🧵 1/ This is the mu-opioid receptor 🧵
It plays a crucial role in attachment, reward, social bonding and pain.
🚀Understanding Borderline Personality Disorder (BPD) as an Interpersonal Pain Syndrome 👇
1/ BPD and Pain Sensitivity: Evidence shows that individuals with BPD often present atypical pain responses, with up to 80% displaying reduced pain perception during non-suicidal self-injury (NSSI) episodes.
This phenomenon may stem from opioidergic system dysregulation, where neurobiological shifts alter pain processing in the brain.
2/Chronic Pain and BPD: Studies reveal that up to 65% of BPD patients experience chronic pain, which not only exacerbates emotional dysregulation but also predicts lower likelihood of remission.
3/ EOS and Emotional Dysregulation: The Endogenous Opioid System (EOS)- a neuromodulatory network crucial for mood, reward, and social bonding- plays a key role in BPD.
Components like mu-opioid receptors (MOR) and kappa-opioid receptors (KOR) modulate pleasure, pain, and the stress response, forming the foundation of pain abnormalities in BPD.
4/ In typical pain processing, MORs provide analgesia and reward signals, while KORs contribute to stress-induced dysphoria.
Childhood trauma and chronic stress disrupt this balance, often leading to hypomethylation of the OPRK1 gene, which boosts KOR expression and contributes to the emotional numbness and dysphoria characteristic of BPD.
5/ Reduced MOR Activity: Neglect or social isolation can lead to under-stimulated MORs, impairing emotional bonding and reward processing.
To compensate, individuals with BPD might turn to behaviours like substance use or self-injury as attempts to restore EOS activity and alleviate emotional pain.
Clinical implications: Clinical trials involving opioid antagonists, such as naltrexone and buprenorphine (KOR antagonist), have shown promising results in reducing self-harming behaviours by blunting the rewarding effects typically associated with these actions.
7/ Interpersonal Pain and Neuroadaptation in BPD: The Allostatic and CReAM Models
Initially, relational stress potentiates dopaminergic trafficking, but over time, prolonged stress shifts patients into a Reward Deficiency (RD) state marked by anhedonia and low motivation.
Neuroadaptations involving the amygdala and brainstem elevate CRF, norepinephrine, and dynorphin, reinforcing an Anti-Reward (AR) State and compounding chronic psychological pain.
8/ Engel’s Lens on Pain: Developmental Roots of Relational Instability in BPD:
"We discover that in the course of the child’s development, pain and relief of pain enter into the formation of interpersonal (object) relations and into the concepts of good and bad, reward and punishment, success and failure. Pain becomes par excellence a means of assuaging guilt and thereby influences object relationships". [Engel, 1959]
In Borderline Personality Disorder (BPD), this link is important as early disruptions in processing pain and comfort within relationships can lead to heightened sensitivity to rejection and a cycle of relational instability.
9/Zanarini’s Perspective: The “Pain of Being Borderline” :
Zanarini et al. highlighted that individuals with Borderline Personality Disorder (BPD) experience 25 distinct forms of distress that are far more prevalent in BPD than in other conditions.
This interpersonal pain may reinforce a “medical victim” identity, where relational distress becomes central to how individuals with BPD experience and seek relief from pain. [Sansone and Sansone, 2007]
This is a little glimpse from the comprehensive review of the Neurobiology and Psychodynamics of BPD.
Full article 👉psychscenehub.com/psychinsights/…
For clinicians, consider the courses (including the psychodynamic psychotherapy courses on the Academy ) 👉academy.psychscene.com
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1/ 🧵 This is your amygdala! It’s tiny-about the size of a shelled peanut at 1.24 cubic cm.
It’s the central hub of stress and trauma responses.
PTSD is one expression of the amygdala’s influence over cognitive, emotional, and behavioural domains
BUT
there’s more to it: the amygdala connects to the autonomic nervous system, hormonal systems inflammatory and even pain pathways.
So, let's explore some key aspects of PTSD 👇
2/ PTSD is diagnosed by symptoms across 4 clusters:
1. Intrusion phenomenon 2. Avoidance 3. Alterations in Cognition and mood 4. Alterations in Arousal and reactivity
3/ The Neurobiology of Fear and Anxiety
Fear processing involves :
👉Rapid Response pathway through the thalamus to the amygdala, triggering autonomic and hormonal responses and
👉Slower response pathway to the cortex for contextual processing.
The Gut-Brain Axis in Play: When Psychiatrists Treat Constipation 💩🚀 🧵1/
How I use Constipation as a Clinical Diagnostic and Management Marker ✅👇
One of the most fascinating aspects of treating depression is the intricate link between mood and the bowels.
Constipation is a very common symptom in severe melancholic and psychotic depression! ( >association with psychotic depression)
So, two things happen
1. Constipation
2. ‘Worry about constipation’ - this phenomenologically is not anxiety but is often misdiagnosed as such.
Note I am not referring to cases where addressing constipation improves mental state, treats confusion.
I’m talking about cases where long standing treatment of constipation has not shifted the bowels.
Phenomenology 👉As part of phenomenological evaluation -
I ask, "What proportion of your day do you think about this?" the answers are often 70%, 80%, even 90% of the day.
This ‘all consuming’ nature is not just anxious preoccupation BUT rather moving toward overvalued ideation. 🔥
But as clinicians, we must dig deeper-
financial ruminations, obsessional guilt, or pervasive feelings of doom are often present as well. ✅
How do we conceptualise this presentation in clinical practice and can it guide treatment? Absolutely! 1/ 👇
The answer lies in the gut-brain axis, a key player in this clinical scenario.
So what are the links between the Gut and the Brain in this scenario?
1️⃣Dopaminergic Dysfunction:
Did you know that dopamine, plays a crucial role in bowel motility?
In fact, guess which symptom often occurs early in Parkinson’s disease? That’s right-constipation.
Dopamine plays an important role in intestinal homeostasis.
Dopamine receptors, including D1, D3, and D5, are distributed in the intestinal wall- not just in the mucosa but also in the nerve endings of the intestinal wall.
Dopamine D2 receptors, are located specifically in the nerve endings within the intestinal wall. Meanwhile, the D4 receptor is found only in the mucosal layer.
When dopamine deficit states occur as in severe depression ( or many neuroinflammatory states) this can lead to reduced gut motility, resulting in constipation.
Thus , by enhancing dopaminergic activity through specific treatments, we can often see improvements in both the depression construct and bowel function. ✅
2️⃣Noradrenergic pathways :
The autonomic nervous system (ANS), which controls involuntary bodily functions like digestion, also plays a role in this process.
The noradrenergic descending pathway from the brain influences gastrointestinal motility by acting on the lumbosacral spinal defecation center.
In severe depression, ANS dysfunction may contribute to constipation, and addressing this requires a delicate balance- reducing agitation while potentiating NA to promote ANS homeostasis. 2/
Ok so you might say - well treat the constipation then! And you are right!
BUT
Now what about the ruminations and overvalued ideation about constipation?
Here’s a critical point that’s often overlooked: ruminations and overvalued ideation are frequently unresponsive to antidepressants alone AND rarely in the context of severe depression is there improvement in bowel movements even with multiple laxatives.
This can lead to a common clinical misstep-dismissing these ruminations as mere anxiety or attributing them solely to constipation, which then leads to the prescribing of multiple laxatives without addressing the underlying neurobiological issues. ❌ 3/
The Law of Rare Events: The Suicide Prediction Paradox
Prompted by the discussion around ADs and suicide prevention and predicting suicide in general- i.e. preventing suicide events and the misunderstanding of probability. 🧵 1/ 👇
#SuicidePrevention #Psychiatry #MentalHealth
Imagine we had a nearly "perfect" test to predict suicide – with 99% sensitivity and 99% specificity. Perfect right?
Well....not really!
Let's look at the surprising reality of what such a test might actually do.
First, some definitions:
Sensitivity: The ability of a test to correctly identify individuals who will suicide (true positives TP).
Specificity: The ability of a test to correctly identify individuals who will not suicide (true negatives TN).2/
Now, let's consider the suicide rate in the UK, which is approximately 17 per 100,000 people. (the latest is lower - but let's work with this)
Given a population of 65 million, this means 11,050 individuals would be predicted to suicide in this population.
Here's where it gets interesting – with our "perfect" test (99% sensitivity and 99% specificity), we would correctly identify 10,939 of these individuals as true positives. ✅
But we would also miss 111 (false negatives). ❌ 3/
🌟A Neuroscientific Voyage from Learned Helplessness to Depression 🌟
Here's a summary of my talk as an invited speaker at the Sri Lanka Psychiatry Conference / SAARC, taking the audience on a journey from learned helplessness to the complex realms of depression. 1/ 🧵
1. The Voyage to the 1960s: Was Learned Helplessness Truly Learned?
Seligman and Maier’s experiments demonstrated in animals how uncontrollable stress leads to passivity/anxiety and a cascade towards hopelessness.
Dogs subjected to inescapable shocks showed behaviours mirroring human responses to chronic stress-reduced aggression, social dominance, and exploration, along with heightened anxiety.
Below is a 10-minute video that sets the foundation for the key principles and stages of the Default Mammalian Response to Stress!
2. What is the Hope Circuit?
Hope largely consists of expecting that future bad events will be temporary, local, and controllable.
The key is The Expectation of Control.
The Ventromedial prefrontal cortex-dorsal raphe nucleus circuit is a key player in fostering the perception of control.
1/ In psychiatry, addiction isn't just about substances like alcohol or cannabis.
It's about the brain's response to what's most "salient."
2/ Salience is what the brain finds most attention-grabbing.
When one stimulus dominates, a cascade of addiction-related behaviors can follow.
A shift from liking to wanting to seeking .
3/ Key Takeaway:
The Salience Network which mediates arousal and reward and plays a pivotal role in reward responses and the associated behaviours via connections to the striatum. 🧠
🧵 Twitter Thread: #AKATHISIA Important Points on Akathisia
🧠 1. Akathisia, derived from the Greek word "akathemi," refers to a compelling urge to move, often accompanied by a sense of inner restlessness.
2. Objective restlessness often leads to identification however 1/
3. Subjective restlessness is equally distressing & Clinicians must rule out subjective restlessness and promptly address it, as akathisia is linked to an increased risk of suicide.
4. Akathisia is not limited to antipsychotics & antidepressants; other meds like Azithromycin, diltiazem, reserpine, and metoclopramide can also induce it.
5. The mechanism is multifactorial, with DA blockade leading to NA dysregulation b/w core and shell nucleus accumbens.