Updated: Jul 17, 2008
A personality disorder, as defined in the Diagnostic and Statistical Manual of the American Psychiatric Association, Fourth Edition, Text Revision (DSM-IV-TR), is an enduring pattern of inner experience and behavior that differs markedly from the expectations of the individual's culture, is pervasive and inflexible, has an onset in adolescence or early adulthood, is stable over time, and leads to distress or impairment. Personality disorders are a long-standing and maladaptive pattern of perceiving and responding to other people and to stressful circumstances. Ten personality disorders, grouped into 3 clusters (ie, A, B, C), are defined in the DSM-IV-TR.1
The origin of personality disorders is a matter of considerable controversy. Traditional thinking holds that these maladaptive patterns are the result of dysfunctional early environments that prevent the evolution of adaptive patterns of perception, response, and defense. A body of data points toward genetic and psychobiologic contributions to the symptomology of these disorders; however, the inconsistency of the data prevents authorities from drawing definite conclusions.
Personality disorders affect 10-15% of the adult US population. Individuals may have more than one personality disorder. The following are prevalences for specific personality disorders in the general population:2
Because the DSM-IV-TR criteria are so bound to North American cultural definitions, epidemiologic data about personality disorders in other countries are notoriously unreliable.
Patients with personality disorders are at higher risk than the general population for many (Axis I) psychiatric disorders. Mood disorders are a particular risk across all personality diagnoses. Some comorbidities are more specific to particular personality disorders and clusters.
No differences in prevalence across the races have been noted.
Personality disorders generally should not be diagnosed in children and adolescents because personality development is not complete and symptomatic traits may not persist into adulthood. Therefore, the rule of thumb is that personality diagnosis cannot be made until the person is at least 18 years of age. Because the criteria for diagnosis of personality disorders are closely related to behaviors of young and middle adulthood, DSM-IV-TR diagnoses of personality disorders are notoriously unreliable in the elderly population.
In general, patients with personality disorders have wide-ranging problems in social relationships and mood regulation. These problems have usually been present throughout adult life. These patients' patterns of perception, thought, and response are fixed and inflexible, although their behavior is often unpredictable. These patterns markedly deviate from their specific culture's expectations. To meet the DSM-IV-TR threshold for clinical diagnosis, the pattern must result in clinically significant distress or impairment in social, occupational, or other important areas of functioning. Note that the disorder occurs in all settings (eg, social as well as vocationally), and it not limited to one sphere of activity.1,3
No specific physical findings are associated with any personality disorders. Physical examination may reveal findings related to the consequences and sequelae of various personality disorders.
| Alcoholism | Mental Disorders Secondary to General Medical
Conditions |
| Anxiety Disorders | Mental Retardation |
| Brief Psychotic Disorder | Paraphilias |
| Bulimia | Posttraumatic Stress Disorder |
| Depression | Schizoaffective Disorder |
| Dissociative Disorders | Schizophrenia |
| Ganser Syndrome | Schizophreniform Disorder |
| Hypochondriasis | Social Phobia |
The diagnosis of personality disorders in patients who have comorbid Axis I disorders, including mood, substance abuse, and medical disorders (eg, head injury, seizure disorders), can make the diagnosis of personality disorders more difficult because of overlapping features. Premorbid and developmental history, especially from collateral sources, is helpful in differential diagnosis.
Psychotherapy is at the core of care for personality disorders. Because personality disorders produce symptoms as a result of poor or limited coping skills, psychotherapy aims to improve perceptions of and responses to social and environmental stressors.
The primary care physician should usually consider psychiatric consultation for patients with personality disorders because the ongoing psychiatric care that patients require is not readily provided in the primary care setting.
The focus is on treatment of symptom clusters such as cognitive-perceptual symptoms, affective dysregulation, and impulsive-behavioral dyscontrol. These symptoms may complicate almost all personality disorders to varying degrees, but all of them have been noted in borderline personality disorder.9,10,11,12,13
The assumption is that neurotransmitter abnormalities underlie these symptom clusters that transcend the concepts of Axis I and Axis II disorders. The strongest evidence for pharmacologic treatment of personality disorders has been for borderline personality disorder, but even this is based on a fairly small database of studies.
Because of overdose risk, tricyclic antidepressants and monoamine oxidase inhibitors (MAOIs) are usually not prescribed for patients with personality disorders. The selective serotonin reuptake inhibitors (SSRIs) and newer antidepressants are safe and reasonably effective. However, because the depression of most patients with personality disorders stems from their limited range of coping capacities, antidepressants are usually less effective than in patients with uncomplicated major depression.
Antidepressants are most often prescribed for a limited time in patients with serious depressive episodes lasting longer than a few weeks.
Selectively inhibits presynaptic serotonin reuptake.
50-150 mg/d PO
Not established
Serotonergic agents, such as other SSRIs, meperidine, and MAOIs, can produce serotonergic reactions with sertraline
Documented hypersensitivity; concurrent administration of MAOIs or within the last 2 wk
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in preexisting seizure disorders and those that have experienced recent MI, have unstable heart disease, or hepatic or renal impairment
Potent selective inhibitor of neuronal serotonin reuptake. Also has weak effect on norepinephrine and dopamine neuronal reuptake.
20-60 mg/d PO
Not established
Phenobarbital, phenytoin, and carbamazepine may decrease effects; cimetidine may increase toxicity; because of its effects on the cytochrome P-450 enzyme systems and protein binding, can increase blood levels of antipsychotics, anticonvulsants, other antidepressants, beta-blockers, type 1C antiarrhythmics, and Coumadin; serotonin syndrome may occur when used with other serotonergic agents such as buspirone, meperidine, tramadol, dextromethorphan, triptans, mirtazapine, nefazodone, and other SSRIs, but especially with MAOIs
Documented hypersensitivity; concurrent administration with MAOIs, or within 14 d of discontinuing
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in history of seizures, mania, renal disease, and cardiac disease; adverse effects include drowsiness, headache, weight gain, and sexual dysfunction
Selectively inhibits presynaptic serotonin reuptake with minimal or no effect in the reuptake of norepinephrine or dopamine.
20-80 mg/d PO
Not established
Phenobarbital, phenytoin, and carbamazepine may decrease effects; cimetidine may increase toxicity; because of its effects on the cytochrome P-450 enzyme systems and protein binding can increase blood levels of antipsychotics, anticonvulsants, other antidepressants, beta-blockers, type 1C antiarrhythmics, and Coumadin; serotonin syndrome may occur when used with other serotonergic agents such as buspirone, meperidine, tramadol, dextromethorphan, triptans, mirtazapine, nefazodone, and other SSRIs, but especially with MAOIs
Documented hypersensitivity; concurrent administration of MAOIs or within the last 2 wk
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hepatic impairment and history of seizures; MAOIs should be discontinued at least 14 d before initiating fluoxetine therapy;
adverse effects include insomnia, headache, weight gain, and sexual dysfunction
Enhances serotonin activity because of selective reuptake inhibition at the neuronal membrane.
Selective serotonin reuptake inhibitor (SSRI) and S-enantiomer of citalopram. Used for the treatment of depression. Mechanism of action is thought to be potentiation of serotonergic activity in central nervous system resulting from inhibition of CNS neuronal reuptake of serotonin. Onset of depression relief may be obtained after 1-2 wk, which is sooner than other antidepressants.
10 mg PO qd initially; if needed, may increase to 20 mg/d after 1 wk
Not established
Primarily metabolized by CYP450 3A4 and 2C19; coadministration with alcohol or other centrally acting drugs increases CNS depression; cimetidine increases AUC and maximum serum concentration; coadministration with sumatriptan and SSRIs has caused weakness and hyperreflexia
Documented hypersensitivity; concurrent MAOI therapy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution with history of seizures, mania, suicide; common adverse effects include insomnia, ejaculation disorder (primarily ejaculatory delay), nausea, sweating, fatigue, and somnolence
Antagonist at the 5-HT2 receptor and inhibits the reuptake of 5-HT. Also has negligible affinity for cholinergic and histaminergic receptors.
300-600 mg/d PO
Not established
Increases effects of digoxin, carbamazepine, triazolam, alprazolam, and protease inhibitors through its effect of inhibiting CYP-450 3A4 enzyme. Serotonin syndrome may occur when used with other serotonergic agents such as buspirone, meperidine, tramadol, dextromethorphan, triptans, mirtazapine, and SSRIs, but especially with MAOIs
Documented hypersensitivity; MAOIs within 14 d of initiating treatment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in cardiac disease, cerebrovascular disease, or seizures; discontinue therapy and reevaluate if priapism occurs; adverse effects include drowsiness, headache, and weight gain
Increases availability of serotonin and norepinephrine.
15-60 mg/d PO
Not established
May potentiate effects of alcohol and benzodiazepines; serotonin syndrome may occur when used with other serotonergic agents such as buspirone, meperidine, tramadol, dextromethorphan, triptans, nefazodone, and SSRIs, but especially with MAOIs
Documented hypersensitivity; MAOIs within 14 d of initiating treatment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Common adverse effects include drowsiness, headache, and weight gain
Useful in stabilizing the affective extremes in patients with bipolar disorder but are less effective for that purpose in patients with personality disorders. They have some demonstrated efficacy in suppressing impulsive and particularly aggressive behavior in patients with personality disorder.
Most widely used agent in its class. Modestly effective and generally well tolerated.
Initial: 750 mg/d in divided doses; may increase by 500 mg/d q2-3d to achieve trough serum levels of 50-125 mcg/mL
Not established
Coadministration with cimetidine, salicylates, felbamate, and erythromycin may increase toxicity; rifampin may significantly reduce levels; in pediatric patients, protein binding and metabolism of valproate decrease when taken concomitantly with salicylates; coadministration with carbamazepine may result in variable changes of carbamazepine concentrations with possible loss of seizure control; valproate may increase diazepam and ethosuximide toxicity (monitor closely); may increase phenobarbital and phenytoin levels while either one may decrease valproate levels; may displace warfarin from protein-binding sites (monitor coagulation tests); may increase zidovudine levels in patients who are HIV seropositive
Documented hypersensitivity; hepatic disease/dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Thrombocytopenia and abnormal coagulation parameters have occurred; risk of thrombocytopenia increases significantly at total trough valproate plasma concentrations >110 mcg/mL in females and 135 mcg/mL in males; at periodic intervals and prior to surgery determine platelet counts and bleeding time before initiating therapy; reduce dose or discontinue therapy if hemorrhage, bruising, or a hemostasis/coagulation disorder occur; hyperammonemia may occur, resulting in hepatotoxicity; monitor patients closely for appearance of malaise, weakness, facial edema, anorexia, jaundice, and vomiting; may cause drowsiness; adverse effects include headache, drowsiness, nausea, tremor, dizziness, and alopecia
Some personality disorders produce transient psychotic periods (especially borderline personality disorder), while others (eg, schizotypal personality disorder) feature chronic idiosyncratic ideation of nearly psychotic proportions.
Response to antipsychotics is less dramatic than in true psychotic Axis I disorders, but symptoms such as anxiety, hostility, and sensitivity to rejection may be reduced. Antipsychotics are typically used for a short time while the symptoms are active.
The atypical antipsychotics have almost completely replaced the traditional neuroleptics because of their safety margin, but neurologic risks (including tardive dyskinesia and neuroleptic malignant syndrome) are never absent. Risperidone and olanzapine are described here; however, quetiapine and ziprasidone may also be used. No evidence indicates that any of these has superior efficacy, and each one may have advantages and disadvantages from the standpoint of adverse effects.
Binds to dopamine D2 receptor with a 20-times lower affinity than for the 5-HT2 receptor. Improves negative symptoms of psychoses and reduces incidence of extrapyramidal adverse effects.
0.5-4 mg/d PO
Not established
Coadministration enhances the effects of alcohol and other CNS suppressants; may inhibit effects of levodopa; may increase clozapine levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause extrapyramidal reactions, hypotension, tachycardia, and arrhythmias; adverse effects include pseudoparkinsonism (particularly at doses > 6 mg/d), sedation, dizziness, and rhinitis
May inhibit serotonin, muscarinic, and dopamine effects.
3.75-30 mg/d PO
Not established
Fluvoxamine may increase effects; antihypertensives may increase risk of hypotension and orthostatic hypotension; levodopa, pergolide, bromocriptine, charcoal, carbamazepine, omeprazole, rifampin, and cigarette smoking may decrease effects
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in narrow-angle glaucoma, cardiovascular disease, cerebrovascular disease, prostatic hypertrophy, seizure disorders, hypovolemia, and dehydration; adverse effects include sedation, constipation, weight gain, and postural hypotension; tardive dyskinesia has been reported
May act by antagonizing dopamine and serotonin effects. Efficacy similar to risperidone and olanzapine. Fewer dose-dependent adverse effects and less concern of weight gain.
25 mg PO bid; titrate to 150-750 mg/d PO; not to exceed 800 mg/d
Not established
May antagonize levodopa and dopamine agonists; phenytoin, thioridazine, and other liver enzyme inducers may reduce quetiapine levels; CYP450 3A inhibitors (eg, ketoconazole, fluconazole, erythromycin) increase quetiapine serum concentration
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May induce orthostatic hypotension associated with dizziness, tachycardia, and syncope; the neuroleptic malignant syndrome and tardive dyskinesia has been associated with this treatment; hyperglycemia may occur and in some cases be extreme, resulting in ketoacidosis, hyperosmolar coma, or death; caution in hepatic impairment (decrease dose)
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR). Washington, DC: American Psychiatric Association; 2000.
Widiger TA, Sanderson CJ. Personality disorders. In: Tasman A, Kay J, Lieberman JA, eds. Psychiatry. Philadelphia, Pa: Harcourt Brace & Co; 1997:1291-1317.
Shedler J, Westen D. Refining personality disorder diagnosis: integrating science and practice. Am J Psychiatry. Aug 2004;161(8):1350-65. [Medline].
Raine A, Lencz T, Bihrle S, et al. Reduced prefrontal gray matter volume and reduced autonomic activity in antisocial personality disorder. Arch Gen Psychiatry. Feb 2000;57(2):119-27; discussion 128-9. [Medline].
Lyons-Ruth K, Holmes BM, Sasvari-Szekely M, Ronai Z, Nemoda Z, Pauls D. Serotonin transporter polymorphism and borderline or antisocial traits among low-income young adults. Psychiatr Genet. Dec 2007;17(6):339-43. [Medline].
Britton R. Narcissistic disorders in clinical practice. J Anal Psychol. Sep 2004;49(4):477-90. [Medline].
Beck AT, Freeman A. Cognitive Therapy of Personality Disorders. London, England: Guilford Press; 1990.
Livesley WJ. A practical approach to the treatment of patients with borderline personality disorder. Psychiatr Clin North Am. Mar 2000;23(1):211-32. [Medline].
Kavoussi RJ, Coccaro EF. Divalproex sodium for impulsive aggressive behavior in patients with personality disorder. J Clin Psychiatry. Dec 1998;59(12):676-80. [Medline].
Soloff PH. Psychopharmacology of borderline personality disorder. Psychiatr Clin North Am. Mar 2000;23(1):169-92, ix. [Medline].
[Best Evidence] Binks CA, Fenton M, McCarthy L, Lee T, Adams CE, Duggan C. Pharmacological interventions for people with borderline personality disorder. Cochrane Database Syst Rev. Jan 25 2006;CD005653. [Medline]. [Full Text].
Simeon D, Baker B, Chaplin W, Braun A, Hollander E. An open-label trial of divalproex extended-release in the treatment of borderline personality disorder. CNS Spectr. Jun 2007;12(6):439-43. [Medline].
Herpertz SC, Zanarini M, Schulz CS, Siever L, Lieb K, Möller HJ. World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for biological treatment of personality disorders. World J Biol Psychiatry. 2007;8(4):212-44. [Medline].
Suominen KH, Isometsa ET, Henriksson MM, et al. Suicide attempts and personality disorder. Acta Psychiatr Scand. Aug 2000;102(2):118-25. [Medline].
character disorder, sociopathy, sociopath, psychopathy, hysteria, paranoid personality disorder, schizoid personality disorder, schizotypal personality disorder, antisocial personality disorder, borderline personality disorder, histrionic personality disorder, narcissistic personality disorder, avoidant personality disorder, dependent personality disorder
obsessive-compulsive personality disorder, OCD, Minnesota Multiphasic Personality Inventory,MMPI, psychiatric disorder, mood disorder, substance abuse, suicide, alcoholism, delusionaldisorder, schizophrenia, depression, obsessive-compulsive disorder, anxiety disorder, somatization disorder, posttraumatic stress disorder, bulimia, anorexia nervosa, social phobia
David Bienenfeld, MD, Vice-Chair, Program Director, Professor, Department of Psychiatry, Wright State University School of Medicine
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