Psychosis: An experiential resolution & understanding of first episode psychosis

ABSTRACT: With 34 years of lived experience I present an experiential understanding of

psychosis, as an adaptive psychosomatic process. Enabled by developing a sensate (Levine,
2010) awareness of hidden regulatory processes. (Schore, 2003) Specifically, the role of
visceral state and visceral afferent feedback on the global functioning of the brain, (Porges,
2011) during episodes of affective psychosis. (McGorry et al, 2012) Enabling a psychophysiological understanding of the bidirectional influences between peripheral physiological
state and the brain circuits related to affective processes, (Porges, 2011) during my first
episode psychosis.
Keywords: psychosis, first episode, phylogenetic perspective, assessment, diagnosis
In 2007, after twenty seven years of medicating my bipolar type 1 disorder mood swings,
doing my best to avoid the delusional highs of mania, the despairing desolation of clinical
depression, and the powerful escape impulse of suicidal ideation. I found myself confronting
the depth of my own self-ignorance about my internal structure and function, in a need to
improve my capacity for self-regulation. After almost three decades of experiencing affective
psychoses, whether on or off antipsychotic medications, I have not used any form of
medication since late 2007, after stumbling on Allan N Schores book: Affect Dysregulation &
Disorders of the Self, and noticing the constant references to the autonomic nervous system
and its role in psychiatric disorders. Schores book triggered a seven year experiential research
effort which has been conducted in the spirit of "everyone is right in some way," it is merely a
matter of knowing "how." (Reich, 1973) With a particular focus on how my birth trauma
experience and my phylogenetic predisposition to intense arousal dysregulation, (Schore,
2003) combining a stress/vulnerability model, highlighting the interaction between biological
predisposition and environmental influences, (McGorry, et al, 2012) with phylogenetic model
of threat vulnerability. A model of nervous dis-ease acknowledging a biomedical model of brain
disease, which postulates how neural mechanisms are accepted as underlying mental
disorder. (McGorry et al, 2012) While this polyvagal perspective (Porges, 2006) on nervous
system dysregulation and three neural circuits that regulate reactivity, (Porges, 2004)
suggests a natural nervous dis-ease of non-pathologic causation. With my education into
nervous system structure and function enabling me to gain a physiological awareness of
primary process emotional/affective states, (Panksepp, 2004) and a psychological
understanding: that physiological states support different classes of behavior. (Porges, 2006)
With this phylogenetic perspective bringing an internal sense of how, "everyone is right in
some way," it is merely a matter of knowing "how." (Reich, 1973) Hence, through the
development of an increasing capacity for introception, (Schore, 2003) I gained a psychophysiological awareness of how my social engagement system (Porges, 2011) is vulnerable
to threat and affect dysregulation, (Schore, 2003) after being primed by early life traumatic

experience. With my improved self-regulation resulting from an experiential integration of this

phylogenetic model of organism function, enabling me to understand how the mis-attuning
social environment that triggers an intense arousal dysregulation, (Schore, 2003) does so
through a nervous system neuroception, (Porges, 2004) of both my internal environment and
the external environment:
The model emphasizes phylogeny as an organizing principle and includes the following
points: (1) there are well defined neural circuits to support social engagement behaviors
and the defensive strategies of fight, flight, and freeze, (2) these neural circuits form a
phylogenetically organized hierarchy, (3) without being dependent on conscious
awareness the nervous system evaluates risk in the environment (i.e., neuroception)
and regulates visceral state to support the expression of adaptive behavior to match a
neuroception of safety, danger, or life threat. (Porges, 2004)
Thus, after almost three decades of chronic treatment resistance to presumptions of disease,
knowledge about the internal structure and function of my nervous system, has enabled a
resolution of a profound nervous dis-ease. With an experience dependent integration of the
polyvagal theory (Porges, 2011) resolving the habituated muscular/vascular tension and
pressure of a trauma entrained, internalized sense of life threat. With my experiential
integration of relevant knowledge and progressive resolution, requiring sensate (Levine,
2010) awareness methods of discharging the nervous, sympathetic tone of muscular tension
and vascular pressure, created by unresolved traumatic experience. In raising my level of selfawareness about the non-conscious, self-protective activity of my autonomic nervous system,
a psychological sense of stress vulnerability has been transformed into a psychophysiological
sense of threat vulnerability, coherent with my evolved nature. With an understanding of how
the intense pain and fear-terror (Tomkins, 1995) of my birth trauma, became contained by
an autonomic splitting (Carrol, 2001) within my nervous system. A non-conscious process
explained thus: One way in which the body protects itself from emotional intensity is the
development of chronic muscular tension, which dampens down both external and internal
stimuli. (Carroll, 2001) A self-defensive orientation which prior to my first episode of
psychosis, was habituated to the point of being unnoticed. With a non-conscious split between
feeling and cognition becoming understood as the loss of my: Infants Sixth Sense: Awareness
and Regulation of Bodily Processes, (Porges, 2011) or introception. (Schore, 2003) With this
trauma induced loss of a subconscious capacity for self-regulation (Schore, 2012) resolved
by developing an embodied awareness of how: Muscle tension creates a buffer, which reduces
anxiety but at a cost a loss of contact with oneself and others. It can be a negative loop that
leads to loss of self-regulation. (Carrol, 2001) An embodied awareness which explained the
profound split in my capacity for high cognitive function with a simultaneous problem of Affect
Regulation & the Origins of the Self, (Schore, 1994) because I was unknowingly lost to myself,
through a psycho-physiological (Porges, 2011) split in my self-awareness.

My First Episode Psychosis & Nervous System Dysregulation

The long journey towards this articulation of my lived-experience, has culminated in a
hierarchical, thermodynamic, dysregulation model of psychosis. A model which brings a
phylogenetic context to a Traumagenic Neurodevelopmental Model, (Read et al, 2001) of
psychosis, and the widely held view of underlying neural mechanisms involved in psychotic
experience. A phylogenetic perspective which also brings a sense of how everyone is right in
some way," it is merely a matter of knowing "how," (Reich, 1973) in my opinion. While the
sudden shift in physiological state which precipitated my first episode psychosis, involved three
neural circuits that regulate reactivity consistent with the Jacksonian principle of dissolution.
(Porges, 1995) A dissolution/dysregulation perspective of how, in February 1980 a sudden
attachment loss triggered my first episode of mania and set me off on a three decade long
struggle to understand the hidden nature of my affective states of consciousness. Although at
that time, like normal people everywhere, I had no knowledge or awareness of my internal
structure and function, to understand and accept my immediate experience. No knowledge of
nervous system function to understand how that spontaneous shift in physiological state, was
an innate resolution of my trauma entrained, avoidance orientation to environmental
challenge. The sudden dissolution of "three principal defense strategiesfight, flight, and
freeze," (Porges, 2004) and the muscular, vascular constriction of an internalized life threat,
precipitated by attachment loss and the need to face the challenge of existential isolation. A
nervous system reaction to an existential crisis, that may be considered natures way of
setting things right. (Perry, 1998) Although it would be decades before a determined selfeducation drive, would bring me knowledge of the phylogenetic nature of my autonomic
nervous system, and the Jacksonian principle of dissolution:
Jackson proposed that in the brain, higher (ie, phylogenetically newer) neural circuits
inhibit lower (ie, phylogenetically older) neural circuits and when the higher are
suddenly rendered functionless, the lower rise in activity. Although Jackson proposed
dissolution to explain changes in brain function due to damage and illness, the polyvagal
theory proposes a similar phylogenetically ordered hierarchical model to describe the
sequence of autonomic response strategies to challenges. (Porges, 1995)
Knowledge which allowed me to understand my inherent threat vulnerability and nervous
system dysregulation during life challenges, and the paradox of cognitive processes which can
actively thwart autonomic nervous system activity, and an innate healing response to
traumatic experience. While an experiential integration of the polyvagal theory allowed an
experience dependent healing response to unfold, despite decades of treatment resistance and
chronic mental illness experience. Thus by developing sensation awareness of normally nonconscious and socially denied autonomic processes, my lived-experience resonates with an

eloquent articulation of how the human animal is a unique being endowed with an
instinctual capacity to heal, as well as an intellectual spirit to harness this innate capacity.
(Levine, 1997) Hence, understanding, on a visceral level, the orienting activity of my nervous
system was crucial to my trans-formative psychoses and a psycho-physiological understanding
of what happened (Dillon, 2013) to me in 1980. Particularly how my original diagnosis of
schizophrenia, reflects an understanding that: Schizophrenia is a chronic terror syndrome.
(Karon, 2008) With an embodied understanding of how it was an attempted resolution of early
life traumatic experience, subsequently self-stimulated (Panksepp, 1998) into delusional
mania, through a lack of self-knowledge and embodied awareness. Particularly knowledge of
my vagal system and my innate response to the experience of trauma, described by professor
Stephen Porges:
Trauma is normally associated with unsuccessful attempts to get away. When we cant
get away, we cant use fight/flight; we resort to our most primitive neural circuit, and
that, functionally, is a shutdown circuit. That shutdown circuit is also vagal, but its the
old vagus; its the vagus that we share with reptiles, like turtles. When this circuit goes,
we just reduce our cardiac output and we reduce our mobilization. Again, one of the
critical things that we find when we talk to clients who have experienced trauma is this
immobilization feature. (Buczynski, Porges, 2013)
With my improving awareness of this immobilization feature of my autonomic nervous
system, explaining the existential paradox of my life-long quest to feel secure, and the relative
isolation need that followed a negative experience of attachment, early in my life. The birth
trauma of a protracted and brutal delivery, plus the subsequent life experience of being a
unwanted child. Meant that life was dominated by relative existential isolation, resulting in a
self-protective cardiac orienting response (Porges, 1995) to experiential challenge. An
experience dependent habituation of heart-brain communication, mediated by three neural
circuits that regulate reactivity, in response to a neuroception of "whether situations or people
are safe, dangerous, or life threatening. Because of our heritage as a species, neuroception
takes place in primitive parts of the brain, without our conscious awareness." (Porges, 2004)
The too defensive orientation to life, which was my premorbid, (McGorry et al, 2012)
prepsychotic personality (Perry, 1998) prior to that spontaneous switch in the: Three Neural
Circuits That Regulate Reactivity, (Porges, 2004) in 1980. A sudden switch which entrained a
sustained experience of positive affect, in an implicit need of an expansion of the affect
array. (Schore, 2003) With my subsequent self-nurturing, self-stimulation (Panksepp, 1998)
into euphoric mania, reflecting a lack of self-knowledge, self-awareness and selfdifferentiation:
I sat looking into the mirror, yearning for a new direction, something I could feed with a
sense of dedication. I prayed sincerely, promising I'd do whatever was required if hed

just show me the way, give me a sign, help me please! Nothing happened for what felt
like minutes as I sat there in hopeful expectation while looking at my own reflection,
looking into my face. Then it began, a new sensation, a feeling at the top of my head
which flowed down slowly, down through my face, into my shoulders and down through
my chest, down into my pelvic area. I sat with a sense of "what is it wonder, although
more felt than in any thinking sense. A sense of wonder that was similar to the out of
body experience when I was fourteen, except this slowly descending calm was the polar
opposite of the sudden sharp elevation, when I'd seemly left my body. It felt like I'd
been sitting in a bath of water that was over my head and someone had pulled the plug.
I sat there as calm descended slowly from head to toe, as if a mind numbing tension
were being drained out of me, like waste water flowing down and out through my toes.
Next came a mindful realisation of the experience in a pleasant and very welcomed
surprise. I felt unburdened somehow, refreshed and excited, happy and new. (Bates,
2012)
Hence, the hierarchical switch in neural circuits that regulate the autonomic reactivity of my
internal environment, was mediated by a non-conscious neurorception of safety, as I sat
looking into a mirror at my own face, while simultaneously aware of a more complete image
of the external environment. With the spontaneous dissolution/dysregulation action of the
"three principal defense strategiesfight, flight, and freeze," (Porges, 2004) suddenly
dissolving the muscular/vascular constriction of an internalized life threat, through a
spontaneous rise in the activity of my integrated social engagement system. (Porges 2001)
Bringing a middle path psychophysiological perspective to how: heightened vulnerability to
stress is not, as often wrongly assumed, necessarily genetically inherited, but can be acquired
via adverse life events, (Read et al, 2008) Which in my case was early life experience,
whereby my pre-wired social engagement system was restricted by the loss of the vital
proximity (Porges, 2011) of a:
Mothers right cortex as a template for the imprinting, the hard wiring of circuits in his
own right cortex that will come to mediate his expanding cognitive-affective capacities
to adaptively attend to, appraise, and regulate variations in both external and internal
information. It is important to note that these dyadically synchronized affectively
charged transactions elicit high levels of metabolic energy for the tuning of developing
right-brain circuits involved in processing socioemotional information. Psychobiologists
emphasize the importance of hidden regulatory processes by which the caregivers
more mature and differentiated nervous system regulates the infants open immature,
internal homeostatic systems. (Schore, 2003)
Hence my life-long dichotomy of fear and avoidance stemmed from an habituated internal
constriction, which actively depressed my social engagement system. With my spontaneous

episodes of affective psychoses understandable in a neural mechanism context of how: the

system is capable of dampening activation of the sympathetic nervous system and HPA-axis
activity. By calming the viscera and regulating facial muscles, this system enables and
promotes positive social interactions in safe contexts. (Porges, 2011) While my articulation
here seeks to contribute to a widely held view that: Any meaningful theory about how early
abuse or trauma leads, years later, to psychotic symptoms must integrate biological and
psychological paradigms. A number of theories have been developed. At the psychological level
of analysis the focus has been on cognitive and attributional processes, dissociation and, to
lesser extent, attachment theory. At the biological level the focus has been the recently
discovered neurodevelopmental effects of trauma on childrens brains, particularly damage to
the stress regulation mechanisms in the hypothalamicpituitaryadrenal (HPA) axis. (Read et
al, 2005) With my resolution experience bringing the evolved nature of the body and its
constant feedback signals to the brain, into conflict with a treatment oriented focus on the
brain alone, as a cultural, affect-regulating denial of the instinctive nature of the human body.
A general cognitive denial which, in my opinion, prefers to categorise a continuum of human
experience into labels like schizophrenia, probably because: What makes both professionals
and the general public alike uncomfortable with schizophrenic people is not so much their
difference from us, but their similarity. We do not want to know what they have to teach us
about the human condition (Deikman, 1971). (Karon, 1992) While my experience dependant
resolution took place over a three year period, reflecting the habituated nature of our everyday
behavioural function. Described as a practising period (Schore, 2003) of behavioural
development, through imitation of others, in the first three years of life. With my embodied
awareness of the traumatic wound, which so constrained my own behavioural development
and my self-regulation needs, is explained through a body-mind understanding of autonomic
nervous system activity, and the hidden nature of a split in human cognition and feeling:
We need to recognise that self-regulation in the widest sense (including its
autonomic/emotional aspects) is intrinsically bound up with complex neural and
chemical motor-sensory feedforward and feedback loops. When we use our muscles, for
example, theres not just an instruction from the brain, but feedback from
proprioceptors in the muscles and joints which monitor changes in tension, the speed of
change, changes of pressure in the tissue, the position of joints in relation to each other
etc. Although largely outside awareness the proprioceptors provide a dense, dynamic 3d map of the body in space and in action. Similarly there are interoceptors in the
organs, complex chemical connections between all parts of the body which relay a
constantly updated picture of whats happening in the body.
The Autonomic Nervous System and the Somatic Nervous System: the muscular
system are regulated by sensory-motor loops. The sensory input to the ANS concerns
the exact nature of visceral activity, blood composition etc; the motor output actively

modifies the organs, muscles, blood vessels etc. The pioneering neurologist Antonio
Damasio has emphasised that the brain is dependent on the body for self-knowledge.
Rather than language being the necessary feature of self-knowledge, it is the critical
multiple feedback loops which inform the brain about activity in the body, which
constitutes the basis of all self-knowledge. He argues that the emergent properties of
complex activity in the body are emotional states. Feeling feelings allows us to make
sense of our environment and act appropriately. (Note: self-knowledge is distinct from
self-consciousness [the capacity to reflect on oneself]. Self-knowledge supports
appropriate actions in a survival context, and provides the basis for more sophisticated
reflective activity.)
Putting together some of the implications from Schores and Damasios work, I would
say that when the containing function of relationship fails, there is a correlative
breakdown of the sensory-motor loop. The sensory component (including sensation and
feeling) is split from the motor function which is necessary for acting. Both feeling and
doing are life-saving functions working together they constitute experience.
Interestingly, Bion defines thinking in terms of the capacity to experience, to make
links, and he attributes this to being able to integrate and assimilate sensory images
(the alpha function). Intense feelings always have a correlative motor i.e. muscular
impulse which includes all the primitive urges to suck, to hit, to reach, to cry, to tear,
to cling. Bion argues that restraint upon motor discharge is provided by means of the
process of thinking. I would qualify this by saying that motor restraint needs to be
accompanied by the sensory information of the act of restraint in conjunction with the
image of what is being desired. The linking of the two constitutes thinking. By contrast,
splitting the motor and sensory function reduces the intensity and dilutes the conflict to
make the self in relation to object less overwhelming, less threatening. The splitting
may subsequently be followed by more integrative reflective activity, or not, depending
on the autonomic capacity to contain the charge.
The motor-sensory split will also be reflected in a sensory dysfunction often marked
by numbness or pain; and motor dysfunction typically manifesting in rigidity/flaccidity
of the muscle, or a compulsive motor discharge (hyperactivity). An individuals body will
be characterised by its own particular variations in muscle tone, body awareness,
differentiation of muscle groups, tissue textures etc. The more split the mental
functioning, the more splits are observable to the trained body psychotherapist. The
bringing together of sensory awareness and motility can increase healthy integration
and differentiation of functions. (Carroll, 2001)
The delusion is extraordinary by which we exalt language above nature:-

making language the expositor of nature,

instead of making nature the expositor of language. -Alexander B Johnson
Discussion: My first person account hopes to stimulate a discussion about our common mindbody split and the psycho-physiological nature of human experience. With, in my opinion, a
growing need for an integration of The Polyvagal Theory into clinical diagnostic observations,
and the hidden nature of our self-protective perceptions, based on a common neuroception
(Porges, 2011) of safety. Particularly within the universal existential context of how: The
attempt to regulate affect - to minimize unpleasant feelings and to maximize pleasant ones - is
the driving force in human motivation. (Schore, 2003)
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