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To the Editor: Aripiprazole is the first partial-agonist dopaminergic antipsychotic, with activity on dopamine D2/D3 receptors and a low side-effect profile. As defined in the DSM-IV-TR,1 Borderline Personality Disorder (BPD) is a persistent and highly disabling mental disorder that is characterized by patterns of unstable relationships, self-image, and affect; and marked impulsiveness; often complicated by co-occurring Substance Use Disorders (SUD), including abuse of cannabis.

We report the case of a 32-year-old Caucasian woman with a BPD (first diagnosed 8 years ago) and a cannabis abuse disorder (for 10 years; 6–8 cigarettes daily). She suffered from spastic paraparesia caused by a congenital medullar dysplasia, and explained her cannabis abuse as caused by pain related to her medullar disease and anxiety due to her BPD. During her last hospitalization in our psychiatric unit, for depression and suicidal behavior, she wanted to stop the cannabis use, which was increasing and becoming problematic in her daily life.

Therapeutic modification was necessary, but not easy because of her heavy pain treatment, involving a combination of gabapentin 1,200 mg/day, baclofen 30 mg/day, tramadol 37.5 mg/day, paracetamol 975 mg/day, and tetrazepam 50 mg on demand, and her BDP treatment, marked by a combination of oxazepam 100 mg/day, fluoxetine 40 mg/day, valpromide 600 mg/day, and zopiclone 7.5 mg at night. Urine screen for tetrahydrocannabinol was initially positive, and we then measured responsiveness to aripiprazole for abstinence from cannabis by this test and clinic examination. The patient was started on aripiprazole at a dose of 10 mg/day; and valpromide was decreased and stopped after 5 days.

The aim of our treatment was to obtain a significant improvement of affective symptoms, impulsivity, and cannabis dependence, without somatic pain increase. Affective symptoms and impulsivity improved after the first week of hospitalization, and the patient had no more craving for cannabis after 13 days.

A 9-month follow-up of our patient showed that she has wholly stopped cannabis consumption, and presently shows better functional status. She has not consumed alcohol or other drugs since, and has not developed affective or other BPD symptoms. Her impulsivity and affective instability have significantly decreased.

In this case, gabapentin and baclofen have been administered for years. Both are thought to be effective against SUD, through their GABAergic action.2 However, they appeared to be inefficient in this case before the addition of aripiprazole.

The pharmacological action of aripiprazole is as a partial agonist effect on dopamine D2 receptors in the nucleus accumbens (NA). These receptors are also involved in addictive behavior when stimulated by dopamine.3 Moreover, BPD showed greater μ-opioid receptor concentration in NA and endogenous opioid system deactivation in the left NA.4 A recent Cochrane review indicates some beneficial effects with second-generation antipsychotics in the BPD treatment.5

We think that aripiprazole has helped to treat our patient’s addictive and psychiatric symptoms of affective and behavioral dyscontrol marked by impulsivity and craving. New research need to be conducted, and we may expect promising results with aripiprazole, especially on BPD patients with SUD, and this maybe a new treatment for cannabis addiction.

Lille, France
References

1. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. Washington, DC, American Psychiatric Association, 1994Google Scholar

2 Leggio L, Kenna GA, Swift RM: New developments for the pharmacological treatment of alcohol withdrawal syndrome: a focus on non-benzodiazepine GABAergic medications. Prog Neuropsychopharmacol Biol Psychiatry 2008; 32:1106–1117Crossref, MedlineGoogle Scholar

3 Pilla M, Perachon S, Sautel F, et al.: Selective inhibition of cocaine-seeking behaviour by a partial dopamine D3 receptor agonist. Nature 1999; 400:371–375Crossref, MedlineGoogle Scholar

4 Prossin AR, Love TM, Koeppe RA, et al.: Dysregulation of regional endogenous opioid function in borderline personality disorder. Am J Psychiatry 2010; 167:925–933Crossref, MedlineGoogle Scholar

5 Stoffers J, Völlm BA, Rücker G, et al.: Pharmacological interventions for borderline personality disorder. Cochrane Database Syst Rev 2010; CD005653:CD005653Google Scholar