical cognitions over emotional systems, but by a more harmonious integration of reason and passion in the brain". He defines psychotherapy as "a process through which our neocortex learns to exercise control over evolutionarily old emotional systems".

3.1D,

3.2D

(By-prod. Sociab. Dis., Defens. Sociab. Dis. / Threat-Resp. Arch. Disr.)

Nesse (1990) and Marks and Nesse (1994) argue that syndromes of pathological fear described by DSM-IV correspond to different exaggerations of normal subtypes of fear

The different subtypes of anxiety disorder and their behavioral characteristics demonstrate a remarkable correspondence to the different kinds of danger that humans are likely to have experienced during the course of evolution e.g. if you have just experienced life-threatening danger, it is adaptive to stay close to home or to go out only with a companion.

An evolutionary approach suggests that the various manifestations of anxiety have been partially differentiated by natural selection into incompletely differentiated subtypes, each designed to cope with a particular kind of threat. If this is correct, it becomes less urgent to ask, for instance, whether social phobia and generalized anxiety disorder are essentially different or essentially the same, as both are overlapping response patterns to somewhat related dangers. (Nesse, 1999)

3.1A,

3.1D

(By-prod. Sociab. Dis, Defens. Sociab. Dis.)

Bracha (2006) argues that "stress and fear circuitry disorders" result from "overconsolidation" of "normal fears", phylogenetically prepotentiated predisposition to acquire instantaneously fears of certain objects or situations that may have once have posed a life threat to early simian ancestors, mate choice related stabilising selection, and gene-culture co-evolution. (See Classification Intro)

Bracha quotes a number of studies that provide empirical support for the evolutionary aetiology for most phobias, including that of Kendler et al 2002, who reports in "The Etiology of Phobias" from over 7,500 twins that their results "are more consistent with non-associative models of phobia acquisition than with traditional etiologic theories involving conditioning or social transmission". They did find two phobias where family environment may have an impact on risk.

3.1A,

3.1D

(By-prod. Sociab. Dis, Defens. Sociab. Dis.)

Akiskal 2002 argues that GAD represents an exaggeration of normal personality disposition. He considers GAD "altruistic anxiety" subserving the survival of one's extended phenotype in a kin selection paradigm. The function of worrying is to protect your kin, to resist relaxing, to avoid being prey to danger. He argues that dependency is important for human cohesion & warns against considering it pathological.

Akiskal suggests the following subtypes of the anxious temperament:

3.1D

Anxious phobic style reflects protection against physical dangers.

3.1D

Anxious sensitive avoidant style reflects protection against threats to the self.

3.1B

Shy phobic individuals stay at the periphery of the group, gaining the advantages of the group but away from the critical eye of the leader.

3.1A

3.1C

Generalised anxious harm-avoidant type - they have an exaggerated sense of protection against danger to kin. They worry about harm befalling their family.

3.1A

3.1C

Phobic anxious temperament are hypersensitive to separation & leaving familiar surroundings; creates a dependence that is necessary for the development of the family.

Social Phobia

?3.1B (Sociab. By-prod. Dis. / Rank. Arch. Disr.)

Nesse (2004) views social phobia as an extreme of social anxiety.

Post Traumatic Stress Disorder (PTSD)

1.1A (Mod. Malf. Dis. / Attach. Arch. Disr.)

Schore (2002) argues that attachment experiences experienced early in life may be particularly important in shaping the individual's pattern of stress responses in later stages of life. Just as disorders of affect regulation may result from maternal deprivation or abuse, & contribute to many mental disorders, including anxiety disorders, mood disorders, borderline personality and antisocial personality disorders, PTSD may be a disorder of fear regulation in individuals made vulnerable by maternal deprivation or abuse.

The arguments favour a model of excessive activation of the threat response neural circuitry in infancy due to environmental failure to provide a safe & secure caretaker environment, when the relevant circuits are being sculpted and pruned by experience. In the last decade, a growing body of neurobiological research on PTSD has uncovered dysfunctional frontal-subcortical systems, and altered functional activity of the orbitofrontal cortex, anterior cingulate and amygdala (Schore 2002).

Schore (2002) argues that PTSD occurs due to trauma-induced excessive pruning of right brain circuits in childhood, causing unopposed amygdala excitability (or over-activation of the fear sub-module).

Schore delineates developmental precursors predisposing to post-traumatic stress disorder. He suggests that disorganised-disoriented insecure attachment, a pattern common in infants abused in the first two years of life, negatively impacts on the developmental trajectory of the right brain, which is dominant for attachment, affect regulation, and stress modulation, thereby setting a template for the coping deficits of both mind and body that characterise PTSD symptomatology.

Schore argues that Bowlby's neurophysiological control system involved in regulating instinctive attachment behaviour is located in the right orbitofrontal area and its cortical and subcortical connections. This system is specialised to show a flexible response in stressful contexts of uncertainty. He goes on to argue that early childhood trauma massively dysregulates and alters the developmental trajectory of the right hemisphere and the orbitofrontal system of the frontal lobes.

The higher regulatory systems of the right hemisphere form extensive reciprocal connections with the limbic and autonomic nervous systems. Both the autonomic and central nervous systems continue to develop postnatally, and the assembly of these limbic-autonomic circuits is directly influenced by the attachment relationship. In this manner, the internalised regulatory capacities of the infant develop in relation to the mother, and thus, as Bowlby suggested, the mother shapes the infant's stress coping systems.

Schore (2002) suggests that the infant post-traumatic stress episodes of hyperarousal and dissociation imprint the template for later childhood, adolescent, and adult post-traumatic stress disorders, all of which show disturbances of autonomic arousal, abnormal catecholaminergic function, neurologic soft signs and dissociation. This would be symptomatically expressed as a cycling between intrusive hypersympathetically driven terrifying flashbacks and traumatic images and parasympathetically driven dissociation, avoidance and numbing. Recent models of PTSD refer to stressor-induced oscillations between traumatic and avoidant states, and cycling between the bi-directional symptoms of emotional re-experiencing and emotional constrictedness (Antelman et al 1997).

Supporting this model is a growing body of research demonstrates orbitofrontal dysfunction in PTSD. The right orbitofrontal system is thought to act as the neural basis by which humans control their instinctive emotional responses through cognitive processes, and the emotional disturbances of PTSD are proposed to have their origins in the inability of the right prefrontal cortex to modulate amygdala functions.

3.2D (Defens. Sociab. Dis. / Threat-Resp. Arch. Disr.)

Also supporting Schore's proposal that attachment experiences experienced early in life may be relevant in shaping the individual's pattern of stress responses in later stages of life, is Kandel's ( 2001) research into the molecular biology of learning & memory. Kandel suggests that the underlying biological substrate of the excessive activation of the threat response archetype is sensitisation, a form of learned fear in which a person or an experimental animal learns to respond strongly to an otherwise neutral stimulus. An excessive activation of the threat response neural circuitry leading to hyperarousal & hypervigilence may result from an individual being sensitised by an aversive stimulus. Kandel provides the example of a person being suddenly exposed to an aversive stimulus, such as a gunshot going off nearby, to explain how a person will be sensitised by the unexpected noise. As a result, that person will be frightened and will now startle to an otherwise innocuous stimulus like a tap on the shoulder. He details the biological underpinnings of this process in the sea slug Aplysia, an animal that can learn to enhance its defensive reflex responses to a variety of subsequent stimuli, even innocuous stimuli, following application of an aversive stimulus to it.

1.1D (Mod. Malf. Dis. / Threat-Resp. Arch. Disr.)

Yehuda (2003) conceptualises PTSD as a failure to switch off activation of the threat response archetype.

She notes that exposure to a traumatic stress results in a fear response, which involves the assessment of the level of danger and then an appropriate behavioural response. Most (94%) trauma survivors have some type (or degree) of PTSD response (Rothbaum et al 1993), which gradually recedes over time in most people (Kessler et al 1995).

PTSD may represent the failure to recover from a universal set of reactions. She argues that failure to contain or control the initial biologic response to stress, due to pre-existing risk factors, leads to a cascade of events resulting in symptoms of hyperarousal, recollection of intrusive events and avoidance of reminders.

Yehuda perceives the development of PTSD as an alternative trajectory to the normative response (Yehuda 2003) and she suggests that the challenge, in the aftermath of a major trauma, is to determine who is at risk of failing to recover.

1.2D (Integ. Malf. Dis. / Threat-Resp. Arch. Disr.)

Derrick Silove (1998) also views PTSD as an 'Over-learnt Survival Response'. He hypothesises that a primitive learning centre in the limbic system rehearses traumatic memories immediately following exposure to trauma, inducing involuntary memories of the novel threat. He postulates that the mechanism developed during an evolutionary phase when there was an absence of sophisticated cognitive mechanisms and automatic learning following a single exposure to a potentially fatal novel threat would have conferred a survival value in the species. Further evolution led to the development of the neocortical pathway to process trauma memories. He suggests that PTSD results from asynchrony between the two phylogenetically distinct pathways in vulnerable individuals under conditions of extreme stress resulting in failure of cortical inhibition to limit the trauma rehearsal generated by the limbic lobe.

2.1D (Environ. Dysreg. Dis. / Threat-Resp. Arch. Disr.)

Silove also suggests that a mismatch between archaic biological mechanisms & novel cues in the modern environment may play a role.

3.2D (Defens. Sociab. Dis. / Threat-Resp. Arch. Disr.)

Chris Cantor (2005) describes PTSD as a 'defense in overdrive'. He argues that slow-footed creatures like apes and humans needed to be less conspicuous than large/fast herd animals and needed to be able to flee to sanctuary when predators lurked. Having fled to a refuge, it would have been advantageous to stay there for a considerable period. Canter suggests that retreating to one's home and becoming very resistant to venturing out would have been adaptive and is thereby a defense in action after being exposed to a life-threatening stressor.

1.1D (Mod. Malf. Dis. / Threat-Resp. Arch. Disr.)

LeDoux (2001) argues that a defective orbitofrontal system operates in PTSD. He postulates that a lack of orbital prefrontal feedback regarding the level of threat causes an imbalance whereby the organism remains in an amygdala-driven defensive response state longer than necessary. The emotional learning persists in the form of memories that seize control of mental life and behaviour. He shows that pathways leading from the central nucleus of the amygdala to the brainstem initiate defensive freezing and associated autonomic and endocrine reactions (LeDoux 2001).

I have classified this model as modular rather than integrative because LeDoux postulates that a defective orbitofrontal module is the source of the hyperactivated (unbalanced) defense rather than the problem lying in the interconnection between the two modules.

1.1D (Mod. Malf. Dis. / Threat-Resp. Arch. Disr.)

Hariri (2000) views the right orbitofrontal system as the neural basis by which humans control their instinctive emotional responses through cognitive processes, and the emotional disturbances of PTSD are proposed to have their origins in the inability of the right prefrontal cortex to modulate amygdala functions.

1.1D (Mod. Malf. Dis. / Threat-Resp. Arch. Disr.)

The hypothesised imbalance between the right frontal cortex & the subcortical limbic lobes ( excessive excitation of the amygdala caused by inadequate opposition by the cortex) in PTSD may also be conceptualised as an imbalance within the Triune brain. (This model was inspired by Stevens & Price (2000)'s Model of Conflict Within the Triune Brain.)

The Blocked Middle Level Losing Model of anger-induced depression purports that persistence of this situation may lead to development of a major depressive disorder.

3.1D

or

3.2D

(By-product or Defens. Sociab. Dis. / Threat-Resp. Arch. Disr.)

PTSD may be conceived as a disorder of "flashbulb" memory. The term "flashbulb memory" was coined by Brown & Kulik (1977) to refer to the vivid recollections that humans may experience of events considered to be of particular significance to the individual or group.

Brown & Kulik reported that the flashbulb effect is marked by extremely vivid and durable images containing a common informational structure and evoked by instances of high surprise and consequentiality, representing a unique type of memory. These memories are described as having a photographic quality, with detail-perfect apparel of contextual information (weather, background music, clothes worn, etc.) pertaining to the time and place where the event was first known. They may evoke emotions similar to the ones felt upon hearing the news. There is also evidence that exposure to flashbulb events evokes recall of similar events (Mahmood 1999).

Sierra & Berrios (1999) suggest that flashbulb memories occur in drug flashbacks, palinopsia (perseveration or recurrence of a visual image after the stimulus has been removed), palinacusis (repetition of sounds after the stimulus has been removed), post-traumatic memories, phobias, panic attacks, obsessional disorder, phantom-limb phenomena and depressive melancholia. All of these experiences share clinical features such as paroxysmal repetition, sensory vividness, a capacity to trigger emotions, dysphoria, and a tendency for the rememberer to shift from the role of actor to that of observer and for the reminiscence to become organised in a stereotyped narrative.

It has been suggested that flashbulb memories are formed by the activity of an ancient brain mechanism evolved to capture emotional and cognitive information relevant to the survival of the individual or group.

The emotional arousal serves to enhance the scope of detail of the memory and the source of arousal is an important determinant of an event's memorability (Libkuman et al 1999).

1.1D

(Mod. Malf. Dis. / Threat-Resp. Arch. Disr.)

Kandel (2001) proposes that the underlying molecular mechanism may be the rapid removal of the family repressors that inhibit the conversion of short to long-term memory storage.

3.1D

(By-prod. Sociab. Dis. / Threat-Resp. Arch. Disr.)

Morgan et al (2001) argued, based on their research, that individual variations in neuroendocrine responses may explain some psychological and behavioural responses to acute stress. These individual differences exist before trauma exposure and may be used to test constructs of stress hardiness and stress vulnerability in humans. This type of distinction may promote the exploration of a “selective fitness” hypothesis in the development of PTSD.