Therapeutic implication of a psychobiological model of BPD based on NMDA malfunction
| Treatment modality | Specific treatment | Proposed psychological mechanisms | Proposed NMDA dependent cellular mechanisms |
|---|---|---|---|
| Early prevention and intervention | Education, social support and environment enrichment (63), (100) | Provide opportunities for various corrective emotional experiences and promote mentalization processes. Prevent the negative effect of stress, neglect and chaos. | Increase synaptic number; create new circuitries; potential synaptic strengthening. |
| Rational targeted pharmacotherapy | NMDA partial agonist, (125), (126) NMDA full agonist, (127)– (129) Glycine transporter-1 inhibitor (90) | Improve memory, learning and cognition processes. Limit dissociative vulnerability and psychotic symptoms. | Facilitate synaptic plasticity; improve neurogenesis; correct NMDA downregulation. |
| Targeted psychotherapy | Psychotherapy (9), (23), (46) | Potential for new corrective emotional and symbolic experience. Creation of new contextual and emotional associations (explicit and implicit) (66) and improved mentalization. | Increase synaptic number; create new synaptic circuitries; potential synaptic strengthening (explicit and implicit) (66) and improved mentalization. |
BPD = borderline personality disorder; NMDA = N-methyl-d-aspartate.