“Civil Schizophrenia” is in Distributed Cognition and the Will, D. Ross and D. Spurett, eds. (Cambridge: MIT Press), in press.

[Brief abstract: In this chapter, I explore schizophrenia as a dysfunction (or set of dysfunctions) of a dynamical system, specifically, a recurrent neural network. This is consistent with recent proposals that the illness is a “disconnection syndrome” (as opposed to a specific regional dysfunction). More important, disruption of recurrent circuits in the brain will alter properties fundamental to the background awareness of temporality, and contribute to the struggle to maintain a subjective sense of reality that individuals with schizophrenia face.]

Dan Lloyd
Trinity College, Connecticut

Some farm houses in a farm yard time
With a horse and horseman time
Where going across the field as if they’re ploughing the field time
With ladies or collecting crops time work is
Coming with another lady time work is
And where she’s holding a book time
Thinking of things time work is
And time work is where you see her coming
Time work is on the field and where work is
Where her time is where working is and thinking of people
And where work is and where you see the hills
Going up and time work is
Where you see the grass time work is
Time work is and where the fields are
Where growing is and where work is

(transcript of patient with chronic schizophrenia describing a farming scene, collected by Heidi Allen and quoted in Frith (1992). Line breaks indicate pauses.)

Schizophrenia is a devastating disorder that affects approximately one percent of humankind. It usually strikes in early adulthood, and by every measure, outcomes of schizophrenia are usually poor: About half of discharged patients will be rehospitalized within a year. Two thirds of first-episode patients will continue to have positive symptoms (like hallucinations or delusions) one year later, and one third will still have these symptoms six to ten years later. Less than 20% of individuals with the illness are gainfully employed. Subjective and objective measures of the quality of life with schizophrenia are very low, even when compared to other chronically ill patients. One in ten will end their lives through suicide (Robins, et al., 1984; Karno & Norquist, 1995; Hafner & Heiden, 1997; Weiden et al., 1996).

The humane need to address this illness is clear, and there has long been a massive effort to understand and treat it. For example, the PubMed database currently references more than 66,000 papers on schizophrenia. More than three thousand were published last year alone; that’s about eight schizophrenia papers every day. Yet, despite all this effort, and despite significant progress in managing the illness, schizophrenia has been singularly resistant to explanation. It is elusive for every discipline, including philosophy, phenomenology, cognitive science, and neuroscience. Its elusiveness is frustrating, but also fascinating. Many psychological disorders and diseases have been crucial to discovering the functions of mind and brain in both illness and health. It would seem that a disorder as manifold as schizophrenia would be especially revealing of the machinery of mind, but so far it poses more riddles than answers.

In this paper, I propose that schizophrenic cognition does open a window on the working brain, but what is revealed is seen through a glass darkly. This is in part because schizophrenia is a complex disorder (or group of disorders), and in part because the explanatory frameworks we bring to bear on it are inappropriate for its distinctive complexity. To address its challenges, I’ll recommend a double shift of approach, motivated by dynamical systems and phenomenology. The two perspectives illuminate an aspect of cognition that is often overlooked, but which may be important in understanding schizophrenia.

I. The Deficit Schema and Its Dysfunctions

Cognitive neuroscience is in some ways the oldest of the disciplines of cognitive science. It can be traced to 19th Century neuropsychology, and the clinical genius of researchers like Broca and Wernicke. They and their colleagues inaugurated a search for a physiological implementation of a much older faculty psychology. Their overarching hypothesis was that the faculties reside at specific anatomical addresses, or in other words that the brain was predominantly organized around functional localization. The logic of localization was a logic of lesions, linking the loss of specific brain regions to specific deficits in behavior. If insult to some region R led to a deficit in the behaviors supported by some function f, then, conversely, R’s normal function would seem to be f.

Neuropsychology is full of lesion studies, which provide much of the foundation of modern cognitive neuroscience. An old example that remains germane is the case of H.M., whose hippocampi (and more) were ablated to control his epilepsy. Following his operation, H.M. suffered from severe anterograde amnesia. He was never again able to create long term episodic memories. His case demonstrated the role of hippocampus in memory, and subsequent experiments, many with H.M. as their subject, teased apart distinctions between declarative memory and procedural memory, among others. Many of the lessons of H.M. remain central to cognitive neuroscience and cognitive psychology (Corkin, 2002).

In the case of H.M., it was not hard to fill in the blanks of the deficit schema. A distinct external cause (his surgery) resulted in a specific and observable single lesion in his hippocampi in both hemispheres, and as a further result brought about specific deficits that could be readily observed and described. None of these clean distinctions hold in schizophrenia. It is multiform at each stage in the deficit schema. First, schizophrenia arises from the joint effect of several causes, none of which is fully understood. One factor is genetic. If your identical twin has schizophrenia, your chance of acquiring it will be around 50%; risk tails off as one moves along the branches of the family tree. For example, if you have a cousin with schizophrenia, your own chances double from the baseline rate of 1%. But even as these ratios point to a genetic contribution, they just as clearly indicate that something else is also involved, affecting some stage of pre- or post-natal development, or arising in the environment or experience of those who ultimately acquire the disease. Moreover, there may be multiple paths to schizophrenic disorders. Many potential contributing causes have been discussed, but there is no consensus yet.

The multiple ambiguous causes of schizophrenia lead to multiple and ambiguous differences in the brain. Early in the last century, it seemed that schizophrenic brains were anatomically indistinguishable from healthy brains, but more careful measurement revealed an enlargement of cerebral ventricles in those with the disorder. This then seemed to be due to smaller volumes of gray matter overall, but particularly in the frontal lobe, but also in the temporal lobe. At this point, statistically significant variations in volume have been found in parts of all four lobes, the basal ganglia, and cerebellum (Niznikiewicz, et al., 2003). These volume differences may (or may not) be related to observed differences in cytoarchitecture in several regions (Frith, 1992). Relating all these variations to their expression in the illness would be complicated in any case, but are additionally confounded from two directions. On the one hand, it’s not clear that schizophrenia causes all these differences, as individuals with the illness are also affected by chronic medication and a very different life experience. On the other hand, it’s also unclear that any of these anatomical differences reflect mechanisms of schizophrenic cognition. Many people exhibit similar anatomical variations – siblings of schizophrenics, for example – without developing the illness. Emblematic of both confounds is the relationship of gray matter loss to schizophrenic symptoms. Individuals with schizophrenia have less gray matter volume than those without, but then, between ages twenty and sixty, the average healthy individual will lose around 15% of his or her cortical gray matter (Lim, et al., 1992). Loss of gray matter in itself does not give rise to schizophrenia, fortunately.

In short, the root causes and neural expressions of schizophrenia are both obscure. But perhaps the most perplexing aspect of the illness is its symptomatology. Only in the 1980s were the symptoms organized into positive and negative categories (Crow, 1980). More recently, the positive symptoms were further divided, leading to a “three-compartment” conception of the illness (Liddle, 1987). These are, first, the positive symptoms including delusions of various types and hallucinations. Second, there are the “disorganized symptoms,” including disorganized speech and behavior, impaired attention, or catatonia. Third, there are the negative symptoms, including diminished speech, decreased ability to initiate goal-directed behavior, flattened affect, inability to express pleasure, and social isolation. (These diagnostic symptoms are frequently accompanied with numerous cognitive deficits. See Barch, 2005.)

The clarity of the three compartments is somewhat illusory, however. Individual patients will express the illness in idiosyncratic ways, and furthermore the form the illness takes changes over time. Moreover, under scrutiny some of the symptoms themselves take on the enigmatic cast of the disease overall. For example, a commonsense understanding of delusions might define them as patently false beliefs held by persons who are unaware of that falseness. Bill Fulford has pointed out that the differentia of this definition fail to capture what seems to have gone wrong in delusion (Fulford, 1994). First, delusions are not simply false (or many of us would be in their grip, most of the time) nor are they necessarily false. Someone may suffer the paranoid delusion that the government is spying on him, but the belief may nonetheless be true. More important, Fulford points out that individuals with delusions often have a great deal of insight into their beliefs. They know that they hold the belief and can appropriately relate it to many other beliefs, some delusional and some not. They often know that the delusion is exceptional, that it is denied by everyone around them, that it is radically dysfunctional in the context of practical action and social life, and that it has made life hell for them. Even more perplexing, it’s not even clear that delusions are beliefs. Deluded patients often fail to act on their delusions or to register appropriate affect about them. Citing observations like these, Stevens and Graham propose a unique propositional attitude, the “delusional stance” (Stephens & Graham, 2004). In short, schizophrenic delusion has something to do with falsehood and evidence, something to do with a lack of insight, and something to do with belief, but a precise description of the cognitive dislocation turns out to be elusive.

One indicator of the complex symptomology of schizophrenia is the proliferation of diagnostic tests for the illness and its variants, like “schizotypal disorder” and “schizoaffective disorder.” Some of these can be revealing of assumptions about the subjective experience of schizophrenia. For example, consider the opening questions of the Schizotypal Personality Questionnaire:

1. Do you sometimes feel that things you see on the TV or read in the newspaper have a special meaning for you?
2. I sometimes avoid going to places where there will be many people because I will get anxious.
3. Have you had experiences with the supernatural?
4. Have you often mistaken objects or shadows for people, or noises for voices?
5. Other people see me as slightly eccentric (odd).
6. I have little interest in getting to know other people.
7. People sometimes find it hard to understand what I am saying.
8. People sometimes find me aloof and distant.
9. I am sure I am being talked about behind my back.
   (http://www-rcf.usc.edu/~raine/spq.htm)

Indirect questions dominate this and other tests. Imagine, by analogy, a diagnostic test for pain that asked not “Does it hurt a lot?” but instead asked “Do you find yourself saying ‘ouch’ a lot?” or “Do other people often offer you aspirin?” The circumlocutions imply that self-awareness is impaired in schizophrenic disorders, even in comparison to other mental illnesses. This failure of insight is one facet of the common view that individuals with schizophrenia suffer a “break with reality.” The break with reality, then, is the subjective counterpart of the breakdown of communicative abilities. Many of the signs listed in the three compartments of schizophrenic symptomatology are variants on the twin themes of mistaken perception and derailed expression. Excerpts from schizophrenic discourse, sprinkled through every textbook treatment, offer many particular examples of delusional belief and fractured language. At the limit, the break with reality can seem to exclude schizophrenic experience from any normal understanding. Karl Jaspers, following Franz Brentano, referred to “genetic understanding” to denote the understanding of how one mental state arises from another, and claimed that the mark of madness was the failure of the sane to achieve a genetic understanding of the mad attempts to communicate (Jaspers, 1963). In Jaspers’ account, regarding severely delusional patients the failure was absolute.

Quoted out of context, individuals with schizophrenia will express beliefs that can’t easily fit into the spectrum of typical world views, c. 2006. With all these assumptions – the break in perception and communication and the failure of insight — in mind, then, let us consider the dialogue below, a transcription of five minutes of a hospital interview of a woman with psychosis:

Interviewer: I want you to tell me something about what’s been happening to you.
Patient: Well, I’ve been exposed to guerilla warfare, and some of these Dutch Confusia…
I: Dutch Confusia?
P: Yes, Dutch Confusia, that’s what he is, he’s a con-fus-ia. He will cause confusion. A great deal of British and Dutch use those people in nations where they want to break into, create some strife, oftentimes steal something, or do something, get away with something. They’ve done it for thousands of years. They planned and plot world conquest. About every thousand years, my grandmother says, the confusia overrun the world. They break into nations: that’s what Russia is, and they’re doing it in South America. They’re to blame for the trouble in South America. They will deceive our Royals and Royals cannot fight back and do the things they do. We have to return good for evil—
I: What are Royals?
P: A Royal is a human being as God created him, that lives by God’s law, that will not slay another man, will not touch his person. Lives by the Bill of Rights, in other words, as God gave the commandments for man to conduct himself. It’s come down to us, it’s called the Bill of Rights today, because William the Bastard and the Duke of York came over during the American Revolution and overran this continent, and they meddled around in our civil affairs over here and now we call it the Bill of Rights. He renamed that and they’ve written in death penalty, which is forbidden by God – any man can err, he can change hands, but you cannot take his life. Disprove that, my grandfather the Baptiste’s first wife — he detected Christ’s human rights —
I: What do you mean, your grandfather—
P: Great grandfather, John the Baptiste, St. John.
I: I see —
P: John the Baptiste, great great great grandfather. I can’t repeat the number of patterns of removal, but he is a great great grandfather and really the head of the American, as we say, the house of Aabel, the American nation over here. He was the founding father —
I: What do you mean, the house of Aabel?
P: Aabel — it’s the clan of Aabel, our tribe, as you would say –
I: Would you explain that word, Aabel?
P: The body of Americans carry Aabel blood more than they do Cain and Satan blood —
I: What does that word Aabel mean?
P: Abel, Abel, A with the first Adam and Bel means one that lived by the Bell of Rights, that set down the eighty marked lands by the acorn and the oak, and the acorn became the symbol of our Liberty Bell and that Bell of Rights, or law, set of commandments as God gave us, become known as the Bell of Rights, because they would call Congress, they would ring that bell, they would call, gather ye, hear ye, hear ye — town crier, or the first bell in the harbor up there, holds a torch aloft. Our grandfather was the first to be given light by God. That happened right down here in the Cove of Anton, that’s one reason that we came to this home –
I: The what?
P: The Cove of San Anton is a cave, a volcanic formation, and our grandfather, the first Jo-an and the first Adam—
I: The first what?
P: My great grandfather is Adam. The first Adam, and his son Jo-an and his wife, and his son’s wife. He had a small child already, he had Anton. The T means a crucifix in ancient hieroglyphics.
I: Tell me more about the meaning of the letters —
P: They had wandered around the United States — I’m coming to that — they came down here, to, they call this the Fountain of Youth region. This water here will mend bones, and they had discovered, God said, “Seeking my light and the right water to heal” — our people were homeopathic. Now if you want to cleanse your system, you seek the right water. If you have an ailment, you have to first seek the right water. And some of our people heal with the sun, but they sought this water because if they had broken bones or sores or anything that wouldn’t heal, this water flows through limestone here, the famous Bell Fountain in Ohio here — you’ve heard of that I suppose — those were Grandpa Bell’s Fountains, and the mineral lode is the best right down where we are, and those 13,000 acres were an ancient reserve that belonged to my grandfather when he went to the other side, the General —
I: Now why are you here?
P: I don’t know why I’m being routed out here. I understood some tests were to be made.
I: What kind of place is this?
P: This is Mountain View, a hospital for mentally deficient, or mental patients.
I: Are you a mental patient?
P: No, I am not, but they’re trying to make it appear that I am. The British and Dutch are doing that, the Confusia…

Undeniably, there is something deeply “off” about this patient’s attempt to communicate with her doctor. She seems almost oblivious to the social environment and the pragmatic demands and constraints that normally support successful communication. From this passage one could extract dozens of explicit claims that could serve as textbook examples of deluded belief or logical chaos. But reading the whole passage, slowly, leaves a very different impression. One is struck, I think, by the patient’s urgency to explain herself, by an indefatigable need to make sense of her world. Bleuler (1913) originally characterized schizophrenic thought process by its “loose associations,” but when we settle in with this transcript the associative paths begin to seem rule-governed and thoroughly explored. By the third reading, the passage almost seems like the theoretical discourse of a systematic philosopher, the ruminations of the Leibniz of Dutch confusionism. As Einstein labored on the general theory of relativity in an office across the street from an asylum, he remarked on a feeling of kinship with the inmates: “They were the madmen who did not concern themselves with physics. I was the madman who did.” At the same time, the passage is reminiscent of modernist literature, with echoes of Beckett or Molly Bloom. In short, genetic understanding of this speaker is not impossible. This is not to deny that the speaker’s illness is greatly distorting her discourse, which is neither literature nor philosophy (but compare the non-schizophrenic novels of Kathy Acker, or the non-schizophrenic philosophy of (e.g.) Lacan). But, just as with the understanding of any discourse, this text becomes clearer with the addition of its context. More text yields more understanding, and even the glimmers of the organization of the patient’s worldview, as she returns to her first topic at the end of the passage.

Isolated sound bites from schizophrenic discourse suggest an illness characterized by an incomprehensible break with reality. But the lesson of the passage above is that providing even limited context for those same data suggests a method in the madness, and the possibility of partial understanding. This simple observation, that context renders schizophrenic perception more understandable, is the emblem for the main claim of this paper. Schizophrenia, I will suggest, is a disorder of context (see also Hemsley, 2005). The context in question is the temporal context of episodes of thought and perception, schizophrenic and healthy alike. Time, I’ll suggest, is the fundamental structure of our experience (and essential to every aspect of cognition). It is so basic as to be invisible and thus largely overlooked in both philosophy and cognitive science. My proposal here is that schizophrenia can be approached as a partial dislocation in fundamental temporal cognition. Its symptoms reflect a struggle to stabilize and normalize a shifting framework that we who are fortunate in health call reality.

My “brief history of time” will unfold on two levels at once. The first level is that of dynamical systems with reference to a few main theories of the pathophysiology of schizophrenia. The second level is phenomenological, considering the normally invisible structures of temporality and their emergence from the underlying dynamic architecture. The links across levels will then suggest an interpretation for what is both strange and inexpressible in schizophrenic experience.

II. The brain as a recurrent network, in health and illness

In 1990 Jeffrey Elman introduced the connectionist architecture known as the Simple Recurrent Network (SRN; Elman (1990)). Figure 1 depicts the SRN architecture schematically. Essentially, a recurrent network is based on a standard three layer feed-forward architecture, designed for back-propagation learning. Its innovation is a feedback loop, functionally implemented in an auxiliary set of “neural” units that copy the information in the hidden layer, making it available for the next cycle of information processing. Thus at each processing cycle two inputs are available to determine the output: the occurrent input, and a copy of the pattern of activity in the hidden layer from the immediately preceding cycle.

Figure 1. A Simple Recurrent Network.

The simple recurrent network is a generalized computational architecture and a highly abstract model. But it is at the right level of abstraction, in that it specifies a minimally sufficient architecture to support a class of functions no ordinary feedforward net can handle. Elman’s 1990 paper is entitled “Finding Structure in Time,” and it demonstrated that recurrence gave networks the power to learn temporal contingencies of many sorts. SRNs can accommodate delayed responses, and iterative and recursive structures, like embedded clauses. A moment’s reflection reminds us that almost all our cognitive power depends on finding structure in time, that is, building complex representations from the serial presentation of independently ambiguous “takes”: language, action planning and execution, scene perception and object constancy, reasoning, narrative, and memory of every sort all presuppose an ability to embed temporal information in perception and cognition. The SRN also illustrates how temporal information could be folded into the general information stream. Parallel distributed processing is characterized, as the name suggests, by distributed representation, in which information is spread across units and connections, each contributing to many separate functions. In a recurrent network distributed representations also encode time. Temporal information is not localized in specialized time-keeping units, but rather is folded into whatever other information the network is processing. This enfolding is ongoing, and as a result the temporal depth of information extends beyond the single cycle mirrored in the feedback loop. The current state of the hidden layer incorporates the previous state, which incorporates the state before that, and so on into the past. Through a regular backpropagation learning process a recurrent net learns to maintain a “working memory” as demanded by the temporal contingencies of the task at hand.

Recurrent networks offer a useful  framework for thinking about perception and cognition.  They also remind us of a pervasive feature of  biological brains, in which as many as 90% of all connections are  feedback.  Figure 1 thus also represents  a highly schematized picture of the brain.   Even at this level of abstraction, we can think of ordinary brain  function as the flow of information through a recurrent network.  And we can think of schizophrenia as a  modification of that flow.

One usual suspect in the  pathophysiology of schizophrenia is dopamine, which was implicated in the  disease more than fifty years ago.  The “dopamine  hypothesis” proposes that schizophrenia is an effect of a  dysregulation in neuromodulatory  pathways, originating in midbrain areas (in and near the substantia nigra) and  projecting to many cortical regions, especially prefrontal cortex and the  mesolimbic system (including nucleus accumbens, ventral striatum, amygdala,  hippocampus, entorhinal cotex, medial frontal cortex, and anterior cingulate).  The dopamine hypothesis has been adjusted over the years, and there is room to  question whether the evidence unequivocally points to dopamine  dysregulation,  but these issues will not be discussed here.   (See Byne, et al., 1999.) For present purposes, we need only consider a  schematic translation of neuromodulation into the dynamical system architecture  before us.  Neuromodulatory inputs can be  modeled as a tonic bias input to a recurrent network, as in Figure 2.

Figure 2. Neuromodulation of a recurrent net.

The schematic leaves unspecified, for now, the manner of modulation, but the overall causal cascade is clear enough: change in the modulator system leads to change in the information processing in the main recurrent loop. Altered neuromodulation translates into a dynamical systems hypothesis as interference or noise in a recurrent circuit. At the dynamic systems level, then, schizophrenia is the expression of dysregulated, noisy recurrent processing. This is oversimplified, but perhaps not grossly, as it will provide a way to think about several interesting recent proposals about schizophrenia. I’ll summarize three views, to suggest the range of ideas in play in this literature.

For example, in several papers Nancy  Andreasen (1999) has proposed that some of the symptoms of schizophrenia arise  through “cognitive dysmetria,” “a defect in timing or  sequencing the flow of information as required during normal ‘thought’ or  speech.”  The flow in question is a loop  through thalamus, frontal cortex, and cerebellum.  Andreasen points out that just as action  requires a fine-grained coordination of sensory inputs and motor outputs, so  also thought.  On this proposal, then,  the motor difficulties observed in individuals with schizophrenia are one  expression of dysmetria, and cognitive deficits another.

Christopher Frith identifies recurrent circuits involved  in the initiation and monitoring of willed action, and considers the manifold  effects of disrupting these loops (Frith 1992).   Functionally, the loop includes a “supervisory attentional system,”  responsible for forming goals and plans.   This system communicates with a system for selecting which action to  undertake next, among competing actions.   The resultant choice initiates the action at the same time as it is  communicated back to the supervisory system.   A disruption of the link between the supervisory system and the action  scheduler would explain several of the negative symptoms of schizophrenia.   At the same time, action is accompanied by  self-monitoring, which Frith proposes occurs through a corollary discharge from  the supervisory system.  The corollary  discharge, then, is the signal of an intention to act. As in Andreason’s  proposal, Frith’s involves an analogy between action and thought.  An internal monitoring system compares the  corollary discharge to what actually happens, as indicated by proprioception  and other forms of self-perception.   Disruption of the corollary intention signal would result in actions or  thoughts that appear unintended, a common thread among the positive symptoms of  the illness.  Frith cautiously identifies  the brain areas that may implement the loop, relying on lesion studies, animal  models, and behavioral experiments with subjects who have schizophrenia.  The attentional supervisory system includes  the anterior cingulate cortex, dorsolateral prefrontal cortex, and  supplementary motor area.  The action  selector includes the striatum, especially the putamen, and the globus  pallidus.

Karl Friston’s “disconnection hypothesis” considers the  implications of dysregulated neuromodulation on two areas of the brain which  seem implicated in schizophrenia:  the  ubiquitous prefrontal cortex and the medial temporal lobe, including amygdala,  hippocampus, and parahippocampal gyrus   (Friston 1999).  The effect of  aberrant modulation is to alter long-term synaptic plasticity, i.e.,  learning.  Schizophrenia disrupts the  learning of contingencies in the environment, including the social environment,  and it disrupts the learning of complex action patterns. This could lead to  negative symptoms, especially those involving communication and social  interaction.  It could also lead to  positive symptoms, through misattribution of the relationships between one’s  own intentions and perceived events.

All of the authors above draw on multiple strands of  evidence, which my capsule summaries completely omit.  All reward study and deserve further  discussion, but for present purposes they illustrate a single point:  Each proposal is a variant on the theme of a  disrupted recurrent network.  They vary  in their ideas about the brain regions involved in the circuit, and the  proposed mechanism of the pathophysiology.   (Andreasen and Frith seem to suggest that schizophrenic symptoms are the  immediate effect of a disruption of connectivity among brain areas.  Friston proposes that the symptoms are a  longer term secondary consequence of disrupted modulation of otherwise normal  processes of synaptic change.)

The exemplary theories further develop their proposals to  explain several schizophrenic symptoms and deficits. In these theories,  localized dysfunction is a secondary manifestation of the illness.  No particular component fails in  schizophrenia, they claim, but rather all fail together as their  interconnections unhinge. It happens that the networks they scrutinize comprise  components that are mutually interconnected, and in different ways aberrant  feedback is proposed as part of the mechanism of cognition in schizophrenia.  But there is a deeper consequence of recurrence which the individual theories  omit, but which is prominent in the dynamic architecture of a generic recurrent  network.  In addition to disrupting  inputs and outputs, dysfunction in a recurrent network both accumulates and  spreads.  Returning to Figure 1 and the  Simple Recurrent Network, a modification in one connection in the recurrent  loop can affect one unit, but that unit can affect several others in the next  cycle, and those can affect still others as the cycles continue.  If the connections are plastic, then the  spreading dysfunction embeds itself in many connections between units, and that  in turn contributes to further distortion.   Like compounded interest reinvested in a savings account, dysfunction  accumulates and compounds over time.

In short, the disconnection hypotheses considered above  regard schizophrenia as a modification of neural networks that are distributed  in space and fail to act in concert.  But  recurrence provides the functional architecture to accommodate information that  is distributed in time.  Its failures are  deficits in sequence, with the secondary effect of compounded problems.  If schizophrenia is a consequence of  dysfunction in a recurrent loop, its expression will be quite different from  deficits limited to spatial, synchronous patterns.

III.  Temporality

“The time is out of joint,” complains Hamlet, and in the  previous section I suggested a possible neural network implementation of his  predicament:  Dysfunction in a recurrent  network will distort structures in time.   But to understand how this distortion might appear in schizophrenia, we  must first understand the normal, undistorted starting point.  The basic structures of temporality in  cognition are little discussed in cognitive science, cognitive neuroscience,  and analytic philosophy.  But temporality  is foundational in continental phenomenology, and despite variations over the  decades, the original phenomenological description of temporal experience is  still accepted.

The definitive account of lived is due to Edmund Husserl,  who described it in lectures given in 1905 (although they were only published  in 1928).  His fundamental observation  was that our conscious perceptual experience of a scene before us right now is  not exhaustively constituted by the occurrent sensory information available.  In addition to sensation, all perception  incorporates a non-sensory “apprehension”; Appearances include both sensations  and apprehensions.  The contents of the  apprehension are manifold, but central to all of them is the awareness of the  temporal context of the present sensation.   The presently experienced context enfolds both future and past.  The future “appears” as an anticipation of  what will or might happen in the seconds and minutes,  ahead.   Husserl called this anticipation “protension.”  At the same time, the past appears as a  non-sensory awareness of what has just transpired.  Husserl called this form of primary memory  “retention.”  Between protention and  retention, the incoming stream of sensation is the “primal impression.”  Our experience of the present, then, is not  simply the intake of information before us, but is a triptych of protention,  primal impression, and retention.   Subjective temporality is “thick” with protentive and retentive layers,  in effect adding phenomenal temporal dimensions to the thin line of linear,  objective time.

Husserl claimed not only that temporality was apparent,  but that it was a necessary condition for anything we would recognize as  conscious experience.  For example,  imagine a watch hanging from a watch chain.   Is it moving or stationary?   Present sensation of the watch right there is ambiguous – it could just  as easily be a snapshot of an immobile as of a moving object.  The perception that the watch is moving can  only be achieved by retaining the context of its positions in the immediate  past.  This is equally true of the  perception that the watch is stationary.   Husserl’s deeper point is that we cannot imagine experience of either  change or stasis without temporal information being part of the present  consciousness of things.

Two further points deserve emphasis in this account.  First, this tripartite structure of time is  all packed into the present moment.   Protention and retention are both here now.  Second, this fundamental temporal structure  is distinct from our explicit attention to the future, through conscious  prediction or planning, or to the past, through recollection.  These distinct processes receive their own  analysis (of their own distinctive tripartite structure).