Authors' reply

We welcome the opportunity to respond to Corrigan & Hull's response to our editorial¹ that presented neurobiological evidence for a trauma-related aetiology of dissociative identity disorder (DID). Corrigan & Hull offer an important additional reason to our proposed DID-dismissive perspectives, namely that DID treatment is considered prohibitively expensive. Not only do they point out costs because of the length of phase-oriented treatment² and its unpredictable non-linear course, they also highlight the costs involved in the training of staff because DID treatment requires specialised skills currently not developed during psychiatrists’ training. They conclude that the evidence for DID should be followed by clinicians and that appropriate treatment will cost less overall than leaving disorders involving pathological dissociation untreated.

An important avenue that might reduce treatment length, and therefore treatment costs, is pharmacological intervention. Corrigan & Hull state that medication is of limited value, but to date no double-blind placebo-controlled studies have been performed with the aim to develop evidence-based pharmacotherapy to alleviate pathological dissociative symptoms in DID. However, it has been proposed that kappa-opioid receptor antagonists may be of interest for the selective pharmacological targeting of debilitating dissociative symptoms in post-traumatic stress disorder and trans-diagnostically.³ Abnormal serotonin neurotransmission in frontal and temporal regions has been found in relation to dissociative amnesia in a positron emission tomography receptor binding study³ and therefore serotonergic medication might also be of interest to treat pathological dissociative symptoms. In addition, the authors would like to offer the consideration of a glutamate hypothesis for dissociation on the basis of scientific evidence that (a) the glutamatergic agent ketamine induces dissociative symptoms in humans⁴ and in animal models,⁵ (b) the psychotropic drug lamotrigine can reduce dissociative symptoms induced by ketamine in healthy individuals,⁶ (c) glutamatergic hyperactivity could be relevant in the neurobiology of depersonalisation and (d) lamotrigine can be an augmenting treatment to reduce dissociative symptoms in depersonalisation disorder,⁶ and (e) anterior cingulate glutamate concentration correlates positively with dissociative symptoms in individuals with borderline personality.³ Glutamate concentrations in the brain of individuals with pathological dissociation can relatively easily be measured using magnetic resonance spectroscopy, which may provide information on whether glutamate is a neurochemical biomarker of dissociation.

Although more has become known about what happens in the dissociated brain and functional neurocorrelates of pathological dissociation^{1, 3} are being unravelled, it remains largely unknown how dissociative symptoms are mediated in the brain at a neurotransmitter level. Neurobiological research into the neurochemical biomarkers of pathological dissociation could possibly lead to the development of pharmacological agents that facilitate more rapid symptom alleviation. Although the development of such pharmacological interventions offers a challenge for the scientific community, they are expected to reduce the treatment costs of individuals with DID.