Research Updates
New DP Research at the IoP, London
01/31/12 00:21
Depersonalization Research Unit - Kings College, London
Testing a neurobiological model of depersonalization with Transcranial Magnetic Stimulation.
Why are we doing this research?
Depersonalization disorder (DPD) is a poorly understood condition characterised by a chronic, distressing and often incapacitating alteration in the perception or experience of the self. The aim of this project is to refine and test our neuropsychological model of DPD which will open up a translational pathway to neurobiologically informed treatments. Our work has established that DPD is characterized by attenuated skin conductance responses (SCR), which are functionally related to reduced activation in brain areas underpinning affective responses, and by increased activation in prefrontal areas involved in emotion regulation.
What are we doing?
We are testing the hypothesis that DPD stems from dysfunctionally increased fronto-insula/limbic inhibitory regulation. We using MRI-guided repetitive transcranial magnetic stimulation (rTMS) in two, contrasting, participant-blind interventions (low and high frequency stimulation) in DPD patients and healthy volunteers. We will measure responses to emotional pictures, both objective – autonomic SCRs, and subjective - self-report arousal ratings, and these will be our co-primary outcomes. We predict that:
1. in DPD patients, low frequency (1 Hz) rTMS induced suppression of prefrontal activity will result in: increased SCRs to arousing pictures (i.e. emotional responses will be released from dysfunctional frontal inhibition) and increased subjective ratings of emotional arousal and reduced symptoms;
2. in healthy volunteers, high frequency (10 Hz) rTMS stimulation will activate the same prefrontal regions which will result in blunted subjective and autonomic responses resembling those of depersonalized patients.
For more information visit this link: Kings College, DP Research Unit, Institute of Psychiatry, London
Testing a neurobiological model of depersonalization with Transcranial Magnetic Stimulation.
Why are we doing this research?
Depersonalization disorder (DPD) is a poorly understood condition characterised by a chronic, distressing and often incapacitating alteration in the perception or experience of the self. The aim of this project is to refine and test our neuropsychological model of DPD which will open up a translational pathway to neurobiologically informed treatments. Our work has established that DPD is characterized by attenuated skin conductance responses (SCR), which are functionally related to reduced activation in brain areas underpinning affective responses, and by increased activation in prefrontal areas involved in emotion regulation.
What are we doing?
We are testing the hypothesis that DPD stems from dysfunctionally increased fronto-insula/limbic inhibitory regulation. We using MRI-guided repetitive transcranial magnetic stimulation (rTMS) in two, contrasting, participant-blind interventions (low and high frequency stimulation) in DPD patients and healthy volunteers. We will measure responses to emotional pictures, both objective – autonomic SCRs, and subjective - self-report arousal ratings, and these will be our co-primary outcomes. We predict that:
1. in DPD patients, low frequency (1 Hz) rTMS induced suppression of prefrontal activity will result in: increased SCRs to arousing pictures (i.e. emotional responses will be released from dysfunctional frontal inhibition) and increased subjective ratings of emotional arousal and reduced symptoms;
2. in healthy volunteers, high frequency (10 Hz) rTMS stimulation will activate the same prefrontal regions which will result in blunted subjective and autonomic responses resembling those of depersonalized patients.
For more information visit this link: Kings College, DP Research Unit, Institute of Psychiatry, London
DP Research Project - Participate!
11/06/11 21:14
Depersonalization, Stress, and Hormones
Research Participants Needed!
The Behavioral Endocrinology Laboratory at Hunter College is looking for volunteers with Depersonalization to participate in a study to better understand how stress affects hormone levels. In this study, participants complete questionnaires about their mood and emotions and complete a stress task. Saliva samples are also taken in order to assess hormone levels. This will be a first study in helping to determining whether persons with depersonalization may benefit from hormone treatments.
This study involves 1 visit for 1.5 hours for a clinical evaluation by Dr. Daphne Simeon and another visit for 2 hours of participation in the stress task and saliva samples. Participants receive up to $50 compensation for participation. No treatment will be provided as part of this study. All responses will remain completely confidential.
For more information or to arrange an appointment please contact Kai Monde at 212-650-3838 or kmonde@hunter.cuny.edu
Research Participants Needed!
The Behavioral Endocrinology Laboratory at Hunter College is looking for volunteers with Depersonalization to participate in a study to better understand how stress affects hormone levels. In this study, participants complete questionnaires about their mood and emotions and complete a stress task. Saliva samples are also taken in order to assess hormone levels. This will be a first study in helping to determining whether persons with depersonalization may benefit from hormone treatments.
This study involves 1 visit for 1.5 hours for a clinical evaluation by Dr. Daphne Simeon and another visit for 2 hours of participation in the stress task and saliva samples. Participants receive up to $50 compensation for participation. No treatment will be provided as part of this study. All responses will remain completely confidential.
For more information or to arrange an appointment please contact Kai Monde at 212-650-3838 or kmonde@hunter.cuny.edu
"Anti-Anxiety Circuit" in the Brain
03/24/11 17:19
In the market for a new, functioning amygdala. Will consider any offer. Price negotiable.
Sandy
Scientists discover anti-anxiety circuit in brain region considered the seat of fear
March 9, 2011
“Stimulation of a distinct brain circuit that lies within a brain structure typically associated with fearfulness produces the opposite effect: Its activity, instead of triggering or increasing anxiety, counters it.
That's the finding in a paper by Stanford University School of Medicine researchers to be published online March 9 in Nature. In the study, Karl Deisseroth, MD, PhD, and his colleagues employed a mouse model to show that stimulating activity exclusively in this circuit enhances animals' willingness to take risks, while inhibiting its activity renders them more risk-averse. This discovery could lead to new treatments for anxiety disorders, said Deisseroth, an associate professor of bioengineering and of psychiatry and behavioral science.”
Read the complete article HERE. We’re not just talking “brain chemistry” but brain circuitry. One more step in understanding the most complex organ in the body.
Sandy
Scientists discover anti-anxiety circuit in brain region considered the seat of fear
March 9, 2011
“Stimulation of a distinct brain circuit that lies within a brain structure typically associated with fearfulness produces the opposite effect: Its activity, instead of triggering or increasing anxiety, counters it.
That's the finding in a paper by Stanford University School of Medicine researchers to be published online March 9 in Nature. In the study, Karl Deisseroth, MD, PhD, and his colleagues employed a mouse model to show that stimulating activity exclusively in this circuit enhances animals' willingness to take risks, while inhibiting its activity renders them more risk-averse. This discovery could lead to new treatments for anxiety disorders, said Deisseroth, an associate professor of bioengineering and of psychiatry and behavioral science.”
Read the complete article HERE. We’re not just talking “brain chemistry” but brain circuitry. One more step in understanding the most complex organ in the body.
New DP Medical Text Available!
10/19/09 22:10
A must-read for every mental health professional as well as every DP sufferer out there.
Comprehensive and eye-opening, this has been a long time coming! Thank you Dr. Sierra!
Read More...
New Meds for DP?
06/23/09 11:29
Link to Abstract and Related Articles
Expert Rev Neurother. 2008 Jan;8(1):19-26.
Depersonalization disorder: pharmacological approaches.
Sierra M.
Depersonalization Research Unit, Institute of Psychiatry, King's College, Section of Neuropsychiatry P068, De Crespigny Park, Denmark Hill, London SE5 8AF, UK. m.sierra-siegert@iop.kcl.ac.uk
ABSTRACT:
Depersonalization disorder (DPD) is a chronic and distressing condition with a prevalence in the general population between 0.8 and 2%. Several neurobiological studies in the last decade have shown that patients have suppressed limbic activation to emotional stimuli.
Such findings are in line with a model which suggests that the condition is generated by an anxiety-triggered, 'hard-wired' inhibitory response to threat. Such a mechanism would ensure the preservation of adaptive behavior, during situations normally associated with overwhelming and potentially disorganizing anxiety. In DPD, such a response would become chronic and dysfunctional.
Depersonalization remains a condition for which no definitive treatment exists, and for which conventional medications, such as antidepressants or antipsychotics, have been found to be of little value.
Fortunately, a few promising lines of pharmacological treatment have emerged in recent years, although more rigorous studies are needed. For example, a number of studies suggest that opioid receptor antagonists such as naltrexone and naloxone are useful in at least a subgroup of patients. In spite of initial expectations, the use of lamotrigine as a sole medication has not been found useful.
However, open-label trials suggest that its use as an add-on treatment with selective serotonin reuptake inhibitors (SSRIs) is beneficial in a substantial number of patients. Similarly, the use of clonazepam, particularly in conjunction with SSRI antidepressants, appears to be beneficial in patients with high levels of background anxiety. In line with the stress-related model of depersonalization, those neurotransmitter systems of relevance to depersonalization are known to play important inhibitory roles in the regulation of the stress response.
PMID: 18088198 [PubMed - indexed for MEDLINE]
Expert Rev Neurother. 2008 Jan;8(1):19-26.
Depersonalization disorder: pharmacological approaches.
Sierra M.
Depersonalization Research Unit, Institute of Psychiatry, King's College, Section of Neuropsychiatry P068, De Crespigny Park, Denmark Hill, London SE5 8AF, UK. m.sierra-siegert@iop.kcl.ac.uk
ABSTRACT:
Depersonalization disorder (DPD) is a chronic and distressing condition with a prevalence in the general population between 0.8 and 2%. Several neurobiological studies in the last decade have shown that patients have suppressed limbic activation to emotional stimuli.
Such findings are in line with a model which suggests that the condition is generated by an anxiety-triggered, 'hard-wired' inhibitory response to threat. Such a mechanism would ensure the preservation of adaptive behavior, during situations normally associated with overwhelming and potentially disorganizing anxiety. In DPD, such a response would become chronic and dysfunctional.
Depersonalization remains a condition for which no definitive treatment exists, and for which conventional medications, such as antidepressants or antipsychotics, have been found to be of little value.
Fortunately, a few promising lines of pharmacological treatment have emerged in recent years, although more rigorous studies are needed. For example, a number of studies suggest that opioid receptor antagonists such as naltrexone and naloxone are useful in at least a subgroup of patients. In spite of initial expectations, the use of lamotrigine as a sole medication has not been found useful.
However, open-label trials suggest that its use as an add-on treatment with selective serotonin reuptake inhibitors (SSRIs) is beneficial in a substantial number of patients. Similarly, the use of clonazepam, particularly in conjunction with SSRI antidepressants, appears to be beneficial in patients with high levels of background anxiety. In line with the stress-related model of depersonalization, those neurotransmitter systems of relevance to depersonalization are known to play important inhibitory roles in the regulation of the stress response.
PMID: 18088198 [PubMed - indexed for MEDLINE]