Paranoid personality disorder (PPD) is a Cluster A personality disorder defined by a pervasive distrust and suspiciousness of others such that their motives are interpreted as malevolent, beginning by early adulthood and present across contexts.[1] Patients rarely present for treatment of the trait itself; they more often arrive after interpersonal rupture, occupational conflict, or a comorbid mood, anxiety, or substance use disorder forces contact with care.[2] The clinical task is to distinguish enduring suspiciousness from psychotic disorders, from trauma-related hypervigilance, and from culturally congruent distrust in marginalized groups.[1,3] Evidence to guide treatment is sparse: no medication has a regulatory indication, and psychotherapy trials in PPD specifically are limited, so management leans on generalist personality-disorder principles and targeted treatment of comorbidity.[2,4] Bottom line: PPD is a clinical diagnosis of enduring, ego-syntonic suspiciousness without frank psychosis, and engagement, not cure, is the realistic therapeutic goal.
PPD is uncommon in clinical samples but more prevalent in community surveys than its visibility in clinic suggests, because affected patients avoid help-seeking.[2,5]
Prevalence
- Community 12-month prevalence in the United States National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) was estimated at approximately 2.3 to 4.4 percent, with substantial methodological variation across studies.[5-6]
- Median prevalence across general-population studies is around 1.2 to 1.7 percent using semi-structured interviews.[2,7]
- Clinical psychiatric outpatient samples report rates of roughly 2 to 10 percent, often as a comorbid rather than principal diagnosis.[2]
Demographics and risk factors
- Onset by early adulthood; symptoms must not be limited to episodes of another disorder.[1]
- Sex distribution varies by source: NESARC and several large community surveys report slightly higher prevalence in women, while other community and clinical samples report roughly equal or modestly higher rates in men.[2,5-6]
- Elevated rates among first-degree relatives of probands with and , consistent with the schizophrenia-spectrum literature.[2,8]
- Childhood emotional neglect, abuse, and exposure to threat-laden environments are associated risk factors, though specificity to PPD versus other personality pathology is limited.[2,9]
Comorbidity
- Frequent comorbidity with other personality disorders, particularly , , and .[2,5]
- High rates of comorbid major depressive disorder, , post-traumatic stress disorder, and alcohol or other substance use disorders.[5-6]
- Suicidal behavior is elevated, mediated largely through comorbid depression and substance use.[6,10]
PPD sits within the schizophrenia spectrum on family and genetic grounds but lacks a defined neurobiology of its own; most mechanistic data are extrapolated from broader personality and psychosis research.[2,8]
Genetic and familial
- Modestly elevated rates of PPD and schizotypal traits in first-degree relatives of probands with schizophrenia, supporting partial inclusion in the schizophrenia spectrum.[2,8]
- Twin studies of personality disorder dimensions estimate heritability of suspiciousness traits in the 0.3 to 0.5 range, though PPD-specific twin data are limited.[2,11]
Neurobiology
- No replicated structural or functional imaging signature is specific to PPD; findings are inferred from studies of paranoia as a transdiagnostic dimension.[12]
- Dimensional paranoia is associated with altered threat appraisal in and medial prefrontal circuits and with biases in social-attribution and theory-of-mind tasks.[12-13]
- Dopaminergic models of paranoia developed for psychotic disorders are not established as mechanism for PPD, which is non-psychotic.[2,12]
Psychosocial and developmental
- Early adversity, including emotional and physical abuse, parental hostility, and chronic exposure to threat, is associated with adult paranoid traits, though associations are non-specific across personality pathology.[2,9]
- Cognitive models emphasize externalizing attribution bias, hypervigilance to social threat, and confirmation bias as maintaining mechanisms.[13-14]
- Sociocultural exposure to discrimination, immigration stress, and victimization can shape trust appraisals; these are environmentally appropriate responses and must not be conflated with disorder.[1,3]
places PPD in the Cluster A (odd / eccentric) personality disorders, alongside schizoid and schizotypal personality disorders.[1] Diagnosis requires a pervasive pattern of distrust and suspiciousness present in a variety of contexts, beginning by early adulthood, with at least four characteristic features and an explicit exclusion of psychotic and medical causes.[1]
Required pattern
- A pervasive distrust and suspiciousness of others such that their motives are interpreted as malevolent, beginning by early adulthood and present in a variety of contexts.[1]
- At least four of the following are present.[1]
Characteristic features (four or more required)
- Suspects, without sufficient basis, that others are exploiting, harming, or deceiving them.[1]
- Is preoccupied with unjustified doubts about the loyalty or trustworthiness of friends or associates.[1]
- Is reluctant to confide in others because of unwarranted fear that the information will be used maliciously against them.[1]
- Reads hidden demeaning or threatening meanings into benign remarks or events.[1]
- Persistently bears grudges, that is, is unforgiving of insults, injuries, or slights.[1]
- Perceives attacks on their character or reputation that are not apparent to others and is quick to react angrily or to counterattack.[1]
- Has recurrent suspicions, without justification, regarding fidelity of spouse or sexual partner.[1]
Exclusions and specifiers
- Does not occur exclusively during the course of schizophrenia, a bipolar or depressive disorder with psychotic features, or another psychotic disorder, and is not attributable to the physiological effects of another medical condition.[1]
- If criteria are met prior to the onset of schizophrenia, add the specifier with premorbid, for example, paranoid personality disorder (premorbid).[1]
- DSM-5-TR retains the categorical Section II criteria; PPD is not one of the six personality disorders operationalized as a specific type in the Section III alternative model, and in that framework would be captured under personality disorder-trait specified using impairment in personality functioning plus relevant trait facets (suspiciousness, hostility, withdrawal).[1]
ICD-11 differences
abolished discrete personality disorder categories and now classifies personality disorder by severity (mild, moderate, severe) with optional trait qualifiers; suspiciousness maps onto the negative affectivity and detachment domains rather than a named PPD.[15]
Patients are guarded, litigious, and quick to perceive slight; the suspiciousness is ego-syntonic, stable, and stops short of frank delusion.[1-2] The clinical signature is consistency across contexts and decades, not a discrete episode.
Cognitive features
- Pervasive expectation of harm or exploitation, applied to strangers and intimates alike.[1]
- Hypervigilance to perceived insult and a tendency to read malevolent intent into neutral events; may occur but lack the conviction of delusional thinking.[1-2]
- Reality testing is preserved; transient, stress-induced quasi-psychotic features lasting minutes to hours can occur but do not meet criteria for a psychotic disorder.[1-2]
Affective and interpersonal features
- Restricted, often hostile affect; humor and warmth are uncommon in clinical contact.[2]
- Bears grudges and is unforgiving of perceived slights; relationships are characterized by jealousy, control, and accusation.[1]
- Litigious behavior, workplace conflict, and "pathological" letters or complaints are common downstream features.[2]
Course
- Onset by early adulthood; traits are stable across decades, though intensity fluctuates with stressors.[1-2]
- Symptoms may attenuate modestly with age, paralleling the broader personality-disorder literature on adult trait change.[2,16]
- Decompensation under interpersonal or occupational stress can produce transient psychotic symptoms; persistent psychosis warrants reconsideration of the primary diagnosis.[1-2]
Red flags suggesting a different or additional diagnosis:
- Sustained delusions, , or disorganized thinking — consider delusional disorder, schizophrenia, or a mood disorder with psychotic features.[1]
- Subacute or late-onset suspiciousness in a previously trusting adult — consider a medical, neurologic, or substance-induced cause.[2,17]
- Suspiciousness anchored to a specific traumatic event with intrusive re-experiencing — consider post-traumatic stress disorder.[1]
The central tasks are separating PPD from frank psychosis, from trauma-related hypervigilance, and from culturally sanctioned distrust; and from the other Cluster A disorders that share interpersonal detachment.[1-3]
| Feature | Paranoid PD | Delusional disorder | Schizophrenia | Schizotypal PD | PTSD |
|---|---|---|---|---|---|
| Core feature | Pervasive distrust and suspiciousness | Fixed non-bizarre delusion | Psychosis with positive and negative symptoms | Odd beliefs, magical thinking, social anxiety | Re-experiencing and hyperarousal after trauma |
| Reality testing | Preserved | Impaired within delusion | Impaired | Preserved but eccentric | Preserved |
| Duration / onset | Pervasive since early adulthood | At least 1 month of delusion | At least 6 months including 1 month active phase | Pervasive since early adulthood | Symptoms more than 1 month post-trauma |
| Affect | Hostile, restricted | Often preserved outside delusion | Flat or inappropriate | Constricted, odd | Reactive, numb, irritable |
| First-line management | Psychotherapy; treat comorbidity | Antipsychotic plus psychotherapy | Antipsychotic plus psychosocial | Psychotherapy; low-dose antipsychotic for select symptoms | Trauma-focused psychotherapy; SSRI/ |
First-line management of the principal mimics anchors the clinical reasoning: delusional disorder is treated with an antipsychotic alongside supportive psychotherapy,[18] schizophrenia with an antipsychotic plus psychosocial interventions per APA practice guidelines,[19] and schizotypal personality disorder primarily with psychotherapy, with low-dose antipsychotics reserved for select cognitive-perceptual symptoms.[20]
Other conditions to consider
- Schizoid personality disorder — detachment is driven by indifference, not suspicion; suspiciousness is absent or peripheral.[1]
- Borderline and narcissistic personality disorders — transient paranoid ideation occurs under stress but does not dominate the lifelong pattern; affective instability and identity disturbance predominate in BPD.[1-2]
- Substance-induced paranoia — chronic stimulant, cannabis, hallucinogen, or alcohol use can produce suspiciousness that remits with abstinence.[1,17]
- Secondary paranoia from medical illness — neurocognitive disorders, Parkinson disease, , temporal lobe epilepsy, central nervous system infection, thyroid disease, and B12 deficiency can all present with new-onset suspiciousness.[2,17]
- Culturally sanctioned distrust — appropriate vigilance in response to discrimination, immigration stress, or political persecution is not a personality disorder.[1,3]
SUSPECT
Suspects exploitation; Unforgiving (bears grudges); Spousal infidelity suspicions; Perceives attacks on character; Enmity in benign remarks; Confiding reluctance; Trust in loyalty doubted.
Diagnosis is clinical and longitudinal; structured instruments support rather than replace the interview, and the alliance is itself diagnostic data.[2,22] Patients typically minimize symptoms and externalize blame, so collateral history is high yield when available and consented to.
Interview approach
- Take a non-confrontational, transparent stance; explain documentation, limits of confidentiality, and the purpose of each question to reduce perceived covert agendas.[2,4]
- Avoid premature interpretation of suspiciousness; map onset, pervasiveness, context, and functional impact across work, family, legal, and social domains.[1-2]
- Screen explicitly for psychotic-spectrum symptoms, mood and anxiety disorders, post-traumatic stress disorder, and substance use; comorbidity drives most clinical decisions.[2,5]
- Obtain collateral where the patient consents — partners and employers often surface jealousy, litigiousness, and grudge-bearing the patient minimizes.[2]
History elements not to omit
- Lifetime course of suspiciousness, including childhood and adolescent precursors.[1]
- Trauma history, including childhood maltreatment and adult interpersonal violence, with attention to PTSD criteria.[1,9]
- Substance use history, particularly stimulants, cannabis, hallucinogens, and alcohol.[1,17]
- Medical, neurologic, and medication review, including corticosteroids, dopaminergic agents, and anticholinergics in older adults.[2,17]
- Risk assessment for violence and self-harm, with explicit inquiry into specific targets and access to means.[2,10]
Validated instruments
- Structured Clinical Interview for Personality Disorders (SCID-5-PD) — semi-structured categorical interview.[22]
- International Personality Disorder Examination (IPDE) — research and clinical use, supports DSM and ICD.[23]
- Personality Inventory for DSM-5 (PID-5) — dimensional self-report aligned with the DSM-5 alternative model.[1,24]
- Comorbidity-relevant scales such as the PHQ-9 for depression and the PCL-5 for trauma symptoms are routine adjuncts.[2,21]
Laboratory and imaging
- No laboratory or imaging test confirms PPD; investigations target medical mimics suggested by history and exam.[2,17]
- Reasonable initial workup for new-onset or atypical suspiciousness: complete blood count, comprehensive metabolic panel, thyroid-stimulating hormone, vitamin B12, urine toxicology, and HIV and syphilis serologies where epidemiologically indicated.[17]
- Neuroimaging and electroencephalography are not routine; reserve for focal neurologic signs, , late onset, or cognitive decline.[17]
A primary PPD diagnosis in a patient with new-onset paranoia after age 40 is suspect; pursue medical, neurologic, substance-induced, and primary psychotic differentials before settling on a personality disorder.[2,17]
No medication has a regulatory indication for PPD, and randomized trials in PPD specifically are sparse; management combines a long-arc therapeutic relationship with targeted treatment of comorbidities and adjunctive pharmacotherapy for specific symptoms.[2,4] Limited evidence suggests psychotherapy is the cornerstone, although high-quality PPD-specific trials are lacking.
Pharmacotherapy
- No agent is FDA-approved for PPD; pharmacotherapy targets comorbid depression, anxiety, post-traumatic stress, or substance use disorders per their respective guidelines.[2,4]
- Limited evidence suggests low-dose second-generation antipsychotics may help transient stress-induced quasi-psychotic symptoms and severe suspiciousness with functional impairment, but high-quality PPD-specific trials are lacking.[2,4]
- It is uncertain whether reduce core suspiciousness, but they are commonly used when comorbid anxiety or depression is prominent.[2,4]
- Avoid sedative-hypnotics and high- burden where possible; both can worsen cognitive distortion and confound assessment.[2,26]
Psychotherapy
- Evidence suggests an individual psychotherapy that emphasizes a stable, transparent, predictable frame is the cornerstone; group therapy is generally avoided early because of mistrust of other members.[2,4]
- Some experts recommend cognitive therapy targeting attributional biases and threat-appraisal distortions, though high-quality evidence is lacking.[2,14]
- Some experts recommend supportive and psychodynamic approaches focused on tolerating ambivalence and reality-testing perceived slights, though high-quality evidence is lacking.[2,4]
- Schema-focused, mentalization-based, and transference-focused therapies developed for other personality disorders have been extended to PPD by some clinicians; PPD-specific outcome data remain limited.[2,4]
Neuromodulation
- No role for , , or other neuromodulation in PPD itself; consider only if a comorbid disorder independently meets criteria.[2]
Adjunctive
- Psychoeducation framed around stress, sleep, and interpersonal conflict, rather than "paranoia," is better tolerated than diagnostic labeling early in care.[2,4]
- Treat comorbid substance use disorders aggressively; ongoing stimulant or heavy cannabis use undermines any other intervention.[1,17]
- Couples and family work can be useful when relational conflict is the presenting problem, with attention to safety around jealousy and accusation.[2,4]
Engagement is the first treatment goal; explicit, written-down agreements about appointments, communication, and confidentiality reduce suspicion and improve retention more than any specific therapy modality.[2,4]
| Intervention | Evidence base / Comparator | Benefits | Harms | Certainty | Notes |
|---|---|---|---|---|---|
| Individual psychotherapy (supportive, cognitive, psychodynamic) | Expert consensus and extrapolation from personality-disorder literature[2,4] | Engagement, reduced interpersonal conflict | Premature termination, alliance ruptures | low | Stable, transparent frame; PPD-specific RCTs lacking[2,4] |
| Low-dose | Small open trials, case series, extrapolation[2,4] | Possible reduction of transient quasi-psychotic features | Metabolic, EPS, sedation | very_low | Reserve for severe symptoms; not approved[2,4] |
| SSRI/SNRI for comorbid depression or anxiety | Indication-level evidence for the comorbid disorder[2,4] | Treats comorbid mood or anxiety symptoms | GI, sexual AE, | moderate | Does not target core suspiciousness[2,4] |
| Group therapy as initial modality | Expert opinion[2,4] | Limited; not recommended early | Heightened mistrust, dropout | expert_opinion | Often deferred until trust is established[2,4] |
| Treatment of comorbid substance use | Indication-level evidence for the substance use disorder[1,17] | Reduces secondary paranoia and clarifies primary diagnosis | Withdrawal management as relevant | moderate | Stimulant and cannabis use are common confounders[1,17] |
Harms in PPD arise more from the therapeutic relationship and from off-label pharmacotherapy than from the disorder's natural course; the evidence base itself is the principal limitation.[2,4]
Common and serious harms of management
- Alliance rupture and premature dropout are the most frequent adverse outcomes of psychotherapy in PPD; clinicians may be perceived as covertly aligned with employers, family, or the legal system.[2,4]
- Second-generation antipsychotics carry metabolic, extrapyramidal, sedation, and prolactin-related adverse effects without an approved indication in PPD; monitor weight, lipids, glucose, and EKG per general antipsychotic monitoring guidance.[2,25]
- and other sedatives risk disinhibition, dependence, and worsening cognitive distortion in suspicious patients.[2,26]
- Coerced or involuntary care without imminent risk damages the alliance and rarely changes the trait.[2,4]
Limitations of the evidence
- No adequately powered randomized trial of any pharmacologic or psychological treatment targets PPD as a primary diagnosis.[2,4]
- Most evidence is extrapolated from heterogeneous personality-disorder cohorts in which PPD is often a comorbid label.[2,5]
- Long-term outcome data are scarce; existing follow-up studies have short horizons, narrow samples, and high attrition.[2,16]
- Cultural sampling is limited; instruments and norms derive predominantly from North American and European populations, with risk of pathologizing context-appropriate distrust.[1,3]
Developmental stage, cultural context, and medical comorbidity all reshape diagnosis and management; the diagnosis itself is reserved for adults and is rarely the correct primary label in late-onset presentations.[1-2]
Pediatric
- PPD is not diagnosed before age 18 in routine clinical practice; persistent paranoid traits in adolescents are documented but warrant alternative formulations and attention to trauma, , and emerging psychosis.[1-2]
- Childhood maltreatment is a non-specific risk factor for adult personality pathology, including PPD.[2,9]
Geriatric
- New-onset suspiciousness in older adults more often reflects , delirium, sensory deprivation, medication effect, or late-onset psychosis than a primary personality disorder.[2,17]
- Long-standing PPD may attenuate modestly with age but rarely remits.[2,16]
Perinatal
- Perinatal-specific data on PPD are limited; comorbid depression, anxiety, and trauma symptoms drive most management decisions.[2]
Medical and substance-related considerations
- Chronic stimulant or cannabis use can phenocopy or amplify suspiciousness; abstinence is both diagnostic and therapeutic.[1,17]
- Neurologic disorders including Parkinson disease, Huntington disease, temporal lobe epilepsy, and post-stroke syndromes can produce secondary paranoia.[2,17]
- and neurosyphilis should be considered in epidemiologically appropriate contexts.[17]
Cultural considerations
- Mistrust of institutions can be context-appropriate among individuals exposed to discrimination, displacement, or political persecution and must not be coded as personality pathology.[1,3]
- Clinician concordance with patient cultural and linguistic background, when feasible, reduces diagnostic misattribution.[3]
PPD is a stable, lifelong trait pattern with modest age-related attenuation; functional impairment is driven more by occupational and relational conflict than by overt symptom severity, and comorbidity drives most adverse outcomes.[2,5,16]
Course
- Onset by early adulthood with persistence across decades; remission of the underlying trait pattern is uncommon.[1-2]
- Modest age-related softening of antagonism and reactivity is consistent with the broader personality-disorder maturation literature.[16]
- A small minority progress to a frank schizophrenia-spectrum disorder; most do not.[2,8]
Outcomes
- Functional impairment is common in work, family, and legal domains; litigiousness and chronic conflict are characteristic.[2,5]
- Comorbid major depression and substance use account for most acute morbidity, including hospitalization and suicidal behavior.[5-6,10]
- Mortality data specific to PPD are sparse; excess mortality reported in personality-disorder cohorts more broadly is mediated largely through suicide, substance use, and cardiovascular comorbidity.[2,10]
Acute presentations in PPD are usually driven by interpersonal crisis, intoxication, comorbid mood pathology, or transient stress-induced quasi-psychotic features rather than by the personality disorder per se.[2,10]
Hospitalization criteria
- Imminent risk of harm to self or others, including specific threats, plans, or access to means.[2,10]
- New or worsening psychotic symptoms exceeding transient stress-induced features.[1-2]
- Acute decompensation of a comorbid disorder, including severe depression, , or substance withdrawal, that cannot be safely managed as an outpatient.[2]
Suicide and violence risk
- Comorbid depression, substance use, and recent interpersonal loss are the dominant drivers of suicide risk; assess directly and document.[10]
- Risk for targeted interpersonal violence, particularly toward partners suspected of infidelity or perceived persecutors, is elevated in select cases; assess access to weapons and history of violence.[2,10]
Do not rely on decision tools or rating scales to rule out suicide or violence risk in PPD; structured judgment and direct inquiry, including collateral where appropriate, remain the standard.[10]
Agitation management
PPD's diagnostic validity, its boundary with the schizophrenia spectrum, and its place in evolving nosology are all unsettled.[2,8,15]
Nosology
- ICD-11 abandoned categorical personality disorder diagnoses in favor of a severity-plus-traits dimensional system; DSM-5-TR retained the categories in Section II and offered a parallel dimensional model in Section III.[1,15]
- The DSM Section III alternative model and ICD-11 trait domains differ structurally; clinicians moving between systems should expect non-equivalent labels.[1,15]
Boundary questions
- The degree to which PPD belongs within the schizophrenia spectrum is contested; family data support partial inclusion, but most patients with PPD do not develop a psychotic disorder.[2,8]
- Overlap with paranoid traits in BPD, narcissistic personality disorder, and PTSD complicates discrete categorical assignment.[1-2]
Treatment evidence
- The absence of adequately powered randomized trials in PPD specifically leaves all pharmacologic and psychological recommendations at low or very low certainty.[2,4]
- Off-label antipsychotic use for personality disorders is debated on benefit-harm grounds and is not endorsed as standard practice.[2,4,25]
- PPD is a Cluster A personality disorder defined by pervasive distrust and suspiciousness beginning by early adulthood, with at least four of seven characteristic features.[1]
- Reality testing is preserved in PPD; sustained delusions, hallucinations, or disorganized thinking point to a psychotic disorder instead.[1-2]
- If criteria are met before the onset of schizophrenia, use the specifier with premorbid.[1]
- Family studies show elevated rates of PPD and schizotypal traits in first-degree relatives of probands with schizophrenia, supporting partial inclusion in the schizophrenia spectrum.[2,8]
- Suspiciousness in PPD is ego-syntonic and pervasive across contexts, distinguishing it from the trauma-cued hypervigilance of PTSD.[1]
- Transient, stress-induced quasi-psychotic features can occur but, by themselves, do not warrant a psychotic-disorder diagnosis.[1-2]
- No medication is FDA-approved for PPD; pharmacotherapy targets comorbid disorders, and antipsychotics for core symptoms are off-label and low-certainty.[2,4]
- Group therapy is generally avoided early in PPD because of mistrust of other members; individual psychotherapy with a stable, transparent frame is preferred.[2,4]
- New-onset paranoia after age 40 should prompt evaluation for medical, neurologic, substance-induced, or primary psychotic causes before assigning PPD.[2,17]
- ICD-11 replaced categorical personality disorder diagnoses with a severity-plus-traits dimensional system; DSM-5-TR retained categorical PPD in Section II.[1,15]
- Comorbid major depression and substance use disorders account for most acute morbidity and suicide risk in PPD.[5-6,10]
- Culturally appropriate distrust in response to discrimination or persecution must not be coded as personality disorder.[1,3]
No external funding. No conflicts of interest declared. Peer-review status: pending.
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