The Eclipse of Self-Awareness

Examining Consciousness in the Neuropsychiatric Landscape

THE OTHER SIDE OF THE SHORE

In the book Ars Poetica, Jorge Luis Borges reminds us of rhetorical figures that reappear throughout the centuries. It is the Eternal Return of eFigure 2ssential metaphors: dreams and death, stars and eyes. The Argentinian poet considers the figure of the river as a metaphor for time, which uses the sensory image of the waterway to grasp the meaning of an abstract concept. According to Borges, the English playwright Alfred Tennyson destroyed a poem when he was fourteen years old, but fragments of the page were recovered, and one line survives: Time flowing in the middle of the night. At night the world is silent and human beings sleep, but time continues to flow.¹Oliver Sacks proposed a reworking of this metaphor and left us a posthumous book: The River of Consciousness. The title suggests that consciousness is a process of change, a current in perpetual motion. But a river has boundaries: each bank imposes constraints, formed by an intricate weave of grass, mud, and stones. What structures impose limits on conscious activity? Do we know its spring and its delta?

This essay is about the flow of subjective experience. I want to pause and consider a particular aspect of consciousness: the process of self-awareness. To organize our behavior, we must acknowledge our body, our actions, and the effects we have on the surroundings. According to Frédérique de Vignemont, bodily self-awareness arises from the sense of ownership over one’s body parts, the sense of agency over one’s actions, and the sense of bodily presence.²In neurology and psychiatry, there are profound disturbances in these forms of bodily consciousness, leading to disruptions in the experience of being oneself and inhabiting a familiar world.

What can the science of consciousness learn from studying neuropsychiatric conditions? First, we can examine disorders marked by a loss of self-awareness. One patient, for example, experienced brief, paroxysmal episodes in which she had visual illusions and autobiographical hallucinations and immediately felt that her left limbs were not her own. Although initially labeled as “hysterical,” further investigation revealed a case of epilepsy. The source of the abnormal electrical activity was a parasite located in the occipital cortex of the right cerebral hemisphere.³The spread of the epileptic seizure to the right parietal cortex was causing the state of asomatognosia ―that is, the loss of the sense of ownership over the left arm and leg. In this case, neuropathology offers key insights into a core feature of self-awareness: feeling that my limbs are an intrinsic part of myself.²It also reveals a problem of epistemic injustice: the patient is labeled “hysterical” because the symptoms are unexpected. Clinical research into self-awareness could help prevent this kind of injustice.

Secondly, we can study disorders characterized by the intrusion of abnormal phenomena into the field of conscious experience. Hallucinations are key in this context. For example, a patient lost vision in the lower left part of her visual field due to a brain injury. During epileptic seizures, autobiographical scenes would appear for a minute, but only in the blind, lower left area of her visual field, as phantom images.⁴This case comes from the field of neuropsychiatry, but it resembles an ordinary phenomenon: the fact that we all have a blind spot in our visual field, and yet we do not see it. This invites us to confront both philosophical and scientific explanations of visual experience. I wonder: is our visual experience direct, or is it constructed through a predictive, generative brain model, continually corrected by signals from the sensory organs? What is the role of theories of consciousness in explaining neuropsychiatric disorders? ^5–8

Currently, the investigation of neuropsychiatric conditions is in a preliminary phase, as we do not have a complete scientific explanation of the relationship between consciousness and bodily processes. But we do know that these problems are real. They do not disappear by decree. They are recalcitrant, even if many people deny their existence. Sometimes there are cognitive deficits, but there may also be excesses or distortions in the qualitative dimension of subjectivity. The scientific study and philosophical analysis of disturbances in self-awareness offers a tool for examining human consciousness.^9–11 I suggest that theories of consciousness may carry a deontological commitment to pathologies of self-awareness. If they contribute both to scientific explanation and phenomenological understanding of clinical problems, their value increases. If they remain heuristically barren ―if they lack theoretical fertility for analyzing neuropsychiatric phenomena― their value diminishes.

In the first section of this essay, I define neuropsychiatric conditions and pose two questions: What can the science of consciousness learn from studying these problems? And what can neuropsychiatry learn from engaging with scientific models of consciousness?

In the second section, titled Disintegration, I present a problem that arises at the crossroads of natural disaster and brain disease. I address the phenomenon of nihilistic delusion ―Cotard’s delusion― in the context of autoimmune psychosis. This is a story of hope, grounded in a scientific discovery that clarified a profound disorder of self-awareness. Moreover, effective therapy in this case offers empirical support for causal reasoning. Yet the case also raises a theoretical problem: if intervening on the components of a system explains changes in its emergent properties, such as consciousness, does this inevitably lead us to a reductionist conception? This question is addressed throughout the essay.

In the third section, I explore what I call the unsettling side of consciousness. Through a case study, I undertake the problem of psychalgia and the structure of illness narratives. The story involves a disorder marked by unilateral musical hallucinations that transmit a peculiar litany, experienced by the patient as blue music that degrades his bodily organs: a beautiful and destructive melody. How can we understand such an intricate phenomenal pattern? The case defies clear explanation by the standards of cognitive neurology, prompting us to consider complementary frameworks such as phenomenological psychopathology and affective neuroscience. Ultimately, the most plausible explanation of this case of affective psychosis seems incompatible with neuroscientific reductionism and compels us to take psychological causality seriously.

In the final section, I argue that neuropsychiatry contributes to developing the explanandum of what we call consciousness: in other words, by studying neuropathologies of self-awareness, clinical research helps to characterize the phenomena in need for explanation.⁹ The integrated analysis of autoimmune and affective psychoses obliges us to reflect on the relationship between life and consciousness. I propose an ecological systems framework as an alternative to both holism and reductionism.

When studying neuropsychiatric conditions, we need a dual approach. There is a neuropathological aspect, a tangle of neural processes altered by disease, and analyzing these patterns provides essential clues from a third-person perspective. By this, I mean the perspective of an external observer who applies quality controls to ensure accuracy and precision in measurement. But there is also a psychopathological aspect: behavioral and cognitive dysfunction, and qualitative disturbances in subjective experience. While changes in behavior and cognition are documented through more or less objective methods, an intersubjective approach is mandatory to interpret the patient’s subjective states.

Sometimes, there is a meaningful relationship between neuropathology and psychopathology; when this occurs, we can properly speak of a neuropsychiatric problem. In some cases, neuropathology fully accounts for psychopathology. The classic example is neurosyphilis, once a leading cause of admission to psychiatric asylums in the 19th century. Frequently, however, no observable neuropathological pattern is identified. Or it is present but fails to explain the psychological disturbances. In any case, whether or not a neuropathological substrate is identified, it is worth recalling the statement by German E. Berrios: “The issue is not whether a mental disorder is, or is not, inscribed in the brain, but whether the decision that a given behavior constitutes a mental disorder can be made solely on the basis of brain analysis. The answer is: it cannot.”¹²

How should we understand the words of Dr. Berrios? They point toward the irreducible dimension of the psychological. This does not necessarily imply the existence of a mental essence or substance distinct from the matter and energy of the physical universe. Rather, I would argue that the functional organization of matter and energy in living beings gives rise to emergent properties of the agent as a whole, properties not present in the system's components. For instance, the conscious activities involved in goal-directed behaviors, such as writing and reading this essay.

Technically, inspecting the brain allows us to diagnose a structural pathology, but to answer whether the pathology affects mental function we must investigate whether there is an impact on behavior or conscious experience. This requires an intersubjective evaluation of the patient’s rationality: their cognitive and ecological functioning, their values, goals, and contexts, the level of suffering and their capacity to cope with it.¹³ In other words, the normative dimension in psychopathology, and in general medicine, is inescapable.

The study of pathology leads us down unsettling paths where the intuitions we hold about self-awareness become obscured. I dare to continue Borges’s play on recurrent metaphors. So, I ask: when it comes to disorders of consciousness, what lies on the other side of the river? As a physician in a neurological hospital, my work consists of taking care of people in states of psychosis. For decades, we have observed individuals with delusions and hallucinations, who descend into stages of impenetrable catatonia. I wonder about the other side of the river every time I face a person who remains with eyes open ―rigid, motionless, mute― for weeks or even months. Despite my best efforts to attune with these patients, their subjective experience lies beyond my knowledge. Is it akin to a nightmare, or an ecstatic dream? Or is there a complete absence of phenomenal experience?

Sometimes we observe full recoveries. In other cases, the condition evolves into a coma state, accompanied by seizures, and at times, death ensues. Only in recent years, thanks to immunological research, have we come to understand that some of these patients suffer from a disease caused by antineuronal antibodies. Immunotherapy can lead to awakenings like those narrated by Oliver Sacks in the unusual context of lethargic encephalitis. Once the catatonic syndrome dissolves, we can finally interact with the person to explore the details of their subjective experience. To explain more clearly the problem of autoimmune psychosis, and the challenges it raises for the investigation of consciousness, I will evoke a moment from recent Mexican history: the earthquake of 2017.

DISINTEGRATION

If you don’t live in Mexico City, it’s hard to understand why twenty million citizens harbor so much fear toward a date on the calendar. On September 19, 1985, a devastating earthquake claimed thousands of lives. In response, Mexican society developed an alarm system and organized earthquake drills. Some politicians, with a macabre sense of humor, decided that the annual drill would be held on September 19, as if we were celebrating the earthquake’s birthday. After hearing the alarm, we exit in an orderly fashion to safe gathering points. And that’s exactly what we did on September 19, 2017. But a couple of hours after the drill, we heard a rumble: a prolonged, primal rupture of the Earth, and felt the ground move violently beneath us. The jolt made us scream. We never imagined there would be a real earthquake that day. The coincidence in dates between the 1985 and the 2017 events felt like a sadistic version of Nietzsche’s theory of Eternal Return.

Mexican society came together in solidarity to help the victims of the disaster. Amid the devastation, a 37-year-old chiropractor ―I’ll call him Diego― joined the rescue efforts. As he walked through the ruins, he began to feel weak. While removing debris in search of survivors, he was running out of strength and started taking longer and longer breaks. There was a state of unease, as if something terrible was about to happen: an ominous premonition of inevitable collapse. Fear took hold of him, along with a deep sense of guilt: he couldn’t help others in their time of need. Diego had a constant headache, couldn’t sleep, and stopped eating. Words no longer came out of his mouth; he began to speak in whispers. He grew irritable with others, without fully understanding why. When he finally spoke to his wife, he revealed an intense fear of his relatives. He heard their voices even in their absence: voices that insulted him. He saw people wielding knives, emerging from unexpected places to attack him. Water was poisoned, so he refused to drink. His body stopped functioning: he couldn’t move, speak or breath; his organs had shut down. The heartbeat had ceased. A few days later, he became aggressive towards his family and attempted suicide. His wife took him to the Institute of Neurology.¹⁴

At the hospital, Diego had his eyes open but remained immobile and wordless. He did not react, even when syringes were used to draw blood or administer injections. He gasped and let out guttural sounds and screams that terrified other patients in the emergency ward. Cardiac monitoring showed drastic fluctuations. His skin was drenched in sweat, causing rapid fluid loss. His entire body was rigid, leading to muscle breakdown and a rise in a protein that damaged his kidneys. He developed renal failure and pneumonia and was transferred to the Intensive Care Unit.

Diego was awake, technically, but his brain activity in the electroencephalogram resembled a coma state. Immunological testing in the cerebrospinal fluid revealed the presence of antineuronal antibodies targeting NMDA glutamate receptors. The diagnosis of autoimmune encephalitis was established.¹⁵ We initiated immunotherapy with plasmapheresis, a procedure in which the blood is removed, the plasma is separated to eliminate antibodies, and the blood cells are reinfused with a replacement solution.

Diego regained the ability to speak, but he remained psychotic for several days. At one point, he said that his heart was “on the right side” and had stopped beating. “I have no feelings because I’m dead… All human beings will be dead.” In the next days, he remained muttering short phrases and isolated words. During a medical visit, a doctor asked, “Do you know where you are right now?” He replied, “In a symbology.” “What do you mean, in a symbology?”. Diego answered, “I’m dead among many companions… human beings… complete human beings… it seems like a program… we will be dead… always have been.” He looked deeply dejected, slumped in an uncomfortable position. A nasogastric tube had been placed; he hadn’t eaten in days and was severely malnourished and anemic.

In the following days, the delusional state improved with general care, nutrition, conversation, physical activity, and medications to promote sleep and reduce psychosis. After completing immunotherapy, he was able to walk and eat again and was discharged after forty-two days. As an outpatient, he received maintenance immunotherapy. His wife reported that he had regained his cognitive abilities and returned to work. The psychiatric medication was tapered, and he never experienced a relapse. During follow-up, his memories of the episode were not entirely clear. “I felt very weak after the earthquake, like in those nightmares where you try to speak but your tongue won’t move. You try to react, but your body is completely stiff. I felt time stretching… I was in the rubble, trying to find my family, but he scene repeated over and over, like a broken record. That’s when I tried to kill myself. Time stopped completely… it felt like an eternity… Eventually I opened my eyes, but everything was frozen among the ruins. I truly believed I was a corpse among many, buried in the debris of the earthquake. And I felt the doctors and nurses weren’t real. They were part of a game, or a computer program designed to conceal my death. ” ¹⁴

A couple of decades ago, we treated similar cases of people immersed in delusional, catatonic, and confusional states. According to the medical doctrine of the time, these were psychiatric disorders of unknown origin or viral infections of brain. Unfortunately, the cause was unknown, treatments were ineffective, and mortality was high. The discovery of anti-NMDA receptor antibodies arose in an unexpected context.

Some women develop ovarian tumors called teratomas, which originate from ectodermal tissue and can form rudimentary neurons. The word teratoma comes from the Greek τέρας, τέρατος (téras, tératos), meaning nightmare or monster. These tumors have fascinated people since antiquity because they sometimes contain hair, teeth, or bone, and, in extraordinary cases, body parts like hearts or hands. Occasionally, teratomas form neurons that express NMDA glutamate receptors. The immune system responds by producing antibodies against the tumor’s neuronal receptors. If these antibodies reach the brain, they disrupt glutamate signaling and cause vivid, chaotic states of psychosis. We eventually learned that men could develop this form of encephalitis. For instance, brain infections caused by herpes simplex virus can destroy neurons and release NMDA receptors, inducing the production of antineuronal antibodies.^16–18

To explain a case of autoimmune psychosis we must ask two questions: Can we say that the psychopathological pattern is caused by an antineuronal antibody targeting the NMDA glutamate receptor? And what is neurocognitive mechanism involved in this disturbance of conscious activity? The answer to the first question is that there is a causal relationship between the antineuronal antibody and the altered patterns of mental experience. The relationship between anti-NMDA receptor encephalitis disease and psychosis is strong according to epidemiological from many centers around the world. ^17,19–21 But what about the context of the illness? It is reasonable to assume that the traumatic experience of the disaster contributed to the content of Diego’s delusion: he saw himself dead among the rubble, alongside other corpses. Also, if the patient had circulating antibodies in peripheral blood, traumatic stress could act as a triggering factor, increasing the permeability of the blood-brain barrier and allowing the antibodies to access the nervous system. Animal models have shown that stress alters blood-brain barrier permeability, and clinical reports suggest that some cases of encephalitis are precipitated by psychosocial stress.^22,23 However, the earthquake was a precipitating factor, not a necessary cause, whereas the autoimmune pathology has a causal role in a strong sense. Woodward’s interventionist approach to causal analysis postulates that a factor is causal if and only if an intervention on that factor produces a significant change in the effect. ^24–26 In Diego’s case, a clear response to treatment was observed, but this is not an isolated effect: the analysis of 164 cases of autoimmune psychosis in a prospective study showed significant improvements following immunotherapy. This is consistent with international research.^17,27–29

The second question is more difficult: in Diego’s case, what is the brain mechanism involved in the disturbance of conscious experience? This can be answered on many levels, depending on how deep we want to go. I must say that the relationship between the NMDA receptor and psychosis is well established. Ketamine, a drug blocking this receptor, has been used as a dissociative anesthetic: it blocks sensory signals as powerful as the pain from a surgical wound. A side effect is immersion in a hallucinatory state of great aesthetic intensity. ³⁰ Thus, the NMDA receptor is related to psychosis in a non-trivial way: pharmacological manipulation induces delusions and hallucinations, and genomic abnormalities in this system increase the risk of chronic psychosis: some variants of the GRIN2A gene, which is necessary for the NMDA receptor synthesis, increase the risk of schizophrenia by a factor of 24. ^31–33

Disruption of NMDA receptors, as seen in dissociative anesthesia, impairs the neurocognitive mechanisms underpinning consciousness. What about autoimmune pathology? When the antineuronal antibodies attack the NMDAR receptors, this causes an internalization of these membrane proteins. The subsequent reduction of their density in the synaptic space leads to a decay of glutamate signaling. According to Global Neuronal Workspace theory, the glutamate system is relevant to explain conscious processing. The theory postulates that specialized neuronal populations are connected through a central network of densely interconnected pyramidal neurons with long-range axons, located primarily in parietal and prefrontal cortices. This network enables a global broadcast of neural information through a two-step process. First, a rapid wave propagates feedforward, through the cortex. This bottom-up signaling is mediated through AMPA receptors, which act as sodium channels, changing the neuron's electrical state and enhancing NMDA receptor sensitivity. Then, a slower, feedback-driven phase follows. This is a top-down signaling process mediated by NMDA receptors, which are calcium channels. These feedback signals sustain a global, reverberating state of synchronized corticothalamic activity. Conscious experience is thus instantiated, and the subject gains a flexible, multimodal, and sequential cognitive activity.^34,35 If we rely on predictive coding as a theory of consciousness, NMDA receptors may be crucial for top-down signaling to posterior cortex and pre-activating sensory templates in higher-order sensory areas.^36,37

While NMDA receptor dysfunction is critically important for understanding autoimmune psychosis, we need additional tools to explain the disturbance of large-scale neuronal networks. Molecular neuroimaging through positron emission tomography provides a representation of the human body’s energy metabolism. Figure 1 shows a finding that characterizes anti-NMDA receptor encephalitis. If we examine the image, we observe “cool” colors (blue and green) in the posterior part of the brain. What does this mean? According to the standard color code, there is a metabolic deficit in that region, so severe that it approaches the pattern observed in patients with persistent vegetative state. ³⁸ This indicates an energy deficiency in the inner and posterior cerebral cortex, corresponding to the posterior cingulate cortex and the precuneus. This is not an isolated finding: systematic research using positron emission tomography shows this metabolic pattern in patients with anti-NMDA receptor encephalitis.^39,40 A first question appears: Why does this disturbance in brain metabolism occur?

Figure 1. ¹⁸F-FDG PET/CT scan in a patient with autoimmune psychosis due to anti-NMDA receptor encephalitis. Two brain images are shown: the lateral view on the left, and the medial view on the right. The scan reveals characteristic findings of the disease: severe posterior hypometabolism in the occipital and parietal cortices, along with anterior hypermetabolism in the lateral surface of the frontal cortex.

A neurochemical atlas of the brain built with positron emission tomography, with more than 1,200 healthy individuals, shows the highest concentration of NMDA receptors in the inner surface of the parietal and occipital cortices.⁴¹ This geographical distribution correlates with the abnormalities observed in anti-NMDA receptor encephalitis. In this disease, antineuronal antibodies cause internalization of the NMDA receptor.¹⁷ The subsequent reduction in neuronal activity leads to a decrease in metabolic demand: thus, we see an intense blue color in the parieto-occipital cortex.

A second question arises: does the altered metabolic pattern help explain the disturbance in conscious processing? The approach to this question requires an analysis that goes beyond localizationism. The typical metabolic pattern in anti-NMDA receptor encephalitis, as depicted in Figure 1, is an abnormal anteroposterior gradient.^40,42 A disruption of the functional connectivity between anterior and posterior brain regions if of great interest to self-awareness. On the left side of the image, we see the lateral aspect of the cerebral hemispheres. Anteroposterior connectivity between the prefrontal, parietal, and temporal cortices is critical for detecting salient and unexpected stimuli, and for implementing goal-directed attentional control, which enables us to select and track stimuli.⁴³ According to Global Neuronal Workspace theory, this connectivity supports the global broadcasting of neural information. The framework of predictive coding provides a complementary insight: anteroposterior connectivity is necessary for the top-down and bottom up feedback signaling that enables the updating of internal models prediction error minimization.^{5,8,34,35,44,45}

On the right side of the image, we see the medial aspect of the cerebral hemispheres. The posterior parietal cortex is a key component of the default mode network. It acts as an integrative and distributive hub for multiple bioelectrical signals related to self-awareness: interoceptive and spatial representations of the body, the construction of first-person perspectives, and access to autobiographical memory.^{38,46,55,47–54} The synchronization of posterior and anterior neuronal populations across the cortical–subcortical midline axis is necessary for the representation, monitoring, evaluation and integration of the self-referential stimuli that will become conscious. ^{49,54,56–58} Furthermore, the connection between posterior and anterior regions enables access to motor systems, necessary for interacting with the world. Patients with anti-NMDA receptor encephalitis suffer from severe psychomotor disturbances: catatonic signs such as repetitive patterns, immobility and mutism.^59–61On more than one occasion, I have considered that nihilistic delusions in encephalitis are a way to express the lived experience of catatonia.

So far, antineuronal antibodies disrupt the large-scale connectivity necessary for conscious access and bodily self-representation. But I want to take a step back to view the problem from a broader perspective. Perhaps a look at bioelectric signaling provides insights into how the brain instantiates patterns of meaningful conscious activity. In the book Neural Basis of Free Will: Criterial Causation, Peter Ulric Tse argues that the NMDA receptor is critically important for neurons to detect patterns of energy, not merely quantities of energy. To understand this, consider the analogy of a radio tuning meaningful signals amid surrounding noise. Neurons must detect relevant signals, and NMDA receptors play a seminal role in this process. These receptors are sophisticated ion channels requiring several conditions to allow calcium to enter the neuron: on one hand, it needs the binding of glutamate and glycine. This indicates activity from other neurons. On the other hand, it depends on a minimum postsynaptic voltage, which reflects the activity of the neuron where the receptor is located. Technically, the NMDA receptor detects the coincidence between pre- and post-synaptic activity. This allows it to function as a coincidence detector, and to participate in a process fundamental to life: the detection of stimulation patterns that indicate opportunities for interaction.^62–64 Paraphrasing Peter Godfrey-Smith, the function of consciousness is to enable the agent to deal with environmental complexity.⁶⁵

What does this mean, in a broader sense? What we call life, says doctor Tse, introduced into the universe a new and revolutionary form of causality. Under the laws of physics, events in the universe are explained by interactions of matter and energy, emphasizing the amount of energy. But to understand conscious activity, quantities of energy are not enough. With the emergence of life, a new, emergent form of causality appeared: the activity of living beings depends not only on the amount and frequency of energy, but on patterns of stimulation. By this, I mean patterns of energy that stimulate organisms through phase relationships. The spatial and temporal configurations of stimuli are detected by living organisms and encoded through biological signaling. Cells ―whether unicellular organisms like amoebas or neurons within the human brain― respond to environmental stimuli not simply because those stimuli carry energy, but because the spatiotemporal configuration of the stimuli is meaningful to the organism. These patterns have formal characteristics that rise above background noise and are detected through receptors in the cell membrane, which are sensitive to phase relationships. Pattern detection allows them to react to objects based on shape, location, movement, and value for survival: Do the stimuli signal a threat to the organism’s life, or do they indicate an opportunity for nourishment, respiration, or play? Moreover, the specific response to relevant signals enables many neurons, even millions, to synchronize, a process essential for establishing functional connectivity across large scale neuronal networks. Could there be continuity between this physiological process and the collective organization of human populations through human semiosis? I explore this question in the final section of the essay.

Before concluding this section, I would like to summarize a few ideas. The study of immune-mediated psychosis supports the hypothesis that NMDA receptors act as coincidence detectors, mediating the recognition of meaningful patterns of stimulation. A rupture in the spatial and temporal continuity of anteroposterior connectivity ―due to the effect of antibodies on the NMDA receptor― leads to a collapse of self-representation within the integrated flow of consciousness.⁶⁶ But this raises a theoretical problem: if changes in phenomenal experience are explained by antibodies disrupting the bioelectrical signaling, by disconnections in the large-scale functional networks, and by the effects of immunotherapy, does this imply a reductionist account of consciousness? Can the analysis of subpersonal physiological processes fully explain the clinical changes in self-awareness? In the next section, I address this question through a clinical case involving bodily delusions that emerge in the context of a life trajectory. If psychological causality is real, subpersonal physiological changes can be driven by affective interactions. This brings us to the central question of this essay: how can we reconcile both explanatory frameworks?

PSYCHALGIA AND THE UNSETTLING SIDE OF CONSCIOUSNESS

Perhaps Borges was right: our thinking moves elliptically around a few essential metaphors. Yet these figures can be renewed if we are open to scientific discovery, artistic creation, and philosophical reflection. Then, living metaphors ―as Paul Ricoeur called them― emerge and revitalize our understanding. The French thinker and Borges agree on a key idea: when metaphors age, they eventually become commonplaces of ordinary language. At that point, they become dead metaphors.

I wonder whether the clinical study of self-awareness can take us beyond computational metaphors. Should we accept Putnam’s notion of the mind as software interacting with hardware, that is, logical states that can be dissociated from physical states? Unlike digital computers, human beings construct affective experiences in the service of survival, enacting relevance.⁶⁷ Our very lives, quite literally, unfold between joy and suffering. Allow me to share a case study that leads us to the core of affliction: psychalgia or affective pain.⁶⁸ In this context, pain is an analogy, but we lack words to express the experiential qualities of suffering. In the face of psychalgia, we are left only with unsettling metaphors.

In this story, I find myself in the neuropsychiatry unit; it is the first Monday of the year. I read the file of Jacinto, a 32-year-old man. Two months ago, he stopped drinking alcohol and entered a state of delirium tremens: He saw snakes, centipedes, and tarantulas crawling over his body. The psychotic symptoms persisted for several weeks. On January 1st, the patient walked barefoot into a ravine. His cousin found him with deep cuts on his neck and both wrists, bleeding heavily. The patient said he had gone there following a pickup truck blasting loud music. The song lyrics were inviting him to follow them. He also said they had removed his kidney and lungs, that he was empty and lacked all his organs.

He lies withdrawn in his bed, showing no interest in the courtyard, where other patients go through the motions of the lunchtime ritual. Jacinto remains silent, tense. As the conversation unfolds, he takes interest in my presence. The morning light doesn’t reach the room, and the contours of night remain with us. Some people in his town play music in their cars, he says, and the music takes away parts of his body. “I don’t know how they do it, but little by little my lungs disappear, my kidneys... the song goes: you have a blue pancreas, a blue pancreas, a blue pancreas... and that’s how I find out they’ve taken that organ from me.”

Once, he was asleep when they opened him “down the middle,” from head to legs, to inspect him and remove his body parts. He falls silent, then exclaims: “They’ve already done it! They stole my stomach, and I can’t eat. So, I decided to stop eating. I’ve lost the liver, the intestines, the kidneys. I already lost one lung. Only the other one is left, and my heart. They use very high-pitched, loud music. Today, the lyrics said: Now it’s turned blue. That means my organ is empty, or that there are no more organs, and the body is hollow.”

I ask, astonished: “Does blue mean it’s empty?”

“That’s right. And they do all this through music.”

A few days after admission, Jacinto tells me he can only hear the music with his left ear. On the same side, he constantly hears the voices. “They order me to stand up so they can rape me, but I stay on the edge of the bed and don’t get up.” When he considers taking his medication, they read or see his thoughts. They told him not to take it: You’re fine. The voices are real.

We discovered that the left ear shows a hearing deficit. According to the neuro-otology department, he suffers from left-sided post-traumatic hearing loss, which began after a direct blow to the left mastoid region by third parties, resulting in a constant tinnitus accompanied by slowly progressing hearing loss. Jacinto describes it like this: “I was coming out of the bar and took the wrong path. It was nighttime and the street was completely deserted. Some people wanted to rob me, but I told them they wouldn’t get anything because I didn’t have a single coin. Now you're screwed, they said. They struck my ear with a stone, and I felt the blood coming out. I made it home crawling.”

I ask him if he still has suicidal thoughts, and he says he doesn’t want to take his own life. “Even though they want me to kill myself.” The conversation has shifted to a life story marked by tragic turns. His mother abandoned the family when he was seven. His father assumed responsibility for their upbringing, but was absent most of the time, and his lover belittled and verbally abused them. Jacinto learned to read and write, but he stopped attending school. He moved from house to house, living with his father in Tetela, a community below the volcanoes. The task of raising him fell to his older sister. But the siblings migrated to different towns and the family disintegrated.

His father taught him to drink before he was twelve. They would go out drinking together: beer, aguardiente, or whatever they could get their hands on. Once, they went out with his uncle and drank late into the night. They ended up sleeping in an unfinished building in the forest. At dawn, his father was putting on his pants. Jacinto asked him: "Where are you going, sir?” The father replied: “And what’s it to you? I’m just going outside to pee.” Jacinto looked at him and said: “It’s just… something’s off. When you go to pee, you don’t take your belt, but now you’re holding it.” His father said: “What does it matter if I have a belt or not? Just go back to sleep. Why are you worrying about my business?” He walked out of the room, but Jacinto, uneasy, couldn’t sleep. “I found him outside, hanging from a beam, the belt tied around his neck. We brought him down with my uncle. He wasn’t breathing, but his body was still warm.”

After several days of pharmacological treatment there is a clear improvement: he eats and sleeps well, his mood has recovered, and little by little, he is interacting more with other patients. We have ruled out brain lesions through brain imaging, and the electroencephalogram is normal.

Suddenly he tells us: “I no longer hear the music; it was beautiful, but very loud, like a brass band, and it wouldn’t let me think.” At discharge, verbal hallucinations persist, but they no longer cause a sense of threat. The nihilistic, somatic, and persecutory delusions have disappeared.

Many years have passed since then. To write this account, I searched through my old notebooks: I do not want to distort Jacinto’s words. We found no evidence of a neurological disease. How, then, can we explain the psychopathological constellation? One might propose the onset of a chronic psychiatric condition such as schizophrenia. It would be a reasonable hypothesis, but certain clues invite a more careful explanation: alcohol dependence and withdrawal can produce the transient brain dysfunction of delirium tremens. The loss of hearing in the left ear helps us understand why a buzzing sound —tinnitus— arose there, as a phantom perception, and later, why verbal hallucinations emerged with the same lateralization. Yet the events that precipitated his mental illness are not limited to physiological processes. The life story is characterized by maternal abandonment, family disintegration, neglect during upbringing, rootlessness. This forms the backdrop for a traumatic history of interactions, including childhood abuse and paternal suicide. There is no need to resolve the metaphysical controversies of downward or mental causation; I rely on well-established concepts from psychology and affective neuroscience: above all, psychological causation is explained through the laws of learning. Under the influence of phylogenetic dispositions, processes such as sensitization, classical conditioning, operant behavior, and vicarious learning reshape the functional architecture of the nervous system, through changes in synaptic plasticity, inflammatory processes, and dysregulation of energy metabolism. Taken together, these events lead to learned helplessness: a state of affective psychosis taking the form of Cotard’s delusion.^69–71And yet, the question stands: why does a pathology of self-awareness emerge?

In the years that followed, I came to know Jacinto better and gained a clearer understanding of the factors that shaped his outcome. Once the hallucinatory experience faded, he told me that he had been threatened by unreal people, that it was impossible for music to remove his internal organs; that his illness stemmed from abandonment and chronic loneliness, and that he had improved thanks to the medication. He never drank alcohol again, having made a vow at the church.

During one consultation, we spoke about his suicide attempt. The conversation offered insight into the formation of his mental symptoms. “It was New Year’s Eve. I was barefoot and started walking. I don’t really know why I did it. The memory of my father came over me, how much he suffered. I felt an unbearable pain in my chest and couldn’t breathe. Someone was chasing me. I jumped over a gate and went down into a ravine. I didn’t feel anything. I wasn’t myself. Suddenly, I found a bottle. I broke it on a stone and began cutting myself with the glass in my right hand… it bled a lot, but it didn’t hurt. Then the left hand, then my neck. I kept walking until I reached the streets. That’s where my cousin found me.”

To understand Jacinto’s account, we need to integrate phenomenology and affective neuroscience. According to Naomi Eisenberger’s experimental work, social disconnection and emotional loss activate paralimbic regions, particularly the dorsal anterior cingulate cortex and the anterior insula. These structures express opioid receptors and play a critical role in pain through their connections with the periaqueductal gray, an ancient brainstem nucleus regarded as “the hidden spring” due to its crucial role in affective consciousness. Notably, opioid analgesics have been shown to reduce separation distress. ^72–77

My hypothesis is that Jacinto’s experience of psychalgia arose from separation distress. For many years, alcohol masked his affective pain; however, withdrawal triggered a paroxysm of anguish. According to Sierra and David, overwhelming states of anxiety involve excessive interoceptive signaling ―mediated by the insular cortex― which can disrupt the sense of self when these internal signals become incongruent with other bodily inputs. To resolve this incongruence, paralimbic activity may be suppressed.^78,79 As the interoceptive signaling decays, depersonalization appears, and the emotional processing of pain may also break down, resulting in a condition akin to pain asymbolia. The patient wounds himself but feels no pain. The transition to delusional depersonalization ―the Cotard delusion― requires a disturbance of metacognitive processes. A predictive coding account postulates that unexpected, extraordinary experiences trigger the formation of delusions, which, in turn, engender new expectations that reduce updating and facilitate the assimilation of contradictory evidence. ^78–85

Once, Jacinto missed an appointment, and his cousin told me he no longer wanted to take his medication. “He gets angry easily; he’s been like that since he was a child. He turns around and walks away. He stops talking to us. We checked his medication. He’s not taking it anymore.” One year later, he was brought in by an elderly woman who might have been his mother. As I spoke with her, I realized she truly was. She told me her son had thrown himself into a ravine and fractured several bones.

Jacinto arrived on crutches. His hair had turned gray, his nails were long, and his pallor was alarming, as if he had aged ten or fifteen years. He told me: “Before the fall, I’d spent three or four days hearing the voices. They wouldn’t leave me alone. If you don’t kill yourself, your family will die off one by one. Throw yourself into the ravine. And I did. From there, I don’t remember anything. I just heard that damned buzzing and the voices in my left ear. When I woke up in a hospital in Cuernavaca, I could still hear them. Luckily, they went away with the medicine. All I wanted was to heal, to walk out on my own. But I needed surgery. They operated on both ankles. The bones had shattered into countless parts.”

Can we consider the act of falling into the ravine ―the moment of relapse― from a panoramic view? Perhaps Jacinto suffers from schizophrenia, a chronic condition in which antipsychotics prevent psychotic episodes. However, residual symptoms and varying degrees of cognitive impairment typically persist in this condition, whereas Jacinto had a full recovery after the first episode. A withdrawal of antipsychotic medication is unlikely: the patient stopped the medication a year prior, and withdrawal-induced relapses occur within days or weeks. A third possibility is that Jacinto suffers from a recurrent form of affective psychosis, and the ongoing need for treatment reflects the continued presence of predisposing and precipitating factors such as a vulnerable psychological structure, social dislocation, loneliness, and economic stress.^86,87

Jacinto survived the relapse and was reunited with his family. Physical rehabilitation was slow, but the fractures healed. The consultation room became a space to talk about Puente de Ixtla, the sunlit valleys where he moved with his mother. “She said she would take care of me. We hadn’t seen each other in many years. She feeds me and looks after me. I’ve always loved her; I never had anything to forgive her for.” He began visiting his sister’s house every third day, to enjoy handmade tortillas and spicy salsa with renewed appetite while playing with his twelve-year-old niece. It comforted him to know that at least she would have the protection of a family.

One day, Jacinto told me he had turned 35. His mother made a special meal, and his sisters came too. He was happy that day. He no longer had nightmares, and the desire to take his own life had disappeared. “I don’t hear the voices anymore. The buzzing is still there. I don’t remember what that music was like. I no longer know what blue music means.”

After three years of treatment, Jacinto came to the appointment alone. He now lives with his niece in Puente de Ixtla. Her husband is involved in Alcoholics Anonymous and invited him to attend group sessions. Jacinto was reluctant, but he felt relief in the first meetings. “The group helps because you hear your companions’ reflections, and you think about other people’s lives. It’s not just you who suffers. They told me to drop the pills. Stop them, your illness is only psychological. But I answered: I’ll come to the group, but if I stop the meds, I could relapse. I’m not going to stop taking the medication unless my doctor tells me to. Don’t worry, Jacinto, they said. Take it the way your doctor told you.”

Then he paused, and his expression turned serious. “My enigma was that I’m an alcoholic. Now I have the strength to overcome my illness. The enigma I carry is the disease of alcoholism.” I remember a fleeting look of wonder on his face. Then he told me: “Eventually I went on a retreat. We dedicated ourselves to working, as they say. Telling our childhood stories, writing everything we’d lived through. Since I write very slowly, someone helped me. I felt very happy. They take us with our eyes closed until we arrive at the Hacienda, far from any town. We walked blindfolded through the gardens. There was a song on the air called Light a Light; for a moment it felt like a dream. When they told us to open our eyes, I saw my mother. She came to welcome me and brought me a bouquet of roses. My niece went to the retreat too, but the family members stayed apart, and we only met them at the end, because private things are shared during the alcoholics’ activities. At the end, the writings are burned; no one else should know those things. It’s personal.”

If we take a step back to look at these affairs with historical distance, writes Cristina Rivera Garza, psychiatric stories can take the form of narratives of suffering and redemption. Jacinto’s story follows a narrative structure that suggests a continuity between mental illness and life itself. The tragic dimension marks the process through which human limitations are recognized and accepted, while the emphasis on suffering and the limits of human experience reveals “the encounter of antagonistic forces capable of transforming hierarchies.”⁸⁸ Clinical histories hold transformative potential because they expose the effects of violent hierarchies within a social order shaped by desertion and usurpation.

The relational dimension of this story is a core aspect to be considered. From an anthropological perspective, Mexican thinker Roger Bartra reminds us that “those who belong to the canon of melancholy understand and misunderstand one another, communicate in solitude, and encode the mystery of separation.”⁸⁹ In Jacinto’s case, the double abandonment by both father and mother leads to a state of learned helplessness and supports a hypothesis of separation distress.^90–92Drawing on the work of Thomas Fuchs, the study of childhood reveals that our affective attunement with others depends on a developmental process: “In every social encounter, two cycles of embodied affectivity intertwine, continuously modifying the affective possibilities and the resonance of each participant.”⁹³ This forms an implicit relational knowledge during early childhood, a sense of attunement or social musicality that is essential for the development of intersubjectivity, that is, the ability to understand and share another person’s feelings. ^94,95Neglect in caregiving during childhood can have long-term consequences that help us understand Jacinto’s loneliness and the sources of his mental illness.

In Figure 2, I share a visual metaphor: it is the photograph of a tree that grew among the volcanoes of the central highlands. This is a region of Mexico fractured by the deep ravines where Jacinto attempted to die. The tree has been exposed since its birth to the powerful currents of the high mountains, and its structure is a plastic formation that reveals the impact of the wind.

Figure 2. The tree of consciousness. Courtesy of Grace Quintanilla Cobo (1967-2017

The resolution in Jacinto’s story comes through his reunion with others. This enables him to reestablish affective ties that may lead to restructuring his disposition toward relationships. At the same time, he undergoes a rediscovery of his autonomy. The fracture of his bones has imparted a clear lesson, which he integrates into his sense of self. Jacinto manages to negotiate with his group and defends his right to medication. Otherwise, the ritual experience helps him accept the recalcitrant facts of his past and recover his sense of purpose. Unexpectedly, at least for me, he attains a state of conviviality, the joyful coexistence with others. The term derives from the Latin convivere, which originally referred to a banquet. Thomas Fuchs develops the concept and extends it to “the bodily resonance and empathy we feel not only with other human beings, but also with other living creatures.” Is this the redemption Rivera Garza speaks of? Is there an existential dimension in the reunion with oneself, and in the religare with communal life?

When we analyze the continuity between mental suffering and life problems, we gain a broader understanding of the person experiencing psychopathology. However, it is important to maintain a critical perspective to avoid the trap of meaning, which gives us an illusory sense of knowledge about psychopathology through retrospective sense-making.^96,97 Therefore, we must also consider the discontinuity between problems in living and mental illness. The inhospitable landscapes at the edges of phenomenal experience urge us to pursue the scientific analysis of consciousness.

ACROSS THE RIVER

In this essay, I study the delusion of being dead as an empirical phenomenon in need of explanation. I have sought to document the clinical facts as literally as possible, yet the affinity of psychosis with dreams, poetic experience, and visionary states has long fascinated patients, clinicians, and philosophers. The very concepts of hallucination and delusion compel us to reflect on the relationship between consciousness and the reality of a shared world.

In search of theoretical insight, we might turn to the mythological figure of Ananké, a primordial entity that gives rise to the cosmos by constraining chaos, and who represents the absence of alignment between our desires and the laws of nature.⁹⁸ Our conscious experience is constrained by physiology, and yet we have the subjective sense of building a life story beyond determinism. Is this nothing but a teleological illusion? According to Thomas Fuchs, “subjectivity manifests itself in the living body in terms of spontaneity, as the emergence of an order that is underdetermined by physical causes.” Conversely, nature is expressed in our phenomenal experience “as the appearance of mental processes that are underdetermined by the will and whose origin and underlying basis lie beyond our consciousness.”⁹⁹

We must acknowledge the limits of introspection as a source of self-knowledge, without underestimating the feeling of spontaneity that animates our actions. For it is precisely this experience that withers in nihilistic delusions: the feeling of being alive, of being able to enact change in the world to reclaim the project of selfhood.

The problem of bodily delusions raises important questions for the study of self-awareness. The investigation of autoimmune psychosis led us to examine NMDA receptors, which in turn prompted us to consider the neural processes that enable the detection of meaningful patterns of matter and energy. This requires the suppression of surrounding noise, one of the processes disrupted in psychosis. In autoimmune encephalitis, the physiological cause is undeniable: anti-neuronal antibodies disrupt the glutamate system and lead to psychosis. However, there are significant contextual factors. The earthquake, and the rescue efforts amid the ruins, were elements of a traumatic experience that triggered pathology and influenced the content of the delusion.

I also shared a case of affective psychosis emerging from a tragic life history, but the therapeutic response to a medication that modulates dopamine signaling suggests the involvement of physiological factors in the causal cycles of psychopathology.^100,101 Psychological causality is dominant in this case, but a feedback loop between physiological and interpersonal processes can be postulated. Psychological dynamics disrupt homeostatic balance, but once a pathophysiological mechanism is established, it has effects on mental processes. More broadly, there are feedback relationships between physiological mechanisms, psychological processes, and social contexts. This is why I do not advocate for theoretical autonomy at each level of explanation, but rather I call for the development of integrative theories. At this juncture, a systems approach offers an alternative to the dichotomy between holism and reductionism.

The reductionist perspective assumes that analyzing the lower levels of a system ―the physiological factors― offers inherently superior explanatory power to that of higher levels, like psychological or social dimensions. In contrast, holism presumes that the agent’s interactions are sufficient to explain the clinical problem, without requiring input from lower-level mechanisms. In neuropsychiatry, both views have limitations: holism overlooks disturbances rooted in physiology, while reductionism fails to account for clinical patterns shaped by psychosocial interactions. A coherent alternative is the systemic approach, which holds that everything is a system or part of a system: each person can be understood as a collective intelligence composed of millions of cells acting in concert to form an agent. While we do not know the ultimate principles that enable this unification, the cognitive agent possesses emergent properties absent from its individual parts. These properties involve qualitative novelty and arise from the integrated system dynamics.^102–104 For instance, some neuronal populations process auditory signals, others process language, and others handle prosodic vocal patterns. Yet only the integrated person can sing a musical piece synchronizing with other fellows in a concert.

The contents of consciousness, although they seem to have properties beyond the physical world, can be understood as Real Patterns ―real psychophysiological phenomena― through Daniel Dennett’s framework. One might assume that only the physical components of the body are real. But according to Dennett’s pragmatic conception, a pattern of mental activity is real insofar as recognizing it offers advantages to predict the cognitive agent’s behavior. Some claim that only the physical vehicle of information is real, not the informational content. But this is a false dichotomy. For the physical process to be effective, it must specify the informational content through the formal organization of energy in temporal and spatial patterns of signaling.^62,105–107

Dennett envisioned an “illusionist” theory of consciousness, but I find that label misleading. While ordinary experience includes illusions and hallucinations, Dennett acknowledges that we are not typically victims, but beneficiaries, of the “user illusion,” which enables genuine cognitive operations. Thus, mental patterns of conscious activity, and their informational content, are real psychophysiological events contributing to the causal cycles sustaining behavioral interaction.

How does an agent’s subjective experience arise? There is currently no definitive answer to the problem of psychopoiesis: the emergence of psychological life in the universe. The mind–life continuity thesis focuses on autopoiesis: the process of self-construction of living beings leading to increasing levels of autonomy. ^108,109 Biosignaling cycles are essential for mapping the organism’s internal states, environmental conditions, and their dynamic interactions.⁵⁰ The process of assigning value to signals from the body or environment is key to explain the feeling of what happens. According to homeostatic and affective theories of consciousness—following Damasio and Panksepp—homeostatic feelings were the inaugural phenomena of consciousness in biological evolution. They were selected for their capacity to provide explicit guidance for vital self-regulation, representing an advance over the implicit regulation of homeostatic behavior. ^{50,90,110,111}

Interactive cycles produce consistent changes in the organism’s internal feedback systems, forming the basis for the plastic, associative mechanisms underlying memory. Learning may enable the causal emergence of an integrated agent by coordinating cellular activity to generate organized responses.¹¹² This allows the organism to anticipate environmental states and the consequences of its own behavior. As Lisa Feldman Barrett has proposed, the evolution of intermediary neural processing enables homeostatic regulation ―both physiological and behavioral― to become predictive and allostatic. This shift provides an extraordinary capacity for life development through anticipation, flexibility, and creativity.^113–118

Within the Active Inference framework, the sense of self is constructed through predictive coding and involves multiple levels of organismal representation, including physiological allostasis, bodily integrity, spatial position and movement, and the consequences of one’s actions.^85,119–122 According to Philip Gerrans, the brain constructs a model of the organism that functions as an avatar: a simplified interface for managing countless physiological interactions that we cannot directly control, such as cellular energy, but which give rise to qualitative experiences like hunger, fatigue or desire. These homeostatic and affective feelings arise from interoceptive active inference. When homeostatic behaviors, such as drinking when thirsty or resting when tired successfully restore balance, the model is reinforced; if they fail, it is updated. Ultimately, the sense of being a unified organism is a tool for survival: it enables self-regulation through goal-directed behavior.^{57,121,123,124}

Collective behavior has driven a major transition in the history of life: from molecular signaling to ecological biosemiotics, and ultimately to cultural semiosis. In his Anthropology of the Brain, Roger Barta proposed that symbolic systems, developed through cultural evolution, serve as a mediation ―a cultural prosthesis― for consciousness. The collective inscription of signs and symbols into physical matter enables intersubjective feedback. While we cannot directly access another person’s subjectivity, we can attune and understand each other through embodied simulation, with the resources of verbal language, manual sign systems, visual arts, dance and music.^95,125–127 The role of semiosis in fostering intersubjective attunement is supported by Pauline Pérez’s research on psychobiological rhythms: she showed that conscious attention to narratives can synchronize fluctuations in heart rate between individuals. This cardiac synchronization predicts recall of the story.¹²⁸

According to the social cognition model developed by Uta and Christopher Frith, our bodily systems integrate exteroceptive, interoceptive, and proprioceptive signals through feedback and control mechanisms. These processes generate prediction error signals when something deviates from expectation. Thus, a form of nonconscious monitoring—or implicit metacognition—is required to regulate the system’s dynamics.^129,130 These implicit processes support the emergence of pre-reflective forms of conscious experience, even though we remain unaware of the underlying physiological mechanisms. We cannot successfully introspect into them.¹³¹ Pain is an example of this kind of phenomenal experience, arguably shared by many animal species. It is a core feature of sentience, which consists of sensory and affective experiences that are typically tacit, minimal, or pre-reflective. In humans, culture introduces an additional cycle of conscious activity: once pre-reflective contents become conscious, they can be enacted or represented through symbolic systems, via cortical networks specialized in gestural, musical, verbal, or mathematical formats. From this perspective, an emergent function of consciousness is to serve as an interface for communicating phenomenal contents ―such as illness experiences― that are relevant to the survival and cooperation of human groups. The communication and enactment of conscious contents enable cycles of social interaction that support the development of normative rationality and, ultimately, explicit metacognition.^57,132,133 This means that we consciously monitor and evaluate our psychological activity, shaped in part by the perspectives of others. Through these intersubjective, recursive cycles, we achieve genuine forms of reflectiveness. To know that I know is one example of this kind of reflective awareness. Symbolic networks provide scaffolding for the formation and sharing of abstract concepts and narrative practices related to self-awareness.¹³³ This, in turn, opens new domains for reflective consciousness, allowing us to address the meta-problem of consciousness, as posed by Chalmers.¹³⁴

A systems perspective helps us understand the relationships that make the advent of consciousness possible. After studying conscious experience in both ordinary and extraordinary states, we must examine its substrate: the structure and function of the neurobiological systems, and the neuropsychological processes that mediate between bodily activity and the environment. We must also consider the organism’s general physiology, its energy metabolism. To grasp the intentionality of the conscious agent, we must look beyond the body, to our interpersonal relationships, the sociocultural world we inhabit, and the ecosystem we belong to. This framework is ecological: the person suffering from a disorder of self-awareness is a living being shaped by a physiological concert, and nested within an ecosocial system of relations.^99,135,136

An ecosystemic approach should consider the phylogeny of organisms, the cultural and social history of communities, and family trajectories. At the individual level, we can contemplate ontogeny, early psychological development, and the history of interactions throughout life. Through the lens of development, we think of collective intelligence from a new light. Following Anna Ciaunica and Katerina Fotopoulou, perceptual experience in ontogenesis is shaped by patterns of stimulation in the womb, where early selfhood emerges through physiological mutuality and shared embodiment. Molecular autopoiesis is thus grounded in co-homeostasis coordinated by the mother’s physiology. The relational dimension of life is therefore co-constitutive of individual consciousness. ¹³⁷

An ecological perspective, grounded in life and relational systems, offers a path for the scientific investigation of self-awareness. But this perspective is not limited to outlining levels of analysis. It has ethical and aesthetic consequences. To ground this ethos, we have conviviality: the fundamental kinship we feel with all forms of life. It is the basis of care and responsibility toward life. If we understand conviviality as intercorporeality, we can establish an ecological ethics that overcomes the separation between culture and nature.¹³⁸ Above all, I long for the science of consciousness to acknowledge those who suffer from these ailments, fulfilling Neruda’s vision: There is no impregnable solitude. All paths lead to the same point: communication of what we are. As the poet would say, we need to cross through incommunication and silence to clumsily dance or sing with melancholy, but in that dance and in that song, the oldest rites of consciousness are consummated: the awareness of being human and the conception of a common hope.

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