
The overall aims of this research were to firstly use low frequency TMS stimulation to test a neurobiological model of DPD, whereby the VLPFC was the target site of stimulation, the TPJ taking the role as active control site of stimulation, and secondly compare the potential therapeutic utility of these two sites of stimulation for future controlled clinical trials in DPD. In addition there was no offline-testing of behavioral or physiological markers. Unfortunately, none of these studies utilized either sham or active control conditions, so it is not possible to exclude placebo effects. Five out of the six responders showed a 68% reduction in symptoms after a total of six weeks treatment. The TPJ region was chosen due to its relevance in out of body experiences (OBEs), researched previously using TMS.
#DEPERSONALIZATION TEST TRIAL#
Finally, a trial in twelve DPD patients reported that half responded to temporal parietal junction (TPJ) TMS after three weeks of treatment. rTMS was delivered to the left DLPFC, and a 28% reduction in symptoms was reported after 6 sessions. The scan showed hypoperfusion bi-temporally and in the left frontoparietal region. In a second case study, a 24 year-old male with comorbid DPD and MDD who had not responded to pharmacotherapy also received an SPECT scan. It was reported that her self-awareness increased and depersonalization symptoms decreased.

The first was a woman with co-morbid DPD and major depression (MDD) whose single photon emission computed tomography (SPECT) scan showed right frontal hyperactivity, which was the target of 1Hz rTMS. There have been two single case reports, and one trial reporting the usage of TMS in DPD. These studies indicate that rTMS can modulate behavior and motivational states by enhancing or attenuating inhibitory prefrontal mechanisms. High frequency (excitatory) rTMS to the left DLPFC can reduce food craving, cigarette smoking and cocaine craving compared to sham TMS. Other studies found that low frequency (inhibitory) rTMS to the right DLPFC in healthy participants could induce risk-taking behavior on a gambling paradigm and reduce participants' willingness to reject unfair offers on ‘the ultimatum game’. A single session of rTMS to the right DLPFC induced impairments in participants' ability to inhibit negative emotion processing in a facial evaluation task. Of relevance to DPD, rTMS has been used to examine the role of the prefrontal cortex in emotional regulation. Transcranial magnetic stimulation (TMS), a non-invasive brain stimulation technique, is well established both as a research tool and therapeutic intervention in a range of psychiatric disorder. This body of work appears to point to a mechanism for the emotional numbing frequently experienced by DPD suffers and may even relate to a core abnormal experiencing of the sense of self. Finally, preliminary work shows that reduced right VLPFC (and increased insula) activation on fMRI corresponds to symptomatic improvement in DPD patients treated with lamotrigine. Work combining fMRI and SCR has shown a correlation between dorsolateral and ventral prefrontal and ‘limbic’ activation in response to emotional faces in DPD which is consistent with the functional (reciprocal) interaction seen between VLPFC and insula in healthy volunteers, and patients with anxiety states.
#DEPERSONALIZATION TEST SKIN#
Psychophysiological studies using skin conductance response (SCR) measures have found reduced autonomic responses in patients with DPD to unpleasant, emotive stimuli, in comparison to those with anxiety disorders and to healthy controls. This model is consistent with neurological case studies and has been refined by neuroimaging research using fMRI, which has demonstrated reduced insula, limbic and visual association cortical activation in response to emotive pictures, and increased VLPFC activation. Ī neurobiological model of DPD has also been proposed, hypothesizing dysfunctionally increased fronto-insula/limbic inhibitory regulation. A cognitive behavioral model has been developed but has not been subjected to a randomized controlled trial.

A variety of pharmacological treatments have been tried but most fail to show substantial benefits. Secondary forms are also well described in patients with neurological conditions, such as temporal lobe epilepsy and following substance misuse. Depersonalization is frequently a transient phenomenon in states of fatigue or fear and can appear as a symptom of other psychiatric disorders including panic disorder. It often begins in adolescence and has a tendency for chronicity. It is found in many cultures and the condition affects around 1% of the population.

Depersonalization disorder (DPD) is a psychiatric syndrome characterized by persistent and distressing feelings of unreality and alterations in a person's sense of self as defined in DSM-IV-TR.
