The Schizo-Stroller

It’s Mel and Colly,
The invisible cunts.
The Beth
of the Unknown Verneinung.
There’s always at least two.
The girls from another planet
Cumming to blow my world.
Boys will be boys.
Hands up if you’re not the only ones.
It’s all fucked up.
I’m not
your mum!
*you’re.

When Nietzsche writes ‘God is dead’. It is not the same sentence structure and therefore a different semantic meaning to the phrase ‘There is no God”.

Historical background for a Nietszchean exegesis:

Around that time in the burdening Wessenschaft relation between anthropology and archaeology, a theory emerged that the earliest god’s were old chieftans or Kings (Ur-Kings) when earlu differences in wealth emerged, with emerging longer periods of settlement that would be returned to, even amongst still semi-nomadic groups. These burial mounds would be then be worshipped and stories told of this King for generations after any lived memory of the King survived. Later temples would be built around these burial mounds and the dead God-King would emerge, leading to hereditary living God-Kings (eg later (but now ancient) Egypt).
This temple would also be the place that as agrarian techniques developed so would the storage of grain, this storage would soon last more than two years. The ‘clerical’ priests would be in charge of distribution and a religious ‘economy’ related to writing, maths, status and labour emerged. Thus, for example, famines were still related to religious beliefs, where the strength of the economy and thus religious faith was related to how long a drought, famine, or plague of locusts the stores could survive. Thus today in modern anthropological psychological dynamics and their relation to the economy, scapegoating is still related ot this ‘hangover’ (best described by Azazel as scapegoat in Leviticus 16 and it’s relation as a relation to the community’s fears).

So with regards such economic, social and religious organisation, this is still a relation to the phrase ‘God is dead’.
(This is related with regards to violence in Nietzsche and Freud’s mythology with regards the killing of the father by the Band of Brother’s. In these mythologies this God-King in this buriial mound was orginally killed and then mourned, as explained in Totem and Taboo. Anthropologically and archeologically the Band of Brothers theory has been put in doubt, but the burial mound theory not so much. Which leaves room for a relation to a more utility based theory of emergence, although still not to divest oneself of the entirety of any violence/ death wish theory (such as Bowlby, although there are other evidence based aspects of Bowlby etc etc)).

If we are to return to Rocjiewicz and Rocjiewicz Jr’s phenomenology after exploring Lisa Blackman’s ‘problem of hallucination’ it is worth exploring Ver Eecke’s ‘dualist’ view of mental health that embraces both phenomenology and the bio-medical model (he does this in his introduction to Der Waelhen’s combination of phenomenology and Lacan so a nice segue on the return through phenomenology back to Lacan’s idea of the ideal ego and ego ideal that we took a detour from some time ago).  On the face of it Ver Eecke’s argument is just another, theory that says, sure there’s a social aspect to mental health but it’s underpinned by a biological cause. This is an issue that The British Psychological Society’s Power, Threat, Meaning Framework deals with and looks at several different approaches to criticise this stance, and we will come to this after. However, Ver Eecke’s is slightly different to some of these more psychological versions in that it deals with phenomenology and Lacanian psychoanalysis. So, for that reason I would like to examine it.
Ver Eecke starts by noting a certain dual causality model to theories of psycho-somatic illnesses within the medical profession. He quotes Van Der Kolk in saying “It is thus no longer scientifically justifiable to make clear distinctions between psychologic and biologic processes; rather we need to define our understanding of the degree which genetic, developmental, toxic and social factors converge to result in certain clinical syndromes!”. He also mentions that Finnish psychiatrist Pekka Tienari suggests that it is time “to move forward to attack the question of how genetic and environmental factors transact to influence development” (p.39-40).
Ver Eecke then spends time disagreeing with the claims that neurobiological disease is the sole cause of schizophrenia, arguing that they are not as strong as they claim, and furthermore that the evidence argues positively against it. One of the first criticisms is that twin studies of monozygotic twins show a 40-50% concordance between the twins, were the cause to be solely genetic, there would be higher concordance as they are genetically the same. Moreover, with regards such genetic causation given the lower insistence of marriage and procreation amongst people with the diagnosis, the incidence of the ‘disease’ would drop, die out. Ver Eecke quotes Portin And Alanen who, after analysing twin studies, adoption studies, environmental studies, and brain imagining findings say “in the light of the evidence provided by the epidemiological studies of the genetics of schizophrenia, it seems that the present-day conclusion is that genes are neither sufficient nor a necessary cause of schizophrenia, but a risk factor for it. Interaction between the genetic factors on the one hand physical, psychological, and psychosocial factors on the other appears to be important in the aetiology of the disease.”. Ver Eecke then goes on to quote Kendler and Diehl: “Schizophrenia is clearly a complex disorder in that gene carriers need not manifest the illness (incomplete penetration), affected individuals need not have the gene (environmental forms or phenocopies), diagnostic uncertainties cannot be avoided, and different families may carry different susceptibility genes (genetic heterogeneity)… These conclusions… are not inconsistent with the hypothesis that in some individuals, schizophrenia is largely environmental in origin, while in others the disorder is caused largely by genetic factors.” (p.40-41).
Ver Eecke then turns to studies that he argues provide direct proof that genetics are not the sole cause of schizophrenia. He refers to some a Danish study that noted differences in diagnostic rates dependent on several cultural factors: increased risk for children born to Danish mothers outside Denmark; and increased risk with unknown fathers but no maternal history of schizophrenia.
Ver Eecke then looks at the dopamine hypothesis. He argues there is as yet no satisfactory dopamine hypothesis, and that dopamine hypotheses are compatible with psychosocial factors. He points out that there are two main neurological development arguments of the dopamine hypothesis as mono-causal. Neither is satisfactory, one is a neurodegenerative one which can explain increasing negative symptoms from positive symptoms but not early onset or season of birth differences. It also fails to fully account for how this neurological degeneration occurs. The other hypothesis suggests dopamine is due to early insult or trauma (including possible in utero), and this can explain early onset but not later negative symptoms. Thus Ver Eecke moves on to examine co-causality theories of the dopamine hypothesis. He notes that the dopamine hypothesis is a theory that developed out of investigating the apparent effectiveness of medications, he then notes that clinicians have observed “that at times those medications work minimally or not at all… [and] many patients continue to have cognitive deficits and negative symptoms despite having had marked response to treatment” and that “amphetamine-induced psychoses… lack a number of features commonly associated with schizophrenia, such as the presence of negative symptoms, the specific kinds of auditory hallucinations that occur in schizophrenia, and a chronic course.” (p.42). he notes that scientists using animal research have concluded that “stress-induced dopamine release could play a role in psychotic decompensation.” (p.43). Ver Eecke  notes that in such a version of the dopamine hypothesis “stress is conceptualised as a causal factor in which dopamine is the mechanism. The theory of schizophrenia presented… implies that persons with a prepsychotic structure are vulnerable to the consequences of stress. This claim goes hand in hand with claims made by Lacanian-inspired therapists that prepsychotic persons are prone to create repeated self-inflicted stress.” (p.43).
After discussing dopamine, Ver Eecke turns to theses involving norepinephrine and serotonin. With regards norepinephrine he notes research that states that studies “do not contain sufficient evidence to suggest that a defect in the norepinephrine system is primary to the development of schizophrenia… however, the studies implicate an alteration in norepinephrine metabolism or response to stress in at least some schizophrenic patients. The noradrenergic system not only is integral to the body’s response to stress but is also involved in modulating the dopaminergic system.” With regards serotonin, he notes the same researchers state that “studies of patients with schizophrenia have failed to convincingly demonstrate that abnormalities in 5-HT [serotonin] neurotransmission mediate the expression of symptoms.” (p.43). So with regarding theses involving norepinephrine and serotonin, Ver Eecke, suggests that if one were searching for “an exclusive biological explanation for schizophrenia, it is important to remember that serotonergic neurotransmission is not believed to be a causal explanation of schizophrenia and that the possible function of the neuro noradrenergic system is explicitly linked to the body’s response to stress. One can therefore conclude that consideration of the function of these two systems in the brain includes psychological stress as a possible factor in schizophrenia.” (p.43).
Ver Eecke then turns his attention to glutamate theories. He notes that Phencyclidine (PCP, angel dust) can produce schizophrenia-like symptoms by blocking one glutamate receptor (NMDA). He notes that post-mortem studies have shown that an increased number of NMDA receptors is associated with acute psychotic states from an excess of dopamine transmission as a result of a change to the nucleus accumbens from damage to the hippocampus and amygdala (potentially prenatal). Ver Eecke notes this again results in a neurobiological appeal to psychological factors relating to stress.
Ver Eecke also looks at other chemical agents, he looks at one example each from four categories. With regards biogenic amines (eg physostigimine, DFP), an increase in cholinergic activity increases negative symptoms, whereas anticholinergic agents improve negative symptoms. With regards endogenous psychotogenes, studies show schizophrenics have a relatively low incidence of allergies as well as decreased responses to histamine. As for neuropeptides, researchers have noticed that high levels of CCK (creatinine phosphokinase) in the limbic system of schizophrenics. With regards more miscellaneous chemical agents, studies have shown that gluten-poor diets decrease psychiatric admissions, or correlate with improvements in psychiatric patients.
Ver Eecke then changes the focus from chemical agents to gender, and that the sex of the person makes a difference in the age of onset as well as possibly course and recovery outcome. He notes that Wyatt claims that “some estrogens appear to have antipsychotic effects and estrogens are known antagonists of D2 receptors. Conversely, dopamine regulates the biological effects of estrogens by decreasing the binding of that hormone to its receptors…” however “there are numerous social demands that could interact with an already altered substrate to increase the risk of developing schizophrenia.” (p.44).
In conclusion to the section I am looking at here, Ver Eecke’s notes that in the conclusion to the overview article “Schizophrenia: Neurochemical, Viral, and Immunological studies” in the Comprehensive Textbook of Psychiatry, Wyatt and his coauthors claim in defence of a medication approach that “the overwhelming beneficial effect of antipsychotic medications in schizophrenia cannot be overlooked. Regardless of the original cause of illness, the neurochemical outcome appears to be a perturbation of the dopamine neurotransmitter system” (p.44). Ver Eecke notes that in investigating these issues Wyatt et al. acknowledge stress as a variable. Thus Ver Eecke argues that “a critical evaluation of the argument for a neurobiological basis of schizophrenia needs to distinguish between, on the one hand, non-interpreted facts and, on the other hand, theoretical explanations of the facts. The survey articles that summarise the theories which attempt to understand the neurobiological basis of schizophrenia do not exclude psychosocial factors. Rather, psychosocial factors are included in the reasoning of how the major neurobiological factor (dopamine system) works.” (p.44). Ver Eecke uses the acknowledgment by researchers who observe the beneficial influences of gluten-poor diets and the low incidence of allergies that these observations do not alone indicate a cause of schizophrenia. “Rather, these non-interpreted facts indicate that there is a neurobiological factor at work in schizophrenia. But such a claim can co-exist with claims derived from other observations in both the neurobiological and psychosocial domains… thus, theoretically, the neurobiological explanation for schizophrenia does not exclude the possibility of psychosocial factors. In some neurobiological explanations, positive appeal is made to these factors.” (p.45).
I will conclude this post here and continue with Ver Eecke’s dualist model in the next post. I will say here, that the purpose of this foray into biomedical theories is to dive in deeper momentarily after looking at an embodied theory, before using the Power Threat meaning Framework to look at the issues with some of the models Ver Eecke raises here (not least the dopamine model), not least that whilst Ver Eecke makes a good case for a method of taking both biological, as he argues non-interpreted facts into account, his interpretation and distinction does not go far enough, as such I will in the future also be looking at the social construction of mental illness, around diagnosis, but also around social, economic and ideological factors, not just psychological stress models. However it is clear Ver Eecke’s conclusion paves the way for this possibility.

We were outside the chippy
And I tried to impress her
I said

My stories are embellished
Like your
Pawn shop jewels.

I run with the pawn shop jewels
Like Goldie Lookin Chains
Newhaven State of Mind.

She looked at me,
Generic brand ketchup
smeared across her red lips
And said

*you’re porn shop jewels

My signifiyng chains
Left strung out like a
Glistening pearl necklace.
The remains of my poet’s trophy
A mere half imagined
Bukkake interruptus.

He was signifier surfing
When a shark approached.

Fortunately,
It wasn’t a Great White,
It was a Bakhtin shark

Blackman then turns her critical gaze to the relation of the psychological to the social. She points out that “psychology, like psychiatry, is not a unified discipline, and it’s made up of a range of disparate therapies, concepts, explanatory structures and techniques and understandings. Many different theories within psychology have been deployed in order to understand the problem of hallucination. Many of them have similarities with psychiatric understandings, attempting to locate the exact psychological, rather than strictly neurological mechanisms, which are seen to underpin the hallucinatory experience. Again, like psychiatry, only some concepts have the status of science-ready-made, and there is much dissent and controversy surrounding many of the theories offered to explain the nature of hallucination.” (p.43-44). It is worth looking at the British Psychological Society’s Power Threat Meaning Framework for an overview of both psychiatric and psychological theories of mental distress. According to Blackman, though, within the conceptual framework of psychology, hallucinations are viewed as a disorder of consciousness. These theories are called ‘seepage’ theories, that is they frame hallucinations as some kind of ‘seepage’ into consciousness of mental activity that would normally be preconscious. “Therefore, the problem of hallucination is construed within the terms of consciousness and its preconscious workings… within this framework hallucinations are experiences related to dreams, originating in the preconscious imaginary realm of the mind. When the rational mind is relaxed then these subterranean forces are brought into play… the difference between hallucinations and dreams within this framework is that the state of consciousness, which occurs during the dreamstate, is considered a normal function of sleep… however, the neuro-physiological mechanism underpinning hallucination is considered deficient, whereas during sleep the mechanism is merely relaxed.” (p.44-45).
Other theories base themselves on hyper-arousal, so whilst it is considered within the bounds of normality, a pseudo-hallucination to hear voices in hostage situations, “these theories suggest that schizophrenia is akin to a state of hyper-arousal, which deleteriously affects cognitive information-processing capacities. The state of hyper-arousal is used to explain attentional deficits, which lead the ‘schizophrenic’ to inadequately screen and process input from the external environment. It is this state which leads to the focus of the internal as opposed to the external, where a person misattributes and confuses the location of the stimuli.” (p.45-46).
Another framework is that of hallucinations as a continuum of ‘normal’ mental imagery. “’Normal’ mental imagery has been defined as a non-veridical experience involving the sensory or perceptual organs” (p.48). Blackman suggests this structure consists of two concepts, the first views hallucinations as extremely vivid mental imagery. So hallucinations are in some respects similar to normal forms of mental imagery such as ‘daydreaming, hypnosis, dreams’ etc., they are also paradoxically quantitatively different. “In other words, although hallucinations are viewed as proximate to other forms of imagery they are also, by definition, the negation of ‘normal’ mental imagery.” (p.48). However, Blackman points out that within this continuum theory, with regards the second concept “the ‘problem of hallucination’ is delimited further by incorporating and redeploying one of the main modes of psychiatric explanation, ‘a belief in the reality of the experience’.” (p.49). Thus “the empirical problem is individualised, and the two concepts conflated through attempting to classify and measure ‘reality testing’ (the ability to judge between real and imaginary events) and the ‘quality of mental imagery’.” (p.49). Blackman goes on to quote Rose saying “’they (psychologists) domesticate and discipline subjectivity, transforming the intangible, changeable, apparently free-willed conduct of people into manipulable, coded, materialised, mathematised, two-dimensional traces which may be utilised in any procedure of calculation’… The paradox is that nowhere in the literature are the norms of ‘normal’ mental functioning defined. Mental imagery is presumed to be a mental picture of the world as produced internally, thus not dependent upon actual representations of external events. However, the laws governing normal mental imagery functioning are not explained. The ‘norm’ of mental imagery is a lack of hallucination. Thus ‘abnormal’ mental imagery is a negation of ‘normal’ mental imagery, which in turn defines and classifies the limits of ‘normal’ mental imagery.” (p.50). In contrasting Hilgard’s 1965 definition of altered states of consciousness to the psychiatric definition of hallucination, both ‘focus upon the involvement of imagery or fantasy production whilst ‘awake’, or at least in a certain state of consciousness. However, hallucinations are differentiated from ‘normal’ mental imagery by invoking the notion of ‘self-conscious’ awareness. However, this criterion or mode of explanation does not suffice to delimit the definition of altered states of consciousness from the psychiatric definition of hallucination. In both definitions the subject loses volition, the willingness to act independently and attention becomes redistributed or refocused. Therefore, what is the conceptual difference between hallucinations and an altered state of consciousness such as hypnosis?” (p.50). It is here that Blackman questions the role of vividness in the distinction, not just ‘self-awareness’. As if vividness of imagery is present in both hallucination and hypnosis, then “the fundamental difference or division is that hallucinations are viewed as inherently pathological and hypnosis is not. Hypnosis is viewed as a transitory state or role, whereas hallucinations are a symptom or index of pathology, and become an integral part of the identity of the person. Thus, in order to understand why hallucinations are constituted within this framework as a continuum of ‘normal’ mental imagery, one needs to understand the antecedent for this statement to exist. Neisser has highlighted that there is no a priori reason for believing that imagery vividness is an underlying condition for a hallucinatory experience to occur – the paradox being that ‘normal’ mental imagery is defined by what is abnormal, i.e. hallucinations. Thus, although psychology aims to extend its knowledge of normal mental functioning to deal with what is constituted as individual and social pathology, the questions are posed in terms of deviation from certain norms. As Rose suggests, in relation to this argument, ‘individual psychology would seem to diagnose social pathology in terns of deviation from statistical norms. Its conception of normal and abnormal mental functioning would be constructed from the point of view of a theory of populations, averages and correlations, not from a conception of the psyche itself.’.” (p.51).  
Continuing Blackman’s argument with regards the alignment of concepts in psychology and psychiatry she states “they focus less on the brain and more on those cognitive capacities which are viewed as existing within the mind. They are attempts to locate the psychological, as opposed to the psychiatric mechanisms, which underpin the hallucinatory experience. They claim to be based upon general theories of mental functioning, which are then extended to understand these so-called deviations from normal functioning. However… it is actually the ways in which deviations, understood as pathology, are articulated, which make possible what we understand normal mental functioning to be.” (p.52). She cites Foucault, “it must not be forgotten that ‘objective’ or ‘positive’ or ‘scientific’ psychology founds its historical origin and its basis in pathological experience. It was an analysis of duplication that made possible a psychology of the personality; an analysis of compulsions and of the unconscious that provided the basis for a psychology of consciousness; an analysis of deficits that led to a psychology of intelligence”. (Blackman, p.52).
Blackman then turns to the social elements of the hallucinatory experience. But we will return to these later. Much of these debates as well as more contemporary one’s are covered by The British Psychology Society’s Power, Threat, Meaning Framework in the literature review that precedes the discussion on practice. I will be covering this Framework later, its relation to some problems of contemporary governance. But for now, I hope that my notes on Lisa Blackman cover some issues in what is considered the ‘problem of hallucination’, and in the next article I will return to some problems of phenomenology and the work of Ver Eecke, before returning to Rocjiewicz Jr and Rockjiewicz’s ‘intentional arc’.

The firmament
Of the lower abdomen
Made public.
The shame!

Who gets to judge the better man,
If the better man doesn’t judge?
It won’t be the better man,
Because the better man’s not for judging.

It’s merely an exploitative,
Disciplinary action
From a legitimation crisis
Of those who are for judging.

To investigate problems with the conception of schizophrenia in psychiatry, Blackman talks of the use of what are called Type 2 syndromes in the psychiatric literature. Type 2 in schizophrenia often refers to the negative symptoms observed in schizophrenia. As Blackman points out this distinction is often contested, however she argues it is a “good example of the ways in which psychiatry, despite its heterogeneity, is attempting to provide coherent causal explanations of psychotic experience. Thus the complex constellation of behaviours and thought processes which are problematised within the discursive practice, could be viewed as originating from two distinct disease categories.” (p.25-26). Thus symptoms such as hallucinations are considered indicators of type 1 syndrome. This phase is considered to be acute but responsive to neuroleptics. This is distinguished from a second phase, type 2, which is considered with more chronic with flattened affect and poverty of speech. This phase is thought to be more intractable, with a poor response to neuroleptics and thought to be possibly irreversible and permanent. Blackman continues “within this particular conceptual framework hallucinations appear as temporary markers of pathology which are amenable to ‘cure’, thus offering a trajectory which is used to explain why ‘hearing voices’ appears across the disease classes as a ‘symptom” (p.26). Blackman argues that this conceptual framework imposes a ‘grid’ that orders the symptom of ‘hearing voices’ encountered in practice (but not in theory). What she means by this is that the problems that stem from encountering contradictions in attempting to distinguish between ‘real’ and pseudo-hallucinations can be reorganised within a different rubric providing a theory of disease that takes into account neuro-physiology alongside the context of experience. Again, the categories that were previously used to think through this theory of disease are duration, severity and chronicity (along with insight). Blackman argues that this means psychiatry can no longer be thought of in terms of control, vividness, duration etc. (as do Rosciewicz Jr. and Rosciewicz) that more finely comprehend the complexities of hallucination, even if the medical model still requires that the patho-physiology of the individual be raised as a causal factor.
Thus in this new framework of explanation hearing voices is seen as an indicator of possible psychosis but not necessarily as definitive of schizophrenia, neither the sole diagnosis not the sole marker of a diagnosis. Blackman suggests this is a sign of a shift within psychiatry of the understanding of the phenomenon of hearing voices, but one where psychiatry is still invested in issues of genetics and heredity, but that leaves space for the creation of new perspectives, and from the point of view that I am writing from, new ways for psychiatric survivors to write their own experience into the discursive space opened up.
Blackman points out that there are particular assumptions in the perspective, gaze, which psychiatry turns on the diagnosis of hallucinatory experiences. She argues that what makes a hallucination, outside organic factors or religious experience, is the lack of any other plausible explanation. The symptoms are not to ‘speak of themselves’, instead there is a “conceptual grid used to divide the normal from the pathological within psychiatric discourse, the psychiatric gaze concerns itself with what is ‘absent’ to the immediate gaze of the psychiatrist.” (p.28). “Psychiatric discourse has… produced a taxonomy of natural diseases, of which certain symptoms, such as hearing voices are viewed as first rank signs. The ‘pure’ psychotic states are those where psychotic symptoms are viewed as signs of disease and illness, such as schizophrenia. These are often viewed as degenerative and linked either to structural changes in the brain, or biochemical or neurological deficit or imbalance (the type 2 syndromes).” (p.29). However, on noting this Blackman moves on to another aspect of the psychiatric gaze, the ‘enfeebled personality’. “This is based on a notion that there are certain persons deemed constitutionally lacking in the so-called normal propensities to equip them to deal with the stresses and strains of life.” (p.29). the method by which this enfeebled personality is ‘discovered’ is the psychiatric interview.
Blackman argues that there are two phases of the psychiatric interview; “the first is a description of the present mental state and involves a ‘provisional’ diagnosis. The second phase of history-taking is undertaken to pinpoint any ‘patho-features’ of the person’s biography, which may have made them vulnerable, or in psychiatric terms, ‘at risk’ to a disease process.” (p.30). It is worth noting here that in a sense this is little difference to ‘formulation’ as an alternative to diagnosis that is currently being promoted as a radical new approach to mental poor health and distress. “This ‘social history’ is then used as part of the grid of perception for making sense of the person’s experience. The discursive space opened up to make the distinction between what is deemed normal and what pathological is disparate and heterogeneous. It is a complex assemblage of concepts, which attempt to make it conceptually possible to ‘think’ in terms of disease and pathology. These include the status of the ‘personality’ of the individual, and the context of the experience, which is rendered in relation to the key concepts of source, vividness, control and duration. However, the most general specification, which underpins the dispersal of concepts within psychiatric discourse is the notion of the ‘enfeebled personality’; one who is viewed as unable to maintain particular kinds of relations with themselves and ‘others’. This personality is one whose ‘psychology’ is directly linked to biological inferiority or inadequacy’.” (p.31).
Blackman suggests that there is a split in psychiatric discourse between the natural and the social. “The natural (body) is made intelligible through particular ways of thinking about the body and biology, derived in part from evolutionary theory. Biology is viewed as a static, invariant set of characteristics which predispose persons to particular forms of thought, behaviour and conduct. Biology then sets limits on how a person is able to interact with the social and also the levels to which the social can impact or impinge upon the individual.” (p.31). these assumptions are then overlaid by other dualisms such as “inherited/ environmental, somatic/ psychological, psychotic/ neurotic and even the pseudo-hallucination/ hallucination.” (p.31-32). Blackman reminds us that psychiatry is not simply biologically reductive, but that it combines this ‘hard’ biology with ‘softer’ psychologically oriented science. Psychiatry makes possible its particular way of thinking about ‘hearing voices’ by targeting biology and the social in a way that conceives biology as its originary point. “Biology is opposed to the social, and the social becomes a measure of the individual’s competence in social interactions. Social and psychological life ultimately is explained with reference to biological causes.” (p.32). It is from this position in psychiatry, that I hope to move to the conception of voice hearing in ‘psychology’ before returning to phenomenology of voice haring ,and from thence a return to the dreamwork of Freud as an approach to voicework in hearing voices.

Springtime.
Taking a Dionysian stroll
During Rogation.
The air is fecund.
Twice-wyrded
As a bistort.