4 - Dissociative, Somatoform, and Paranoid Disorders

Editors: Shader, Richard I.

Title: Manual of Psychiatric Therapeutics, 3rd Edition

Copyright 2003 Lippincott Williams & Wilkins

> Table of Contents > 4 - Dissociative, Somatoform, and Paranoid Disorders

4

Dissociative, Somatoform, and Paranoid Disorders

Richard I. Shader

Katharine A. Phillips

This chapter reviews a group of disorders that are among the more interesting and challenging disorders that clinicians encounter. In addition, dissociative disorders should be considered in the differential diagnosis of patients with dementia, delirium, confusion, and amnesia (see Chapter 5). In some ways, this cluster of disorders is prototypical of what would have in the past been considered the nonorganic forms of mental disturbance. The paranoias are included here because of some overlapping features. Patients with obsessive-compulsive disorder may also show features similar to those of several somatoform disorders (i.e., body dysmorphic disorder and hypochondriasis). Because of the severity of obsessive-compulsive disorder and the availability of treatments approved for this specific diagnosis, obsessive-compulsive disorder is discussed separately in Chapter 6.

I. Dissociative and Somatoform Disorders

For many of the following disorders, patients' complaints or behaviors may suggest physical illness, dysfunction, or impairment. For some of these disorders to follow or to occur during the course of a physical illness or after an injury (e.g., seizure disorders, head injury) is not unusual. They may occur as distinct disorders, in conjunction with each other, or as partial features of other disorders. Unconscious coping styles (see Chapter 1) and conscious motivation and behavior may be factors in their development.

Clinicians are often frustrated or even angered by these patients because generally they do not respond to reassurance when the workup does not reveal a serious underlying physical disorder; the patients may respond by doctor shopping. A clinician who receives requests for records from another clinician or facility may find that contacting the new doctor to review concerns and impressions is worthwhile. When clinicians do not compare notes consistently, a few patients may consume unwarranted amounts of clinician time and health care dollars, and they may be exposed to unnecessary tests, medical treatment, or surgery.

A. Dissociative Disorders

These conditions involve alterations or disturbances in memory, consciousness, and identity. Some may have a sudden onset and they may be temporary; others may be gradual in onset and chronic in course. When these disorders have a sudden onset and a brief duration, some clinicians prefer to use the terms acute stress reaction and brief reactive dissociative disorder to describe dissociative fugue and dissociative amnesia.

  • Dissociative amnesia involves the selective exclusion of important personal information or experiences from the memory, usually after a stressful or traumatic experience. The lost memories may not be retrieved for hours; in rare instances, they may remain unrecovered for a lifetime. The extent of the anterograde memory loss, which is sudden in onset, in dissociative amnesia is too extensive to be dismissed as mere forgetting. A single episode of dissociative amnesia is most common, but, if repeated experiences of extreme stress or trauma occur, multiple episodes are possible. The precipitating stress or trauma is usually quite severe (e.g., a threat to one's life, combat, injury, or being the perpetrator or victim of an unacceptable act).

    The recovery of memory may be spontaneous, or it may be aided by hypnosis (see Chapter 23) or the use of intravenous amobarbital. (Note: Although procedures for the amobarbital interview were widely known and taught in the post-World War II era, this diagnostic method is rarely used today.) Once memory is recovered, the return of what was excluded

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    from the individual's consciousness is generally complete; by contrast, the memory loss from a concussion is usually retrograde and the recovery is gradual. However, for dissociative amnesia to follow an injury, including a head injury, or a seizure disorder is not unusual. Posttraumatic stress disorder with concomitant dissociative amnesia may develop as a sequela of certain stressful traumatic experiences (see Chapter 14).

  • Dissociative fugue and dissociative amnesia are sometimes considered forms of what used to be called dissociative hysteria. Dissociative fugue is also sudden in onset, and it involves an inability to recall one's identity, rather than memory loss for a period of time. Unplanned travel, usually to a distant location where the affected person is not likely to be recognized or known, occurs; and a new identity, either partial or complete, is assumed. The travel is purposeful; it does not appear to be aimless wandering. The loss of knowledge of one's real identity and past almost invariably includes a loss of knowledge of one's birthplace and birth date. As with dissociative amnesia, dissociative fugue may occur after an acute stress. Alcohol consumption or substance abuse at the time of onset is common.

    Dissociative fugue is rare. Its prevalence rate in the United States is under 0.3%. Nevertheless, most large urban emergency or psychiatric departments can recount a few such cases. As with dissociative amnesia, hypnosis or intravenous amobarbital may prove helpful. Supportive discussion and psychotherapy that encourages remembering usually lead to a gradual recovery of the patient's true identity and the events preceding the onset of the fugue. Concomitant central nervous system pathology (e.g., seizure disorder) may also be present. Some persons who appear to have dissociative fugue may actually be malingering or lying for obvious secondary gain (e.g., after embezzlement); in contrast, dissociative fugue and other dissociative disorders are generally thought to arise from unconscious reality-distorting coping mechanisms.

    Dissociative fugue may overlap with certain culturally syntonic states, such as amok among Pacific Island peoples, pibloktoq or Arctic hysteria among Greenland Eskimos, or grisi siknis among the Miskito Indians of Nicaragua.

  • Dissociative identity disorder (DID; formerly called multiple personality disorder) involves the coping strategy of developing two or more distinct personalities unconsciously, each of which usually has a distinct name, as a way of living with overwhelming circumstances. Typically, this dissociative adaptation develops in the aftermath of intrafamilial childhood sexual or physical abuse. Whether thinking of such patients as defensively forming additional personalities or, alternatively, seeing them as having an incompletely or inadequately formed personality (i.e., one that permits different aspects of an unintegrated and unregulated personality to emerge) is more accurate remains unresolved. Most DID patients are not forthcoming about their various personalities, which are sometimes called alters, even when they are aware of them. The various personalities tend to be distinctive and to dominate or control the patient's behavior when they are operant. Some patients experience a sense of struggle for dominance among their alters. A shifting importance to the role of each personality over time and of the time spent in each alter may be seen. Each personality may have its own set of relationships.

    Personalities may emerge during religious or magic-related rites. Some clinicians believe these latter patients should be in a distinct diagnostic category (i.e., trance or possession disorder). For one personality to be good and highly moral and for at least one other to be willful, irresponsible, mischievous, sexual, carefree, or bad is not uncommon. The formation of multiple personalities is likely a way of emotionally managing betrayal by a trusted parent or parental figure. One personality remains unstained by the events from childhood; another

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    part perpetuates or justifies them as follows: I wasn't betrayed; I like the immoral life.

    Pediatricians, emergency department clinicians, and others involved in the acute care of victims of sexual and physical abuse should make appropriate referrals to try to prevent the development of DID (see Chapter 27). Clinicians who learn of childhood sexual and physical abuse from their adult patients should be alert to the possibility of DID. Treatment of DID is complex; it is best undertaken by a specialist in DID, so referral is indicated.

  • Depersonalization disorder is another dissociative disorder. Depersonalization as a symptom refers to an altered sense of self. One may feel unreal, like an automaton; as if in a dream or detached or estranged from one's body or its mental representations or from one's surroundings; or as if one is outside of oneself and is looking in, observing one's own mental processes or body. Derealization refers to a change in one's relationship to or awareness of one's environment that creates a feeling of unreality or estrangement. To describe depersonalization, one might say, I feel strange. When describing derealization, one might say, My world or my surroundings feel strange.

    Depersonalization and derealization may be transient phenomena; however, they also can occur together. Both symptoms may be noted by patients who are taking particular medications or drugs (e.g., tricyclic antidepressants, medications with antihistaminic properties, lysergic acid diethylamide [LSD]), many of which alter the serotonergic systems. Patients who are extremely anxious or depressed may report depersonalization. Childhood trauma appears to be an additional risk factor. Some authors note the co-occurrence of depersonalization with obsessive-compulsive and panic-like symptoms, which suggests a linkage to perturbations in serotonergic activity. Some support for this hypothesis derives both from the reduction in depersonalization experiences that some patients have with proserotonergic agents and from the production of depersonalization experiences by the 5-hydroxytryptamine (HT)2c agonist m-chlorophenylpiperazine. Limited data from imaging studies suggest that depersonalization represents a dissociation of perceptions; functional abnormalities have been noted in sequential hierarchical areas of the sensory cortex and in areas responsible for an integrated body schema.

    Depersonalization disorder is diagnosed when depersonalization or derealization persists or recurs episodically, it does not occur exclusively during the course of another mental disorder, and it is not due to use of a substance. In depersonalization disorder, reality testing is intact; therefore, depersonalization disorder is not a delusional state. In addition to the descriptions of feelings noted above, patients with depersonalization disorder may complain of difficulty feeling their own emotions, or they may see others as lifeless, less dimensional, or cardboard-like. Body parts, particularly limbs, may feel distorted in size or shape. Most patients are distressed by these experiences.

    Typically, clinicians are alerted to this disorder by the difficulty the patients have in describing what they have been feeling and how they resort to metaphor to try to explain it. Generally, no readily apparent experience-linked or stress-linked etiology or precipitant is present in depersonalization disorder. In the authors' experience, it occurs in susceptible people at times of transition (physiologic, psychic, or environmental), and it is associated with impaired arousal.

    Treatment for depersonalization disorder is based on anecdotal and case reports. One pattern emerges from these reports a suggestion that medications that increase synaptic dopamine (e.g., amphetamines, methylphenidate, monoamine oxidase inhibitors, bupropion) may be beneficial. Another treatment approach involves the use of proserotonergic

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    agents (e.g., clomipramine, selective serotonin reuptake inhibitors [SSRIs]) combined with a benzodiazepine (e.g., clonazepam). This latter strategy is supported by several small sample nonblinded studies, case reports, and unverified testimonials on the World Wide Web (Internet). The co-occurrence of obsessive-compulsive symptomatology with depersonalization may suggest a positive response to proserotonergic agents. Because no criteria for when and how to treat depersonalization disorder are universally accepted, a conservative approach is recommended. Medication trials may be considered for patients who are distressed or impaired by their symptoms, but only when the symptoms persist. When appropriate, patients may need to be informed that their condition is not a customary indication (see Appendix I) for these medications. A good step for risk management is obtaining and documenting a second opinion.

  • Acute amnesia or memory impairment from drugs and alcohol

    • Pathologic intoxication with alcohol, which is sometimes called the syndrome of alcohol idiosyncratic intoxication or mania potu, may also be a cause of amnesia; it is discussed here for perspective. Some of these cases may actually be cases of dissociative disorder. The amnesia is manifested as an anterograde loss of episodic memory and not as a loss of information in long-term storage. Affected people (usually males), who may have an idiosyncratic sensitivity to alcohol, behave in a disinhibited manner that typically involves senseless violent acts after drinking small amounts of alcohol, amounts that are usually so little that the person does not appear to others to be intoxicated. (Note: In some instances, patients may merely be using their consumption of alcohol as an excuse for unacceptable behavior.) Such outbursts are generally followed by a period of extended sleep that again is out of proportion to the amount of alcohol ingested and by amnesia for the events.

      When a patient is in this state, anyone who is trying to help should approach the patient in a calm, nonchallenging way, as confrontation usually escalates the patient's potential for violence. Because the state will pass, the safest route may be no intervention. Nevertheless, small parenteral doses of benzodiazepines (e.g., diazepam, lorazepam, midazolam) may be used for sedation. Once a predisposition for pathologic intoxication with alcohol is recognized, prevention by abstinence is the best treatment (see Chapter 11 for a brief perspective on alcoholism).

    • Drug-induced amnesia or the impairment of registration and retention of memory without accompanying violence or excessive sleep can be seen after the ingestion or parenteral use of alcohol, scopolamine, and many benzodiazepines (e.g., diazepam, lorazepam, triazolam, midazolam). Usually, the individual has a memory gap for some hours after drug administration. New experiences and new learning may not be retained. This form of memory impairment may be dose related, and sensitivity to it varies among patients. Repression does not seem to be involved in these drug-induced amnesic states. Because of their potential for amnesic effects, the use of oral benzodiazepines is not recommended to reduce the anxiety associated with learning speeches, studying for examinations, or other similar situations.

B. Somatoform Disorders

  • Conversion disorder is considered a form of somatoform disorder in which the unconsciously motivated dysfunction or impairment involves the voluntary muscle or sensory nervous systems. Patients present with impairments, usually of acute onset (e.g., I woke up and couldn't move my right hand ), which on physical examination do not conform to the expected patterns of muscle groups or dermatomes or to known

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    pathophysiologic mechanisms (e.g., glove or stocking pattern anesthesia may be present). Conversion disorder involves motor impairment (e.g., gait disturbance or ataxia, tremor, paralysis or weakness, swallowing, or aphonia) or sensory impairment (anesthesia, usually in the form of numbness; hyperesthesia in the form of burning sensations in the head or abdomen; blindness or diminished visual fields [tunnel vision]; or deafness). Episodic seizures or vomiting may also be encountered.

    With conversion disorder, in addition to the lack of correspondence to known bodily dysfunctions, information obtained from the patient (or others when necessary) should reveal a temporal connection between the onset or exacerbation and some stressful experience or heightened emotional state. The impairment unconsciously allows avoidance, gets the patient off the hook, or sanctions access to support or care. Once the patient's history is understood, seeing that the patient's symptoms have meaning and derive from unconscious motivations (e.g., a fear of being aggressive) and produce some form of gain for the patient (e.g., control of others) should be possible. However, the reader should note that the motivations involved often reflect complex needs and concerns and that the underlying unconscious factors and their significance or meaning may not be readily apparent without extensive exploration. Alternatively, one can see the dysfunction in conversion disorder as a nonverbal communication that should be understandable once the message is decoded.

    Treatment is directed at symptom removal, and it is most likely to succeed when the disorder is of recent onset. Because conversion disorder may occur in response to some distressing physical illness, treatment of the underlying disorder, when possible, is usually the first step. As with the dissociative disorders, hypnosis (see Chapter 23) or intravenous amobarbital or benzodiazepines may be helpful (at the present time, these drugs are used only infrequently in the United States). As in other somatoform disorders, an effort should be made to redirect the patient's attention and focus away from the impairment and to shift them toward the events and issues that provoked it. If an identifiable stressor is involved, the patient may need help in resolving or mastering it. Any reinforcing factors should be identified and reduced or eliminated. This process may be particularly problematic in treating the somatoform disorders, because the very tests (e.g., electromyogram, computed tomography, magnetic resonance imaging) needed to rule out or establish contributing physical factors may spur the patient on to find another clinician with an even more sophisticated test.

  • Somatization disorder is the current diagnostic term for many patients that were previously said to be suffering from hysteria or, more recently, from Briquet syndrome. (Note: Somatization disorder should be differentiated from the overarching term somatoform disorders, of which somatization disorder is one diagnosis.) Occurring more frequently in females, this disorder is estimated to have a prevalence in the general population of 0.5% to 2%; some studies suggest that male family members may have higher than expected frequencies of antisocial personality disorder and substance-related disorders. Onset generally is in the late teens to 20s; and, by the age of 30, these patients believe they are sickly. By 30 years of age, they have visited multiple clinicians and other health-related practitioners, such as chiropractors and naturopaths. Patients with somatization disorder are often quite distressed, and they have chronic or recurrent complaints involving multiple organ systems. Typically, at least 13 complaints are noted when the clinician sequentially reviews the organ systems. Table 4.1 lists some common complaints of patients with somatization disorder.

    Patients with somatization disorder are particularly difficult to treat. Because of their multiple complaints, their poor or incomplete response to reassurance, and their resistance to accepting emotional and stress-related

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    factors as contributory, many clinicians consider these patients to be impossible. The frustration and anger experienced by the doctor usually are not well masked, and they may further reinforce the patient's prior pattern of doctor shopping. An important element of treatment is conservative support and reassurance with a minimum of other interventions. Studies have suggested that psychiatric referral can reduce the total health care costs for these patients, especially if the psychiatrist can gain the confidence of the patient and can establish a working alliance that acknowledges the seriousness of the concerns while shifting the dialogue away from the patient's health to his or her relationships, job, or life. In addition, regular visits (as opposed to only when symptoms occur or increase) to a supportive primary care clinician who adequately attends to the patient's physical health status without pursuing unnecessary diagnostic procedures or treatments may be helpful. Unfortunately, many of these patients may have already undergone an excessive number of expensive tests or have managed to obtain unnecessary surgeries (e.g., laparoscopy).

    TABLE 4.1. COMMON COMPLAINTS OF PATIENTS WITH SOMATIZATION DISORDER

    System Symptom
    Cardiopulmonary Shortness of breath in absence of exertion
    Gastrointestinal Vomiting
    Nervous Pain in extremities
    Difficulty swallowing
    Amnesia
    Reproductive or sexual Painful menstruation
    Burning sensation in sexual organs or rectum other than during sexual intercourse

    Pharmacologic treatment is not indicated for somatization disorder unless the patient has concomitant anxiety or depression; medication use is then directed at these comorbid conditions.

  • Hypochondriasis refers to a belief, either an unsubstantiated fear or a false belief, that one has a serious physical disease that is based on misinterpretation of bodily symptoms. Such unsubstantiated fears are usually associated with symptoms of anxiety, and they may be associated with depression. Particularly when depression is present (see Chapter 18), the false beliefs may be of delusional proportions. Onset is usually gradual, and it occurs most commonly in early adulthood. Once present, hypochondriacal preoccupations typically persist. This contrasts with the episode-related exacerbations of fear of illness that may wax and wane in patients with depression. Some clinicians believe that patients with hypochondriasis suffer more from their illness concerns than do depressed patients. An acute onset of hypochondriasis may be seen after the death of a loved one (see Chapter 16). Some hypochondriacal patients are self-preoccupied and invested in the sick role; others (i.e., those with hypochondriacal symptoms more similar to the symptoms of obsessive-compulsive disorder) generally are not. Patients with hypochondriasis appear to be overinterpreting and magnifying bodily sensations as representing disease, and some appear motivated by a need to persuade the clinician that their complaints are genuine and serious. Focusing on the body is a habit for these patients. Many have low self-esteem, feel incomplete, and believe that their emotional needs are not being met.

    Emerging research findings indicate that SSRIs and cognitive-behavioral therapy may be effective for hypochondriasis. Psychoeducation

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    is an important adjunct. When underlying anxiety or depression is present and appears primary, treatment should be directed toward these underlying disorders or symptoms. The overall treatment goal is to reduce the dysfunction and disability that ensue from hypochondriasis and to minimize the effects on the patient's family and others. Sometimes these patients respond to efforts to provide them with a better understanding of how the body works and to reassurance that most symptoms are transient and that they do not portend serious disease. The clinician must remember, however, that hypochondriacal patients have the same probability as others of developing a serious illness. In addition, hypochondriacal patients are extremely apt to believe they are not being taken seriously. Any tests should be carefully scheduled because delays and postponements feed the patient's insecurity. Patients should also be enlisted in formally tracking their pain or dysfunction. Charts that identify the timing and character of symptoms may be useful, and they may assist the clinician and the patient in discovering temporally related stress factors (e.g., the death of a close relative). History taking should also include eliciting whether other relatives or key persons in the patient's life have had similar symptoms. Clinicians who undertake the treatment of hypochondriacal patients must recognize that short-term interventions often will not work.

    For many patients, the balance struck by the clinician over time when providing psychoeducation, reassurance, support, concern, limited testing, and clarification is the key to helping these patients overcome their impaired self-concept and feelings of being damaged or incomplete.

  • Body dysmorphic disorder (BDD) was previously known as dysmorphophobia. These patients are preoccupied with a nonexistent or minimal appearance flaw (e.g., a blemish, hair loss, the shape of their ears or nose, facial asymmetry) to the point where their appearance concerns cause significant distress or impair functioning. Nearly all patients perform repetitive and time-consuming appearance-related behaviors, such as mirror checking, excessive grooming, skin picking, or reassurance seeking. Patients with BDD often are initially seen by dermatologists and plastic surgeons; however, such treatment does not appear to be effective. Patients with the delusional form of BDD are completely convinced that their view of their appearance defect is accurate (i.e., they have an encapsulated or circumscribed false belief of delusional proportions that typically occurs in the absence of an obvious precipitant or other evidence of psychosis). These patients are diagnosed with delusional disorder, somatic type (formerly known as monosymptomatic hypochondriacal psychosis); they may also receive a diagnosis of BDD.

    • Onset and course. Most patients with BDD date the onset of their preoccupations to early adolescence, a time when appearance is often a paramount concern. Others date the onset to childhood or the 20s or 30s. If BDD is left untreated, it can be a chronic condition, although exacerbations while under stress are common.

    • Pharmacotherapy. A medication may be useful in the treatment of patients with BDD. Once this disorder has been identified and the patient accepts that a medication may alleviate his or her preoccupation, distress, or difficulty functioning (this is not always an easy step for the clinician to get the patient to take), a carefully monitored medication trial may prove beneficial.

      • Proserotonergic agents. Considerable evidence from case reports and series, small sample clinical trials, and controlled studies indicates that proserotonergic antidepressants, such as clomipramine and SSRIs (e.g., fluoxetine and fluvoxamine), are beneficial in BDD. Adding buspirone to an SSRI has been shown to benefit some patients. Although fixed-dose studies have not been published, higher SSRI doses and longer trials

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        (e.g., 12 weeks) than those that are typically used for depression appear to be required to achieve efficacy (see Chapter 18). Of note, SSRIs alone have been shown to be as effective for delusional patients as they are for nondelusional patients with BDD.

        Patience is required on the part of both the treating clinician and the patient because improvement may not be noted for 6 to 8 weeks. No empirically based guidelines for maintenance or continuation therapy exist. Treating for at least 1 year beyond the attainment of maximal improvement seems reasonable.

      • Antipsychotic agents. Some clinicians (including the editor) have had occasional success with pimozide, an infrequently used, nonstandard antipsychotic agent with a dopamine-2 (D2) receptor antagonist, a serotonin (5-HT2a) receptor antagonist, and T-type calcium channel blocking properties (see Chapter 7, section IX.B.2.b.(2), and Chapter 20). Although this drug is marketed as a second-line treatment for the phonic and motor tics of patients with Tourette disorder, pimozide has been found to be effective in some patients in a small number of anecdotal and case-based reports. (Note: Some case reports also indicate a lack of efficacy for pimozide in BDD.) A positive response to use of olanzapine has been reported in one patient. An unanswered question is whether the combination of an SSRI with a conventional antipsychotic agent, the nonstandard antipsychotic agent pimozide, or an atypical antipsychotic agent may be effective, especially for delusional patients.

    • Cognitive behavior therapy. This approach may also be beneficial for some patients with BDD. This treatment generally consists of cognitive restructuring, exposure (e.g., to avoided social situations), and response prevention (i.e., avoidance of repetitive behaviors, such as reassurance seeking).

II. The Paranoias

A. Paranoia

Paranoia is a complex multifaceted symptom. The term derives from the Greek para (beside) and nous (mind). As with delirium (see Chapter 5), paranoia has at times been considered synonymous with insanity. Many people, particularly when they feel disappointed and under stress, have brief experiences of paranoia a feeling that somehow they have been singled out for victimization. Paranoia exists on a descriptive continuum that includes transient feelings that most adults and many children experience, more enduring traits that do not dominate the personality, clear symptoms in several forms of psychotic disorder (e.g., bipolar disorder, schizophrenia), and a personality disorder in which paranoid thinking controls relationships and interferes with functioning. Paranoia should not be used to refer to mistrust or suspiciousness that is based on a lack of adequate cues or information, one's past experiences, or the learned (or culture-bound) expectations of one's family or group.

The central features of all paranoid states or conditions are excessive self-referential thinking (everything is linked to me ), self-consciousness, and concerns with distrust or mistrust and about one's autonomy. For these features to be coupled with exaggerated sensitivity to rebuff and humiliation is common. The patient rejects or avoids responsibility for events, often blaming other people or fate. Underlying feelings of inadequacy or an unusual degree of concern with powerlessness or power may be present. Combativeness, irritability, and aggressiveness are frequently present the patient seems to believe that the best defense is a good offense. Other paranoid people are quiet and remote, and they isolate themselves. Alternatively or sometimes concomitantly, they may exaggerate their self-sufficiency to defend against feelings of vulnerability and easily threatened autonomy. Resentment, litigiousness, and suspicion are common.

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People subjected to sensory deprivation or separated from familiar surroundings or persons often become transiently paranoid (e.g., visually or hearing-impaired people; migrant workers; immigrants and refugees; prisoners, especially those kept in isolation; and people with delirium and dementia, particularly when they are transferred to an unfamiliar setting). In other people, the onset is gradual, with paranoid traits emerging during adolescence or early adulthood. Drug-induced or toxin-induced and stress-related paranoias rarely occur in childhood, but they may appear at any age thereafter.

One way to understand paranoia is to see the ego as protecting the self (see Chapter 1) through denial and projection. Feelings of vulnerability related to fear; powerlessness; or feelings of inadequacy, inferiority, or distrust may be dealt with in this manner. These distortions may then be elaborated by some into ideas or even delusions of reference (e.g., I am noticed may mean I am not as insignificant or as alone as I feel or They are noticing what I would rather not have others observe ). Delusions of persecution, jealousy, or grandiosity may be present. Grandiosity typically presents in two forms. In one, the individual has a sense of being chosen and invested with special powers; in the other, the person has a false belief that he or she is rich or famous.

B. Delusional Disorder

This condition is diagnosed when persistent nonbizarre delusions that are not related to a known toxic or metabolic underlying condition exist. Delusional disorder has historically been considered a form of paranoia. The delusions are usually persecutory, they include seemingly plausible feelings of being conspired against or cheated, and they are not determined by the current or prevailing mood (i.e., they are not affect-congruent or affect-consonant). Other types of delusional disorder may involve nonpersecutory delusions as discussed below. Delusions that are keyed into prevailing mood suggest a mood disorder with psychotic features (see Chapters 18 and 19). Auditory hallucinations may be present in delusional disorder, but they should not be prominent and no other significant evidence of thought disorder should be present. The Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV), indicates that delusional disorder may be further subclassified according to the predominant delusional theme and content (i.e., erotomanic, grandiose, jealous, persecutory, somatic, and mixed and unspecified types). Some overlap may be present among delusional disorder (somatic type), obsessive-compulsive disorder, and hypochondriasis.

C. Delusional Disorder, Somatic Type

As was discussed above, delusional BDD is also one type of delusional disorder, somatic type. Other forms of the somatic variant of delusional disorder include the belief that one emits a foul body odor (i.e., olfactory reference syndrome) and delusions of infestation (i.e., a belief that one's body is infested with bugs or some other type of crawling organism also known as parasitosis, dermatozoonosis, or Ekbom syndrome). Although tactile hallucinations may be a component of parasitosis, the fixed belief is what is central to this disorder. Thus, delusions of infestation differ from the tactile hallucinations experienced by patients with alcohol withdrawal or cocaine intoxication (formication) or from the visual hallucinations of bugs crawling on the skin that are experienced by those with toxicity secondary to anticholinergic agents.

D. Erotomania

Sometimes known as de Cl rambault syndrome or psychose passionnelle, erotomania involves a delusional belief that one is loved by a public or prominent figure (typically a politician, entertainer, or disk jockey) who is constrained from revealing his or her love. Typically, the individual also has a sense that the public figure is indirectly communicating with the patient (e.g., He is telling me he loves me from the titles of the songs he chooses to play ). The patient frequently contacts the loved person by telephone or letter; the intensity of this contact may vary from an annoying nuisance to

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frank harassment. Erotomania occurs far more frequently in women than in men. In DSM-IV, such patients are classified as having delusional disorder, erotomanic type. The relationship between erotomania and obsessive love, which is typically seen in young men, is unclear (see Chapter 6).

E. Treatment Considerations in Paranoid Disorders

  • General considerations. Treatment for paranoia is as complex as the concept itself. Because the paranoid symptomatology becomes manifest in situations of both literal and figurative isolation, addressing this dimension is part of any first step. The clinician's initial approach should be one of tempered concern and understanding. Paranoia does not usually yield to confrontation. Interest, tolerance, and impartiality may help to establish an initial connection with these patients, who are often distrustful, suspicious, and guarded. Helping patients to understand that they are overinterpreting experiences because they are feeling isolated may be beneficial. Practical steps, such as providing better eyeglasses or a hearing aid, improving lighting, and increasing stimulation and contact with other people, should be considered, particularly with elderly patients who are showing paranoid features of recent onset. When more intensive psychotherapy is possible, trying to move the patient toward a recognition that self-protective mechanisms and low self-esteem are present and that depression may be the cause contributes to improvement in a few patients.

  • Pharmacotherapy. Based on limited, case-based, or anecdotal experiences, a carefully monitored trial of an atypical antipsychotic agent (e.g., risperidone) or pimozide, either alone or in combination with an antidepressant and in conjunction with psychotherapy may be beneficial to some patients with paranoid or erotomanic features. A Chilean group found no useful clinical benefits from pimozide in a 6-week trial of patients with erotomania. Conventional antipsychotic agents have not been as consistently effective for erotomania, although the evidence is limited to individual case studies. Although no placebo-controlled studies specifically on the use of low doses of atypical antipsychotic agents (e.g., risperidone, olanzapine) or mood stabilizing anticonvulsants (e.g., divalproex sodium, gabapentin) for delusional disorder have been published, preliminary evidence suggests that these agents may reduce paranoid ideation in some patients with disorders of personality (see Chapter 13). A well-monitored clinical trial may be considered.

    When the paranoia is part of a mood disorder (e.g., hypomania or mania), lithium, divalproex sodium, or carbamazepine may be useful (see Chapter 19), as may both conventional and atypical antipsychotic agents (e.g., when schizophrenia or schizoaffective disorder is present [see Chapter 20]); more specifically, risperidone appears to be beneficial.

    Clomipramine and other antidepressants, as well as pimozide and other antipsychotic agents, have been noted in case reports to be beneficial for patients with olfactory reference syndrome. Pimozide, haloperidol, and risperidone have been reported to be helpful for parasitosis. As was previously discussed, the delusional variant of BDD has been shown to respond to an SSRI alone.

    Paranoia leads to altered relationships; the preformed distrust of the clinician by the patient likely will complicate any form of medical care.

ADDITIONAL READING

Allen JJ, Movius HL 2nd. The objective assessment of amnesia in dissociative identity disorder using event-related potential. Int J Psychophysiol 2000;38:21 41.

Barr LC, Goodman WK, Price LH. Acute exacerbation of body dysmorphic disorder during tryptophan depletion. Am J Psychiatry 1992;149:1406 1407.

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Barsky AJ, Wyshak G, Klerman GL. Psychiatric comorbidity in DSM-III-R hypochondriasis. Arch Gen Psychiatry 1992;49:101 108.

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Manual of Psychiatric Therapeutics Paperback
Manual of Psychiatric Therapeutics: Practical Psychopharmacology and Psychiatry (Little, Browns Paperback Book Series)
ISBN: 0316782203
EAN: 2147483647
Year: 2002
Pages: 37

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