Download Revisiting unitary psychosis, from nosotaxis to

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project

Document related concepts

Psychiatric and mental health nursing wikipedia , lookup

Generalized anxiety disorder wikipedia , lookup

Antisocial personality disorder wikipedia , lookup

Asperger syndrome wikipedia , lookup

Conduct disorder wikipedia , lookup

Mental health professional wikipedia , lookup

Depersonalization disorder wikipedia , lookup

Mania wikipedia , lookup

Deinstitutionalisation wikipedia , lookup

Child psychopathology wikipedia , lookup

Antipsychotic wikipedia , lookup

Thomas Szasz wikipedia , lookup

Narcissistic personality disorder wikipedia , lookup

Conversion disorder wikipedia , lookup

Political abuse of psychiatry in Russia wikipedia , lookup

Cases of political abuse of psychiatry in the Soviet Union wikipedia , lookup

Dissociative identity disorder wikipedia , lookup

History of psychiatric institutions wikipedia , lookup

Bipolar disorder wikipedia , lookup

Anti-psychiatry wikipedia , lookup

Emergency psychiatry wikipedia , lookup

Mental disorder wikipedia , lookup

Spectrum disorder wikipedia , lookup

Mental status examination wikipedia , lookup

Emil Kraepelin wikipedia , lookup

Bipolar II disorder wikipedia , lookup

Schizophrenia wikipedia , lookup

Dementia praecox wikipedia , lookup

Schizoaffective disorder wikipedia , lookup

Diagnostic and Statistical Manual of Mental Disorders wikipedia , lookup

Causes of mental disorders wikipedia , lookup

Political abuse of psychiatry wikipedia , lookup

Psychosis wikipedia , lookup

Abnormal psychology wikipedia , lookup

Critical Psychiatry Network wikipedia , lookup

Sluggish schizophrenia wikipedia , lookup

Glossary of psychiatry wikipedia , lookup

History of mental disorders wikipedia , lookup

Social construction of schizophrenia wikipedia , lookup

Classification of mental disorders wikipedia , lookup

Controversy surrounding psychiatry wikipedia , lookup

History of psychiatry wikipedia , lookup

Pyotr Gannushkin wikipedia , lookup

Transcript
Salud Mental 2012;35:101-113
Revisiting unitary psychosis, from nosotaxis to nosology
Revisiting unitary psychosis,
from nosotaxis to nosology
Carlos Rojas-Malpica,1 Néstor de la Portilla-Geada,1 Adele Mobilli-Rojas,1 Danilo Martínez-Araujo2
Original artícle
SUMMARY
RESUMEN
The concept of psychosis as known today comes from the late nineteenth century, and was developed from ancient notions, such as insanity, alienation and dementia. Four dichotomies can be registered
in the evolution of the concept: Psychosis vs. Neurosis, Unitary vs.
Multiple, Functional vs. Organic, and Endogenous vs Exogenous. The
purpose of this research is to rethink the issue of unitary psychosis from
a new scientific and epistemological reading. Toward this objetive, the
terms of nosotaxis, nosography and nosology are discussed, as well
as the role of major classification systems of contemporary psychiatry.
It also imposes a historical review of the concept from Aretaeus of
Cappadocia to the present. Through a rigorous hermeneutic exercise,
we discuss the problem of the positivist Kraepelinian conception of
psychoses and its epistemological resolution through complex thinking
theory, and chaos theory, with empirical reference to hallucinations
and delusion as well as the biological basis of schizophrenia and bipolar disorder, but emphasizing their common components. Essential
to perform this exercise are theoretical developments from Bartolome
Llopis and Henri Ey, enriched by the latest findings of neuroscience. It
seems clear that mental illness is a loss of complexity, leaving little of
the fresh and unexpected chaotic health behavior. While asserting the
existence of a unitary psychosis is controversial with current available
data, it is equally true that the assertion of a schizophrenia/bipolar
disorder dichotomy is also difficult to sustain. However, the axial syndrome common to all psychoses, Bartolomé Llopis´s brainchild, remains a fertile idea, as well as the concept of Henri Ey, to understand
mental illness as a condition of loss of freedom.
El concepto de psicosis, tal como hoy se le conoce, viene del siglo
XIX tardío, y fue elaborado a partir de nociones más antiguas, como
insania, alienación y demencia. Se pueden registrar cuatro dicotomías
en la evolución del concepto: psicosis vs. neurosis, unitaria vs. múltiple,
funcional vs. orgánica y exógena vs. endógena. El propósito de la presente investigación es replantear el tema de la psicosis única o unitaria
desde una nueva lectura científica y epistemológica. Para ello se discuten los términos de nosotaxia, nosografía y nosología y el papel de los
sistemas clasificatorios más importantes de la psiquiatría contemporánea. Se impone también una revisión histórica del concepto desde Areteo de Capadocia hasta la actualidad. Por medio de un riguroso ejercicio hermenéutico, se discute el problema de la concepción positivista
kraepeliniana de las psicosis y se plantea su superación epistemológica desde el pensamiento complejo, la teoría de sistemas y la teoría del
caos, tomando como referencia empírica las alucinaciones y el delirio,
así como los fundamentos biológicos de la esquizofrenia y el trastorno bipolar, pero haciendo énfasis en sus componentes comunes. Para
realizar dicho ejercicio resultan fundamentales los desarrollos teóricos
de Henri Ey y Bartolomé Llopis, enriquecidos por los más recientes
hallazgos de las neurociencias. Parece evidente que en la enfermedad
mental hay una pérdida de complejidad, quedando muy poco para
lo fresco y caóticamente inesperado del comportamiento saludable.
Aunque afirmar la existencia de una psicosis única resulta polémico
con los datos disponibles en la actualidad, no es menos cierto que la
afirmación categórica de una dicotomía esquizofrenia/trastorno bipolar también es difícil de sostener. Sin embargo, el síndrome axil común
a todas las psicosis de Bartolomé Llopis, sigue siendo una idea fértil,
como también la idea de Henri Ey de entender la enfermedad mental
como una patología de la libertad.
Key words: Unitary psicosis, hallucination, delusion, anankastic
phenomena, nosology.
Palabras clave: Psicosis única, alucinación, delirio, fenómenos
anancásticos, nosología.
EPISTEMOLOGICAL INTRODUCTION
Nosological debate spans all the history of psychiatry and
its offshoots. For the purposes of this article, we are more
concerned with the concept of psychosis, and in particular,
1
2
that of unitary psychosis. The concept of psychosis, as it is
known today, comes from the late 19th century and was developed from older ideas such as insanity, alienation and
dementia. There are four distinct dichotomies in the evolution of this concept: psychosis vs. neurosis, unitary vs.
Department of Mental Health, Faculty of Health Sciences, Universidad de Carabobo, Valencia, Venezuela.
Women’s Hospitalization Area, “Dr. Carlos Arvelo” Military Hospital, Caracas, Venezuela.
Correspondence: Dr. Carlos Rojas-Malpica, Departamento de Salud Mental, Facultad de Ciencias de la Salud, Universidad de Carabobo. Uslar 92-50, Urb.
El Trigal centro, 2002-005, Valencia, Venezuela. E-mail: [email protected]
Received: August 3rd, 2011. Accepted: October 28, 2011.
Vol. 35, No. 2, March-April 2012
101
Rojas-Malpica et al.
multiple, functional vs. organic and exogenous vs. endogenous.1 The term “unitary psychosis” itself is derived from
the German einheitpsychose. It is known in Spanish as both
“psicosis única” and “psicosis unitaria.” The term has been
used to mean several things: a) to refer to the idea that there
is just one kind of psychosis, b) resulting from impairments
to an invariable structure, and c) that clinical differences are
pathoplastic effects of personal and environmental components.2 The debate on this issue is far from settled. For the
Cambridge School, the concept of unitary psychosis refers
to the collective denomination of a group of distinct doctrinal positions, whose central idea is that there is only one
form of psychosis, whose myriad clinical expressions can
be explained by the action of endogenous and exogenous
pathoplastic factors.3
Classificatory proposals, which have varied over time,
such as the APA’s DSM and the WHO’s ICD, are designed
to simplify and improve scientific communication, unify criteria, and shorten distances between the many theoretical
positions. Such proposals receive strong criticism from different points of view, resulting in the need to make multiple
adjustments over the course of time. While they are taken as
atheoretical models, they all retain some element from the
botanical naturalist classifications of Linnaeus’s time. Classifications must be understood as transitory models that
express representations of clinical reality with virtues and
defects, carrying the ideological and cultural markings of
the spaces in which they are produced. So they are not to be
seen as geologically consistent truths from which we might
derive indisputable results. It is important this distinction
be noted, given that (on behalf of these proposals) research
of all kinds (clinical, epidemiological, biological, psychopharmacological, neurobiological, etc.) has been conducted,
which tends to be presented as indisputable truth, ignoring
the fact that their basis is epistemiologically lax.3,4 We must
recall that the “disorders” described in the DSM are not natural structures; nor are they discrete entities with no relation
to other conditions. Rather, they are “groupings which are
agreed upon based on algorithms, symptoms, and behaviors
that disable the individual to a varying degree, and whose
classification does not amount to an etiopathogenesis”.
In addition, “not only are they compatible with the ideas
that gave birth to the theory of unitary psychosis, but also
they require these ideas be reestablished in many aspects
(etiopathogenetic, clinical, therapeutic, and rehabilitational,
among others)”.5 A more humble approach would be to accept that there are no findings to be heralded as Truth, but
only credible knowledge to be debated, as we see in the rest
of the health sciences.
In light of this debate, it is appropriate that we revive
three commonly used terms in medicine: nosography, nosotaxis and nosology. The common Greek origin of these terms
is nosoç (nosos), which means disease. According to the
Spanish Royal Academy Dictionary (translated to English)6
102
nosography is the part of nosology that deals with the classification and description of diseases. However, it would be
more accurate to say that nosography deals with description
of disease, while nosotaxis deals with classification, although
“nosotaxis” does not appear in the aforementioned dictionary. In reality, all three activities are inseparable, as they all
form part of a diagnosis (from the Greek diagnostikoç),
while remembering that said concept has been expanded
to multiaxial and idiographic diagnosis.7 When we speak
of mental disease or disorder, we are conducting nosography, as it is necessary to describe the symptoms through
which such disease manifests itself. Likewise, we are also
conducting nosotaxis, in stressing that the central and common point to these disturbances is the mental impairment
by which they are classified. Furthermore, we must also
conduct nosology, because everything will be accompanied
by an effort to explain and/or understand the relationships
between symptoms and the personal, biological, genetic,
emotional, experiential, social and psychological substratum that make these symptoms possible. In this way, the
most inclusive practice of all is nosology, through which the
clinician seeks to grasp the logic inscribed in nature, which
explains the disturbance or condition.8,9 But logic requires
nuance. Contemporary scientific debate admits that not all
processes can be understood through the mechanistic logic
that drives the natural sciences, born and structured within
the positivism of modern times, now criticized and questioned by complexity theorists and systems theory.10,11 The
innovation, as well as the difficulty, of complex thought, is
that it does not aspire to eliminate contradiction, obscurity
or uncertainty, but rather establishes these things as basic
elements of the order/disorder of nature. We cannot ignore
the chaos of madness (and nor can we assume they are synonymous). On this level of reflection, psychiatry must be
heteroclite and heterological, that is, it must take its logical
framework from both natural and spiritual sciences (heterological), while also assuming that among its subjects of
study (in this case, subjectivity and its processes of disease),
at times cannot be understood when combined in adherence
to common standards, and so expressed only through language and metaphor (heteroclite). To perform nosography,
statistics and frequency analysis have often been used. In
following research that is based on a supposedly “atheoretical” model (as is the DSM), one runs the risk of defining the
disease by its symptoms and the frequency with which they
appear, and not by its structure. So we must advise that the
most important thing is not necessarily that which is repeated, but that which is indispensable for the support of the
structure. In no way is a disease more completely described
by referencing the frequency with which its symptoms appear, as opposed to that which is essential to its process. It
was toward this end that Karl Jaspers, making use of the
phenomenological method, defined his general psychopathy.
Therefore, mere symptomatological alliteration must not
Vol. 35, No. 2, March-April 2012
Revisiting unitary psychosis, from nosotaxis to nosology
be confused with phenomenology, as the latter seeks and
proposes to arrive at the essential and/or structural which
cannot be achieved through simple analysis of frequency. It
is for this reason that the clinician must make use of hermeneutic rigor to interpret the symbolic processes and contents
that structure the psyche, which cannot be understood by
conventional readings.
Other terms which deserve attention from a nosological angle include that of “spectrum” and “comorbidity.” The
former seems to derive from physics. When a beam of light
is projected, one part can be seen as clearly illuminated,
while another is faded, ending with darkness. This parallel with light would indicate that many nosological entities
overlap along the edges, in many cases becoming indistinguishable. An example of these blurry edges lies in the concept of borderline. Regardless of whatever truth there may
be in these assessments, the real difficulty lies in the fact that
most of the time the resemblance is in the clinical core and
not in the periphery, as we will discuss later with regard to
bipolar disorder and schizophrenia. In this regard, it is very
likely that there is more overlapping between disease and
health than there is between mental disorders themselves.
So, the term “spectrum” can also be confusing, both for its
intentions and for the reality it seeks to describe. The psychoanalytic definition of spectrum, proposed by Tutte, is
very interesting. He posited that “at one end are disorganized, invasive and paralyzing conditions, and at the other
are conditions which are close to normalcy.” Between these
ends there are all kinds of intermediary situations, conditions that produce effects of greater or lesser mental harm,
including more or less mild states forming symptoms in the
organization of neurosis, to that which is corresponds to
veritable gaps in symbolization, which can lead to the psychic silence of psychosis.12
With regard to “comorbidity,” there are a few critical
points to be made. When we treat a bipolar patient with a
severe personality disorder and abuse of addictive drugs,
must we consider this person to suffer from three or four
“comorbid” pathologies? Or is it more accurate to consider that the entire condition comes from a common thread,
which our nosotaxic parceling does not allow us to see? Can
it be that the patients we so often see suffer from schizophrenia, anxiety disorder, depression and obsessive compulsive
disorder? Is the terrible anxiety suffered by our depressive
patients “comorbid,” or is it as central as the deep sadness
they experience? We will try to discuss these questions in
more detail later in this article.
The need to measure, weigh, and quantify the “facts”
of science, as well as the exclusion and confiscation of subjectivity have been imposed restrictively since the times of
Auguste Comte.13 We can state that traditional scientific positivism epistemologically governs the better part of biomedical research. However, thanks to psychoanalysis, phenomenology, existential analytics, medical anthropology, and
Vol. 35, No. 2, March-April 2012
other qualitative developments, we have managed to open
a space for subjectivity in medical research, and (in particular) in psychiatry. Thanks to this knowledge we have a hermeneutic tool that allows us to better penetrate psychotic
existence, without which neither communicative efforts nor
therapeutic relationships would be possible. Today, it is accepted that the data from positivist research are useful in
explaining many biological regularities. However, they are
insufficient when used to analyze more complex phenomena, such as human behavior and its myriad determinations.
This occurs because the linear mathematical systems lose
their predictive capacity in the complex systems that require
the logic established in Chaos Theory.14 According to Edgar
Morin and his theory on complexity, the positivist method
presents us with a reality that is cut into slices, which while
producing knowledge, also produces ignorance. So, the
alternative to the simplistic, reductionist and disjunctive
thinking of positivism, must be complex thought.15
History of the concept
of unitary psychosis
The notion of unitary psychosis began much earlier than the
founding of psychiatry as a medical specialization, dating
back to the 1st century in the work of Aretaeus. Bartolomé
Llopis affirms that the Cappadocian suggested a fundamental form of madness (melancholy) from which all other forms
derived.16 The approach is complex. Let us follow an already
fruitful path to understand this history.17 If we seek to define
this concept in a simple way, we could say that he affirms
that the different psychotic conditions represent no more
than different levels of intensity of the same fundamental
disorder. It was in the 18th century that Vincenzo Chiarugi
(1759-1826) wrote, in 1793, his famous “Della pazzia.” It is
important to note that the term “pazzia” is the equivalent to
madness in English, and he used this word despite the fact
that in Italian the word for insanity did exist.18 This Italian
author, unjustly criticized by Pinel, proposed that “madness” follows an evolution that spans from melancholy to
mania, and from mania to dementia.
Heinrich Neumann (1814-1884), who is considered by
some to be the “father” of unitary psychosis, said in his Lehrbuch der Psychiatrie, published in 1859: “There is one sole
form of psychic impairment, we call it madness (das Irresein).
Madness does not have different forms, but rather different
stages, which are called: the delirious stage (der Wahnsinn),
mental confusion (die Werwirtheit) and mental breakdown
(der Biodsinn).”19
Georget EJ (1795-1828), one of the disciples of Esquirol,
defined madness as “an idiopathic brain disorder, whose
symptoms can vary greatly.” This definition appeared in
“De la folie”, which was published in 1819, and translated
by Heinroth to German just one year later.20 It had signifi-
103
Rojas-Malpica et al.
cant influence on psychiatrists such as Zeller, who was later
a teacher to Griensinger and Neumann, the latter of whom
became the most passionate defender of the paradigm of
unitary psychosis in Germany. Hence the famous phrase attributed to this Berliner, that “mental diseases are diseases
of the brain,” also attributed by some authors to Georget.21
Another francophone author, the Belgian Guislain J
(1797-1860), believed that all mood disorders were a result of
one morbid excitement of one’s sensitivities (feelings), which
constitute the origin of all mental pathology. He greatly influenced German psychiatry, which at the time was still
governed by knowledge developed on the other side of the
Rhine, although not long after this was to change radically.
It was through Albert Zeller (1804-1877), a teacher of
Griesinger, that the concept of unitary psychosis became
German. The consolidation of the idea of unitary psychosis
was enshrined in a text by Griesinger W (1817-1868), written
in 1845 when the author was just 28 years old, which quite
soon became the most important psychiatry book of its time.
The “Pathology and Therapy of Mental Diseases” would
be translated to French in 1864, to English in 1867, and to
Spanish by 1880, later seeing many subsequent releases in
all these languages, evidence of its broad influence.22 There
would be questioning of this hypothesis, one of the most important being the concept of “paranoia,” a term which was
proposed by Kahlbaum.
According to Lanteri-Laura, “until the middle of the
19th century, all the world followed the paradigm of absolute unitary psychosis, and the works of JP Falret and others were what opened the door to the idea of a plurality of
mental conditions.”23
Also in France, and almost simultaneously, in 1854, two
prominent “alienists” used the names “folie circulaire” (Falret JP) and “folie à double forme” (Baillarger) to describe
the entities which later would be detached from the root
of unitary psychosis and Kraepelin would subsequently
call “manic-depressive madness.” Later, the enormous influence of the classificatory work of Emil Kraepelin was
what finally buried (although not entirely, which we will
discuss later) the old idea of unitary psychosis.24 However,
it was also Kraepelin who in 1920 wrote: “No experienced
diagnostician can deny that the cases in which it is impossible to make a clear decision are lamentably frequent.”24 It
was words like these which brought Angst to affirm, perhaps somewhat boldly, that “it is very likely that Kraepelin
would have changed his concept of this dichotomy had he
lived longer.”25
Given these cases of difficult distinction, Eugen Bleuler
spoke of “mixed psychoses” while Kurt Schneider used the
term “cases in the middle.”26 Kretschmer even affirmed that
“close to half of all psychotic patients suffer from mixed
psychoses.”27 Schule showed the existence of cases that begin as manic-depressive, and end as schizophrenic, as well
as the other way around.
104
In 1928, the Spanish psychiatrist Sanchís Banús highlighted the conceptual difficulties in separating dementia
praecox from manic-depressive psychosis. Five years later,
the American psychiatrist Jakob Kasanin (1933) coined the
term “schizoaffective psychosis” to refer to these cases of
mixed symptoms, in what Alarcón called the first American
contribution to psychiatric nosography.28
Without a doubt, in the Spanish-speaking world it was
Barolomé Llópis who most distinguished himself in defending the paradigm of unitary psychosis. He did so from the
disadvantaged position he occupied due to his political convictions in Spain during the 1940s. Based on his observations
on the mental pathology of patients with pellagra, he developed his theory on the axial syndrome common to all psychoses.
His book continues to be, more than half a century later, an
extraordinary example of psychopathological science, and so
has been revived for new generations in a new release. Here
we might recall Kuhn TS (1962), who has shown us the destiny of paradigms in the sciences, while Lanteri-Laura indicates
that something always survives from the replaced paradigm.
Flor-Henry, in 1969, studying schizophreniform and affective cases in patients with epilepsy, found himself unable
to differentiate clinically between the schizophrenic and
manic-depressive cases, while also finding something very
interesting: a greater incidence of epileptic foci in the dominant hemisphere in the first group, and in the non-dominant
hemisphere in the second. This was confirmed by many authors, as Trimble points out.29
The paradigm of unitary psychosis, as we can see, reemerges in the 21st century, and for many reasons. “Thus
we return to the possibility (never fully abandoned) that the
brain mechanisms underlying the occurrence of psychotic
symptoms are shared, and that the value of the symptomatology must be established based on the function of the patient, not the condition,” as Baca affirms.30
We find authors such as Menniger, Ellenberger and
Pruiser, who hypothesized that neuroses and psychoses
are different stages of dyscontrol.31 On the other side of the
world, in the Soviet Union, Gannushkin PB, one of the leading figures of the so-called Moscow School of Psychiatry,
in a classic monograph from 1931, affirmed that there was
a continuum between neuroses, psychopathic personalities
and psychoses.32
Hueso Holgado states: “These proposals are important
in understanding how psychotic episodes can occur in people whose normal functioning is neurotic, or that of a personality disorder, as I believe there is a continuum between
the psychotic and neurotic.”33 Also Peralta et al.34 described
psychoses as continual processes in a schizoaffective spectrum. Or, is it possible to admit that a patient suffers from
schizophrenia and bipolar disorder as comorbid entities?
For Villagrán, authors like Bonhoefer, Hoche, Kretschmer,
Conrad, Ey, Menninger, Rennert, Janzarik, can be considered
unitarists in one way or another. To this list we can add Ber-
Vol. 35, No. 2, March-April 2012
Revisiting unitary psychosis, from nosotaxis to nosology
rios, Timothy Crow and Robin Murray. The master of Bonneval, Henri Ey, proposed that all mental disorders result
from changes in the longitudinal axis (diachronic) or transversal axis (synchronic) of the structures of consciousness.35
Likewise, Timothy Crow as well as Murray and Duta36 affirm on multiple occasions that there is a continuum in psychoses, proposing that “we accept that the neo-Kraepelinian
vision that schizophrenia and bipolar disorder are totally
distinct entities is not supported by available scientific evidence.” To this we must add that spoken by Renato Alarcón:
“It is, in reality, impressive that the dichotomy that underlies
the apparent clinical separation between schizophrenia and
bipolar disorder has survived almost a century.” Similarly,
Murray and Duta go so far as to affirm that the history of
psychiatry can be seen as the story of efforts made to overcome the notion of unitary psychosis. Other authors agree
that the results of research conducted are inconsistent with
the classification of psychoses, and in some cases, as with
Craddock and Owen,37 they offer that current classifications
inhibit both research and clinical practice. This statement
coincides surprisingly with the words of Heinrich Neumann, written in 1854, more than a century and a half ago:
“We cannot believe in the true progress of psychiatry before making the decision to throw away all classifications.”
In the field of psychology, the unitary theory has also had
its distinguished followers, such as Hans Eysenck, of the
Maudsley Hospital, and Gordon Claridge, from Oxford.38
However, Emil Kraepelin had a very interesting
thought which deserves to be studied carefully. In their extensive study on this author, Berríos and Hauser39 say that
in his “Research Programme” from 1897, Kraepelin already
proposed a plan for the classification of psychoses, which he
developed from 1896 to 1898. Very soon he incorporates the
problem of the evolution in the classification of psychoses,
announcing that he had found a new way to study mental
disease, describing early predictors of the clinical course.
The Kantian category of time enters the door to psychiatry
through the work of Kraepelin. Diagnosis was a way to understand the connections between the clinical case and the
underlying anatomical impairment. With his procedure, he
wanted to link etiology, pathology and symptomatology.
For Berríos and Hauser, contemporary psychiatry lives in
a “Kraepelinian world”. The authors translate to English an
extensive paragraph from his work, which reads as follows:
“¿... to what extent and with what clinical methods can
we understand with the greatest clarity the manifestations
of madness? The symptoms and signs that correspond to the
base conditions are extraordinarily varied, which implies
that the conditions preceding the process must have been
complex. Even when external agents are clearly involved
(for example, an injury to the head or intoxication)... there
is a group of forces working in the mechanism: the nervous
system of the affected individual, the deficit inherited from
past generations, and their own personal history... these
Vol. 35, No. 2, March-April 2012
prior conditions are especially important in considering the
manifestations of the disorder that are not derived from external injuries, but from the circumstances of the individual
in question... it seems absurd to propose that syphilis causes
patients to believe they are the proud owners of cars... and
not that the general desires of people are reflected in these
delusions... if these observations approach the truth, we will
have to seek the key to understanding the clinical case primarily in the characteristics of the individual patients... because their expectations play a defining role.”
The work of Berríos and Hauser, and the writings of
Kraepelin, not only illustrate the depth of their thinking,
but also give important epistemological clues for the clinical
practice that they propose in their time. On the one hand,
they want to integrate the personal history of the patient in
the interpretation of the psychopathological phenomenon.
This anthropological approach should not surprise us, coming from an author who was one of the first to conduct
trans-cultural psychiatric studies. On the other hand, Kraepelin does not seem to feel satisfied with the psychopathological exploration techniques, as they do not allow him to
articulate with the underlying condition. We believe that the
study of the representations, with the most recent findings
provided by neurophenomenology and the neurosciences,
together with systems theory and in consideration of chaos,
represents a good chance at transcending the epistemiological obstacles that hinder Kraepelinian research, as well as
articulating the issue of the “underlying impairment” with
clinical practice in treating disease and its pathoplastic expression.40 We will touch on this in the next section.
The representations approach
Reading a text from Michael Trimble,41 we come across this
phrase from Lombroso: morbus totius substantiae, which could
be translated as the total essence of the disease or as the disease
is the essence of all. We mention this because when speaking
of unitary psychosis, we are grasping for nothing less than the
total essence of mental illness, which in Latin, Greek, German,
Spanish and French can be written as: “totum essentiam mentis
morbum”, “to su1nolo thç ousi1aç thç yucikh1ç asqe1neiaç”,
“die gesamte Substanz der Geisteskrankheit“, “la esencia total de la
enfermedad mental” and “le produit total de la maladie mentale”,
respectively. Now, among the clinical entities of psychiatry, which of them contain the greatest amount of the substance we are after? We believe there would be a consensus
that schizophrenia and bipolar disorder best answer this
question. Unitary and dichotomous classifications contain
within their structure the greatest expression of the whole
of mental illness. Following this inevitable circumlocution,
we can add that for the ancient Greeks, the human body is
apomimesis tou hólou, that is, a copy of everything, imitation
of the universe, which is very much in keeping with the
105
Rojas-Malpica et al.
theoretical postulates of complexity and its hologramatic
principle, which affirms that “not only is the part in everything, but also everything is in the part.” That being said, let
us study “the parts” that contain the greatest amount of the
whole that makes up the psychoses, which, in our opinion,
together with autism and fear of death, are hallucinations
and delirium.42,43
In traditional psychology, the concept of representation
accepts a certain polysemy. It is thus that the apprehension
of an immediately present object can be understood, as occurs in perception, but also the reproduction in the awareness of a past perception; likewise, the representation can
be made to anticipate a future event, which brings it toward
imagination.44 In some cases, there is a poietic representation, through which reality is resemantized with novel
subjective additions and, in intense contrast with that reality, there is the mineralized representation that characterizes hallucinations. For Wittgestein, the best representation
must share a structural or logical form similar to reality,
bringing it closer to the isomorphic conceptions whose best
empirical expressions are found in mathematics and chemistry. Ricoeur distinguishes between image and memory,
for which he proposes an appropriate eidetic analysis.45
It is based on Husserl and his terms Vorstellung, Bild and
Phantasie. Here, Vorstellung is equivalent to representation,
Bild corresponds to the presentifications that describe something indirectly, like sculptures and paintings; while when
speaking of Phantasie one thinks of the angels and demons
of legend, thereby tying the concept to fiction and beliefs. In
any case, past events tend to become present as something
already perceived or lived by the subject, or to the contrary,
it is not recognized as one’s own. If hallucinations and delirium must be admitted as representations, then we must
immediately point out a deficient piece of data regarding
the majority of cognitive representations: they fail to adhere
to what Kant refers to as triple subjective synthesis, consisting of traversing, joining and recognizing, which guarantees
the cohesion and appropriation of what is perceived.46
Representing is not understanding, but it is a prior and
important step toward understanding reality. In the process
of understanding, the represented is assimilated and enriched by consciousness, until it becomes part of the Ego.
For Plato, ideas and things are not the same. Ideas belong
to the reign of Being, while things have been created by a
demiurge to the image and likeness of ideas. These kinds of
considerations have given rise to a debate on the relationships between the concepts of eidólon, eikón and phantasia,
that is, between the world of ideas and concepts, icons and
the imagination, or fantasy. Although some debate whether
representations were a subject of discussion in the world of
the ancient Greeks, Foucault’s research seems to show that
they were. In effect, when he examines the spiritual exercises recommended by the stoic emperor Marcus Aurelius, in
his Meditations, he finds a recommendation “that the object
106
that we represent and capture in its objective reality, pass
through description and definition, to the thread of suspicion, of the possible accusation, of the moral reproaches, of
the intellectual relationships that dissipate illusions, etc.”47
To capture the objective contents of the representation,
it will then be necessary to have a moment of both eidetic
and onomastic meditation. In our words, we would say that
the exercise recommended by Marcus Aurelius requires a
lucid and self-critical awareness, not to be fooled by the first
perceptive instant, and to examine the object until transforming the perception into an apperception, where the
guarantee of having arrived at the truth is achieved when
reflection drives and forms part of the Reason that presides
over and organizes the world. To represent, then, is a mental
activity that requires the integrity of the processes that make
consciousness possible, which ought to be studied through
the light of contemporary neuroscience.
For their part, Crick and Koch48 propose aspects of great
relevance in understanding the so-called Neural Correlates
of Consciousness. On the one hand, they are concerned with
very quick reaction times, of an order that goes from milliseconds to a handful of seconds, in which there is only
the possibility of already-developed behaviors, which the
frontal area of the cortex seems, in large measure, to control,
where some inputs from the sensory zones activate stereotypical and unconscious responses, which for their speed
do not require significant conscious elaborations. This indicates that a large part of the frontal activity runs and is
dedicated to unconscious processes. On the other hand, they
propose that the main function of the sensory cortex consists
of constructing and utilizing detectors for specific traits or
qualities, like those that are activated for orientation, movement, and facial recognition. In this way, we could affirm
that most of the sensory and motor activities are already
made and available throughout the cerebral cortex, by way
of global prior representations.49 For Libet, nearly one half second must pass in order for a situation to be registered in the
consciousness, so that we are we unaware of certain behaviors, as the unconscious brain has carried them out.50 It is not
necessary, for example, for an animal to explore between a
wide variety of behavioral possibilities in order to know that
there is a predator and that it is at risk. Instead, immediately
the unconscious neural registries are consulted, leading to
fight or flight behaviors. It is not only a matter of emotional
or flight responses that are innate or learned, but also of
neuronal groups of niches where unconscious behaviors are
stored, which are very necessary for the preservation of the
species and the perfection thereof among individuals. Crick
and Koch speak even of an unconscious homunculus and of
“zombie modes” that can be seen as cortical and structured
unconscious reflections, such as rapid and stereotypical responses. It is accurate to use the word zombie, a word of
Haitian origin, which is used to refer both a person who is
supposedly dead, but that has been revived by witchcraft,
Vol. 35, No. 2, March-April 2012
Revisiting unitary psychosis, from nosotaxis to nosology
as well as to designate an automated behavior in a subject
with a certain level of alteration in consciousness, which at
the same time appears void of voluntary initiative and vivid
reflections in behavior. The zombie metaphor makes sense,
because if, effectively, all behavior were not illuminated
with the living light of consciousness, it would seem to be a
kind of neuromotor robot. Consciousness is achieved much
more slowly and with broader and less stereotypical sensory input, often configured in images, and it takes longer
to decide between thoughts and appropriate responses that
require complex processes. This process of conscious qualification of the different sensory nuances and its progressive
complexity is a progressive trait, which, within phylogenetic
evolution, leads up to the homo sapiens sapiens. Phylogenesis
is characterized by increasing complexity, subjectivity and
individuality. In fact, in the so-called half-conscious, driven
by thalamocortical activation, when a task is performed that
requires effort and attention, we find spontaneously co-activated neural structures that are coordinated in space and
time, of the kind called prior global representations by Changeux, in such way that we can affirm that most sensory and
motor activities are already made and available throughout
the cerebral cortex. It must be admitted that there are visual,
auditory, tactile, olfactory, motor, linguistic, mathematical,
and aesthetic representations of different levels of complexity, which are constantly adjusted in the personal organization of the subject. Some are psychomotor and/or cognitive
habits whose automation and availability save the subject
some effort, allowing him energy for other realizations,
while others require an autopoietic completion that implies
contrasting prior representations to process novel behavioral emergencies, which involve several levels of initial chaos,
as well as new possibilities for organization of life and of the
person. As such, we accept with other authors that perception, hallucination, and delirium, as well as other cognitive
and neuromotor activities, are representations, and that, as
such, they cannot be considered as conceptually opposed
categories, while they can be differentiated. But we also recognize that all representations imply the joint activation of
complex cortical connections related to thought, language,
and imagination, and at a vertical and deeper level, of the
regions that regulate and harbor needs, drives, and desires.
Research by Kandel51,52 on memory and its neurobiological
basis, refers to processes relating to ontogenesis. However,
research on the human genome shows that there is a vast
genetic heritage shared between the homo sapiens sapiens
and other living beings. The effect on behavior of certain
genotypic and phenotypic attributes is understood, as well
as their relationships with neuroplasticity and the environment, but we still know very little about the effect that the
common heredity of our species can have on the symbolic
products of the individual. The way we see it, Sarró’s approach to the issue of delirium, which he considered to be
expressive mythologems of the universal fears and desires of
Vol. 35, No. 2, March-April 2012
the human race, which feed both delirium and myth, means
they can also be considered to be archetypal representations
whose neurobiological basis is only beginning to be understood.31,32,53,54 Téllez-Carrasco says that the “archetypal”
voice comes originally from Saint Augustine, who uses it in
his work De Div Quest, and is an explanatory periphrasis of
the Platonic eidos. Jung later used it in his famed theory of
the collective unconscious. For Téllez-Carrasco, “archetypes
would be symbols that shine through the same forms to reveal the vitality in time and in space, and I suggest naming
them with the neologism timofanías.”55
The hallucinatory phenomenon had been considered,
since Esquirol, as a “perception without an object.” The definition had not been substantially modified until recently
Alonso-Fernández questioned Esquirol’s idea in affirming
that “the hallucination is anything but a perception without an object, because it is not a perception and it does have
an object (...). Contrary to the activity of sensoperception,
which comes from the outside to the inside, in its capacity as
the centripetal mental function par excellence, the hallucination is produced by objectivizing a mental image, providing it with sensoriality, and then projecting it outward, in
brief, an objectifying projection, in a distinctly centrifugal
way.”56 In addition, today it is accepted that there are hallucinatory phenomena in healthy subjects, which are related
to certain personality traits, including imagination.57 Likewise, one aspect of the hallucinatory phenomenon has been
brushed aside, that which was indicated by Falret JP, in La
Salpêtrière, from 1864, where he states: “hallucinations of
the insane refer only to one sense, to an object or an identical series of objects. To the contrary, in dreams, fantastical
perception of absent things cannot be predicted, they occur
at random, with no discontinuity, and in the field of all the
senses... hallucination, this perception without an object, or,
if you prefer, this rumination of sensations...”58
That is to say, dreams present a subjective richness that
is absent in the hallucinatory phenomenon, which constitutes a distinctive and fundamental piece of information in
the semiology of both states. The phenomenology of hallucinations is best described as the rumination of sensations,
as Falret so correctly calls it. We can conclude with Amaral,
that hallucinations would be representations equipped with
all the characteristics of normal perception, including the
power of convincing us of the existence of the represented
object,59 although it must be stressed that the most significant
differences would be subjective richness, the greater level of
complexity of conscious phenomena, and the sensation of
the ego in control, all which characterize the representations
of lucid consciousness.
From England, Hughlings Jackson began to propose
a Darwinian reading of the phenomenon of delirium: “the
disease only causes the physical condition for the negative
element of the mental condition; the positive element, that
is, delirium, obviously an elaborate delirium, as absurd as
107
Rojas-Malpica et al.
it may be, means activity of the healthy available nervous
system, it means evolution moving toward what remains
intact of the highest cerebral centers.”60 Later, in the times of
the great clinical structures, the neo-Jacksonian theory proposed by Henri Ey only considered psychotic or delirious
hallucinations to be true hallucinations, which constitute a
free and positive aspect, a product of a global destructuring
of the activities of the neo-cortex, which has as a negative
trait the loss of the ability to distinguish between reality and
the interior fantasy that makes hallucination possible. In this
way, for Ey it is not a matter of simple cortical irritation, nor
of the projection of a repressed affection in the unconscious,
but one of a very complex alteration that severely impacts
the subject and restricts his/her freedom.
The topic of delirium has been subject to many different
reflections. We know that the term was coined by Chiarugi
in 1795, defining it as a disturbance in the ability to judge or
as a feverless fantasy with no alteration in consciousness. A
formal description of delirium is later developed by Jaspers,
in 1913, who in addition to indicating the impossible content
of delirium, insists on its character of absolute evidence and
its incorrigibility by way of logical argument or experience.61
Other authors have insisted on the primary or derived character of the delirious experience, from which comes the description of the delirious occurrence or feeling, delirious cognition, and delirious perception. The problem of the genesis
and understanding of delirium is also debated, referring to
the possibility of understanding delirium based on a specific
experience that changes radically throughout the life of the
subject, or if to the contrary, it is a matter of a primary experience, not derived from any other, which would allow us to
speak of primary and secondary delirium. Another debate
on the problem of delirium consists of understanding it as
a separate entity, with clearly defined compartments within
mental activity, or if, to the contrary, these boundaries are
blurred with passions, fantasies and beliefs. Clearambault
insisted on the automatic character of the delirious phenomenon. In obsessive disorders, the patient is besieged by intrusive thoughts which are perceived as having come from
outside the desire and intention of the Ego, but in so-called
psychic hallucinations, there is a true xenopathic emancipation, by which thoughts become foreign, strange, intervened, imposed, intercepted, published, stolen, divulged;
the boundaries of the Ego are confused and mental activity
seems to come from another place; there is no clear separation between what comes from outside by way of the senses,
and what is developed within, in one’s personal privacy. In
Clérambault’s mental automatism syndrome, there is a true
amalgamation between delirium and the hallucinatory phenomenon. Acoustic-verbal hallucinations, such as imperative phonemes, talking voices, enigmatic words and hearing
one’s thoughts, become structured as a whole in delirium,
until being broken down in the final stages of schizophrenic
disorder.62 Amaral performs an interesting exercise63 in es-
108
tablishing the debate between delirious perception and apperception. But the perspectives of Castilla del Pino and of
Dörr Zegers must also be highlighted, who used very different methodological means to arrive at similar conclusions
on the function of delirium. The former proposes that delirium would have an orthopedic function for a starved and
ill-structured Ego, while the latter, wanting to see beyond
the disease, considers that delirium can be another human
possibility through which a person transforms an unbearable existence into a different less painful reality.64
In our case, we are interested in studying the phenomenon by which delirium comes to install itself at the center of
the life of the patient, as a mineralized representation of the
world of himself, until structuring most of his behavior and
his life, which we propose be called anankastic representations, clarifying that this concerns a separate approach that
in no way seeks to diminish or discount different possible
approaches to this phenomenon. Diachronic study of the
topic shows that said anankastic representation comes from
a series of prior phenomena, such as Griesinger’s pre-delirium, the primary experience of Moreau de Tours, or Conrad’s trema, until the delirium constitutes a unitary world in
the conscious mind.64,65 To understand the phenomenon, it
seems to us that Llopis’ idea is fundamental, regarding the
fact that nature does not have different laws for producing
similar phenomena, in such way that the delirium and the
hallucinations that are observed in different clinical entities,
must obey one pathogenetic mechanism, and so, “thought
disorders and perception disorders are not, in reality, qualitatively different, but just means of expressing the different
levels of intensity of a disorder.”
Thanks to brain research techniques like fMRI and
SPECT imaging, electronic microscopes, histochemistry,
etc., the neurobiological basis of hallucinations is better understood. A decrease in the activity of the left dorsolateral
prefrontal cortex, together with the activation of some areas
of the sensory cortex, seem to be the most notable traits of
this process. In any case, what must be stressed is that what
is activated in the hallucinatory phenomenon is a sensory
network carrying a threatening signal to the patient, which
is only possible because it has left his/her control. Everything points to this being a matter of representations that are
presentified before a conscious mind that does not recognize
them as its own, because they have evaded the coinciding
detection mechanism for afferent and re-entrant signals that
support conscious perception, according to the findings of
neuroscientists. This is a critical finding for this debate, and
so neurophysiology must take on the issue of representations, the storing of information, engrams, and the recognition of the constitutive memories of the individual.66
Processes of simulation and supervision intervene in
the many states of consciousness that allow global access to
the past, present and future. The subject is not only receiving stimuli from their environment, to which they respond
Vol. 35, No. 2, March-April 2012
Revisiting unitary psychosis, from nosotaxis to nosology
from their brain with the innate patterns encoded in their
genome, but they are also an agent that makes new realities and behaviors. They are a poietic and autopoietic factor. And for that reason they have dignity. In the dialogue
regarding genetic traits, environment and the constitution
of the epigenetic, consciousness and neuroplasticity are fundamental.67 In order for everything to work harmoniously,
a balance of activity is needed between the sensory and
primary motor cortex and the association areas scattered
throughout the cerebral cortex which, it would seem, are
organized from the prefrontal cortex. The constructs contained in prior representations must be reviewed at every
chance and undergo some circumstantial adjustment or profound transformation, as the case may be. This is a process
of metacognition through which the mind examines its own
contents, in a similar way to that recommended by Marcus Aurelius in his exercises from the 2nd century. When
a pathological situation alters this process, the constructs
can become raw material for hallucinations and delirium.
The autopoiesis is interrupted and the mental dynamic is
trapped by anankastic representations. Crick’s zombies, the
prior representations of Changeux, or Téllez’s timofanías,
now independent from the Ego, imposed automatically on a
conscious mind that cannot differentiate them from reality,
thus constitute a symptomatic expression of what we have
called mental illness, anánkẽ.68
Authors that study the relationships between chaos and
health propose, contrary to prevalent thinking, that health
has a high level of uncertainty, in the same way that a lack
of variability and physiological and behavioral chaos leads
to a mineralization of the possibilities of existence, just as
occurs in most mental disorders. As such, new therapeutic
strategies must not regularize the behavior of the patient on
the level of his anánkẽ, but rather increase his repertoire of
lost complexity, transforming psychiatry into a true science
of liberty, as Henri Ey once proposed.69
The biological fundaments
of the proposal
The Kraepelinian desire to link symptoms to the “underlying
disorder” is ongoing. Today it has been suggested that the
correlation between biological variables with psychological
dysfunctions, as well as the existence of basic units in psychopathology in so far as common nuclei between different
disorders that show different clinical manifestations, seems
to be more appropriate for classification in psychiatry. However, we must not forget that the history of the patient and
their cultural experiences have a fundamental pathoplastic
value, as Kraepelin himself acknowledged. From the neurobiological point of view, it is well established that the there
are signs of alterations in the metabolism of the neurotransmitters that are not specific to any disorder, which rather are
Vol. 35, No. 2, March-April 2012
related to psychopathological dimensions of certain specificity. In this same way, functional psychopharmacology is
in line with the approach of said dysfunctions, and inevitably will lead to the use of combinations of useful drugs in
different disorders.70
While nosography still holds a place of privilege in psychiatry, it is itself a guide that can become complicated. The
syndromic organization of current psychopathology has
been shown to have faults. It is believed that a functional
organization in this area could be more appropriately used
as a reference framework for research in biological psychiatry, with proposals for a two-tiered diagnostic system. On
the first tier we would find the nosological diagnosis, while
the second would include a detailed description of the psychological and biological components of the dysfunction,
together offering a way to deal with what has become a
problem in the area of psychiatry, which has been called,
rather ironically, nosologomania.71 These criteria support
our proposition regarding the need to read the findings of
psychopathological and clinical research from a new epistemiological point of view.
New systems have been proposed for grouping the
different psychiatric disorders, based on aspects such as
the presence of common genetic findings, the existence of
similar biomarkers, comorbidity, and response to the same
family of medications. Taking into account these proposals,
it is clear that schizophrenics share more dimensions with
bipolar disorder than with other mood disorders.72 More
recent psychopharmacological research offers evidence that
drugs originally proposed for treatment of schizophrenia,
such as olanzapine and quetiapine, are not prescribed for socalled drug-resistant depression.73,74 In the same way, other
medications initially used for epilepsy are now indicated
as mood stabilizers.75,76 Likewise, the so-called “Attenuated
Psychotic Symptoms Syndrome,” which is proposed for the
new DSM-V, seems to respond better to preventive treatment with SSRIs than with antipsychotics.4 This all points
toward a common pathogenetic mechanism that places the
separate entities of the nosotaxis in doubt.
A strong and significant overlap has been found in biomarkers such as the slow tracking eye movement, sensory
openness (P40), prepulse inhibition, the reduction of P300
and a neural synchronization defect both in schizophrenia
and in bipolar disorder.77,78,79,80 Although Del-Ben, Rufino
Armanda, Brandão Fragata et al.81 have used instruments
allowing them to hone the ability of the clinician to make
differential diagnoses in the first psychotic episodes, their
efficacy is clearer in episodes induced by drug abuse. It is
possible that with their instruments one can better distinguish between the different etiologies in the severe stages of
the disorder, but without a doubt, a very similar response has
been activated in all cases. Similarly, Mauricio Kunz, Keila
Maria Ceresér, Goi Pedro Domingues et al.,82 find biological data on inflammatory and immunological activity that
109
Rojas-Malpica et al.
seems to differ between schizophrenics and those suffering
from bipolar disorder, which could indicate a rather severe
expansion of the underlying impairment, which regardless
can exist in both cases, and so can result in false negatives.
Different structures have been indicated, sharing common aspects, both for schizophrenia and for bipolar disorder, especially the tonsil, the hippocampus, and above all the
prefrontal dorsolateral cortex, the supraorbital cortex, and
the anterior cingulate cortex.83 In these structures, alterations
have been described, such as differences in blood flow,84
hippocampal dysfunction that produces an impairment in
declarative memory with hypoactivity of the dorsolateral
prefrontal cortex and variable dysregulation of the anterior
cingulate cortex, as well as the prefrontal cortex, which explains the alterations in abstract thinking, mental flexibility,
and the initiation of an activity, as well as a dysfunction in
the ventrolateral cortex.85 In both entities a decrease has been
noted in the cerebral volume, with diminished gray matter,
evidenced in observable changed in imaging studies such as
nuclear magnetic resonance and FMR.86-93
Epidemiological and biological evidence, both of
schizophrenia and bipolar disorder, indicates more coincidence than difference. It has already been shown that there
is evidence of common basic neurobiological processes for
both disorders, but equally important is the evidence that
indicates a common genetic susceptibility, which would
explain the alterations in neurodevelopment and brain myelination, as well as those observed in brain functions such
as sensory discrimination and visuospatial orientation.94
Likewise, recent epidemiological studies also highlight
common components, making it ever more evident that
the diagnostic division between schizophrenia and bipolar disorder is unable to define different etiological and/or
pathophysiological entities. Large epidemiological studies,
as well as recent genetic studies, reinforce the strong connection between these disorders.95,96
In studies conducted with bipolar subjects that had psychotic symptoms, a relationship to the genome was suggested
in the 8p and 13q chromosomes, which have been implicated
in prior research both on schizophrenia and bipolar disorder. In other association studies for bipolar subjects with psychotic symptoms and subtypes such as bipolar patients with
psychotic symptoms incongruent with mood have shown
weak positive results for several potential dysbindin genes,
DAOA/G30, DISC-1 and neuregulin. This is consistent with
the hypothesis that subphenotypes of bipolar psychotic patients can represent a clinical manifestation of genes overlapping between schizophrenia and mood disorders.97
Specific common genes, or loci, have been implicated
in both disorders. The evidence suggests an overlap in the
genetic susceptibility between traditional systems of classification that dychotomize psychotic disorders into schizophrenia and bipolar disorder. The most notable findings
are the genes DAOA (G72), DISC1 and NRG1. Identifica-
110
tion of genes that make individuals susceptible to psychosis will surely have a large impact on our understanding of
pathophysiology, leading to changes in classifications and
clinical practice.98 More recently, studies have compared the
risk variant to the gene ZNF804A, rs1344706, finding it able
to invoke susceptibility for both disorders, where homozygous subjects showed a reduction in the cortical gray matter
in the superior temporal gyrus and in the anterior and posterior cingulate cortex.99
In a large study involving some 36,000 subjects with
schizophrenia and 40,500 with bipolar disorder, it was
found that immediate family members (parents, siblings
and offspring) of both groups had an increased risk for both
conditions. If a patient suffered from schizophrenia, his/her
siblings were nine times more likely to suffer bipolar disorder and four times more likely to suffer schizophrenia. Half
siblings with the same mother were 3.6 times more likely to
suffer schizophrenia if their half sibling had schizophrenia,
and 4.5 times more likely to suffer bipolar disorder. Half
siblings with the same father were 2.7 times more likely for
schizophrenia and 2.4 times more likely for bipolar disorder. Adopted children with a biological father with either
of the disorders had a significant risk for the other disorder.
This leads to the conclusion that both shared and unshared
environmental factors contribute to risk, but to a lesser extent than genetic predisposition.100
In an extensive association study conducted by the International Schizophrenia Consortium, the genomes of 3,322
Europeans was compared to 3,587 control subjects, showing
the extent to which common genetic variations underlie the
risk of suffering schizophrenia. They found the major histocompatibility complex on chromosome 6, as well as chromosome 4 related to cognition and 11 related to perception,
indicating that there is genetic evidence for a polygenetic
component for the risk of suffering schizophrenia, which involves thousands of common alleles of very little effect. This
component also contributes to the risk of suffering bipolar
disorder, but not for other non-psychiatric disorders.101
All these findings lead us to consider that the relationship between schizophrenia and bipolar disorder could be
described either as two pathologies that present a high level
of overlap, or as a continuum that presents one common nucleus of genetic, neurochemical, and structural susceptibility.102 Some authors103 suggest that as a model of the relationship between schizophrenia and bipolar disorder, extended
endophenotypes should be established, which, based on a
common genotype, would share one neuroanatomy, one
physiopathology and certain cognitive impairments that
would present a particular clinical manifestation. Other
authors104 have come to suggest that the current model of
schizophrenia includes multiple phenotypically juxtaposed
syndromes and that, as such, the unitary concept of schizophrenia may have come to an end, meaning we must configure the known facts on genomic, environmental, endo-
Vol. 35, No. 2, March-April 2012
Revisiting unitary psychosis, from nosotaxis to nosology
phenomic and phenotypic dimensions to identify groups of
etiopathologically significant and empirically demonstrable
entities. It can be concluded that the findings described on
the relationship between schizophrenia and bipolar disorder constitute a challenge for the conception that they are
unrelated diagnostic entities. These disorders represent a
continuum of deficits in neurodevelopment influences both
genetically and environmentally, more than etiologically
separate entities.105 Major clinical syndromes, in part for the
severity and for the predominant pattern of abnormal brain
development, result in functional deficits, modified in turn
by other genetic and environmental factors.106,107
Current classifications are based on symptoms and ignore etiology. It is said that these classifications have a high
level of reliability, an uncertain validity, and a variable utility. Biological criteria must be established for the current
diagnostic entities. The biological variables and the endophenotypes established could validate the diagnostic entities following quantitative and qualitative methods. There
is no doubt that contemporary neurosciences are close to
bringing clinical practice to identify the “underlying impairment,” as Kraepelin desired. But psychiatry does not read
symptoms as they do in neurology, a more topographical
and synchronic discipline, where the relationships are clearly established between injury, symptom and sign. Access to
the experiential world of the patient requires, in addition
to an understanding of his/her body, a diachronic exercise
that reveals the meanings and their value in the subjectivity
of the patient. In summation, it is a matter of a hermeneutic
with a higher level of complexity.
Final Reflections
Affirming the existence of a “unitary psychosis” would be a
controversial act given the clinical and neurobiological data
we have reviewed. However, the proposal of Llopis regarding the axial syndrome common to all psychoses (in plural, and so
multiple), seems to us an idea that sheds a lot of light on the
phenomenon, and one that is not theoretically exhausted. In
the same way, it seems difficult to construct clinical structures
as separate entities by virtue of recent research. At best, the
solution would be to do more nosology and less nosotaxis.
The historical approaches toward unitary psychosis
indicated by Berríos have in common their basis on a naturalist focus on the phenomenon, inherent to the positivism
so present in the sciences, even today. From this perspective, everything points to an enormous symptomatological,
biological and even therapeutic overlap between schizophrenia and bipolar disorder. However, another epistemiological possibility is opened by way of systems theory,
chaos theory, and complex thought. This is how we want
to suggest the possibility of a new reading of psychopathological phenomena, as a tension between the stochastic and
Vol. 35, No. 2, March-April 2012
the anankastic, which underlies many biological and social
happenings. Both in health and in disease, many processes
coexist, which are inherently linked to life. Apostosis must
occur, while neuroplasticity and neurogenesis must occur at
the same time. Using complex thought, it is easier to understand and accept the dynamics of programmed regularities
and emerging chaos.
Although from a mechanical and determinist point
of view, there are strong reasons to think that human behavior is overdetermined by cerebral biological conditions,
we cannot deny the processes which lead to the forming of
self-consciousness and that occur in the connection between
the sociodependent internal circuits and the so-called “exobrain,” represented in the myriad symbols that circulate in
our culture and that allow us to “conceive” objects, unlike
signs and signals, which only announce them. This is relevant, because Bartra believes that there is found the seed
of our own free will, which he believes to have a miniscule
representation in the entirety of our behavior.108 So, it bears
mention the importance of the hermeneutic effort in interpreting this symbolic world, and its value for the understanding of the psychotic existence. Although the so-called
“free will” has a quantitatively miniscule share of overall
behavior, its specific weight in the organization of subjectivity is enormous and fundamental. In some way we could
see it as the apex of the processes of autopoiesis that lead
to the expression of subjectivity, arrested by the anankastic
impositions of the psychotic process.
We believe that in the psychotic structure of world, mental life is anchored to some anachronic place of the physis,
from which it is anankastically regulated and subjected to a
progressive sclerosis that suspends the autopoietic systems. It
is a process where the many expressions of the entropic (energy seeking to organize itself) end up absorbed by a mineralizing structure, leaving very little for the fresh and chaotically
unexpected of healthy behavior. It is evident that in mental
illness there is a loss of complexity. As such, nineteenth century positivism must be transcended if the search for mental
health seeks to arrive at a restitution of subjectivity with all its
richness. An understanding of these phenomena will result in
new therapeutic practices, both psychosocial and biological,
and psychiatry will come closer to the concept of the science
of liberty, as Henri Ey once proposed.
REFERENCES
1. Berríos G. Historical aspects of psychoses: 19th Century issues. Br Med
Toro 1987;43(3):484-488.
2. Berríos G. Unitary psychosis in English speaking psychiatry: A conceptual history. En: Fur und wider die einhetspsychose. Mund C, Saβ H
(eds). Gerog theme Verlag. New York: Stuttgart; 1992.
3. Berríos G. The notion of unitary psychosis: a conceptual history. History
Psychiatry 1994;5(17):13-36.
4. Hueso-Holgado H. Riesgo del síndrome de síntomas psicóticos atenuados en DSM-V. Norte Salud Mental 2011;IX(39):19-26.
111
Rojas-Malpica et al.
5. Santo-Domingo J. La psicosis única en la actualidad: de H. Ey y B. Llopis
a la ICD-10 y la DSM-IV. Arch Neurobiol 1998;61(3):175-186.
6. Real Academia Española. Diccionario de la Lengua Española (DRAE).
Madrid: Espasa Calpe; 2001.
7. Mezzich J, Berganza C, Ruiperez M. Culture in DSM-IV, ICD-10, and Evolving
Diagnostic System. Psychiatric Clinics North America 2001;24(3):407-419.
8. Laín E. La medicina hipocrática. Madrid: Ediciones de la Revista de Occidente; 1984.
9. Moya J. Psicosis única y trastornos del lenguaje. Rev Asoc Esp Neuropsiq 1998;XVIII(66):219-234.
10. Morin E. El pensamiento complejo. Barcelona: Editorial Gedisa, SA; 2003.
11. Letelier J. Los derroteros científicos De Francisco Varela. Biol Res
2001;34(2):7-13.
12. Tutte J. ¿Es posible una psiquiatría dinámica? Aportes desde el psicoanálisis. Rev Psiquiatr Urug 2010;74(2):139-158.
13. Comte AU. Discurso sobre el espíritu positivo. Editorial Aguilar: Buenos
Aires; 1975.
14. Romanelli L. Teoría del caos en los sistemas biológicos. Rev Argent Cardiol 2006;74:478-482.
15. Morin E. La epistemología de la complejidad. CNRS, París, Fuente:
Gazeta de Antropología Nº 20, 2004 Texto 20-02. http://www.ugr.
es/~pwlac/G20_02Edgar_Morin.html, available at: www.pensamientocomplejo.com.ar
16. Llopis B. La psicosis única, escritos escogidos. Fundación Archivos de
Neurobiología. Madrid: Editorial Triacastella; 2003.
17. De la Portilla Geada N. Psicosis única en la actualidad. Salud Mental
2010;33(2):107-109.
18. Huertas R. Nosografía y antinosografía en la psiquiatría del siglo XIX: En
torno a la psicosis única. Rev Asoc Esp Neuropsiquiatr 1999;XIX(69):63-76.
19. Benitez I. La evolución del concepto de hebefrenia (primera parte). Alcmeon.1992;2(2):182–205. Available at:: http://www.scielo.org.mx/scielo
Org/php/reflinks.php
20. Zilboorg GG. Historia de la psicología médica. Buenos Aires: Librería
Hachette SA; 1945.
21. Villagrán J. Psicosis: Análisis histórico y conceptual. Revista Gallega Psiquiatría Neurociencias 1997;1:9-25.
22. De la Portilla N. Reseña histórica de las traducciones en psiquiatría. Valencia, Venezuela: Ediciones de la Universidad de Carabobo; 2003.
23. Lanteri-Laura G. Ensayo sobre los paradigmas de la psiquiatría moderna. Madrid: Editorial Triacastela; 2000.
24. Kraepelin E. Die erscheinungs formen des irresseins. Z Gesamte Neurol
1920;62:1-29.
25. Angst J. Psychiatric diagnosis: the weak component of modern research.
World Psychiatry 2007;6(2):94-95.
26. Arenas A, Rogelis A. Revisión de la historia del trastorno esquizo-afectivo y su relación con los rasgos de personalidad. Universitas Médica
2006;47(2):47-56.
27. Kretschmer E. Gedankenüber die fortentwicklung der psychiatrischen
systematik bemerkungen zu vorrstehender abhandlung. Z Gesamte
Neurol Psychiatr 1919;48:317-371.
28. Alarcón R. When the paradigms languish. World Psychiatry 2007;6(2):97-98.
29. Trimble MR. The psychoses of epilepsy. New York: Raven Press; 1991.
30. Baca B. Lo psicótico. Historia conceptual de las psicosis. En: Trastornos
psicóticos (ed). Barcelona, España: Ars Médica; 2007.
31. Meninger K, Ellenberger H, Pruyser P, Mayman M. The unitary concept
of mental illness. Bull Menninger Clin 1958;22:4-12.
32. Lavretsky H. The Russian concept of schizophrenia. A review of the literature. Schizophr Bull 1998;24(4):537-557.
33. Hueso Holgado H. Psicosis histéricas o trastorno disociativo psicótico. El problema de la nosología psiquiátrica. Academia Biomedicina
Digital. 2008:34(1-8). Available at: http://dialnet.unirioja.es/servlet/
articulo?codigo=2877424. Access date: August 13, 2011.
34. Peralta V, Basterra V, Zandio M, Cuesta M. Psicosis cicloide; etiopatogenia, características clínicas y nosología. Ediciones 1: Aula Médica Psiquiatría; Mexico: Grupo Aula Medica; 2008.
112
35. Crow TJ. A continuun of Psychosis, one human gen, and not much elsethe case for homogeneity. Schizoprh Res 1995;(2):135-145.
36. Murray R, Dutta R. The right answer for the wrong rehaznos. World
Psychiatry 2007;6(2):93-94.
37. Craddock N, Owen M. Rethinking Psicosis: the disadvantages of a dicotomus
classification now outweigh the advantages. World Psychiatry 2007;6(2):84-91.
38. Claridge G. Lecture of the Annual Conference in Cardiff. Psychologists
2006;19(11):656-658.
39. Berríos G, Hawser R. The early development of Kraepelin’s ideas in classification: a conceptual history. Psychological Medicine 1998;18:813-821.
40. Rojas-Malpica C. Las alucinaciones y el delirio como representaciones
anancásticas. Salud Mental 2010;33:379-387.
41. Trimble MI. The soul in the brain; the cerebral basis of language, art, and
belief. Baltimore: The Johns Hopkins University Press; 2007.
42. Rojas-Malpica C. El enfermo mental ante la muerte; Estudios clínicos de
antropología psiquiátrica. Valencia, Venezuela: Ediciones del Rectorado; Universidad de Carabobo; 2002.
43. Marina JA. Anatomía del miedo. Barcelona, España; Editorial Anagrama
SA; 2007.
44. Ferrater-Mora J. Diccionario de filosofía. Barcelona, España: Ariel; 2004.
45. Aristegui-Urkia I. La intencionalidad en la representación mental: Esbozo
de dos modelos. Citado 2008 feb. 08. Available at: http://www.sc.ehu.es/
yfwtahum/web/N.4/8.%20Aristegi.pdf. Access date: February 8, 2008.
46. Ricoeur P. La memoria, la historia, el olvido. Buenos Aires: Fondo de
Cultura Económica; 2000.
47. Foucault M. La hermenéutica del sujeto. Madrid: Akal SA; 2005.
48. Crick F, Koch C. A framework for consciousness. Nature Neuroscience
2003:6(2):119-126.
49. Changeux JP. El hombre de verdad. México DF: Fondo de Cultura Económica; 2005.
50. Libet B. Mind time; The temporal factor in consciousness. Harvard: Harvard University Press; 2004.
51. Kandel E. A new intellectual framework for psychiatry. Am J Psychiatry
1998;155:457-469.
52. Kandel E. Biology and the future of psychoanalysis: A new intellectual
framework revisited. Am J Psychiatry 1999;156:505-524.
53. Soto-Sedek JM. Consideraciones en torno al delirio y otras psicosis. Caracas: Fundación Editorial el Perro y la Rana; 2007.
54. Sarró R. Análisis temático de los delirios endógenos. Rev Psiquiatr Psicol
Med Eur Am Lat 1987;18(2):65-79.
55. Téllez-Carrasco P. Las timofanías, arquetipos de la vitalidad. Revista
Psiquiatría Psicología Médica Europa América Latina 1979;14(3):197.
56. Alonso-Fernández F. La objetivación alucinatoria: una alternativa entre
la vulnerabilidad psicopatológica y la estética comunicativa. Psicopatología 2006;26(3-4):69-103.
57. López A, Paíno M, Martínez P, Inda M et al. Alucinaciones en población normal. Influencia de la imaginación y la personalidad. Psicothema
1996;8(2):269-278.
58. Lanteri-Laura. Las alucinaciones. México DF: Fondo de Cultura Económica; 1994.
59. Amaral M. Alucinações: a origem e o fim de um falso paradoxo. J Bras Psiquiatr 2007;56(4):296-300. Serial on the Internet. Available at: http://www.
scielo.br/scielo.php. Access date: April 1, 2010.
60. Berríos G, Fuentenebro de Diego F. Delirio; Historia. Clínica. Metateoría.
Madrid: Trotta SA; 1996.
61. Dörr O. Psiquiatría antropológica. Santiago de Chile: Universitaria; 1997.
62. De Clérambault GG. Automatismo mental. Buenos Aires: Polemos; 2004.
63. Amaral M. Alucinações: a origem e o fim de um falso paradoxo. J Bras
Psiquiatr 2007;56(4):296-300.
64. Castilla del Pino C. El delirio, un error necesario. Oviedo: Nobel, SA; 1998.
65. Conrad K. La esquizofrenia incipiente. Madrid: Fundación Archivos de
Neurobiología; 1997.
66. Díaz J. Persona, mente y memoria. Salud Mental 2009;32(6):513-526.
67. González Valenzuela J. Genoma humano y dignidad humana. Barcelona: Anthropos; 2005.
Vol. 35, No. 2, March-April 2012
Revisiting unitary psychosis, from nosotaxis to nosology
68. Rojas Malpica C, Gómez-Jarabo G, Villaseñor S. La enfermedad mental
como anánkẽ. Inv Salud 2004;6(3):159-164.
69. Ey H, Brisset B. Tratado de psiquiatría. Barcelona: Toray-Masson; 1969.
70. Andrews G et al. Consistency of diagnostic thresholds in DSM-V. Aust
N Z J Psychiatry 2010;44(4):309-313.
71. Van Praag HM. Two-tier diagnosis in psychiatry. Psychiatry Res
1990;34(1):1-11.
72. Andrews G. 164th Annual meeting. Honolulu, Hi: American Psychiatric
Association; 2011.
73. Shelton RC, Williamson DJ, Corya SA, Sanger TM et al. Olanzapine/fluoxetine combination for treatment-resistant depression: a controlled study of SSRI and nortriptyline resistance. J Clin Psychiatry
2005;66(10):1289-1297.
74. Bauer M, El-Khalili N, Datto C, Szamosi J et al. A pooled analysis of two
randomised, placebo-controlled studies of extended release quetiapine
fumarate adjunctive to antidepressant therapy in patients with major
depressive disorder. J Affect Disord 2010;127(1-3):19-30.
75. American Psychiatric Association. Practice guideline for the treatment
of patients with bipolar disorder (revision). Am J Psychiatry 2002;159(4
supl.):1-50.
76. Smith LA, Cornelius V, Warnock A, Bell A et al. Effectiveness of mood
stabilizers and antipsychotics in the maintenance phase of bipolar disorder: a systematic review of randomized controlled trials. Bipolar Disord
2007;9(4):394-412.
77. Hong LE, Mitchell BD, Avila MT, Adami H et al. Familial aggregation of
eye-tracking endophenotypes in families of schizophrenic patients. Arch
Gen Psychiatry 2006;63(3):259-264.
78. Sánchez-Morla E, García-Jiménez M, Barabash A, Martínez-Vizcaíno V et al. P50 sensory gating deficit is a common marker of vulnerability to bipolar disorder and schizophrenia. Acta Psychiatr Scand
2008;117(4):313-318.
79. Swerdlow NR, Light GA, Cadenhead KS, Sprock J et al. Startle gating
deficits in a large cohort of patients with schizophrenia: relationship to
medications, symptoms, neurocognition, and level of function. Arch
Gen Psychiatry 2006;63(12):1325-1335.
80. Bramon E, McDonald C, Croft R, Landau S et al. Is the P300 wave an
endophenotype for schizophrenia? A meta-analysis and a family study.
Neuroimage 20051;27(4):960-968.
81. Del-Ben C, Rufino C, Teixeira B, Azevedo-Marques J et al. Diagnóstico
diferencial de primeiro episódio psicótico: importância da abordagem
otimizada nas emergências psiquiátricas. Rev Bras Psiquiatr [periódico na Internet]. Available at: http://www.scielo.br/scielo.php. Access
date: April 8, 2011.
82. Kunz M, Ceresér K, Goi P, Fries G et al. Serum levels of IL-6, IL-10 and
TNF-α in patients with bipolar disorder and schizophrenia: differences
in pro- and anti-inflammatory balance. Rev Bras Psiquiatr (periódico na
Internet]. Available at: http://www.scielo.br/scielo.php. Access date:
April 8, 2011.
83. Schloesser R, Huang J, Klein P, Manji H. Cellular plasticity cascades in
the pathophysiology and treatment of bipolar disorder. Neuropsychopharmacology 2008;33(1):110-133.
84. Schultz S, O’Leary D, Boles Ponto L, Arndt S et al. Age and regional cerebral blood flow in schizophrenia: age effects in anteriorcingulate, frontal
and parietal cortex. J Neuropsychiatry Clin Neurosci 2002;14(1):19-24.
85. Eisenberg D, Berman K. Executive function, neural circuitry, and genetic
mechanisms in schizophrenia. Neuropsychopharmacology 2010;35(1):
258-277.
86. Thompson P, Vidal C, Giedd J, Gochman P et al. Mapping adolescent brain
change reveals dynamic wave of accelerated gray matter loss in very early-onset schizophrenia. Proc Natl Acad Sci USA 2001;98(20):11650-11655.
87. Drevets W, Price J, Simpson J, Todd R et al. Subgenual prefrontal cortex
abnormalities in mood disorders. Nature 1997;386(6627):824-827.
88. Altshuler L, Bookheimer S, Proenza M, Townsend J et al. Increased
amygdala activation during mania: a functional magnetic resonance
imaging study. Am J Psychiatry 2005;162:1211-1213.
89. Weinberger D, McClure R. Neurotoxicity, neuroplasticity, and magnetic
resonance imaging morphometry: what is happening in the schizophrenic brain? Arch Gen Psychiatry 2002;59(6):553-558.
90. Connor C, Guo Y, Akbarian S. Cingulate white matter neurons in schizophrenia and bipolar disorder. Biol Psychiatry 2009;66(5):486-93.
91. Drevets W, Savaz J. The subgenual anterior cingulate cortex in mood
disorders. CNS Spectr 2006:13:8.
92. McDonald C, Bullmore E, Sham P, Chitnis X et al. Regional volume deviations of brain structure in schizophrenia and psychotic bipolar disorder: computational morphometry study. Br J Psychiatry 2005;186:369-377.
93. Arnone D et al. Magnetic resonance imaging studies in bipolar disorder
and schizophrenia: meta-analysis. Br J Psychiatry 2009;195:194-201.
94. Ellison-Wright I, Bullmore E. Anatomy of bipolar disorder and schizophrenia: a meta-analysis. Schizophr Res 2010;117(1):1-12.
95. Maier W, Zobel A, Wagner M. Schizophrenia and bipolar disorder: differences and overlaps. Curr Opin Psychiatry 2006;19(2):165-170.
96. Gottesman I. Complications to the complex inheritance of schizophrenia. Clin Genet 1994;46(1):116-123.
97. Tsuang M, Lyons M, Faraone S. Heterogeneity of schizophrenia. Conceptual models and analytic strategies. Br J Psychiatry 1990;156:17-26.
98. Goes F, Sanders L, Potash J. Putative psychosis genes in the prefrontal
cortex: combined analysis of gene expression microarrays. Curr Psychiatry Rep 2008;10(2):178-189.
99. Craddock N, O’Donovan M, Owen M. The genetics of schizophrenia and
bipolar disorder: dissecting psychosis. J Med Genet 2005;42:193-204.
100.Voineskos A, Lerch J, Felsky D, Tiwari A et al. The ZNF804A gene: Characterization of a novel neural risk mechanism for the major psychoses.
Neuropsychopharmacology 2011 (en prensa).
101.Lichtenstein P, Yip B, Björk C, Pawitan Y et al. Common genetic determinants of schizophrenia and bipolar disorder in Swedish families: a
population-based study. Lancet 2009;373:234-239.
102.Purcell S, Wray N, Stone J, Visscher P et al. Common polygenic variation contributes to risk of schizophrenia and bipolar disorder. Nature
2009;460:748-752.
103.Craddock N, O’Donovan M, Owen M. Psychosis genetics: modeling the
relationship between schizophrenia, bipolar disorder, and mixed (or
“schizoaffective”) psychoses. Schizophr Bull 2009;35(3):482-490.
104.Prasad K, Keshavan M. Structural cerebral variations as useful endophenotypes in schizophrenia: do they help construct “extended endophenotypes”? Schizophr Bull 2008;34(4):774-790.
105.McHugh PR, Slavney PR. Methods of reasoning in psychopathology:
conflict and resolution Compr Psychiatry 1982;23(3):197-215.
106.Keshavan S, Nasrallah H, Tandon R. Schizophrenia, “Just the Facts” 6.
Moving ahead with the schizophrenia concept: from the elephant to the
mouse. Schiz Research 2011;127:3-13.
107.Owen M, O’Donovan M, Thapar A, Craddock N. Neurodevelopmental
hypothesis of schizophrenia. Br J Psychiatry 2011;198:173-175.
108.Bartra R. Antropología del cerebro: Determinismo y libre albedrío. Salud
Mental 2011;34(1):1-9.
Declaration of conflict of interests: None
Vol. 35, No. 2, March-April 2012
113