Adolescent Nonsuicidal Self-Injury: Evaluation and Treatment

June 1, 2008

In working with adolescents, mental health care professionals often draw on their own developmental experiences to help guide their patients; however, nonsuicidal self-injury (NSSI) is not likely to be a personal experience that psychiatrists can often draw on.

In working with adolescents, mental health care professionals often draw on their own developmental experiences to help guide their patients; however, nonsuicidal self-injury (NSSI) is not likely to be a personal experience that psychiatrists can often draw on. In fact, today's youth face new challenges, including increasing exposure to the practice of self-injury. We can best help adolescents by being aware of this problem, asking directly about self-injury, understanding basic therapeutic approaches, and having knowledge of more specific evidence-based psychotherapeutic and psychopharmacological interventions that can be used to treat NSSI.

In this article, NSSI, which is used interchangeably with self-injury, is defined as deliberate, self-directed tissue injury inflicted without conscious intent to kill oneself.1 In most studies, skin cutting is the most common form, followed by burning and self-hitting or banging; the forearms, wrists, and thighs are common locations of self-injury.2,3 Other forms of self-injury include scratching and interfering with wound healing. Klonsky4 reports that many individuals who engage in NSSI practice more than one method.4 The prevalence of self-injury in adolescents and young adults, including the nonclinical population, may be increasing.4-7 One out of 3 self-injurers reports an onset of self-injurious behavior in childhood, with a peak incidence in mid- to late-adolescence.8 Relatively late development of brain circuits (pruning and myelination) involved with emotion, judgment, and inhibitory control may explain the heightened propensity of adolescents to act impulsively and ignore the negative consequences of their behavior.9 Studies have found that approximately 15% of high school adolescents and 17% of college students engage in self-injury, with estimates as high as 40% to 60% for adolescent inpatients.5,6,10 In one study, researchers found that 1 out of 5 students attending an Ivy League school endorsed these maladaptive behaviors, and 1 in 10 respondents were repeat self-injurers.5

Risk factors

Other psychiatric conditions often predispose patients to self-injurious behavior. Borderline personality disorder (BPD) and other personality disorders, anxiety, eating disorders, and substance abuse are all risk fac-tors for NSSI.11-14 Additional risk factors include adolescence to college age, maltreatment, and family turmoil.5,12-14 A recent study noted that identification with Goth subculture is also a risk factor.15 Although most studies report females as being more likely to engage in NSSI, a number of studies have found no significant differences between females and males.2-6 There are several potential reasons for this disconnect. First, a majority of the earlier studies were completed with patients who had BPD, a disorder that is more common in females. Second, self-hitting and banging, which may not have been included in analyses of NSSI, may be more common among males; females are more likely to cut themselves. Third, a significant increase in male NSSI may have made a strong contribution to the overall increasing prevalence of NSSI in adolescents and young adults.5,6

Possible reasons for increased prevalence

An increase in some risk factors (eg, child abuse, substance abuse, family turmoil, anxiety) may explain the possible increase in incidence of NSSI in the adolescent population. Likewise, the phenomenon of contagion may be affecting rates of NSSI. "Behavioral contagion" is an increased tendency to engage in a behavior when socially related people also engage in that behavior.16 Contemporary routes for transmission include direct contact with self-injurers (often friends or family), direct or indirect exposure over the Internet, exposure via the media, and role modeling through the cult of celebrity, including adolescent antiheros.17,18In addition to risk factors and modes of transmission, there are variables that motivate and reinforce the behavior of each individual. Nock and Prinstein1 hypothesized that NSSI may be automatically reinforced (eg, emotion regulation) or socially reinforced (eg, avoidance/escape, attention/communication of distress). The primary function of most NSSI appears to be reinforced by the individual, involving an affect-regulation function (reduction of negative affect).4 There is also strong support for a self-punishment function.4 Additional functions with more modest evidence include antidissociation, interpersonal influence, antisuicide, sensation seeking, and interpersonal boundaries functions.4


What should you do when there is a new adolescent patient seated in your office? Ask directly about self-injury, "Have you ever cut or done other damage to your skin on purpose?"5 In my experience, most adolescents will be forthcoming about a number of risky behaviors, including NSSI, when directly questioned without their parents present. If the adolescent seems particularly guarded under direct questioning, you may consider having the patient fill out a written self-report scale on NSSI.19-21 You should also assess the general appearance of the adolescent, noting any obvious scarring on visible skin and unusual dress, such as a Goth look or wearing long-sleeve shirts in hot weather.

After NSSI is disclosed, or if the adolescent was specifically referred for this issue, it is important to proceed with the interview and approach the patient in a nonjudgmental manner. Families (and sometimes clinicians) may overreact when they learn of self-injury. In many cases, NSSI may be a form of brief experimentation causing superficial tissue injury as part of the separation-individuation process; rarely does the self-mutilation involve suicidal intent.4,22 I would be reluctant to recommend psychiatric hospitalization with NSSI as the chief concern in the absence of other signs or symptoms of severe disturbance. However, even though NSSI usually does not constitute an acute emergency involving imminent danger, it does increase overall suicide risk, and clinicians should react accordingly.23,24 Following disclosure of NSSI, the clinician should attempt to ascertain why the patient is engaging in such behaviors and the function(s) of NSSI (Table 1). Because NSSI is nonspecific, like a fever, it is necessary to understand the motivation behind the behavior to develop a treatment plan. Similarly, it is important to inquire about the emotions that precede and follow the NSSI.

Also, it may be helpful to ask, "How did you learn to hurt yourself?" This examines both the functions of NSSI and the possibility of contagion. Contact with peers who also engage in NSSI may positively reinforce this maladaptive behavior. Knowledge of active behavioral contagion suggests the need for changes in the adolescent's social environment, which may include limiting unsupervised access to certain friends or the Internet. While the clinician will likely view NSSI as a serious issue, the adolescent may not see it as a problem. It is extremely important to ask, "Do you think this is a problem?" Discovering where the adolescent is on the Stages of Change (Transtheoretical) model will inform the therapeutic approach that will most likely be successful.25 The Stages of Change model is a general approach to helping patients change behavior.25 It recognizes that changes in behavior may involve a patient moving gradually from being uninterested in change (precontemplation) to considering change (con-templation) to deciding and preparing to make a change.25 Other helpful questions for the interview are included in Table 1.

General therapeutic approaches

Information gathered about the self-injurious behavior, especially core psychological problems and triggers, can be used to develop interventions. Asking questions using the Stages of Change model as a framework may allow a patient to begin thinking about change as well as the benefits and barriers to change (Table 1). In addition, it is useful to help patients identify alternative ways to reach goals associated with this behavior, such as feeling strong, connected, in control, and independent.26 Clarifying questions may be very powerful, such as, "Who is in control of your life-the cutting or you?" It is also wise to highlight the other aspects of NSSI that may be distasteful to the patient, including scarring, secrecy, shame, wound infections, doctor visits, stigma, the potential for addiction to the behavior, and accidental death.

In my experience, the majority of NSSI cases improve following disclosure and supportive therapeutic techniques. NSSI also may be reduced through the treatment of comorbid mental health conditions. Therapeutic approaches involving cognitive restructuring, behavioral modifications, motivational interviewing, assertiveness training, and teaching alternative coping mechanisms are the common practice. Several comprehensive guidebooks discussing self-injury and its treatment are available. Walsh27 and Conterio and Lader28 describe contingency management, including treatment participation agreements and replacement skills; cognitive-behavioral assessment of self-injury, using the terms "Self-Injury Log" and "Impulse Control Log," respectively; and ways to address common cognitive distortions for self-injurers.

Treatment participation agreements involve the terms, structure, goals, and rewards of the recovery plans. Replacement skills cover alternative coping strategies to soothe or manage anxiety and tension, or at the very least temporarily deflect attention from self-injury; such activities include writing in a journal, mindful breathing, muscle relaxation, exercise, communicating with others, listening to music, and visualizing pleasant scenes.27,28 Logs chart the antecedents, the behavior itself, and the consequences of self-injury (or not self-injuring) in an attempt to eventually make the connection between thoughts, feelings, and behaviors.27,28 Often the logs later incorporate replacement skills; in which case, it may be known as a "Brief Skills Practice Log."27,28

The use of negative replacement skills, such as snapping a rubber band against the wrist or writing on the arm with a red marker (which may symbolically resemble self-injury without causing tissue damage), is controversial.27,28 Understanding the Stages of Change model and how to assess for motivation to change is important given Conterio and Lader's requirement for their program that "in the initial screening the patient must demonstrate a heartfelt and internal motivation to stop injuring."28If self-injury continues despite attempts with the interventions already described, or if the self-injurious behavior is severe, then pharmacotherapy and/or other more specific and intensive psychotherapeutic interventions should be considered.

Psychotherapy for self-injury

Dialectical behavioral therapy (DBT) is perhaps the best-studied psycho-therapeutic intervention for NSSI. Although a thorough explanation of DBT is beyond the scope of this article, it is a variation of cognitive-behavioral therapy (CBT) that also includes mindfulness training. Through individual and group skills training, patients learn emotional regulation, how to cope with negative affect, and problem-solving techniques. DBT has demonstrated direct and sustained effects for individuals with BPD and self-injury in at least 7 well-controlled trials with different patient populations, including adolescent inpatients.29-31 In these studies, researchers found decreases in the percentage of patients with self-inflicted injuries, number of self-inflicted injuries, and medical risk of injuries.

However, traditional DBT may not be unique in its ability to treat NSSI. In randomized controlled trials, a program that uses CBT techniques called "manual-assisted cognitive treatment" demonstrated efficacy for reducing both the severity and frequency of deliberate self-injury in patients with BPD.32There is also some evidence for therapeutic interventions that do not rely on the principles of CBT. In a recent long-term trial comparing DBT with nonbehavioral community treatment, NSSI was reduced equally by both protocols.30 A psychoanalytically oriented partial hospital program also showed reductions in self-injury.33

Pharmacotherapy for self-injury

There is evidence, albeit limited, for pharmacotherapy. It should be noted that there are no medications currently labeled for the treatment of self-injury or BPD. Medications are used to target the neurotransmitter systems most likely to contribute to self-injury. Opioid, serotonin, and dopamine receptors are commonly implicated.

The opioid system is implicated because of higher pain thresholds and stress-induced analgesia in BPD, likely mediated by increased activity of the dorsal prefrontal cortex with deactivation of the anterior cingulate and amygdala.34 NSSI may also involve addictive qualities, including postcessation withdrawal dysphoria.14 Open-label studies of the opioid antagonist naltrexone have shown reduced self-injury.35,36

Decreased serotonin levels have been linked to impulsive, aggressive, and suicidal behaviors.37 Self-injury is usually an impulsive act, with half of cutters thinking of the behavior less than an hour before committing the act.22 Fluoxetine is the serotonergic medication with the most evidence for use in NSSI, with at least 2 controlled trials showing reductions in impulsive aggression.38,39 In an open-label trial, venlafaxine was also beneficial.40Self-injury may also present in syndromes that involve the dopamine system, such as Lesch-Nyhan syndrome and Tourette syndrome.41 Self-biting behaviors may be elicited by stimulants that primarily work through a dopaminergic mechanism of action. The use of dopamine antagonists has been studied for NSSI. Although there is some evidence for the efficacy of all of the atypical antipsychotics for reducing aggression and/or impulsivity, olanzapine has had the best results in the most rigorous trial designs.39,42-46

There is a paucity of literature regarding combination therapy. Surprisingly, adding fluoxetine to DBT was not found to give any additional benefit.47 A trial of olanzapine plus DBT reduced the frequency of impulsivity/aggressive behavior more than placebo plus DBT, although self-injurious behavior did not decrease significantly.48In addition to serotonergic, dopaminergic, and opioid medications there are other drug categories being studied for NSSI. There are promising case reports for glutamate-decreasing agents, including riluzole, N-acetylcysteine, and topiramate.49 Similarly, the glutamate-modulating agent lamotrigine was found to decrease behavioral dyscontrol, impulsivity, and anger in open-label trials, retrospective trials, and controlled trials.50-52 There have been controlled studies of lithium, divalproex, carbamazepine, and omega-3 fatty acids, which have all demonstrated decreases in impulsive aggression, but not NSSI specifically, in individuals with BPD.53-56 There was also an open-label study of oxcarbazepine that demonstrated statistically significant decreases in impulsivity, affective instability, and outbursts of anger in small sample populations with BPD.57 Clonidine, an a2-agonist, decreased the urge to commit self-injurious behavior in an open study.58


NSSI is common and its prevalence may be increasing in adolescents. There are a number of known risk factors for NSSI, and NSSI may be a risk factor for later suicide attempts and completion. NSSI has a number of psychological functions and may be contagious and/or addictive. DBT, when available, can be considered the standard treatment for cases of NSSI that do not respond to initial interventions.

Medications should be considered the second line of treatment in most instances. The serotonin, opioid, and dopamine systems have been implicated, so medications that target these systems have potential benefit. Before pharmacological treatment is initiated for NSSI, preexisting medications for other mental health concerns should be optimized. In the absence of an existing psychotropic regimen or clear indications for pharmacotherapy of comorbid mental health conditions, fluoxetine, currently the best-studied antidepressant for NSSI, is a good first option. If fluoxetine is poorly tolerated or of insufficient benefit, consider switching to olanzapine, which appears to be the most effective atypical antipsychotic for NSSI.

The suggestion of first initiating a trial of an SSRI, as opposed to an atypical antipsychotic, has more to do with side-effect profile than potential efficacy. In fact, a recent meta-analysis of randomized controlled trials of pharmacotherapy against core traits of BPD found that antidepressants and mood stabilizers did not produce significant benefits against impulsivity and aggression or suicidality (although they were effective against affective instability and anger).59 On the other hand, antipsychotics, as a class, had a positive effect in reducing impulsivity and aggression. For severe and/or refractory cases, consider other SSRIs, serotonin-norepinephrine reuptake inhibitors, other atypical antipsychotics, naltrexone, clonidine, mood stabilizers, or glutamate-modulating agents (Table 2).

Given our growing awareness of the magnitude of the NSSI problem and the limited evidence base for its treatment, there are many future directions for research. Studies that specifically target the symptom of self-injury, especially in individuals without BPD, are sorely needed. We must also construct new studies that overcome limitations of past studies including small sample sizes, with a predominance of female, white, and adult participants, lack of controls, over reliance on self-report, low dosing of medications, and short trial durations. There needs to be further investigation of new generation antidepressants, naltrexone, clonidine, omega-3 fatty acids, atypical antipsychotics, mood stabilizers, glutamate-modulating agents, and polypharmacy to target NSSI. Finally, there must be further investigation of the potential efficacy of combined medication and psychotherapy, especially DBT.



1. Simeon D, Stanley B, Frances A, et al. Self-mutilation in personality disorders: psychological and biological correlates. Am J Psychiatry. 1992;149:221-226.

2. Favazza AR, Conterio K. Female habitual self-mutilators. Acta Psychiatr Scand. 1989;79: 283-289.

3. Briere J, Gil E. Self-mutilation in clinical and general population samples: prevalence, correlates, and functions. Am J Orthopsychiatry. 1998;68: 609-620.

4. Klonsky ED. The functions of deliberate self-injury: A review of the evidence. Clin Psychol Rev. 2007; 27:226-239.

5. Whitlock J, Eckenrode J, Silverman D. Self-injurious behaviors in a college population. Pediatrics. 2006;117:1939-1948.

6. Muehlenkamp JJ, Gutierrez PM. An investigation of differences between self-injurious behavior and suicide attempts in a sample of adolescents. Suicide Life Threat Behav. 2004;34:12-23.

7. Hawton K, Fagg J, Simkin S, et al. Trends in deliberate self-harm in Oxford, 1985-1995. Implications for clinical services and the prevention of suicide. Br J Psychiatry. 1997;171:556-560.

8. Zanarini MC, Frankenburg FR, Ridolfi ME, et al. Reported childhood onset of self-mutilation among borderline patients. J Personal Disord. 2006;20:9-15.

9. Volkow ND. What do we know about drug addiction? Am J Psychiatry. 2005;162:1401-1402.

10. Nock MK, Prinstein MJ. Contextual features and behavioral functions of self-mutilation among adolescents. J Abnorm Psychol. 2005;114:140-146.

11. Zanarini MC, Gunderson JG, Frankenburg FR, Chauncey DL. Discriminating borderline personality from other axis II disorders. Am J Psychiatry. 1990; 147:161-167.

12. Guertin T, Lloyd-Richardson E, Spirito A, et al. Self-mutilative behavior in adolescents who attempt suicide by overdose. J Am Acad Child Adolesc Psychiatry. 2001;40:1062-1069.

13. Sansone RA, Levitt JL. Self-harm behaviors among those with eating disorders: an overview. Eating Disord. 2002;10:205-213.

14. Favazza AR. Self-injurious behavior in college students. Pediatrics. 2006;117:2283-2284.

15. Young R, Sweeting H, West P. Prevalence of deliberate self harm and attempted suicide within contemporary Goth youth subculture: longitudinal cohort study. BMJ. 2006;332:1058-1061.

16. Jones MB, Jones DR. Testing for behavioral contagion in a case-control design. J Psychiatr Res. 1994;28:35-55.

17. Taiminen TJ, Kallio-Soukaninen K, Nokso- Koivisto H, et al. Contagion of deliberate self-harm among adolescent inpatients. J Am Acad Child Adolesc Psychiatry. 1998;37:211-217.

18. Whitlock JL, Powers JL, Eckenrode J. The virtual cutting edge: the internet and adolescent self-injury. Dev Psychol. 2006;42:407-417.

19. Nock MK, Prinstein M. A functional approach to the assessment of self-mutilative behavior. J Consult Clin Psychol. 2004;72:885-890.

20. Gutierrez P, Osman A, Barrios F, Kopper B. Development and initial validation of the Self-harm Behavior Questionnaire. J Pers Assess. 2001;77:475-490.

21. Sansone R, Wiederman M, Sansone L. The Self-Harm Inventory (SHI): development of a scale for identifying self-destructive behaviors and borderline personality disorder. J Clin Psychol. 1998;54:973-983.

22. Rodham K, Hawton K, Evans E. Reasons for deliberate self-harm: comparison of self-poisoners and self-cutters in a community sample of adolescents. J Am Acad Child Adolesc Psychiatry. 2004;43:80-87.

23. Cooper J, Kapur N, Webb R, et al. Suicide after deliberate self-harm: a 4-year cohort study. Am J Psychiatry. 2005;162:297-303.

24. Nock MK, Joiner TE Jr, Gordon KH, et al. Nonsuicidal self-injury among adolescents: Diagnostic correlates and relation to suicide attempts. Psychiatry Res. 2006;144:65-72.

25. Zimmerman GL, Olsen CG, Bosworth MF. A "stages of change" approach to helping patients change behavior. Am Fam Physician. 2000;61:1409-1416.

26. Suyemoto KL, MacDonald ML. Self-cutting in female adolescents. Psychotherapy. 1995;32:162-171.

27. Walsh BW. Treating Self-Injury. New York: Guilford Press; 2006.

28. Conterio K, Lader W. Bodily Harm. New York: Hyperion Press; 1998.

29. van den Bosch LM, Koeter MW, Stijnen T, et al. Sustained efficacy of dialectical behaviour therapy for borderline personality disorder. Behav Res Ther. 2005;43:1231-1241.

30. Linehan MM, Comtois KA, Murray AM, et al. Two-year randomized controlled trial and follow-up of dialectical behavior therapy vs therapy by experts for suicidal behaviors and borderline personality disorder. Arch Gen Psychiatry. 2006;63:757-766.

31. Lieb K, Zanarini MC, Schmahl C, et al. Borderline personality disorder. Lancet. 2004;364:453-461.

32. Weinberg I, Gunderson JG, Hennen J, Cutter CJ Jr. Manual assisted cognitive treatment for deliberate self-harm in borderline personality disorder patients. J Personal Disord. 2006;20:482-492.

33. Bateman A, Fonagy P. Treatment of borderline personality disorder with psychoanalytically oriented partial hospitalization: an 18-month follow-up. Am J Psychiatry. 2001;158:36-42.

34. Schmahl C, Bohus M, Esposito F, et al. Neural correlates of antinociception in borderline personality disorder. Arch Gen Psych. 2006;63:659-667.

35. Roth AS, Ostroff RB, Hoffman RE. Naltrexone as a treatment for repetitive self-injurious behavior: an open-label trial. J Clin Psychiatry. 1996;57:233-237.

36. Sonne S, Rubey R, Brady K, et al. Naltrexone treatment of self-injurious thoughts and behaviors. J Nerv Ment Dis. 1996;184:192-194.

37. Coccaro EF, Siever LJ, Klar HM, et al. Serotonergic studies in patients with affective and personality disorders. Correlates with suicidal and impulsive aggressive behavior. Arch Gen Psychiatry. 1989;46:587-599.

38. Rinne T, van den Brink W, Wouters L, van Dyck R. SSRI treatment of borderline personality disorder: a randomized, placebo-controlled clinical trial for female patients with borderline personality disorder. Am J Psychiatry. 2002;159:2048-2054.

39. Zanarini MC, Frankenburg FR, Parachini EA. A preliminary, randomized trial of fluoxetine, olanzapine, and the olanzapine-fluoxetine combination in women with borderline personality disorder. J Clin Psychiatry. 2004;65:903-907.

40. Markovitz PJ, Wagner SC. Venlafaxine in the treatment of borderline personality disorder. Psychopharmacol Bull. 1995;31:773-777.

41. Winchel RM, Stanley M. Self-injurious behavior: a review of the behavior and biology of self-mutilation. Am J Psychiatry. 1991;148:306-317.

42. Bogenschutz MP, Nurnberg HG. Olanzapine versus placebo in the treatment of borderline personality disorder. J Clin Psychiatry. 2004;65:104-109.

43. Zanarini MC, Frankenburg FR. Olanzapine treatment of female borderline personality disorder patients: a double-blind, placebo-controlled pilot study. J Clin Psychiatry. 2001;62:849-854.

44. Bellino S, Paradiso E, Bogetto F. Efficacy and tolerability of quetiapine in the treatment of borderline personality disorder: a pilot study. J Clin Psychiatry. 2006;67:1042-1046.

45. Pascual JC, Oller S, Soler J, et al. Ziprasidone in the acute treatment of borderline personality disorder in psychiatric emergency services. J Clin Psychiatry. 2004;65:1281-1283.

46. Nickel MK, Muehlbacher M, Nickel C, et al. Aripiprazole in the treatment of patients with borderline personality disorder: a double-blind, placebo-controlled study. Am J Psychiatry. 2006;163:833-838.

47. Simpson EB, Yen S, Costello E, et al. Combined dialectical behavior therapy and fluoxetine in the treatment of borderline personality disorder. J Clin Psychiatry. 2004;65:379-385.

48. Soler J, Pascual JC, Campins J, et al. Double-blind, placebo-controlled study of dialectical behavior therapy plus olanzapine for borderline personality disorder. Am J Psychiatry. 2005;162:1221-1224.

49. Pittenger C, Krystal JH, Coric V. Initial evidence of the beneficial effects of glutamate-modulating agents in the treatment of self-injurious behavior associated with borderline personality disorder. J Clin Psychiatry. 2005;66:1492-1493.

50. Pinto OC, Akiskal HS. Lamotrigine as a promising approach to borderline personality: an open case series without concurrent DSM-IV major mood disorder. J Affect Disord. 1998;51:333-343.

51. Tritt K, Nickel C, Lahmann C, et al. Lamotrigine treatment of aggression in female borderline-patients: a randomized, double-blind, placebo-controlled study. J Psychopharmacol. 2005;19:287-291.

52. Preston GA, Marchant BK, Reimherr FW, et al. Borderline personality disorder in patients with bipolar disorder and response to lamotrigine. J Affect Disord. 2004;79:297-303.

53. Links PS, Steiner M, Boiago I, et al. Lithium therapy for borderline patients: preliminary findings. J Clin Psychopharmacol. 1990;4:173-181.

54. Hollander E, Tracy KA, Swann AC, et al. Divalproex in the treatment of impulsive aggression: efficacy in cluster B personality disorders. Neuropsychopharmacology. 2003;28:1186-1197.

55. Gardner DL, Cowdry RW. Positive effects of carbamazepine on behavioral dyscontrol in borderline personality disorder. Am J Psychiatry. 1986;143:519-522.

56. Zanarini MC, Frankenburg FR. Omega-3 fatty acid treatment of women with borderline personality disorder: a double-blind, placebo-controlled pilot study. Am J Psychiatry. 2003;160:167-169.

57. Bellino S, Paradiso E, Bogetto F. Oxcarbazepine in the treatment of borderline personality disorder: a pilot study. J Clin Psychiatry. 2005;66:1111-1115.

58. Philipsen A, Richter H, Schmahl C, et al. Clonidine in acute aversive inner tension and self-injurious behavior in female patients with borderline personality disorder. J Clin Psychiatry. 2004;65:1414-1419.

59. Nose M, Cipriani A, Biancosino B, et al. Efficacy of pharmacotherapy against core traits of borderline personality disorder: meta-analysis of randomized controlled trials. Int Clin Psychopharmacol. 2006;21: 345-353.