Erika Paradiso, MD

Borderline personality disorder (BPD) is characterized by a pervasive pattern of instability of interpersonal relationships, self-image, and affect, in addition to marked impulsivity.

 Although psychotherapy plays a significant role in the treatment of borderline patients by focusing on maladaptive personality traits and patterns of interpersonal relationships, 

 pharmacotherapy is indicated by the American Psychiatric Association guidelines to manage vulnerability traits, symptoms, and crises.

Treatment strategies for BPD target different domains of psychopathology, such as cognitive-perceptual, affective, and impulsive-behavioral symptoms. Guidelines specify the use of antidepressant agentsin particular, selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitorsand mood stabilizers for affective dysregulation; SSRIs and mood stabilizers for impulsive-behavioral dyscontrol; and antipsychotics for cognitive-perceptual symptoms. This article focuses on data concerning the efficacy of mood stabilizers in the treatment of BPD.

A consensus definition of mood stabilizer remains to be established, and international regulatory authorities do not officially recognize the term as a mode of drug activity.

 Clinicians and researchers apply the concept of mood stabilization to a range of compounds used in the treatment of bipolar disorder, although considerable variability can be found in the literature concerning the meaning and use of the term.

 In its broadest form, a mood stabilizer has been operationally described as an agent that is useful in at least 1 of the 3 phases of bipolar disorder (mania, bipolar depression, or long-term maintenance) while not increasing the frequency or severity of any of the other phases of the illness.

Although no drugs used as mood stabilizers have been approved by the FDA for the treatment of BPD, these drugs are often prescribed off-label in clinical practice and are suggested for treating BPD-related symptoms by the guidelines of the American Psychiatric Association.

 Some investigators have proposed that the same mechanism may drive both the affective instability of BPD and the rapid mood cycling of bipolar disorder and that this could be a rationale for the use of mood stabilizers in BPD.

To date, several open-label and controlled trials have been undertaken to test the efficacy of these agents in BPD and to define their effects on different dimensions of borderline psychopathology (

The first mood stabilizer considered for the treatment of patients with BPD is lithium carbonate; its effectiveness has been reported in 3 reviews since the late 1980s.

 Concerning the mechanism of action, 3 interacting systems appear critical for lithium activity: modulation of neurotransmitters, which may contribute to neuroprotection by readjusting excitatory and inhibitory activity balance; modulation of signals impacting on the cytoskeleton, including glycogen synthase kinase-3β, cyclic AMP-dependent kinase, and protein kinase C, which may be critical for the neural plasticity involved in mood stabilization; and regulation of second messengers, transcription factors, and gene expression.

The results of a 6-week, doubleblind, placebo-controlled crossover study that compared lithium with desipramine in 10 patients with BPD showed the efficacy of lithium on core features of borderline psychopathology, such as irritability, anger, and selfmutilation.

 concerning lithium and the anticonvulsant agent carbamazepine in the treatment of patients with BPD or antisocial personality disorder pointed out the effectiveness of both agents on behavioral dysregulation and aggressiveness.

At about the same time, further data concerning treatment of BPD with carbamazepine were published. This agent blocks voltage-gated sodium channels and is indicated by the FDA as an anticonvulsant.

 Although its use in the treatment of BPD is common in clinical practice, this has not been officially approved. In a crossover trial with a sample of 11 female outpatients with BPD, Gardner and Cowdry

 demonstrated decreased frequency and severity of behavioral dyscontrol. Their results were confirmed by other studies: a 6-week controlled investigation comparing carbamazepine (mean dose, 820 mg/d), alprazolam (4.7 mg/d), trifluoperazine (7.8 mg/d), and tranylcypromine (40 mg/d) in the treatment of 16 patients with BPD and comorbid hysteroid dysphoria,

 and a review of double-blind clinical trials.

 Both showed that carbamazepine induced a marked improvement in impulsive aggression.

Controlled trials suggest the efficacy of carbamazepine not only in reducing impulsive-aggressive behaviors

 which is often the main goal of mood stabilizer use in the treatment of BPD. A clinical practice survey by Denicoff and colleagues26 compared carbamazepine with many other agents (lithium, valproate, neuroleptics, clonazepam, phenytoin, calcium antagonists) and electroconvulsive therapy in 1257 patients with different neurologic and psychiatric disorders, and found a significant global improvement in the subgroup of patients with BPD treated with carbamazepine.

 Oxcarbazepine is another anticonvulsant structurally related to carbamazepine, with the same mechanism of action of blocking voltage-gated sodium channels, but it is less likely to induce cytochrome P-450 and drug interactions.

 A series of studies indicated the efficacy of oxcarbazepine in the treatment of several psychiatric disorders, such as bipolar disorder, substance abuse, resistant psychosis, and schizoaffective disorder. 

 However, as in the case of carbamazepine, oxcarbazepine has been approved by the FDA for treating only seizure disorder.

Our research group recently performed a 12-week pilot study of oxcarbazepine in 13 outpatients with BPD.

 A statistically significant improvement was observed in global psychopathology; anxiety; interpersonal relationships; and BPD core features, including impulsivity, affective instability, and outbursts of anger.

Among mood stabilizers, divalproex sodium has been extensively studied in patients with BPD. Its mechanism of action consists of facilitating transmission of y-aminobutyric acid.

 was the first to suggest the role of divalproex in reducing agitation in patients with BPD. In 1994, Wilcox

 tested the efficacy of valproate in a group of patients with psychomotor agitation caused by various underlying psychiatric conditions. The decrease in agitation after treatment was particularly evident in patients with bipolar disorder or BPD. These data were replicated in a subsequent study by Wilcox

 concerning the treatment of BPD with divalproex sodium.

An 8-week open-label trial of valproate (daily dose titrated to reach blood levels of 50 to 100 μg/mL) in 11 patients with BPD by Stein and colleagues

 provided further data on this agent. Of the 8 who completed the study, half were responders on clinician-rated measures of overall psychopathology, mood, anxiety, anger, impulsivity, and rejection sensitivity.

 administered valproate (up to 2000 mg/d) to 10 patients with several Axis II diagnoses who had failed to respond to an SSRI (2 patients met criteria for BPD). After 8 weeks of treatment, irritability and impulsive aggressiveness were significantly reduced.

Subsequently, 3 placebo-controlled trials were published. Hollander and colleagues

 performed a 10-week double-blind study of valproate (plasma level of 80 μg/mL) in 16 patients with BPD and found a marked improvement in global symptomatology; social functioning; and BPD features, such as depressive symptoms, aggressiveness, irritability, and suicidal ideation or behavior. However, a high dropout rate precluded finding significant differences between treatment groups.

More recently, the same study group confirmed the efficacy of valproate (mean daily dose, 1325 mg) on impulsive aggression of 52 outpatients with BPD in a 12-week double-blind trial.

 included 30 women with BPD and comorbid bipolar II disorder in a 6-month controlled study and showed that valproate (plasma level of 50-100 μg/mL) had significant effects on interpersonal sensitivity, anger, hostility, and aggressiveness.

The anticonvulsant lamotrigine has been considered in recent years for treating depressive episodes of bipolar disorder and preventing recurrences. This drug inhibits neuronal excitability and modifies synaptic plasticity by inhibiting voltage-activated sodium channels. Indirectly, these effects would be expected to regulate aberrant intracellular and intercellular signalling in critical regions of the limbic forebrain.

The use of lamotrigine for treating BPD was initially reported by Pinto and Akiskal

 in a 1-year open-label trial focused on 8 outpatients. Their results showed that 40% reported a significant improvement in global functioning, sexual impulsiveness, substance abuse, and suicidal behavior. A review by Green

 of patients with mood disorders suggests the efficacy of this agent in also treating mood instability of BPD.

 investigated the frequency of comorbid BPD in 35 patients with bipolar disorder who had previously participated in 2 open-label trials with lamotrigine, in order to evaluate the effects of this drug on BPD dimensions. BPD was retrospectively diagnosed in 40% of the patients. Results of the study showed the efficacy of lamotrigine on all BPD traits, with a marked improvement in impulsivity and mood instability.

 compared the efficacy of lamotrigine and placebo in the treatment of aggression in 24 women meeting the criteria for BPD. Highly significant improvements in anger were observed after 8 weeks in patients treated with lamotrigine.

Novel antipsychotics as mood stabilizers in BPD

Second-generation antipsychotics antagonize both dopamine and serotonin- 2 (5-HT2) receptors. Because dopamine receptor blockade has been associated with antimanic properties and 5-HT2 antagonism with antidepressant effects, it has been postulated that novel antipsychotics may be effective in the treatment and prevention of bipolar mania and depression.

 These hypotheses have been substantiated by a number of studies.

The mood-stabilizing properties of second-generation antipsychotics have also been considered for treatment of BPD-related symptoms (

). Although this indication has not yet been approved by the FDA, these agents are indicated by BPD treatment guidelines both for their antipsychotic effects on cognitive-perceptual disturbances and for their mood stabilizing action on affective instability, anger, and impulsive aggression.

Clozapine was found to be efficacious on overall symptomatology, aggressiveness, and severe psychotic symptoms related to BPD.

 However, patients with BPD treated with clozapine frequently had Axis I comorbidities and had been refractory to previous treatments. These patients did not have pure BPD and they had already been treated unsuccessfully with other drugs.

To date, studies on risperidone in BPD are sparse and derive from some case reports and an open-label trial.66-69 In their 8-week open-label trial of risperidone (3.3 mg/d) in 15 outpatients with BPD, Rocca and colleagues

 outlined the efficacy of this agent on aggressive behavior, affective instability, and global psychopathology.

More extensive data suggesting mood stabilizing properties have been reported for olanzapine and quetiapine. Olanzapine is a thienobenzodiazepine with a high affinity for dopamine (D2 through D4) and serotonin receptors (5-HT2A), and a lower affinity for histamine (H1), muscarinic (M1 through M5), and α-adrenergic (α1) receptors. Antagonism at D2 through D4 and 5-HT2A receptors is supposed to be the basis for its therapeutic efficacy, while antagonism at H1, M1-M5, and α1 receptors is probably responsible for adverse effects.

 performed the first open-label study of olanzapine in a sample of 9 outpatients with BPD who had comorbid dysthymia. After 8 weeks of treatment, patients reported a significant improvement in impulsivity, hostility, global psychopathology, and global functioning.

Since then, the findings from several controlled trials have been published. A 6-month double-blind, placebo-controlled trial of olanzapine (mean dose, 5.33 mg/d ± 3.43) in 28 women with BPD was undertaken by Zanarini and Frankenburg,72 who pointed out the efficacy of this agent on anxiety, paranoid ideation, and interpersonal sensitivity. Bogenschutz and Nurnberg

 recently reported similar findings in a 12-week double-blind, placebo-controlled trial of olanzapine (5 to 10 mg/d) in 40 outpatients with BPD. A significant improvement in borderline psychopathology and anger was found after the fourth week of treatment.

 compared the efficacy of fluoxetine, olanzapine, and the olanzapine-fluoxetine combination (OFC) in the treatment of 45 women meeting criteria for BPD. In their 8-week randomized double-blind study, the investigators found that all 3 treatment options significantly ameliorated chronic dysphoria and impulsive aggression. However, olanzapine monotherapy and OFC were found to be superior to fluoxetine monotherapy in treating both features of borderline psychopathology.

 recently compared the efficacy of olanzapine and placebo in a combined treatment with dialectical behavioral therapy. In their 12-week double-blind study of a group of 60 outpatients with BPD, they found that olanzapine (mean dose, 8.83 mg/d) led to a significant reduction of impulsive- aggressive behavior, depression, and anxiety.

Quetiapine is a dibenzothiazepine characterized by low affinity for and rapid dissociation from postsynaptic D2 receptors, which reduces the incidence of adverse events, such as extrapyramidal symptoms, prolactin elevation, and weight gain.

 described the impact of this agent (400 to 800 mg/d) on 2 women with BPD with severe episodes of self-mutilation and found positive effects on impulsive behavior and overall functioning.

A few pilot studies on quetiapine in BPD treatment have appeared in recent years. Adityanjee and Schulz

 evaluated the efficacy of quetiapine (25 to 300 mg/d) in 10 patients who completed an 8-week open-label trial. Results suggested a significant improvement in overall symptomatology, hostility, impulsivity, and functioning. Villeneuve and Lemelin

 recently replicated these findings. They investigated the effects of quetiapine (175 to 400 mg/d for 12 weeks) in a group of 23 outpatients and found a significant improvement in impulsivity, hostility, depression, anxiety, and social functioning. 

 performed a 12-week pilot study on the efficacy of quetiapine (mean dose, 309 mg/d  83) for the treatment of BPD in 14 patients. Our results were mostly concordant with previous findings and confirmed the improvement of global symptomatology, impulsivity, outbursts of anger, anxiety, and social functioning.

Recent investigations of mood stabilizers in the treatment of BPD are promising and suggest that these drugs can be useful in clinical practice, particularly for controlling affective instability and impulsive aggression. However, further studies are needed to confirm the initial results and to ascertain whether some novel antipsychotics can be used for their mood-stabilizing effects in patients with BPD.

Future investigations should focus on a list of relevant topics: pilot studies of new drugs; controlled trials of drugs already tested in open case series; comparisons of new anticonvulsant agents with better-known mood stabilizers, such as lithium or valproate; head-to-head comparisons of novel and traditional antipsychotics to verify which differences in clinical effects and adverse events specifically occur in patients with BPD; maintenance studies to assess persistence of therapeutic effects in longlasting disorders such as BPD; add-on trials of mood stabilizers and novel antipsychotics in samples of patients with BPD who do not respond to firstline therapy with serotonergic antidepressants; and the relationship of clinical subtypes of patients with BPD (eg, affective labile, self-injurious, psychotoform) with response to drug treatment.

Dr Bellino is assistant professor of psychiatry, Dr Paradiso is a resident in psychiatry, and Dr Bogetto is professor of psychiatry and chairman in the department of neuroscience at the University of Turin in Italy.

Drs Bellino, Paradiso, and Bogetto report that they have no conflicts of interest with the subject matter of this article.

Carbamazepine (Carbatrol, Tegretol, others)
Clonazepam (Klonopin, Rivotril)
Clozapine (Clozaril)
Divalproex (Epival, Depakote)
Fluoxetine (Prozac)
Lamotrigine (Lamictal)
Lithium (Eskalith)
Olanzapine (Zyprexa)
Oxcarbazepine (Trileptal)
Phenytoin (Dilantin)
Quetiapine (Seroquel)
Risperidone (Risperdal)
Tranylcypromine (Parnate)
Trifluoperazine (Stelazine)
Valproate/valproic acid (Depakote, others)




1. American Psychiatric Association. Diagnostic andStatistical Manual of Mental Disorders, Fourth Edition,Text Revision (DSM-IV-TR). Washington, DC:American Psychiatric Association; 2000.
2. Clarkin JF, Yeomans FE, Kernberg OF. Psychotherapyfor Borderline Patients. New York: John Wiley& Sons; 1999.
3. Livesley WJ. A practical approach to the treatmentof patients with borderline personality disorder.Psychiatr Clin North Am. 2000;23:211-232.
4. American Psychiatric Association. Practice Guidelinesfor the Treatment of Patients With BorderlinePersonality Disorder. Washington, DC: AmericanPsychiatric Association; 2001.
5. Vieta E. Mood stabilization in the treatment ofbipolar disorder: focus on quetiapine. Hum Psychopharmacol.2005;20:225-236.
6. Sachs GS. Bipolar mood disorder: practical strategiesfor acute and maintenance phase treatment.J Clin Psychopharmacol. 1996;16:32S-47S.
7. Keck PE Jr, McElroy SL, Richt N, Tohen M. Whatmakes a drug a primary mood stabilizer? Mol Psychiatry.2002;7(suppl 1):S8-S14.
8. Ketter TA, Calabrese JR. Stabilization of moodfrom below versus above baseline in bipolar disorder:a new nomenclature. J Clin Psychiatry. 2002;63:146-151.
9. Grof P. "Mood-stabilizers: the archeology of theconcept" by M Harris, S Chandran, N Chakrabortyand D Healy: a commentary. Bipolar Disord. 2003;5:453-455.
10. Harris M, Chandran S, Chakraborty N, Healy D.Mood stabilizers: the archeology of the concept.Bipolar Disord. 2003;5:446-452.
11. Keck PE Jr, McElroy SL. Redefining mood stabilization.J Affect Disord. 2003;73:163-169.
12. Mackinnon DF, Pies R. Affective instability asrapid cycling: theoretical and clinical implications forborderline personality and bipolar spectrum disorders. Bipolar Disord. 2006;8:1-14.
13. Zanarini MC, Frankenburg FR, Gunderson JG.Pharmacotherapy of borderline outpatients. ComprPsychiatry. 1988;29:372-378.
14. Gardner DL, Cowdry RW. Pharmacotherapy ofborderline personality disorder: a review. PsychopharmacolBull. 1989;25:515-523.
15. Goldberg SC. Prediction of change in borderlinepersonality disorder. Psychopharmacol Bull. 1989;25:550-555.
16. Jope RS. Anti-bipolar therapy: mechanism ofaction of lithium. Mol Psychiatry. 1999;4:117-128.
17. Links PS, Steiner M, Boiago I, et al. Lithium therapyfor borderline patients: preliminary findings.J Clin Psychopharmacol. 1990;4:173-181.
18. Stein DJ. Drug treatment of the personality disorders.Br J Psychiatry. 1992;161:167-184.
19. Ghaemi SN, Ko JY. Oxcarbazepine treatment ofbipolar disorder: a review of the literature. PrimaryPsychiatry. 2002;9:55-59.
20. Gardner DL, Cowdry RW. Positive effects of carbamazepineon behavioural dyscontrol in borderlinepersonality disorder. Am J Psychiatry. 1986;143:519-522.
21. Cowdry RW, Gardner DL. Pharmacotherapy ofborderline personality disorder: alprazolam, carbamazepine,trifluoperazine, and tranylcipromine. ArchGen Psychiatry. 1988;45:111-119.
22. Hori A. Pharmacotherapy for personality disorders.Psychiatry Clin Neurosci. 1998;52:13-19.
23. Mattes J. Comparative effectiveness of carbamazepineand propranolol for rage outbursts. J NeuropsychiatryClin Neurosci. 1990;2:159-164.
24. Kravitz HM, Fawcett J. Carbamazepine in the treatmentof affective disorders. Med Sci Res.1987;15:1-8.
25. Blumer D, Heibronn M, Himmelhoch J. Indicationsfor carbamazepine in mental illness: atypical psychiatricdisorder or temporal lobe syndrome? ComprPsychiatry. 1988;29:108-122.
26. Denicoff KD, Meglathery SB, Post RM, TandeciarzSI. Efficacy of carbamazepine compared with otheragents: a clinical practice survey. J Clin Psychiatry.1994;55:70-76.
27. Emrich H. Studies with oxcarbazepine (Trileptal)in acute mania. Int Clin Psychopharmacol. 1990;5(suppl 1):83-88.
28. Hellewell JS. Oxcarbazepine (Trileptal) in the treatmentof bipolar disorders: a review of efficacy andtolerability. J Affect Disord. 2002;72(suppl 1):S23-34.
29. Hummel B, Walden J, Stampfer R, et al. Acuteantimanic efficacy and safety of oxcarbazepine in anopen trial with an on-off-on design. Bipolar Disord.2002;4:412-417.
30. Dietrich DE, Kropp S, Emrich HM. Oxcarbazepinein the treatment of affective and schizoaffectivedisorders. Fortschr Neurol Psychiatr. 2003;71:255-264.
31. Evins AE. Efficacy of newer anticonvulsantmedications in bipolar spectrum mood disorders. JClin Psychiatry. 2003;64(suppl 8):9-14.
32. Ghaemi SN, Berv DA, Klugman J, et al. Oxcarbazepinetreatment of bipolar disorder. J Clin Psychiatry.2003;64:943-945.
33. Perugi G, Toni C, Frare F, et al. An open casestudy in Italy of oxcarbazepine, an effective moodstabilizer, in patients with drug resistant/intolerant bipolar I disorders. Poster presented at the XVI Congressof European College of Neuropsychopharmacology;September 20-24, 2003; Prague.
34. Raja M, Azzoni A. Oxcarbazepine versus valproatein mood and schizoaffective disorders. Int J Neuropsychopharm.2003;6:409-414.
35. Benedetti A, Lattanzi L, Pini S, et al. Oxcarbazepineas add-on treatment in patients with bipolar manic, mixedor depressive episode. J Affect Disord.2004;79:273-277.
36. Spina E, Perugi G. Antiepileptic drugs: indicationsother than epilepsy. Epileptic Disord. 2004;6:57-75.
37. Stahl SM. Anticonvulsants as mood stabilizersand adjuncts to antipsychotics: valproate, lamotrigine,carbamazepine, and oxcarbazepine and actionsat voltage-gated sodium channels. J Clin Psychiatry.2004;65:738-739.
38. Yatham LN. Newer anticonvulsants in the treatmentof bipolar disorder. J Clin Psychiatry. 2004;65(suppl 10):28-35.
39. Gentry JR, Hill C, Malcolm R. New anticonvulsants:a review of applications for the management of substanceabuse disorders. Ann Clin Psychiatry. 2002;14:233-245.
40. Leweke FM, Gerth CW, Koethe D, et al. Oxcarbazepineas an adjunct for schizophrenia. Am J Psychiatry.2004;161:1130-1131.
41. Bellino S, Paradiso E, Bogetto F. Oxcarbazepinein the treatment of borderline personality disorder:a pilot study. J Clin Psychiatry. 2005;66:1111-1115.
42. Polc P. Enhancement of GABAergic inhibition: amechanism of action of benzodiazepines, phenobarbital,valproate and L-cycloserine in the cat spinalcord. Electroencephalogr Clin Neurophysiol. 1982;36(suppl):188-198.
43. Wilcox JA. Divalproex sodium in the treatment of aggressivebehaviour. Ann Clin Psychiatry. 1994;6:17-20.
44. Wilcox JA. Divalproex sodium as a treatment forborderline personality disorder. Ann Clin Psychiatry.1995;7:33-37.
45. Stein DJ, Simeon D, Frenkel M, et al. An opentrial of valproate in borderline personality disorder.J Clin Psychiatry. 1995;56:506-510.
46. Kavoussi RJ, Coccaro EF. Divalproex sodium forimpulsive aggressive behavior in patients with personalitydisorder. J Clin Psychiatry.1998;59:676-680.
47. Hollander E, Allen A, Lopez RP, et al. A preliminarydouble-blind, placebo-controlled trial of divalproexsodium in borderline personality disorder.J Clin Psychiatry. 2001;62:199-203.
48. Hollander E, Swann AC, Coccaro EF, et al. Impactof trait impulsivity and state aggression on divalproexversus placebo response in borderline personalitydisorder. Am J Psychiatry. 2005;162:621-624.
49. Frankenburg FR, Zanarini MC. Divalproex sodiumtreatment of women with borderline personalitydisorder and bipolar II disorder: a double-blindplacebo-controlled pilot study. J Clin Psychiatry.2002;63:442-446.
50. Xie X, Hagan RM. Cellular and molecular actionsof lamotrigine: possible mechanisms of efficacy in bipolardisorder. Neuropsychobiology. 1998;38:119-130.
51. Pinto OC, Akiskal HS. Lamotrigine as a promisingapproach to borderline personality: an open caseseries without concurrent DSM-IV major mood disorder.J Affect Disord. 1998;51:333-343.
52. Green B. Lamotrigine in mood disorders. CurrMed Res Opin. 2003;19:272-277.
53. Preston GA, Marchant BK, Reimherr FW, et al.Borderline personality disorder in patients with bipolardisorder and response to lamotrigine. J AffectDisord. 2004;79:297-303.
54. Tritt K, Nickel C, Lahmann C, et al. Lamotriginetreatment of aggression in female borderline-patients:a randomized, double-blind, placebo-controlled study.J Psychopharmacol. 2005;19:287-291.
55. Bowden CL, Brugger AM, Swann AC, et al. Efficacyof divalproex vs lithium and placebo in the treatmentof mania: the Depakote Mania Study Group. JAMA.1994;271:918-924.
56. Jarema M, Sartorius N. Treatment of bipolar disorderswith second generation antipsychotic medications.Neuro Endocrinol Lett. 2005;26(suppl 1):5-7.
57. Malhi GS, Berk M, Bourin M, et al. Atypical moodstabilizers: a typical role for atypical antipsychotics.Acta Psychiatr Scand Suppl. 2005;(426):29-38.
58. Muzina DJ, Calabrese JR. Maintenance therapiesin bipolar disorder: focus on randomized controlledtrials. Aust N Z J Psychiatry. 2005;39:652-661.
59. Vieta E, Goikolea JM. Atypical antipsychotics:newer options for mania and maintenance therapy.Bipolar Disord. 2005;7(suppl 4):21-33.
60. Conus P, Berk M, McGorry PD. Pharmacologicaltreatment in the early phase of bipolar disorders:what stage are we at? Aust N Z J Psychiatry. 2006;40:199-207.
61. Frankenburg FR, Zanarini MC. Clozapine treatmentof borderline patients: a preliminary study.Compr Psychiatry. 1993;34:402-405.
62. Chengappa KN, Baker RW, Sirri C. The successfuluse of clozapine in ameliorating severe self-mutilatingin a patient with borderline personality disorder.J Personal Disord. 1995;9:76-82.
63. Chengappa KN, Ebeling T, Kang JS, et al. Clozapinereduces severe self-mutilation and aggression inpsychotic patients with borderline personality disorder.J Clin Psychiatry. 1999;60:477-484.
64. Benedetti F, Sforzini L, Colombo C, et al. Lowdoseclozapine in acute and continuation treatmentof severe borderline personality disorder. J ClinPsychiatry. 1998;59:103-107.
65. Swinton M. Clozapine in severe borderline personality.J Forensic Psychiatry. 2001;12:580-591.
66. Kouzam HR, Donnelly NJ. Remission of selfmutilationin a patient with borderline personalityduring risperidone therapy. J Nerv Ment Dis.1997;185:348-349.
67. Szighethy EM, Schulz SC. Risperidone in comorbidborderline personality disorder and dysthymia.J Clin Psychopharmacol. 1997;17:326-327.
68. Hirose S. Effective treatment of aggression andimpulsivity in antisocial personality disorder withrisperidone. Psych Clin Neurosci. 2001;55:161-162.
69. Rocca P, Marchiaro L, Cocuzza E, Bogetto F.Treatment of borderline personality disorder withrisperidone. J Clin Psychiatry. 2002;63:241-244.
70. Bhana N, Foster RH, Olney R, Plosker GL.Olanzapine: an updated review of its use in the managementof schizophrenia. Drugs. 2001;61:111-161.
71. Schulz SC, Camlin KL, Berry SA, Jesberger JA.Olanzapine safety and efficacy in patients with borderlinepersonality disorder and comorbid dysthymia.Biol Psychiatry. 1999;46:1429-1435.
72. Zanarini MC, Frankenburg FR. Olanzapine treatmentof female borderline personality disorder patients:a double-blind, placebo-controlled pilot study.J Clin Psychiatry. 2001;62:849-854.
73. Bogenschutz MP, Nurnberg HG. Olanzapineversus placebo in the treatment of borderline personalitydisorder. J Clin Psychiatry. 2004;65:104-109.
74. Zanarini MC, Frankenburg FR, Parachini EA. Apreliminary randomized trial of fluoxetine, olanzapine,and the olanzapine-fluoxetine combination inwomen with borderline personality disorder. J ClinPsychiatry. 2004;65:903-907.
75. Soler J, Pascual JC, Barrachina J, et al. Doubleblind,placebo-controlled study of dialectical behaviortherapy plus olanzapine for borderline personalitydisorder. Am J Psychiatry. 2005;162:1221-1224.
76. Kufferle B, Tauscher J, Asenbaum S, et al. IBZMSPECT imaging of striatal dopamine-2 receptors inpsychotic patients treated with the novel antipsychoticsubstance quetiapine in comparison toclozapine and haloperidol. Psychopharmacology.1997;133:323-328.
77. Hellewell JSE, Cameron Hands D, McKellar J.Seroquel: an effective atypical antipsychotic with nogreater EPS than placebo across the full dose range.Schizophr Res. 1998;29:154.
78. Brecher M, Rak IW, Melvin K, et al. The longtermeffect of quetiapine ('Seroquel') monotherapyon weight in patients with schizophrenia. Int JPsychiatry Clin Pract. 2000;4:287-291.
79. Kapur S, Zipursky R, Jones C, et al. A positronemission tomography study of quetiapine in schizophrenia:a preliminary finding of an antipsychoticeffect with only transient high dopamine D2 receptoroccupancy. Arch Gen Psychiatry. 2000;57:553-559.
80. Hilger E, Barnas C, Kasper S. Quetiapine in thetreatment of borderline personality disorder. WorldJ Biol Psychiatry. 2003;4:42-44.
81. Adityanjee A, Schulz SC. Clinical use of quetiapinein disease states other than schizophrenia.J Clin Psychiatry. 2002;63(suppl 13):32-38.
82. Villeneuve E, Lemelin S. Open-label study of atypicalneuroleptic quetiapine for treatment of borderlinepersonality disorder: impulsivity as main target.J Clin Psychiatry. 2005;66:1298-1303.
83. Bellino S, Paradiso E, Bogetto F. Efficacy andtolerability of quetiapine in the treatment of borderlinepersonality disorder: a pilot study. J Clin Psychiatry.In press.

 Green B. Lamotrigine in mood disorders. Curr Med  Res Opin. 2003;19:272-277.

Hollander E, Swann AC, Coccaro EF, et al. Impact of    trait impulsivity and state aggression on divalproex    versus placebo response in borderline personality    disorder. Am J Psychiatry. 2005;162:621-624. . 

Articles

This article focuses on data concerning the efficacy of mood stabilizers in the treatment of BPD.

Erika Paradiso, MD

Articles

Mood Stabilizers and Novel Antipsychotics in the Treatment of Borderline Personality Disorder