eMedicine Specialties > Psychiatry > Adult

Personality Disorders: Treatment & Medication

Author: David Bienenfeld, MD, Vice-Chair, Program Director, Professor, Department of Psychiatry, Wright State University School of Medicine
Contributor Information and Disclosures

Updated: Jul 17, 2008

Treatment

Medical Care

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.

  • Psychodynamic psychotherapy examines the ways that patients perceive events, based on the assumption that perceptions are shaped by early life experiences. Psychotherapy aims to identify perceptual distortions and their historical sources and to facilitate the development of more adaptive modes of perception and response. Treatment is usually extended over a course of several years at a frequency from several times a week to once a month; it makes use of transference.6
  • Cognitive therapy (also called cognitive behavior therapy [CBT]) is based on the idea that cognitive errors based on long-standing beliefs influence the meaning attached to interpersonal events. It deals with how people think about their world and their perception of it. This very active form of therapy identifies the distortions and engages the patient in efforts to reformulate perceptions and behaviors. This therapy is typically limited to episodes of 6-20 weeks, once weekly. In the case of personality disorders, episodes of therapy are repeated often over the course of years.7
  • Interpersonal therapy (IPT) conceives of patients' difficulties resulting from a limited range of interpersonal problems including such issues as role definition and grief. Current problems are interpreted narrowly through the screen of these formulations, and solutions are framed in interpersonal terms. Therapy is usually weekly for a period of 6-20 sessions. Though empirically validated for anxiety and depression, IPT is not widely practiced, and therapists conversant in the technique are difficult to locate.8
  • Group psychotherapy allows interpersonal psychopathology to display itself among peer patients, whose feedback is used by the therapist to identify and correct maladaptive ideas, communication, and behavior. Sessions are usually once weekly over a course that may range from several months to years.
  • Dialectical behavior therapy (DBT): This is a skills-based therapy (developed by Marsha Linehan, PhD) that can be used in both individual and group formats. It has been applied to borderline personality disorder. The emphasis of this manual-based therapy is on the development of coping skills to improve affective stability and impulse control and on reducing self-harmful behavior. This treatment is also being used with other cluster B personality disorders to reduce impulsive behavior.2

Consultations

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.

Medication

Medications are in no way curative for any personality disorder. They should be viewed as an adjunct to psychotherapy so that the patient may productively engage in psychotherapy.

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.

Antidepressants

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.


Sertraline (Zoloft)

Selectively inhibits presynaptic serotonin reuptake.

Adult

50-150 mg/d PO

Pediatric

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

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in preexisting seizure disorders and those that have experienced recent MI, have unstable heart disease, or hepatic or renal impairment


Paroxetine (Paxil)

Potent selective inhibitor of neuronal serotonin reuptake. Also has weak effect on norepinephrine and dopamine neuronal reuptake.

Adult

20-60 mg/d PO

Pediatric

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

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in history of seizures, mania, renal disease, and cardiac disease; adverse effects include drowsiness, headache, weight gain, and sexual dysfunction


Fluoxetine (Prozac)

Selectively inhibits presynaptic serotonin reuptake with minimal or no effect in the reuptake of norepinephrine or dopamine.

Adult

20-80 mg/d PO

Pediatric

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

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

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


Escitalopram (Lexapro)

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.

Adult

10 mg PO qd initially; if needed, may increase to 20 mg/d after 1 wk

Pediatric

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

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution with history of seizures, mania, suicide; common adverse effects include insomnia, ejaculation disorder (primarily ejaculatory delay), nausea, sweating, fatigue, and somnolence


Nefazodone (Serzone)

Antagonist at the 5-HT2 receptor and inhibits the reuptake of 5-HT. Also has negligible affinity for cholinergic and histaminergic receptors.

Adult

300-600 mg/d PO

Pediatric

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

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiac disease, cerebrovascular disease, or seizures; discontinue therapy and reevaluate if priapism occurs; adverse effects include drowsiness, headache, and weight gain


Mirtazapine (Remeron)

Increases availability of serotonin and norepinephrine.

Adult

15-60 mg/d PO

Pediatric

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

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Common adverse effects include drowsiness, headache, and weight gain

Anticonvulsants

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.


Valproic acid (Depakote)

Most widely used agent in its class. Modestly effective and generally well tolerated.

Adult

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

Pediatric

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

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

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

Antipsychotics

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.


Risperidone (Risperdal)

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.

Adult

0.5-4 mg/d PO

Pediatric

Not established

Coadministration enhances the effects of alcohol and other CNS suppressants; may inhibit effects of levodopa; may increase clozapine levels

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause extrapyramidal reactions, hypotension, tachycardia, and arrhythmias; adverse effects include pseudoparkinsonism (particularly at doses > 6 mg/d), sedation, dizziness, and rhinitis


Olanzapine (Zyprexa)

May inhibit serotonin, muscarinic, and dopamine effects.

Adult

3.75-30 mg/d PO

Pediatric

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

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

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


Quetiapine (Seroquel)

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.

Adult

25 mg PO bid; titrate to 150-750 mg/d PO; not to exceed 800 mg/d

Pediatric

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

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

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)

More on Personality Disorders

Overview: Personality Disorders
Differential Diagnoses & Workup: Personality Disorders
Treatment & Medication: Personality Disorders
Follow-up: Personality Disorders
References
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References

  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR). Washington, DC: American Psychiatric Association; 2000.

  2. Widiger TA, Sanderson CJ. Personality disorders. In: Tasman A, Kay J, Lieberman JA, eds. Psychiatry. Philadelphia, Pa: Harcourt Brace & Co; 1997:1291-1317.

  3. Shedler J, Westen D. Refining personality disorder diagnosis: integrating science and practice. Am J Psychiatry. Aug 2004;161(8):1350-65. [Medline].

  4. 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].

  5. 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].

  6. Britton R. Narcissistic disorders in clinical practice. J Anal Psychol. Sep 2004;49(4):477-90. [Medline].

  7. Beck AT, Freeman A. Cognitive Therapy of Personality Disorders. London, England: Guilford Press; 1990.

  8. 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].

  9. 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].

  10. Soloff PH. Psychopharmacology of borderline personality disorder. Psychiatr Clin North Am. Mar 2000;23(1):169-92, ix. [Medline].

  11. [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].

  12. 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].

  13. 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].

  14. Suominen KH, Isometsa ET, Henriksson MM, et al. Suicide attempts and personality disorder. Acta Psychiatr Scand. Aug 2000;102(2):118-25. [Medline].

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Further Reading

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Contributor Information and Disclosures

Author

David Bienenfeld, MD, Vice-Chair, Program Director, Professor, Department of Psychiatry, Wright State University School of Medicine
David Bienenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, and Association for Academic Psychiatry
Disclosure: Nothing to disclose.

Medical Editor

Sarah C Aronson, MD, Associate Professor, Departments of Psychiatry and Medicine, Case Western Reserve School of Medicine/University Hospitals of Cleveland
Sarah C Aronson, MD is a member of the following medical societies: American Academy of Family Physicians, American Medical Association, and American Psychiatric Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Iqbal Ahmed, MBBS, Professor, Department of Psychiatry, John A Burns School of Medicine, University of Hawaii
Iqbal Ahmed, MBBS is a member of the following medical societies: Academy of Psychosomatic Medicine, American Association for Geriatric Psychiatry, American Neuropsychiatric Association, and American Psychiatric Association
Disclosure: Nothing to disclose.

CME Editor

Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer  Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research

Chief Editor

Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.

 
 
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