This volume makes the point that every patient with psychosis requires a careful differential diagnosis, and that there is more to diagnosis than just the monolithic concept of “schizophrenia.” Moreover, the ancillary anxiety and depressive symptoms of psychotic disorders are not just “understandable” artifacts of a distressing disease. For example, DSM-5 notes that “anxiety and phobias are common” in schizophrenia. But it could well be that five specific anxiety and depressive subtype syndromes may be the core of five corresponding psychotic disorders, and they may be the key to understanding and categorizing discrete psychosis subtypes. Each one requires careful and informed clinical evaluation, each has its own phenomenology and prognosis, and each has a specific treatment approach that can be much more effective than antipsychotic medications alone.
The idea that comorbid syndromes could play a central role in psychotogenesis goes back more than 100 years. Early observers tended to view anxiety as a predecessor and contributor to schizophrenia, although more recent scholars have been more likely to consider anxiety and depression as comorbid syndromes that may result from schizophrenia.
Schizophrenia
Of the five core comorbidity syndromes in this book, the one that looks much like classic paranoid schizophrenia with auditory hallucinations is schizophrenia with comorbid panic anxiety. Indeed, the name “Panic Psychosis” has been proposed for this syndrome. In addition, there can be other psychosis comorbidities such as obsessive-compulsive disorder ( Chapter 3 ) and social anxiety disorder ( Chapter 5 ; focusing primarily on Persecutory Delusional disorder).
Schizophrenia is defined in DSM-5 1 ( Table 4.1 ).
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When viewed as a single entity, lifetime schizophrenia prevalence is estimated at 0.7%. It is important to remember that schizophrenia diagnosis requires at least 6 sustained months of illness. Shorter durations with similar symptoms include brief reactive psychosis and schizophreniform disorder, and do not necessarily progress to schizophrenia. Importantly, the differential diagnosis includes delusional disorder ( Chapter 5 ), psychotic depression ( Chapter 6 ), bipolar psychosis ( Chapter 7 ), substance-induced psychosis ( Chapter 8 ), medical illness and iatrogenic psychosis ( Chapter 9 ), as well as the concepts of schizo-obsessive disorder ( Chapter 3 ) and the panic psychosis discussed in this chapter.
Recent research has suggested that there may be a genetically influenced susceptibility to schizophrenia underlying five distinct subtypes of schizophrenia. Two studies each used factor analysis of common symptoms to propose their similar five subtypes. On the surface, there is some suggestion that they may correspond with the same five psychoses previously proposed clinically, documented in a small pilot study of schizophrenia comorbidity subtype diagnosis, and now considered here (along with substance and medically related psychoses).
Schizophrenia is a chronic, progressive, and debilitating disease. Symptoms are typically grouped into positive psychotic symptoms and negative social symptoms. The positive symptoms can include auditory hallucinations, paranoid delusions, and ideas of reference. Ideas of reference include self-referential belief that there are special personal meanings in radio or television broadcasts, glances or sounds from strangers, or in news events. Negative symptoms can include apathy and limitations in affective display, speech output, social interaction, capacity for pleasure, and motivation. Schizophrenia symptoms produce substantial social and cognitive limitations. With onset typically in adolescence or early adulthood, education and social development are seriously disrupted, and the disruption typically continues even with decent response to antipsychotic medications.
These medications can reduce psychosis and rehospitalization, but schizophrenia remains a life-changing illness. To be sure, some people do return to a more normal life and function, and some may even experience substantially full recovery. But research and anecdotal evidence presented in this volume suggest that the degree and duration of improvement can be substantially increased with diagnosis and treatment of comorbid, and perhaps underlying, psychiatric disorders.
There are financial costs to society as well. Schizophrenia impairs occupational and social function, contributes to homelessness, and to needs for external family, community, and financial support. There is also a significant cost of medical and psychiatric care. Any increased cost of improved diagnosis and treatment would be offset by reductions in some of these other costs, not to mention the personal, familial, and societal benefits.
Panic Disorder
This chapter focuses on comorbidity of panic disorder with schizophrenia, panic exacerbation of schizophrenia, and the proposed notion of a panic psychosis. Panic disorder is defined in DSM-5 1 ( Table 4.2 ).
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Panic disorder (panic anxiety) diagnosis requires a specific and detailed clinical inquiry about paroxysmal onset episodes of panic anxiety, and about related symptoms. For example, panic underlies most phobias, and is often associated with chronic anticipatory anxiety (commonly experienced as generalized anxiety). Anticipatory anxiety is understood as ongoing non-panic anxiety unwittingly caused by fearful uncertainty about when the next panic will occur. Research suggests that a significant percentage of those with generalized anxiety disorder have underlying but unrecognized panic disorder.
Panic attacks can’t be quantified by clinician observation, as only rarely are they outwardly visible to other people. Until diagnosis, people with panic attacks often experience them as merely an escalation of anxiety, rather than as a discrete and paroxysmal subtype of anxiety. In addition, they often attribute panics to being trapped, and thus unable to escape from some kind of physical danger. The perceived danger can also be related to actual panic symptoms, and so lead people to other physicians before psychiatrists. For example, chest pain can lead to concerns about heart attacks, shortness of breath to asthma, and other symptoms to many more medical concerns. After diagnosis, patients become more able to experience panics as internally generated, as discrete episodes, and often in response to some known or unknown symbolic emotional threat.
Panic disorder is common in the general population, with an estimated US population prevalence of 4.8%. It is generally thought that most people are not able to panic, even in response to laboratory challenge procedures known to provoke panic in people who have the syndrome. So, if you include all those people who report even one lifetime panic attack, the population prevalence for panic susceptibility may be closer to 23%. Even in a large sample of corporate employees, the lifetime prevalence of at least one panic attack was 15%, disproportionately occurring in lower-level job categories.
Panic disorder typically begins in early to mid-adolescence, but is sometimes preceded by an earlier period of separation anxiety in toddlers. Individual panic attacks typically last for several minutes, but can last for hours or even days. Prolonged panic attacks contribute to agitation and agitated behavior. Untreated, panic disorder symptom severity waxes and wanes over a lifetime, frequently with lengthy panic-free periods, and often with development of coping skills that reduce some of the emotional and functional impediments to social and occupational accomplishment. Panic is also a predictive risk factor for some medical diagnoses, including heart disease and stroke.
Psychosis-Like Symptoms in Non-Psychotic Panic Disorder
Two studies have reported that ideas of reference and paranoid ideation, drawn from the psychoticism and paranoia subscales of the SCL-90, were significantly more common in panic patients with no psychosis history than in no-panic controls. These same symptoms are also among those considered markers for psychosis-proneness.
Schizophrenia with Auditory Hallucinations and Comorbid Panic
Many studies have noted a high prevalence of comorbid panic anxiety in schizophrenia. In the Epidemiological Catchment Area study (ECA), 45% of schizophrenia patients had a lifetime history of panic attacks. In one small sample of patients with schizophrenia with voices, 100% had panic associated with their voices, as well as carbon dioxide challenge test induced panic. Many other studies have reported a significantly increased panic prevalence rate in schizophrenia. Where there is variation in prevalence rate, it may be due to different methods for panic diagnosis, less specific criteria for schizophrenia diagnosis (i.e., sometimes including other psychotic disorders), the difficulty of diagnosing panic when it appears in psychotic form, or when cognitive impairment clouds awareness. Panic, like the other comorbidities in this volume, is easiest to diagnose when psychotic patients have been stabilized, and by including a careful history of panic that preceded psychosis onset. Importantly, an earlier history of prodromal panics suggests ongoing chronic panic disorder, or at least chronic susceptibility.
Compared to other schizophrenia patients, comorbid panic and schizophrenia is associated with earlier age of onset, more severe illness course, more severe symptoms, more positive psychotic symptoms, more paranoid features, more suicidal thought, and lower quality of life.
Panic can itself appear in psychotic form, notably as auditory hallucinations, but also as acutely exacerbated paranoid delusions. As noted below, specific interview techniques are essential for evaluating these possibilities. This approach is used by the semi-structured Panic and Schizophrenia Interview (PaSI). In two small PaSI studies, the voices also met DSM panic criteria in 73% and in 100% of patients. In the second of those studies, PaSI interview findings were confirmed in the laboratory by a randomized and blinded carbon dioxide panic challenge test. Carbon dioxide provoked panic in all eight subjects, while placebo provoked panic in only one. Not surprisingly, some patients describe more panic attacks when they become non-hallucinatory. At that point, many patients will understand the concept of their now ordinary panic attacks as “voices without the voices.” Consistent with the notion of ongoing anticipatory anxiety in ordinary panic, some patients with voices experience ongoing paranoid fears about the recurrently frightening characters and messages in their voices.
Recent research on both panic and schizophrenia has looked at pathophysiology of the GABA neurotransmitter system, prefrontal cortex function, and at genetic and familial observations. To start, one study has shown that unselected schizophrenia patients, as compared to controls, have a nearly five times higher prevalence of panic disorder among their first-degree relatives. When healthy relatives of schizophrenia patients were given low-dose alprazolam, they had a distinctive GABA response as compared to healthy relatives of normal controls. The GABA neurotransmitter system regulates anxiety, with different GABA receptor subtypes influencing varied anxiety subtypes. In general, reduced GABA activity is associated with increased anxiety. Not surprisingly, genetic research shows that panic disorder is associated with GABRA5 (alpha 5 receptor subunits) and GABRB3 (beta 3 receptor subunits) genes and associated dysfunction. Similarly, panic disorder patients have decreased GABA levels in the prefrontal cortex. Another study showed reduced GABA receptor binding in the prefrontal cortex (primary site of conscious thought), which correlated with panic symptom severity.
Schizophrenia research similarly suggests deficient GABA activity in the prefrontal cortex. A study of first-episode patients found comparable results, along with compensatory increased glutamate activity. Schizophrenia patients with reduced prefrontal cortex size (associated with psychosis susceptibility) had a stronger clinical response to alprazolam. While much research is still needed, these paired panic and schizophrenia findings suggest that some specific form of deficient GABAergic transmission could be an underlying mechanism that connects panic with some schizophrenia. Clonazepam, or similarly acting present and future medications, may help by acting on this shared mechanism.
Fictional Case
Helen, an 18-year-old high school graduate from Texas, began feeling more anxious at age 14, especially when she was away from home and family. At first, she just thought this was just occasional distress about going to school, or about getting stuck in traffic jams. But soon the anxiety became more constant, though with varying intensity. Grades and social life began to suffer. At 16, Helen’s parents brought her for counseling. She learned helpful techniques for understanding and coping with the anxiety, but it did not go away. She also came to realize that the worst part of the anxiety came on as very sudden panic, with sweating, an urge to flee, racing heart, shakiness, shortness of breath, and a fear that something dreadful would happen.
At 18, she began to hear a voice talking to her. The voice would also begin very suddenly, together with her other panic symptoms. This harsh and critical voice was quite real to her, and far more troubling than the other symptoms. She found it increasingly hard to motivate herself, to enjoy anything, or to socialize. After some months of increasingly paranoid fears, social withdrawal, and emotional detachment, she was brought to see a psychiatrist.
Evaluation included careful psychiatric history from Helen and family, medical consultation, evaluation of possible substance abuse and suicide risk, and consideration of elective hospitalization. At first, her acute psychosis was treated as an outpatient with risperidone, and after a month (6 months from illness onset) she had a significant reduction in her voices and paranoid fears. At that point, the psychiatrist reviewed her psychosis history and her potential comorbid and premorbid symptoms. Helen was newly able to recall and describe the panic attacks that had started at 14. When asked, she was also able to describe the paroxysmal onset of her auditory hallucination episodes, and how they were accompanied by the same sudden symptoms as her panic attacks. Now that the voices were far less common, she also began to notice the return of panic attacks without voices. Other common comorbidities were not present.
Helen’s risperidone was augmented with clonazepam q12h fixed dose (no PRNs). Medications were given by her family, and the initial clonazepam dose was small. She was warned that she might feel drowsy for a few days each time the clonazepam dose was raised. Over the course of a few weeks, her dose was slowly raised to the point where even mild voices and panics had fully ceased at 2 mg q12h. The paranoid fears steadily faded in importance. Helen remembered them only when asked, and they were of rather little concern. Little or no drowsiness remained. Ironically, as she reached the point where her symptoms were essentially gone, she became quite concerned about medication side effects, and wanted to stop treatment. This concern was addressed in psychotherapy by carefully explaining the difference between illness and treatment. Therapy also discussed her dread of a serious illness, as well as her uncertainty about the likelihood of continuing to feel well.
Feeling her best since age 14, Helen was soon able to start college. She remained in weekly therapy with a local psychiatrist, established a social network, and did well in class. After a year or so, her risperidone dose was reduced. Three years later, fully compliant with treatment, she continued to do well, and was hopeful for the future.
Interview Technique
A skilled interview requires clinical training and expert familiarity with schizophrenia and panic diagnostic criteria and phenomenology. The detailed assessment below is typically more effective after acute psychosis is already stabilized. Some basic guidelines for interviewing psychotic patients are included in Chapter 1 . After establishing a diagnostic alliance with the patient, ask patients if there are times when they are not actively hearing voices. Then ask if, at least sometimes, the voices return with a paroxysmal onset (regardless of any reported triggering events at those moments). While repeatedly focusing on that paroxysmal moment, ask about concurrent panic, fear, or anxiety, as well as the other DSM-5 panic symptoms. A detailed semi-structured clinical approach to DSM-5 panic diagnosis in schizophrenia is included in the PaSI, intended as a supplement to a full psychiatric history. Like any diagnostic interview, the sensitivity and specificity of diagnostic data may be limited by clinicians’ experience, and by patients’ cognitive impairment, personality, and fearfulness. Since the PaSI focuses on careful evaluation of psychotic symptoms for concurrent panic symptoms, this part of the clinical interview may need 15 minutes to complete.
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