From love to pain: is oxytocin the key to grief complications?

While most adults confronted with the death of a loved one manage to grieve, about 10-20% of individuals develop complicated grief, characterized by persistent distress and impaired social skills, or pathological grief, defined by the onset or decompensation of a psychiatric disorder. Little is known about the biological causes of these grief complications. Recent work suggests that oxytocin, a major neuroendocrine hormone regulating many neurocognitive mechanisms, may be involved in this process. Oxytocin is widely studied and well known for its impact on the mother-child bond and hormonal and brain systems related to attachment and social interactions. In this article, we propose a neurocognitive model of grief complications based on existing data on the role of oxytocin in interpersonal attachment and its impact on brain activity. We suggest that complicated grief is associated with dysfunctional cerebral oxytocinergic signaling and persistent hyperactivation of the nucleus accumbens. This mechanism is involved in limiting the reduction of interpersonal attachment to the deceased during acute phases and in searching for new interpersonal relationships during the recovery phase. We show how the exploration of cerebral oxytocinergic signaling would improve the understanding of physiological grief mechanisms in the general population and could allow the development of new therapeutic perspectives against the complications of grief.

Improvement of Tardive Dyskinesia during Mindfulness Meditation.

BACKGROUND: We report the case of a patient presenting with orofacial tardive dyskinesia (TD), following administration of a first-generation antipsychotic (Loxapine). INTERVENTION: Four weeks of repeated sessions of mindfulness-based cognitive therapy (MBCT) and mindfulness-based stress reduction (MBSR) protocols were administered, with TD hetero-quantified before and during each session via the Abnormal Involuntary Movement Scale (AIMS). RESULTS: The dyskinesia ameliorated quantitatively and qualitatively (1) during each session, and (2) at resting conditions in the long term. During some sessions, after which patients' compliance was auto-evaluated as maximal, complete arrest of the TD was observed. Hypothesis and Conclusion: We suggest mindfulness meditation as a novel adjunctive therapeutic approach for tardive dyskinesia, and invite for further clinical and neurological investigations.