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Feb 26 12 tweets 3 min read Read on X
At birth, the brain is a blank slate, but not an empty one.

A newborn's survival depends on basic needs—warmth, nourishment, and safety.

But how does this evolve into complex emotions, consciousness, and psychiatric disorders?

Let's explore how core emotional circuits shape mental health. 👇🧵Image
The Neuroscience of Emotions & Mental Health

Before we feel emotions, we experience affect—raw physiological states.

These early signals shape how we perceive the world before cognition develops.

🔹 Hunger → distress
🔹 Warmth → calm
🔹 Separation → panic

These primal circuits lay the foundation for future emotional responses.
Three Levels of Affects (Panksepp):

🧩 Homeostatic (Drives) – Survival instincts (hunger, thirst).

🧠 Emotional (Instincts) – Innate reactions (fear, attachment).

👁️ Sensory (Reflexes) – Pain, pleasure, and sensory processing.

These systems interact to form the basis of emotions and psychiatric disorders.Image
How Emotions Take Shape

Early experiences sculpt emotional circuits that determine resilience or vulnerability.

🔹 Secure attachment fosters emotional regulation.

🔹 Trauma or neglect disrupts these circuits, increasing psychiatric risk.

💡 Psych Scene Tip: Early interventions improve emotional resilience.
The Seven Core Emotional Systems (Panksepp)

🔎 SEEKING – Motivation & reward
😨 FEAR – Threat response
😡 RAGE – Defensive aggression
💖 CARE – Nurturing & bonding
🔥 LUST – Reproductive drive
😭 PANIC/GRIEF – Attachment & loss
😆 PLAY – Social learning

Each plays a role in mental health, emotional processing, and psychiatric conditions.
Depression: When the SEEKING System Shuts Down

Depression isn’t just sadness. It’s a failure of motivation and reward processing.

- Low dopamine reduces goal-directed behaviour.

- Excess PANIC/GRIEF leads to social withdrawal.

- Neuroinflammation worsens anhedonia.

💡 Psych Scene Tip: Behavioural activation restores motivation and reward.
Anxiety: The Brain Stuck in FEAR Mode

Anxiety isn’t just overthinking. It’s a hyperactive threat system.

- Overactive amygdala = heightened fear response.

- Dysregulated stress hormones = chronic tension.

- Weak prefrontal control = poor emotional regulation.

💡 Psych Scene Tip: Exposure therapy helps rewire fear pathways.Image
PTSD presents in two neurobiological patterns:

⚡ Hyperarousal → High fear response (fight/flight/freeze).
😶 Dissociation → Emotional shutdown due to excessive inhibition.

Treatment must match the subtype for effective intervention.
Addiction: The SEEKING System Hijacked

Substances artificially spike dopamine, creating false reward signals.

- Over time, natural rewards lose their appeal.

- The PANIC/GRIEF system fuels withdrawal.

- Impulse control weakens, reinforcing the cycle.

💡 Psych Scene Tip: Recovery focuses on restoring natural SEEKING behaviours.Image
The Brain Can Rewire

Neuroplasticity allows emotional circuits to adapt with:

✅ Psychotherapy (CBT, EMDR, trauma-focused approaches)

✅ Pharmacotherapy (SSRIs, dopamine modulators)

✅ Lifestyle changes (exercise, mindfulness, social connection)

Mental illness is not a fixed state. The brain can heal.
What Clinicians Need to Know

- Psychiatric disorders reflect emotional circuit dysregulation.

- Depression = SEEKING dysfunction.

- Anxiety = FEAR dysregulation.

- Addiction = SEEKING hijacked by artificial rewards.

Targeting the right emotional circuits is key to effective treatment.
Want to dive deeper into the neuroscience of emotions?

Read the full article, "The Neuroscience of Emotions: Clinical Relevance for Understanding Depression, Anxiety, and Addiction," by Dr Sanil Rege.

Explore how core affective systems shape mental illness and discover evidence-based treatment strategies here:

psychscene.co/4bgG9Ga

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More from @psycheureka

Feb 28
Antidepressant-Induced Sexual Dysfunction (AISD) is one of the most common yet underreported side effects of antidepressants, affecting up to 70% of patients.

AISD can impact libido, arousal, and orgasm, leading to distress, relationship strain, and non-adherence (Montejo et al., 2019).

Here’s how to assess, manage, and treat AISD. 🧵👇Image
What Causes Antidepressant-Induced Sexual Dysfunction?

Neurotransmitter Imbalance:

🔼 Serotonin → inhibits sexual response (5HT2/5HT3 activation).

🔽Dopamine & Noradrenaline → impairs desire and arousal.

Adrenergic & Cholinergic Effects → interfere with orgasm and ejaculation.Image
How Common is AISD?

📉 Prevalence rates:

● Selective Serotonin Reuptake Inhibitors (SSRIs): 25–73%

● Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): 58–70%

● Tricyclic Antidepressants (TCAs) & Monoamine Oxidase Inhibitors (MAOIs): ~30–40%

● Atypical Antidepressants: Lower risk (e.g., bupropion, mirtazapine)

AISD often goes undiagnosed unless directly asked.

💡 Psych Scene Tip: Always screen for sexual dysfunction before starting an antidepressant to establish a baseline.Image
Read 8 tweets
Feb 27
1 in 8 adults meet the criteria for Alcohol Use Disorder (AUD), yet fewer than 10% receive pharmacological treatment. (Grant et al., 2015)

With high morbidity & mortality, why is AUD so under-treated? 

What should psychiatrists know about its neurobiology & evidence-based treatment?

Let’s dive in.👇Image
The Global Burden of Alcohol Use

● Alcohol contributes to 5.9% of all deaths globally (7.6% men, 4% women).

● Leading cause of death in men under 50.

● Strongly linked to CVD, liver disease, cancer, & psychiatric disorders. Image
The Neurobiology of Alcohol Use Disorder (AUD)

🔹 Alcohol activates the mesolimbic dopamine system, reinforcing use.

🔹 Modulates opioid, GABA, & glutamate pathways, amplifying reward.

🔹 Chronic use reduces dopamine transmission, leading to tolerance, escalation & compulsive use.Image
Read 10 tweets
Feb 25
Up to 40% of lithium-treated patients develop nephrogenic diabetes insipidus (NDI), leading to excessive thirst & urination (Stone, 1999).

Chronic Kidney Disease (CKD) occurs in 10-20% of long-term users (McKnight et al., 2012).

Let’s analyse the pathophysiology, risk factors & management of lithium-induced renal dysfunction. 👇🧵Image
Types of Lithium-Induced Renal Dysfunction

➡️ Polyuria (40% of patients)

➡️ Nephrogenic Diabetes Insipidus (NDI) – Polyuria, nocturia, polydipsia, reversible in early years

➡️ CKD & ESRD – Risk increases with long-term use (≥20 yrs)
How Lithium Affects the Kidneys

- Inhibits ADH → Reduces kidney’s ability to concentrate urine → Polyuria

- Increases sodium excretion (↓ ENaC activity) → Natriuresis

- Reduces water reabsorption (↓ AQP2 channels) → Water loss

💡 Psych Scene Tip: Persistent polyuria (>3L/day) in lithium-treated patients? Evaluate for NDI.
Read 10 tweets
Feb 25
Why do conditioned cues drive addiction?

Conditioned cues may trigger more potent dopamine (DA) responses than the drug itself, shifting reinforcement from the substance to the cues. (Volkow et al., 2019)

Here’s how this process fuels persistent substance use. 🧵👇 Image
The Reinforcement Shift

🔹 Conditioned cues surpass the dopamine response to the drug, reinforcing addictive behaviours.

🔹 Anticipated drug effects often fail to match the actual response, leading to repeated use in search of the expected high.

🔹 The anti-reward system engages over time, reducing DA & serotonin while increasing stress-related neurochemicals, causing withdrawal symptoms.
The Cycle of Withdrawal & Relapse

🔹 Withdrawal is marked by reduced D2 receptor levels in the striatum, impairing motivation for natural rewards & increasing relapse risk.

🔹 Sensitivity to both natural rewards & negative reinforcers diminishes, making treatment outcomes more challenging.

🔹 This contributes to compulsive drug-seeking behaviours, even in the face of negative consequences.
Read 5 tweets
Feb 24
SNRIs like Venlafaxine & Desvenlafaxine are widely used in Major Depressive Disorder (MDD) & anxiety disorders, but their pharmacokinetics & mechanisms differ—impacting efficacy & tolerability.

A meta-analysis found both to be effective in depression, with Desvenlafaxine showing a linear dose response. (Norman & Olver, 2021)

Here’s what clinicians need to know about their differences in metabolism, clinical effects & prescribing considerations. 🧵👇Image
Receptor Binding & Neurotransmitter Effects

1️⃣ Venlafaxine: 30:1 serotonin (5-HT) to norepinephrine (NE) ratio, acting mainly as an SSRI at low doses and an SNRI at higher doses (>225 mg).

2️⃣ Desvenlafaxine: 10:1 5-HT:NE ratio, meaning it acts as a dual reuptake inhibitor at standard doses (50 mg+). (Liebowitz & Tourian, 2010)
Pharmacokinetics & Metabolism

1️⃣Venlafaxine XR: Metabolised via CYP2D6 to Desvenlafaxine, with a half-life of ~15±6 hrs.

2️⃣Desvenlafaxine: Minimal CYP metabolism, primarily conjugated by UGT enzymes, with a half-life of ~11 hrs.

💡 Psych Scene Tip: Desvenlafaxine is less affected by CYP2D6 polymorphisms, making plasma levels more predictable.Image
Read 8 tweets
Feb 22
Approximately 1 in 9 U.S. children have been diagnosed with ADHD, yet traditional stimulant medications often fall short in efficacy and tolerability. (CHADD, 2021)

Recent advancements have introduced novel therapies targeting multiple neurotransmitter systems, expanding treatment options and potentially improving outcomes. (Neurolaunch, 2023)

Here are 4 emerging treatments that could improve ADHD management by offering alternatives to stimulants and addressing broader neurochemical pathways 🧵👇Image
The Cortico-Striatal-Thalamo-Cortical (CSTC) Loop & ADHD

ADHD is linked to dopaminergic & noradrenergic dysfunction in CSTC circuits, affecting:

- Attention

- Impulse control

- Executive function

Targeting these circuits is key to optimising treatment strategies.
1. Viloxazine (Qelbree) – A serotonin-norepinephrine modulating agent (SNMA)

- Increases serotonin in the prefrontal cortex

- Modulates norepinephrine & dopamine

- FDA-approved (2021) for ages 6-17

📌 Effective for inattention & impulsivity but carries a black box warning for suicidality.

💡 Psych Scene Tip: Consider Viloxazine for stimulant non-responders, but monitor closely for mood changes.

(Source: Yu et al., 2020)
Read 8 tweets

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