Definition of Functional Psychosis

Primeval social instincts helped safeguard both ancient human groups and modern animal groups of all kinds, but we humans also have an evolutionary advantage when it comes to consciousness. That ability to think about thinking has helped us evaluate environmental and interpersonal situations, readapt, reorganize environments, and inform our social interactions and other needs. So, conscious reason has allowed humans to adapt and prosper beyond the reach of other species. Our consciousness instinct is responsible for moderating our primeval social instincts. However, a decrease of that rational consciousness can allow the reemergence of instinctual perceptions and beliefs, leading to heightened prominence of social instincts and to frightening concerns.

With consciousness, we humans can overcome biological social instincts, and we can better rely on reasoning to achieve better outcomes in both challenging and promising situations. Consciousness and self-awareness are adaptive traits that can improve human life when focused on ourselves and especially when focused on others. However, when consciousness decreases and social instincts emerge, we have a loss of contact with reality and with normal social functioning. When extreme, these unmoderated socially instinctive beliefs can be called “psychosis,” as in the overused but paradigmatically termed “schizophrenia.”

Eugene Bleuler (1857–1939) described “The Group of Schizophrenias” with a presumed biological cause. Considering how our inner unconscious holds much of our social instinct, it is remarkable that Bleuler, in coining the term “schizophrenia” in 1908, understood it as an illness where the brain splits apart between a conscious mind (think conscious reason) and an inner unconscious (think social instinct), so that the inner unconscious then dominates. Although primeval social instincts are adaptive to a point even today, when they are too dominant, they can contribute to psychotic experiences.

Psychosis is a clinical category with various symptoms, and diagnosis is possible only through psychotic clinical manifestations, rather than through laboratory, genetic, and neuroimaging investigation. According to the American Psychiatric Association’s (2013) Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5), psychotic features are defined by such alterations as delusions, hallucinations, disorganized thinking or speech, disorganized or abnormal motor behavior, and negative symptoms.

Although psychosis includes a spectrum of several disorders, schizophrenia is only approximately 30% of the psychotic spectrum. Even so, it has been 10 times more researched than the other 70% of psychotic disorders. In clinical practice and public awareness, the term “schizophrenia” has been used to epitomize the nature of all psychosis types, even those with brief psychotic episodes, and those considered at ultra-high risk (UHR) for schizophrenia. And because schizophrenia is a chronic and progressive disorder, many professionals prefer to substitute diagnoses that suggest a better clinical outcome. Indeed, when psychotic patients do recover substantially, they are usually considered ineligible for the chronic diagnosis called schizophrenia.

In the early editions of the Diagnostic and Statistical Manual of Mental Disorders, psychosis was defined more by the presence of functional limitations than by the role of symptoms in those limitations. Nowadays, schizophrenia diagnosis is made solely based on the presence of hallucinations and/or delusions without insight (i.e., by impairment of reality testing). However, there are other psychotic symptoms also commonly found in nonpsychotic patients that seem to affect severity, intensity, and the co-occurrence of hallucinations and delusions. These can include disorganized thinking, neologism, thought blocking, other disturbances of thought, and negative symptoms. It is also common for adolescents with psychosis to present anxiety, mood changes, and social withdrawal before the onset of the first psychotic episode, which can further explain the relation between nonpsychotic affective symptoms with thought disturbances and the more severe psychotic symptoms.

Alongside psychotic symptoms, patients frequently have other psychiatric comorbidities. Missed diagnoses, and misdiagnoses are also common, despite the seeming homogeneity of psychotic disorders. The core diagnoses in nonpsychotic patients are also the most common comorbidities in schizophrenia: melancholic major depression, atypical major depression, obsessive-compulsive disorder, panic disorder, and social anxiety. In addition, these comorbidities can worsen prognosis and increase symptom severity; therefore adequate diagnosis and treatment of comorbidities can ameliorate positive and negative psychotic symptoms.

A History of Psychosis Differential Diagnosis

Psychosis derives from the Greek word “ psykhe ” (mind) and “ osis ” (diseased state), which means mental disorder. The term “psychosis” was used to explain interactions between physical and mental processes. A German pathologist and neurologist named Nikolaus Friedreich (1825–1882) thought of psychosis as a combination of physical brain anomality and mental vulnerability, with a predominantly organic neurologic basis. Therefore psychosis was used to explain “insanity” and “mental illness.”

Emil Kraepelin (1856–1926) explained how different diseases had similar processes and would produce similar symptoms, pathologic anatomy, and common etiology. People believed each disorder had its own etiology, pathologic anatomy, and symptoms, but Kraepelin believed many disorders had similar symptoms and biological foundations that would follow different courses as illness progressed. He then grouped illnesses such as catatonia, hebephrenia, and dementia paranoides into one condition called “dementia praecox,” with the idea that this illness was present in young people and had symptoms such as inappropriate emotions, stereotyped behavior, distraction or confusion, hallucinations, irrational beliefs or delusions, and a deterioration of mental functions.

Besides dementia praecox, Kraepelin also differentiated dementia praecox from manic depressive illnesses and paranoia, the last two with better prognoses. Manic depressive illnesses were mood disorders, whereas paranoia had symptoms of delusional belief with less severity than in dementia praecox. Inspired in part by Kraepelin’s work, Bleuler then coined the term “schizophrenia,” believing dementia praecox did not adequately define psychosis. His notion of schizophrenia was a pathologic splitting apart of the emotional and rational consciousness parts of psychic functioning. Catatonia, which was once apart from dementia praecox classification by Kraepelin, was then included within schizophrenia. A psychiatrist named Jacob Kasanin (1897–1946) coined the term “schizoaffective disorder,” to reflect symptoms of schizophrenia, mood disorders such as mania and depression, and hallucinations, but with fewer symptoms of passivity.

Just as depressive symptoms can vary in number and severity, there are patients with only a few psychosis-related symptoms but not enough to diagnose a psychotic disorder. A psychosis continuum supposition would encompass the range of psychosis symptom variety and severity in the general population. This range includes the overt psychoses, as well as many people with minor symptoms that can include hallucinations, delusions, and ideas of reference. For example, benign hypnogogic hallucinations typically include a voice calling someone’s name as they fall off to sleep. Because psychosis has several symptom dimensions that overlap with affective and nonaffective disorders, it could be thought of as both an illness continuum and also a heterogeneous disorder.

DSM’s diagnostic criteria for schizophrenia are clinically relevant and useful; however, it does not provide essential information about the nature, etiology, biology, social aspects, risk factors, and structure of schizophrenia. Many professionals have debated the construct validity of schizophrenia, in view of psychotic-like experiences in many other psychotic and nonpsychotic disorders, and even in the normal population.

Current Psychosis Differential Diagnostic Theories

Dopamine-blocking antipsychotic medication treatment has been used for nearly 70 years. Medications that block the effect of dopamine can decrease positive symptoms in all psychotic patients, leading to the realization that all forms of psychosis are somehow related to an increase in dopamine activity. This observation led to the dopamine theory of schizophrenia, and later genetic and epigenetic research further increased our understanding. Although antipsychotics have not shown greatly improved efficacy over time, successive medication generations have had milder side effect profiles than previous antipsychotics. However, studies have not shown whether the increase of dopamine in psychosis is related to an excess of dopamine, an excess of dopamine receptors, a hypersensitivity to dopamine, or a combination of those and other factors.

Individuals with subclinical psychotic features tend to show increased dopamine synthesis capacity. But this increased capacity is only among those who later develop overt psychosis. Increased dopamine synthesis capacity is also associated with severity in psychotic disorders. An increase in dopamine levels is also more commonly found in people who are acutely psychotic, by comparison to people with more stable psychosis. Although higher serum dopamine levels are related to severity in schizophrenia, they are not specific to this disorder, and are present in the whole psychosis spectrum, including subclinical psychotic symptoms.

Dopamine, as part of our reward and limbic systems, increases our satisfaction of appetitive instincts and makes us search for more satisfaction, pleasure, and inspiration. However, it is also responsible for increasing our ability to remember aversive situations, helping us recognize potentially dangerous situations and people, and thus amplifies our fear response. Because intense dopamine activation can intensely stimulate our primeval social instincts, that may diminish the role of our rational conscious thoughts. Faced with great pleasure just out of reach, many people will take reckless steps despite their better judgment. In sum, dopamine is responsible for increasing pleasure and appetites, as well as our fear or anger, supplementing the influence of our conscious rational thoughts.

Dopamine abnormalities are common in both people with schizophrenia and people at high risk of psychosis, and the blocking of dopamine can reduce severity of prodromal symptoms in individuals at high risk. Dopamine synthesis capacity is also increased in individuals at clinical high risk for psychosis, which can cause greater severity of prodromal symptoms. Therefore neuroimaging studies have shown a link between dopaminergic dysfunction in schizophrenia prodrome with the clinical development of the disorder, thus suggesting a possible causal role.

Consciousness is thought to occur in the frontal cortex. The hypofrontality theory of schizophrenia points to a thinning of the frontal cortex that is found both in people with psychosis and in people at high risk for schizophrenia. Because frontal lobe thinning is present before schizophrenia onset and is not later linked to severity or duration of illness, it is not a consequence or result of the illness. Diminished frontal lobe function impairs conscious thought, reduces attention span, and impedes processing of social cues. Similar to Bleuler’s notion of schizophrenia, psychosis may result from this imbalance of consciousness and socially instinctive emotions.

Neuroimaging studies have shown great progress in understanding the neurologic aspects of psychosis. In laboratory neuroimaging studies, people with schizophrenia have shown decreased brain activity and changes in the neuroanatomy of the cerebral hemisphere. This can help explain their decreased ability to understand the intent underlying a human action, to recognize pictures they have already seen, and to explain difficulties with abstract thought. These decreased abilities and cognitive impairments are also present in patients with mood-related disorders and individuals at high risk of schizophrenia.

Since frontal lobe executive function is correlated with both clinical insight and cognitive insight, the cognitive impairment of psychosis results in impaired insight. In general, people at high risk for schizophrenia have poor conscious processing of social and emotional information, facial expressions, and social interactions. This is also shown by their need for intensified brain activity when given theory-of-mind tests (the ability to assess others’ thoughts and emotional state) and further points to diminished consciousness well before the onset of psychosis.

Nonpsychotic people with increased dopaminergic activity or with cerebral cortex hypofrontality are more prone to develop psychosis and are more likely to transition from nonpsychotic anxiety or depressive disorder to a psychotic form. Comorbid anxiety or depressive syndromes may be directly related to diagnostic subtyping of psychosis. Ordinary anxiety disorders that evoke weak quasipsychotic symptoms suggest some overlap between nonpsychotic and psychotic categories and support the psychosis spectrum approach. From this point of view, developmental factors can help determine the severity level along the spectrum. Not surprisingly, minor psychotic symptoms in early life can help predict later psychosis, and untreated comorbidities can increase this risk.

A neurodevelopmental hypothesis of psychosis posits that prenatal and perinatal events can increase the risk for psychosis by interaction with structural brain defects. Indeed, some genetic features of schizophrenia are shown during fetal development, predicting compromised cognitive development in early adult life and later psychotic illness. At the same time, neurodevelopmental hypotheses suggest that the low cognitive performance of people with schizophrenia may also correlate with other prenatal and perinatal risk factors or genetic factors. The cognitive impairment in schizophrenia is determined by a complex interaction of nature, nurture, and the illness itself.

Illustrating this complex interaction, patients with schizophrenia who have more early risk factors show greater sensitivity to everyday trauma in comparison with controls, which in turn can then worsen psychotic symptoms and increase psychosis severity. A comprehensive neurodevelopmental theory would explain not only how biological risk and genetic factors can make someone’s brain more prone to psychosis but also how that risk interacts with psychological development, social environment, and both emotionally and physiologically significant events. The overall sum of these effects determines psychotic disorder occurrence and severity, as well as comorbidities.

Murray et al. highlights a vicious cycle in psychosis where stress can increase dopamine dysregulation, which causes psychotic experiences with yet more stress, and finally more dopamine release. This hypothesis has created a new model emerging from the neurodevelopmental model: The developmental risk factor model, which sees schizophrenia as the severe end of a broad multidimensional psychosis spectrum. Thus the psychosis spectrum would encompass a continuum of subclinical psychotic symptoms that can be present in the general population in different levels of severity and reoccurrence.

Evolutionary Theory and the Group of Schizophrenias

Evolution selects for adaptive genes. Those adaptive genes are contained in DNA and act to increase the likelihood of its own replication and survival in the population gene pool. However, given that psychotic disorders generally lead to fewer descendants, why haven’t psychosis-prone genes disappeared over time? One theory is that, although overt psychosis leads to fewer children, milder versions have some sort of kin group survival and reproductive value. Looking at this from a psychosis spectrum point of view: persecutory delusional disorder (associated with social anxiety) may reduce reproduction, but social anxiety can include mildly psychosis-like oversensitivity to potentially dangerous people. In addition, there may be other kin group adaptive benefits to a mild reduction in rational consciousness. Randolph Nesse refers to the transition point of overt psychosis as the “cliff-edge” of reproductive failure.

The evolved social instincts mentioned earlier primarily have a primeval altruistic value for humans and other species. They are instinctive prompts for social behaviors that may be evolutionarily adaptive for the kin group but often conflict with the perceptions and social values of rational consciousness and modern civilization. The genes behind those instincts have survived because they are adaptive for the kin group as a whole. They still underly our overall perception and behavior, and for affected individuals, they sometimes tend to cause emotional pain and reproductive disadvantage. Primeval instinctive altruism differs greatly from modern conscious altruism.

When psychosis proneness diminishes consciousness, primeval instincts can emerge in their unmodified primeval form. Along the lines of Bleuler’s “group of schizophrenias,” each of the five primeval social instincts may determine a specific psychotic disorder comorbidity, or even specific psychosis subtypes. Diagnosis and treatment of the comorbidities can greatly improve clinical outcome. Those five psychosis-associated disorders are the core of this book, briefly reviewed below in this introduction.

Recent research has taken a “transdiagnostic” look at psychotic disorders. Largely through statistical analysis of psychosis rating scales, at least two studies suggest that there are five psychosis subtypes, as well as a separate factor for psychosis proneness. This resembles the clinically transdiagnostic approach of this volume, with five subtypes and psychosis proneness as the key determinants of more specific and more treatable psychosis subtypes. Although direct comparison of those two sets of five statistical subtypes to the five clinical subtypes in this volume is not yet possible, there is at least face plausibility that they could coincide with the five subtypes here.

Evolutionary theory must ultimately agree with genetic research findings. Thus genetics has found hundreds of gene variants associated with schizophrenia but has had limited success in finding genes for endophenotypes. There has been greater success in finding genes associated with psychosis proneness. One possibility is that genes interact with developmental, environmental, and other factors either epigenetically or otherwise. These secondary forces make finding underlying genes more elusive or less specific. Then again, the endophenotypes may be genetically influenced by genes for the five associated comorbidities.

Transdiagnostic study of symptoms could mean that working on a single symptom can also ameliorate related downstream symptoms, if they are linked through a causal chain. Moreover, understanding psychosis through a transdiagnostic dimension can allow greater comprehension of multifaceted symptoms and their underlying dynamics. Although psychosis is sometimes considered mostly schizophrenia, current researchers again think that there are a variety of psychotic experiences.

Psychosis may be related to other psychiatric disorders and is not exclusively schizophrenia, and milder symptoms can appear in nonpsychotic disorders. When exacting diagnosis and newer subtypes are taken into account, it is even possible that schizophrenia will be mostly redefined as a collection of well-defined psychotic subtypes.

Establishing clear definitions and criteria for those subtypes has many potential benefits. Diagnostically, it would improve diagnostic criteria and precision, as well as knowledge of clinical phenomenology. For research, it would enhance genetic, epidemiologic, neuroimaging, psychotherapeutic, and psychopharmacologic approaches. Most importantly, clinical treatment of subtypes and associated comorbidities will allow greatly improved treatment and outcome. The transdiagnostic approach can have a huge impact on how we view and deal with mental illness, once related comorbidities, such as mood and anxiety disorders, are seen as core syndromes rather than as a hodgepodge of secondary distress symptoms. Many studies have shown a high prevalence of mood and anxiety disorders associated with psychosis spectrum disorders.

Obsessive-compulsive disorder (OCD; Chapter 3 ) is one common comorbidity. Obsessive and compulsive symptoms are often present prior to psychosis onset, often starting in childhood. Similarly, OCD symptoms associate with earlier age of psychosis onset, as well as diminished functioning in psychotic patients. Comorbid obsessive-compulsive symptoms correlate with increased schizophrenia severity, obsessions, mind-reading concerns, and inappropriate sexual impulses. As noted in the OCD chapter, criteria for a “schizo-obsessive disorder” have been proposed.

Panic disorder ( Chapter 4 ) is also a common comorbidity in schizophrenia, occurring in 7.1% to 47.5% of schizophrenia patients, and panic attacks are often masked when they are component parts of psychotic symptoms. Sometimes, panic anxiety precedes and triggers such psychotic symptoms as auditory hallucinations and paranoid delusions. When psychosis-masked panic is closely evaluated, the panic comorbidity in schizophrenia with voices may be 100%. In addition, panic is also associated with guilty delusions, which can be found in nonpsychotic anxiety disorders as well. As noted in the Panic chapter, although a panic psychosis has been proposed, much research remains to be done.

Social anxiety ( Chapter 5 ) is also associated with schizophrenia generally and with delusional disorder in particular. Social anxiety correlates with paranoia, social withdrawal, feelings of inadequacy, negative assessment by others, and mind reading in both patients with schizophrenia and with persecutory delusional disorder. This can also cause symptoms of mind reading and social-phobic delusions of negative assessment.

Depression in psychosis is commonly associated with greater positive and negative symptoms. Depressive symptoms are also common with earlier psychosis onset, and both can diminish coping and heighten psychotic experience.

Melancholic depression ( Chapter 6 ) another specific depressive subtype, may underly psychotic (delusional) depression. This syndrome includes greater psychological distress, feelings of guilt and victimization, and persecutory delusions. As noted in its chapter, this subtype has long been formally established, and dual treatment of depression and psychosis are typically the best treatment.

Atypical depression ( Chapter 7 ) a specific depressive subtype, is the most common depression in true bipolar I disorder. Mania, with its delusions of grandeur, can be considered a psychosis, and it is often misdiagnosed as schizophrenia. Mania is associated with certain markers of psychosis-proneness. In addition, some manic patients have auditory hallucinations and more elaborated delusions. However, mania is a recurrent component, whereas atypical depression is an ongoing illness. The association of the two has no well-defined mechanism. Even so, manic delusions are typically focused on saving the world, while the rejection sensitivity of atypical depression leads to avoidance of offensive behavior, thus saving social harmony.

With these five subtypes in mind, as well as those psychoses related to substance abuse ( Chapter 8 ) and to medical illness and treatment ( Chapter 9 ), the evolutionary and transdiagnostic perspective can allow us to better understand and individually treat each patient. Psychosis is not a specific and unitary disorder with variable symptoms. Rather, there are several overlapping symptoms related to nonpsychotic disorders. This perspective can help professionals avoid treat overt psychotic symptoms, while also addressing those contributory comorbid syndromes that can aggravate or cause psychosis.

Psychosis and Mixed Comorbidities

Isolated psychotic experiences found in nonpsychotic patients have been typically found in patients with anxiety or depression and may even occur in the general population, ranging in prevalence from 0.6% to 84%. These experiences are often related to psychiatric disorder severity and poor treatment outcome. Therefore, if psychotic experiences can worsen prognosis, it is beneficial to understand how symptoms interact, to clarify diagnostic criteria.

Although disorders are organized through symptoms and clusters, each patient will manifest them in different ways. This broad range of symptom manifestations, the ability to find those symptoms in the general population, and the overlap of symptoms in different disorders can hinder and cloud diagnosis. So, it is extremely common for people within the psychosis spectrum to have affective symptoms, as it is common for people with mood disorders to have different but overlapping affective symptoms and present such manifestations of other disorders as psychotic symptoms and anxiety.

Patients with schizophrenia often present comorbidities such as obsessive-compulsive disorder, social anxiety, depression, and other anxiety disorders. Many of these disorders occur at a rate higher in schizophrenia than in the general population. And, just as nonpsychotic patients with one of these syndromes often have more than one, the same phenomenon of multiple comorbidities occurs in schizophrenia. That makes full and accurate diagnosis more important and more confusingly difficult.

It is common for schizophrenia patients to have panic anxiety, which tends to begin before schizophrenia onset. Higher panic anxiety levels make patients more likely to hear more voices and have more delusions, just as nonpsychotic patients with panic disorder have increased brain activity to experimental noise. Emerging data suggest that voices usually occur together with panic symptoms in patients with psychosis.

Although not categorized as a symptom for a psychosis diagnosis, cognitive biases such as jumping to conclusions (JTC) and liberal acceptance (seeking less information to reach a decision) are associated with psychosis and delusions; they are also seen in other psychiatric disorders with delusion-like experiences. This implies a transdiagnostic process, where cognitive biases may have a role in forming delusions.

In addition, individuals at UHR for schizophrenia show higher than normal rates of depression and anxiety, and conversely, psychotic-like experiences are more common in individuals with anxiety and depressive disorders. Some research points to melancholic and atypical major depression, obsessive-compulsive disorder, panic disorder, and social anxiety as the five core diagnoses in nonpsychotic patients and commonly found in schizophrenia as both single and multiple comorbidities.

Depressive symptoms in schizophrenia may be associated with diminished coping, heightened psychotic experiences, greater psychological distress while deluded or hallucinating, and the obsessional guilt and victimization commonly found in delusional depression. These may also increase risk for suicide when compared with patients with nonpsychotic depression, and especially during the most acute phase of the illness. Studies show that depression is often found in UHR individuals with nonpsychotic comorbid mental disorder at baseline.

OCD can also increase schizophrenia severity with ego-dystonic obsessive delusions of aggressive, sexual, or guilt content and formal thought disorder of mind reading. Panic is also related to guilty delusions, as well as increased suicidal ideation, auditory hallucinations, early onset, and hospitalization. Lastly, social anxiety can be associated with social-phobic delusions of negative assessments and decrease in social anxiety instincts by the hypofrontality common in psychosis.

A study investigating clinical outcomes of UHR patients ( N = 74) at 6-year follow-up found that 28% of the UHR patients transitioned to psychosis and 56.8% presented at least one nonpsychotic comorbid mental disorder. UHR patients with affective symptoms have better prognosis when treatments aim at reducing not only psychotic symptoms but also mood and anxiety symptoms. Therefore psychosis might arise from nonpsychotic subthreshold psychopathology that can develop into a more severe disorder under some circumstances.

Although it is likely that comorbidity diagnostic assessment is often hindered by cognitive impairment, the effort is worthwhile. The ability to define psychosis comorbidities can help professionals differentiate among treatable and discrete syndromes. In turn, this helps to improve prognosis with more accurate and specific diagnoses that focus on psychosis, as well as on comorbidities. Recognition of the comorbidities requires awareness that they can both precede and coincide with psychotic processes.

To work preventively in psychosis, professionals must be able to identify UHR patients and develop a holistic strategy to predict illness onset, early course, and subsequent evolution. The different comorbidities that can precede and coincide with psychosis may have different outcomes and pathways. UHR patients usually already have at least one comorbid diagnosis, such as anxiety or depressive disorders. In addition to other contributing factors, these early syndromes can also be part of a negative feedback loop. Anxiety and depression can decrease functional levels, causing more distress, thus aggravating themselves toward a psychotic outcome.

Basic Interview Guidelines for Acutely Psychotic Patients

Diagnostic interviews of psychotic patients are not always easy and are more difficult still during acute psychosis. With that in mind, some basic guidelines can improve the odds of obtaining detailed and accurate symptom and syndrome history. Each of the diagnosis chapters in this book includes some additional guidelines specific to the different psychotic and comorbid diagnoses.

Because not every guideline is appropriate for every patient and interview, each suggestion should be considered in the context of each particular patient and interview. That said, here are some basic guidelines for interviewing actively psychotic patients:

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  Be friendly, supportive, and professionally detached

  
  
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  Too friendly or emotionally close can be threatening

  
  
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  Emphasize and explain evaluation process and confidentiality rules

  
  
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  Recruit a family member who may retain some of the patient’s trust

  
  
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  Everyone should avoid words such as “paranoid,” “psychotic,” “crazy,” etc.

  
  
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  Be honest, but carefully phrase questions and comments

  
  
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  Start with a bit of small talk

  
  
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  Then proceed to less emotionally loaded material (i.e., medical history, living arrangements, work history)

  
  
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  Neither contradict nor agree with psychotic beliefs

  
  
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  Recognize patient’s point of view and perceived circumstances, even if psychotic

  
  
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  Usually express empathic concern about their difficult situation

  
  
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  Clinical knowledge of their diagnostic construct also shows empathy

  
  
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  Some patients will slowly develop some fragile trust and open up a bit

  
  
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  Always review both prepsychotic and psychotic history for comorbidities

  
  
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  Review all symptoms of each psychotic and nonpsychotic syndrome considered

  
  
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  Always carefully assess potential violence and self-harm risk

  
  
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  In some cases, consider a weapons check

  
  
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  Always remember that there may be unrevealed symptoms

  
  
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  Conduct interview in a secure setting safe for patient and yourself

  
  
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  Medication can be accurately proposed as an aid to their perceived struggle

  
  
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  Usually repeat the diagnostic interview after acute psychosis is diminished

Summary: Limitations of Existing Research, Increasing Research Interest

Schizophrenia has long been seen as a collection of psychotic disorders. Various subtyping methods have been proposed and discarded over time. Meanwhile, at least three functional subtypes have been recognized as separate and distinct conditions: psychotic depression, delusional disorder, and bipolar I mania. Even so, those three conditions are often mislabeled as schizophrenia when the haze of patient psychosis and limited evaluation time combine to make specific subtyping difficult. Each of the three appears to have a commonly comorbid condition, while two more novel psychoses may also have comorbid determinants (obsessive-compulsive schizophrenia and panic psychosis). In addition, there are psychoses associated with substance abuse and with medical illness and treatment.

Alas, only some of this diagnostic schema are fully established, and much research remains, although it is clear that the comorbidities are common in psychoses. However, few genetic and neuroimaging studies used these comorbidities as markers to look for differing physiopathology in schizophrenia. Similarly, although psychotic-like experiences are included as markers for UHR for schizophrenia, studies do not usually evaluate anxiety and depressive subtypes, nor do they associate these syndromes with risk or phenomenology of schizophrenia. Longitudinal studies that follow up the symptom transformation from nonpsychotic to psychosis may be a frontier for new understanding of psychopathology and methods to avoid psychotic evolution. Finally, the study of comorbidities hidden among psychotic symptoms has been of increasing clinical interest. What is anecdotally clear to some clinicians is the vital importance of diagnosing and treating those comorbidities at the same time as the psychosis itself.