How Stress And Trauma Impact The Brain ▶ Trauma And The Brain - Neurobiology of PTSD 2020

Dr Sanil Rege takes you through the impact of trauma and stress on the brain.
This video presents how stress and trauma impacts the brain but also covers the following subjects:
-Trauma and the brain - neurobiology of PTSD
-Trauma and the nervous system
One thing I observed when I was looking for info on how stress and trauma impacts the brain was the lack of pertinent information.
Hope this is relevant and of interest to you.
The hypothalamic-pituitary-adrenal (HPA) axis in the brain is the central coordinator of how humans respond to stress and trauma. The stress response starts in the hypothalamus where paraventricular neurons (PVN) secrete corticotropin-releasing hormone (CRH).
This hormone stimulates the release of adrenocorticotropin hormone (ACTH) from the anterior pituitary, which in turn stimulates the release of glucocorticoids (e.g. cortisol) from the adrenal cortex.
Cortisol exerts negative feedback control of the HPA. Cortisol also reduces the noradrenergic stress response.
In Post-traumatic stress disorder (PTSD), there exists a dysregulation of glucocorticoid signalling underpinned by heightened negative feedback sensitivity of the HPA. This results in low cortisol levels and blunted ACTH responses to CRH due to elevated levels of CRH resulting in down-regulation of CRH receptors on the anterior pituitary.
Two genes that are thought to be involved are NR3C1 (encoding the glucocorticoid (GC) receptor) and FKBP5 (role in immunoregulation and regulating the amount of GC available to the GC receptor)
The dynamic interaction between the medial prefrontal cortex and the amygdala creates two distinct phenotypes in PTSD patients.
In many patients, a phase-oriented therapy is more appropriate focusing on reducing hyperarousal in the short term allowing them to engage in trauma-related psychotherapies after emotional dysregulation and hyperarousal are addressed.--------------
If you want to discover more regarding trauma and the brain neurobiology of PTSD or other topics on psychiatry please have a look at our various other videos: / @psychiatrysimplified
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Please like the KZbin vid to assist your friends looking for trauma and the brain neurobiology of PTSD or trauma and the nervous system :)
Read more: psychscenehub.com/psychinsigh...
To learn more about how stress and trauma impact the brain visit: 👉 psychscenehub.com

[@sovereignsoulutions6612]

This is THE BEST video on explaining PTSD and HPA dysregulation. 🙏🏼

[@PsychiatrySimplified]

Thank you for your feedback. 🙏🏼

[@randdee6042]

EXCEPTIONAL TEACHING VIDEO!!!!!! Thank You!

[@PsychiatrySimplified]

Thanks for your feedback 🙏🏻

[@philholding6905]

At last, a good neurological explanation for PTSD. As a recently retired NHS high intensity EMDR/CBT therapist, this appears to converge with my research studies. Not so keen on the background music though, appears a bit incongruent. Would be nice to see a future clip on trauma related dissociation. This clip has passed my strict recording criteria.

[@PsychiatrySimplified]

Phil Holding thanks for the feedback. Was wanting to fill in the white noise through some soft music. Appreciate the comments. We’ve covered the neurobiology in more detail here psychscenehub.com/psychinsights/post-traumatic-stress-disorder/

[@a.b.2850]

Excellent. Exactly the information I was looking for. Thank you.

[@AgentKodak]

Great job with the video Doc! I really appreciate it. I’m trying to understand this condition more and more by the day and although it’s hard it’s good to know that somebody’s out there studying it and educating other veterans

[@monicacabrera9215]

omg. this is so helpful!! the involvement of hpa axis in ptsd was clearly explained. thank you so much!! i needed this for my reporting huhu

[@PsychiatrySimplified]

Thank you for the feedback. Glad you found it useful.

[@godwatching1515]

It will drive you crazy..seek help ASAP if you going through it

[@NearlyNomads]

Thank you, this is exactly what a nerd like me needed today. I would love to see your explanation of the impact of norepinephrine being released into the system and what happens if it is at elevated levels over a long timeframe.

[@PsychiatrySimplified]

Sure will do one. Very good question. Elevated noradrenaline on one hand as explains prevents the fear extinction response due to amygdala hyper activation ( which has very high levels of NA neurons) . 2. It has systemic effects - Beta receptors in periphery - palpitations, increases heart rate and hence ANS responses. Longer term can add ‘pressure on the heart. 3. Alpha receptors periphery - increased peripheral vascular resistance - increase in BP - again can lead to cardiac issues if not Rx. 4. Excess NA in PFC - moves prefrontal cortex decision making from flexible to more rigid, difficulty coping with stressors etc. Hope this helps.

[@Frisson391]

Theres also something about one of these meds causing an unexpected hypertension if started in the wrong order such as guanfacine/clonidine or prazosin. Can never keep it quite straight. (Think its guanfacine) but not sure!

[@themysticmuse1111]

Excellent video,sir.

[@alicerose9140]

Thank you! Such a good, concise explanation of why this condition is so hard to get over.

[@PsychiatrySimplified]

Thank you for the feedback. We have covered psychological therapies in more detail that are evidence based in this article - mainly focusing on complex trauma. psychscenehub.com/psychinsights/complex-post-traumatic-stress-disorder-cptsd-impact-of-childhood-trauma-assessment-and-management-principles-2/

[@alicerose9140]

@@PsychiatrySimplified Thank you for this link. Yes, I've read the full article now, it's very comprehensive. I also enjoyed your interview with David Nutt on use of psychadelics. You are a breath of fresh air.

[@PsychiatrySimplified]

@@alicerose9140 thank you 🙏

[@SabiLewSounds]

Thank you for this

[@simply.mimi0]

This video is amazing, thank you so much!

[@PsychiatrySimplified]

Thanks for your feedback 🙏

[@1voiceinthecrowd]

Ty. This is such a clear explanation

[@PsychiatrySimplified]

Thank you for the feedback 🙏🏻

[@ananigalindo7092]

amazing video! so informative :) thank you!

[@PsychiatrySimplified]

Thank you for your feedback.

[@horatiogrant8018]

Hello Dr Rege, I have tried to find this but cannot. Sure hope you can resolve: HDAC inhibition of Valproic acid to reverse epigenetic change from childhood trauma. Could you advise if those reversals hold or does one have to keep taking valproate indefinitely? Thank you kind Sir

[@MaxWaldron]

Well presented !

[@PsychiatrySimplified]

Thank you for the feedback. We appreciate it

[@MaxWaldron]

@@PsychiatrySimplified I can tell you love your subject. So do I. A noteworthy channel indeed.

[@drkhan5401]

Thanks a lot sir for this great explanation. Keep up the good work and try to cover all common psychiatric disorders and their treatments. Which book would you recommend sir for common psychiatric disorders and their treatment, that would be easily understood and retained. Thanks

[@PsychiatrySimplified]

Thank you for your feedback. There are many textbooks available but you might find this digital textbook useful - this has all the various disorders arranged in sections with links so you can visit the respective disorders psychscenehub.com/psychpedia/psychiatry-digital-textbook-free-download-article-and-video-catalogue/

[@drkhan5401]

@@PsychiatrySimplified thank you so much sir. Much needed ❤️

[@victorrodionoff9184]

Thank you for the excellent video. One quick point of clarification. Around minute 6, you introduce alpha-2 agonists including clonidine and prazosin. My understanding is that the latter agent is an alpha-1 agonist/inverse agonist. Is that true? Thanks!

[@PsychiatrySimplified]

You are correct. Prazosin is an alpha 1 antagonist at post synaptic receptors. We covered alpha 1 and 2 receptors and clonidine and prazosin in more detail here kzbin.info/www/bejne/iprSfmyErtKNjsU

[@CreatingYourPurpose]

This is great information! Can you explain to me why there is typically reduced brain volume in patients with PTSD? I have tried to find this info; however, I cannot seem to get a clear explanation. I am doing some research for an assignment for grad school. Any info you have on this would be great...even if you can point me to an article that discusses this, I would really appreciate it!

[@PsychiatrySimplified]

Sure - it is linked to cortisol and impaired neurogenesis. You will find information in these articles I've written - 1. PTSD neurobiology psychscenehub.com/psychinsights/post-traumatic-stress-disorder/ 2. Neuroplasticity - psychscenehub.com/psychinsights/what-is-neuroplasticity-a-simplified-guide/ 3. Neurobiology of depression (in HPA axis section you will also find - Stress - which links to PTSD) psychscenehub.com/psychinsights/neurobiology-of-depression-3/ 4. You can further read about inflammation and depression if additional points are required. Good luck with your assignment.

[@CreatingYourPurpose]

@@PsychiatrySimplified oh thank you so much!!! I appreciate you. 😄

[@janechu]

To reduce noradrenaline, is it common that guanfacine is also used? Theoretically, if a person is on an alpha 2 agonist and never resolves their trauma/anxiety through other therapeutic means, would the body/brain build a tolerance to the alpha 2 agonist? Wondering if it’s considered as a long term solution.

[@PsychiatrySimplified]

Here is a video on guanfacine clonidine. Latter part it's not tolerance ; depending on nature and severity of the trauma psychological therapies can be added. kzbin.info/www/bejne/iprSfmyErtKNjsU

[@Frisson391]

Feedback loop cortisol does not shut off CRH RELEASE FROM THE HYPOTHALAMUS. CRH CONTINUES TO BE RELEASED FROM HYPOTHALAMUS BUT …Pituitary does not respond to CRH “the pituitary is sensitized”. Did you mean desensitized? ALSO WHAT RECEPTOR CHANGES ARE HAPPENING at the pituitary that cause it to not respond to continued CRH release from the hypothalamus?

[@PsychiatrySimplified]

Yes they are desensitised. Essentially the receptors do not get stimulated to the signals generated from the hypothalamus.

[@bpggg]

Is there a similar process that happens in Bipolar Disorder (or Major Depression for that matter) ? I thought cortisol in excess amounts induces hippocampal atrophy. Does this also happen in PTSD (hippocampal atrophy) or in PTSD have an opposite effect (hippocampal neurogenesis)? I know people can have residual cognitive issues even after considered to be in remission in mood disorders. Can people with PTSD have traumatic memories that are strong and yet have general impairment in encoding new memories?

[@PsychiatrySimplified]

Yes absolutely. PTSD can have cognitive deficits in various dosing while having vivid memories of trauma. Overlap b/w bpad and ptsd as well.

[@jamescullen-657]

Hi Sanil, Is there a link between pots and PTSD? Can PTSD potentially bring about symptoms that can be seen in postural orthostatic tachycardia syndrome?

[@PsychiatrySimplified]

Yes there is a link. Covered in more detail in the POTS video on the channel

[@jamescullen-657]

@@PsychiatrySimplified thank you doctor !

[@jocs8824]

I had an overnight metyrapone (blocks the enzyme just before cortisol of adrenal hormones) test done to check if the hpa axis was intact as I have low but within range morning blood, saliva midnight and saliva and urine all day cortisol despite feeling stressed most of the time. The result of the test was that the pituitary definitely responds as the precursor to cortisol shot right up and stayed up well into the next morning. Does that rule out PTSD then? I also have very limited memories of my traumas from childhood and since then even as my memory is generally low overall. I have had trouble tolerating ssri antidepressants for depression(too much anxiety side effect) and dr wondered if it was ptsd so we had the adrenal tests to find out. Does it sound like this is not PTSD? My DHEA is within range but high end and it normally travels with cortisol. Acth is not high. There is some research on PTSD saying a faster deactivation of cortisol to cortisone occurs when childhood trauma epigenetically changes the enzymes for life aftet that. Is that the explanation I wonder and are the alpha 2 blockers still applicable then in my case despite not having a good memory but certainly feel on high alert from noradrenaline maybe? Can very high noradrenaline also cause low memory formation? Maybe bit like adhd where I cannot filter out irrelevant stimuli so cannot focus to form the memory?? They use guanfacine for that type of ADHD I think. My son has adhd but no traumas like me BTW. He does well on stimulants however. I tried them but couldn't sleep. Is Prazosin still going to help if I don't have nightmares or flashbacks as I don't recall the traumas in detail and generally don't think about them either. My issues are depression with anxiety/agitation/sleep difficulty. I worry constantly about everything and everyone. Sad about the world and cry easy. Is this just depression now from lowish cortisol/inflammation? I don't have any elevated inflammation markers on my blood tests like crp or esr. I take fish oil daily and eat gluten free as my gut hurts with gluten. Not celiac though.

[@PsychiatrySimplified]

In general blood tests do not help in conclusively diagnosis as they can be cause or effect. If trauma is present it can affect a number of systems. Cogntion, hyerarousal at night , mood, pain, fatigue etc - thus an assessment is needed to understand and then target these symptoms appropriately. For example complex ptsd affects a number of these domains. Cognitive aspects can present like ADHD - in the video on amber heard and Johnny Depp 1 I cover the overlap between ptsd / CPTSD and BPD. In fact amber heard had responded to a stimulant prescribed - and I explain why that might be the case. In short multiple domains should be looked at and targeted. Prazosin or clonidine can help with nightmares .importantly if agitation is present then antidepressants can activate - so it’s important to address this mesolmibic system or firing amygdala and then add AD if needed. I’ve covered this in the mixed features video

[@jocs8824]

why are there no 5ht2a blockers that don't effect histamine, dopamine or 2c(like mirtazepine and anti-psychotics do-these were too sedating/brain fogging/appetite causing weight gain)? these are not desired effects in me but blocking 2a seems like it would relieve the depression if it's mixed features bp2d (alongside perhaps cptsd but hypervigilence isn't something I have unless on ssri, hence why its more bp2d I feel). The prazosin taken day and night as trialed for PTSD was way too tiring physically.

[@PsychiatrySimplified]

@@jocs8824 Agomelatine is one such agent - 5HT2C - increased dopamine. No serotonergic or histaminergic action - Covered this in another video

[@jocs8824]

@@PsychiatrySimplified tried that 10 weeks. did nothing for depression. slept well though. it doesn't touch 2a though. why is there nothing for that alone?

[@PsychiatrySimplified]

@@jocs8824 it depends on what symptoms are being targeted? Antidepressants on their own in mixed features unlikely to work effectively unless the mesolimbic system is addressed. So antidepressants work very differently when the mesolimbic system is addressed as opposed to when it isn't.

[@Demi_Marie564]

If the negative feedback loop is sensitised then why is there CRH still being released from the hypothalamus? Also if it’s sensitised then why is there a cross going through it in your image, doesn’t sensitised just mean that less cortisol is needed to shut off the stress response in the hypothalamus?

[@PsychiatrySimplified]

Thanks for your comment. The sensitisation is that the level of the adrenals . So stress activates the stress response increasing CRH but adrenal receptors sensitised and not responding to elevated CRH - hence the Red Cross. Hope that makes sense.

[@Demi_Marie564]

@@PsychiatrySimplified Okay, thank you but I still don't get how the adrenal receptors being sensitized would reduce negative feedback, wouldn't the receptors have to be desensitized? I thought that the lack of ACTH due to its blunted reaction to CRH would cause less cortisol release and thus reduce negative feedback (explaining the red cross).

[@PsychiatrySimplified]

@@Demi_Marie564 while HPA axis dysregulation is considered a key component the exact nature is still not known. “ Stress activates a complex network of hormones known as the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis is dysregulated in chronic stress and psychiatric disorders, but the origin of this dysregulation is unclear and cannot be explained by current HPA models.” this article does into more detail if interested. But www.ncbi.nlm.nih.gov/pmc/articles/PMC7364861/ Low(ish) cortisol levels could be due to partial primary adrenal insufficiency, hypothalamic-pituitary-adrenal (HPA) axis underactivity, increased negative feedback sensitivity and/or changes in glucocorticoid metabolism - in context of stress. So yes the negative feedback should be reduced but note the crh activation and acth activation would be coming from stress response to amygdala

[@rwdestefano]

According to a number of other neuroscientists, the hippocampus down regulates during trauma, which makes the traumatic memory unlikely to be consolidated, nor given a memory stamp. These memories, sights, sounds, feelings, thoughts, bodily sensations, are then stored in implicit memory circuits. Thus, these memories, when triggered in the future, are not consolidated and have no memory stamp. According to Dr. Daniel Siegel, there is then nothing about the experiencing of the memory that would indicate to the experiencer that it is a memory. The person experiences the thoughts, feelings, sensory information, bodily sensations, as if they are happening in the present, rather than as a memory. The person then is trapped into reliving experiences, rather than remembering them. Therefore, I disagree with this video's interpretation of memory function in trauma and PTSD.

[@PsychiatrySimplified]

That is not true. Consolidation occurs in the hippocampus and this is seen clinically - smells of the perpetrator, visual flashbacks, intrusive memories as if the event is happening all over again. Implicit memory is in basal ganglia - but note hippocampal consolidation plays a part in this as well. And in treatment we see this change - the appraisal changes as safer memories are substituted. Sometimes it's best not to hang on to one persons explanation as clinical practice and patient experiences Trump all of that. This is why clinical practice is important - linking neuroscience and clinical practice. It's not what one thinks or wants to think - it's about what patients tell us. I wouldn't invalidate your memories and patients memories shouldn't be either

[@rwdestefano]

@@PsychiatrySimplified I am not relying on one person’s experience. Dr. Cozzolino’s work highlights the same phenomenon of the degradation of the hippocampus during traumatic events, thus leaving memory to be stored in implicit memory circuits. Dr. Joseph LeDoux is another voice echoing this. The people I mentioned are neuroscientists, not psychiatrists. We must respectfully agree to disagree on this one.

[@rwdestefano]

“Under conditions of extreme stress, there is failure of ..memory processing, which results in an inability to integrate incoming input into a coherent autobiographical narrative, leaving the sensory elements of the experience unintegrated and unattached. These sensory elements are then prone to return when …activated by current reminders.” Van der Kolk, Hopper, & Osterman