I love this module. The case, video, and discussion questions are so great. Dr. Dwyer does such a great job explaining things in the video. I also love using this module to talk to residents about their countertransference to patients with borderline personality disorder, and that thinking about the biology/neuroscience underlying the BPD sx helps me to manage that countertransference.
I have used it in the clinical setting (inpatient unit) and now in classroom setting. I used it today as part of our psychiatric genetics workshop. We are also using our neuroscience workshops (several per year) to practice writing case formulations. The case in this module worked great for showing residents how to incorporate neuroscience aspects into their formulations – they came up with impulsivity (possible OFC issues), poor response to medications (might consider pharmacogenomic testing), and of course the epigenetic changes discussed in the module’s video.
I love the video in this module. I think the methylation concept is really cool. Amazing how we can track the molecular pathways of how experience affects our brain chemistry! I have used the video to teach residents as well as some sophisticated patients to help understand the science of early adversity.
Good video but this does not explain why in PTSD clinically there is lower cortisol levels. One would think that trauma would leave the HPA axes unchecked as described in this video.
Thanks for your thoughtful comment regarding potential links between the HPA dysregulation described here in models of early life neglect, and the hypocortisolism described in patients with PTSD. Early life neglect can predispose to a variety of conditions, including depression, borderline personality disorder, or PTSD, and there are likely specific neurobiological changes that determine which disorder, if any, develops over time. There are also multiple levels of negative feedback that can be altered. Adult PTSD has been associated with enhanced hypothalamic and pituitary GR sensitivity to negative feedback (assessed by the dexamethasone suppression test), whereas the early life neglect model produces impaired negative feedback at the circuit level (i.e. hippocampal inhibition of the hypothalamus, likely by way of the BNST). Great question!
I love this module. The case, video, and discussion questions are so great. Dr. Dwyer does such a great job explaining things in the video. I also love using this module to talk to residents about their countertransference to patients with borderline personality disorder, and that thinking about the biology/neuroscience underlying the BPD sx helps me to manage that countertransference.
I have used it in the clinical setting (inpatient unit) and now in classroom setting. I used it today as part of our psychiatric genetics workshop. We are also using our neuroscience workshops (several per year) to practice writing case formulations. The case in this module worked great for showing residents how to incorporate neuroscience aspects into their formulations – they came up with impulsivity (possible OFC issues), poor response to medications (might consider pharmacogenomic testing), and of course the epigenetic changes discussed in the module’s video.
I love the video in this module. I think the methylation concept is really cool. Amazing how we can track the molecular pathways of how experience affects our brain chemistry! I have used the video to teach residents as well as some sophisticated patients to help understand the science of early adversity.
Good video but this does not explain why in PTSD clinically there is lower cortisol levels. One would think that trauma would leave the HPA axes unchecked as described in this video.
Thanks for your thoughtful comment regarding potential links between the HPA dysregulation described here in models of early life neglect, and the hypocortisolism described in patients with PTSD. Early life neglect can predispose to a variety of conditions, including depression, borderline personality disorder, or PTSD, and there are likely specific neurobiological changes that determine which disorder, if any, develops over time. There are also multiple levels of negative feedback that can be altered. Adult PTSD has been associated with enhanced hypothalamic and pituitary GR sensitivity to negative feedback (assessed by the dexamethasone suppression test), whereas the early life neglect model produces impaired negative feedback at the circuit level (i.e. hippocampal inhibition of the hypothalamus, likely by way of the BNST). Great question!
This remains one of my favorite lectures! I have had really positive resident feedback. Thank you!