Postpartum psychosis affects 1-2 per 1000 births. 72% of cases emerge within 2 weeks postpartum (Bergink et al., 2016).

If misdiagnosed, it can lead to infanticide or suicide.

Here’s how to recognise, differentiate, and manage it effectively. 🧵👇 What is Postpartum Psychosis?

It’s a severe psychiatric disorder occurring post-birth, characterised by:

🔹 Acute onset: Symptoms develop over hours to days.

🔹 Rapid mood & cognitive shifts: Mania, depression, confusion.

🔹 Psychotic symptoms: Delusions, hallucinations, disorganised behaviour.

🔹 Severe risk of harm: Suicide, infanticide, neglect.

🚨 72% of cases occur within 2 weeks postpartum—early recognition is crucial!

Fasting triggers neurobiological processes that support brain health and mental health.

It shifts metabolism, activates autophagy, and increases brain-derived neurotrophic factor (BDNF)—mechanisms linked to cognitive function, mood regulation, and neuroprotection...

Here’s what clinicians need to know about its impact on the brain and mental health. 🧵👇 The Science Of The Metabolic Switch

Fasting shifts brain metabolism from glucose to ketones, activating pathways that regulate synaptic plasticity, inflammation, and oxidative stress.

This switch increases:

1️⃣ BDNF

2️⃣Mitochondrial biogenesis

3️⃣ Synaptic plasticity

Which are the keys for cognition and emotional regulation.

Does ADHD and OCD stem from the same neural circuitry?

Despite their opposing clinical features, ADHD and OCD share frontostriatal circuit dysfunction, suggesting a neurobiological overlap rather than entirely distinct conditions. (Cabarkapa et al., 2019)

Let’s dive in. 🧵⬇️ ADHD vs OCD

● ADHD: Impulsivity, inattention, disinhibition.
● OCD: Compulsivity, cognitive rigidity, overcontrol.
● Both impact executive function and self-regulation, but in different ways.

Clinical trials reveal that some antidepressants are over 100% more effective than placebo, while others barely outperform it.

The largest meta-analysis (Cipriani et al., 2018) compared 21 antidepressants in 116,477 patients, revealing striking differences in efficacy and tolerability.

Here’s what the study shows 🧵👇 For response rates (≥50% symptom reduction), these were the top performers:

- Amitriptyline
- Mirtazapine
- Duloxetine
- Venlafaxine
- Escitalopram

These consistently outperformed others.

Note: Just because a drug ranks high in efficacy doesn’t mean it’s the best choice for every patient. Prescribing should consider symptom severity, patient history, and tolerability.

Cognitive symptoms in major depressive disorder (MDD) often persist even after mood improves, affecting memory, processing speed, and executive function.

Vortioxetine has been investigated for its potential pro-cognitive effects, independent of its antidepressant properties (McIntyre et al., 2016).

Here’s a review of the mechanisms and clinical findings. 🧵👇 Pharmacological Profile & Multimodal Mechanism

Vortioxetine is a serotonin modulator and stimulator with a multimodal mechanism:

● SERT inhibition (~50%) → Increases synaptic serotonin with a lower risk of sexual dysfunction vs SSRIs (Adamo et al., 2021).

● 5-HT1A Agonism → Facilitates serotonergic transmission.

● 5-HT1B Partial Agonism → Enhances dopamine, noradrenaline, and histamine.

● 5-HT3 & 5-HT7 Antagonism → May contribute to cognitive benefits.

A 60-year-old woman with a history of heavy alcohol use presents with confusion, disinhibition, and memory impairment. Despite significant cognitive deficits, her language remains intact.

Neurological findings suggest an underlying pathology, but an unexpected serological result complicates the picture.

Could this be Wernicke-Korsakoff Syndrome, or is an overlooked autoimmune process at play?🧵👇 Full Symptom Profile

🧠 Cognitive & Psychiatric

● Profound anterograde amnesia (impaired new learning)
● Confabulation
● Disorientation with paranoid themes

🦵 Motor & Neurological

● Ataxia, dysdiadochokinesis, past pointing
● No ophthalmoplegia or autonomic instability

17.9 million people die from cardiovascular disease (CVD) annually (WHO, 2023). 

Yet, stress—a key driver of autonomic dysregulation, inflammation, and atherosclerosis—is rarely addressed in clinical care.

Stress isn’t just psychological; it accelerates CVD. 

Here’s what clinicians need to know about the brain-immune-heart axis and why stress management should be part of cardiovascular prevention.🧵👇 Stress as a Cardiovascular Risk Factor

Chronic stress is a significant predictor of cardiovascular disease, comparable to smoking (Rege, 2017).

• Dysregulates autonomic, endocrine, and immune functions.
• Increases blood pressure and heart rate.
• Triggers systemic inflammation, worsening atherosclerosis.

Dissociation isn’t just a symptom – it’s a neurobiological survival mechanism.

Research shows 30% of PTSD patients experience dissociation (Stein et al., 2013). 

The Polyvagal Theory (Porges, 2009) highlights the dorsal vagal complex as key in triggering shutdown when fight/flight fails.

Recognising dissociation in PTSD is crucial for tailoring therapy. Let’s explore how understanding dissociation improves outcomes👇🧵 Two PTSD Phenotypes

Dissociation in PTSD manifests as two phenotypes (Yehuda et al., 2015):

1️⃣ Emotional undermodulation: Hyperarousal & intense emotional responses.
2️⃣ Emotional overmodulation: Numbing, detachment, derealisation.

Understanding these phenotypes enables targeted interventions like grounding for undermodulation and trauma-focused therapy for overmodulation.

1/ PTSD: Two frameworks, distinct approaches.

Ever wondered how DSM-5 and ICD-11 differ in diagnosing PTSD?

Let’s explore their criteria, clinical implications, and their differences. 🧵👇 2/ DSM-5 defines PTSD using 4 key symptom clusters:

📌 Intrusion
📌 Avoidance
📌 Negative Cognitions/Mood
📌 Hyperarousal

This broad approach captures diverse trauma responses, making it ideal for complex clinical presentations. 

Here’s a breakdown of Criterion A 👇

Varenicline (Champix) is nearly twice as effective as nicotine replacement therapy (NRT) for smoking cessation (Cahill et al., 2013).

It targets the brain’s addiction pathways, reducing cravings while blocking nicotine’s rewarding effects.

Here’s how it works and why it’s so effective 🧵👇 Neurobiology of Nicotine Dependence

Nicotine binds to α4β2 nicotinic acetylcholine receptors (nAChRs) in the ventral tegmental area (VTA) → triggers dopamine release in the nucleus accumbens (NAc) → reinforces addiction & craving (Benowitz, 2010).

Varenicline disrupts this cycle by acting as a partial agonist & antagonist.

A doctor dies by suicide every day in the U.S.

🔹 Male physicians: 1.41x higher risk than the general population

🔹 Female physicians: 2.27x higher risk—one of the highest among any profession

Here’s a detailed look at the systemic and psychological factors driving this crisis. 👇🧵 The Scope of the Problem

📊 300–400 physicians die by suicide each year in the U.S. (Schernhammer & Colditz, Am J Psychiatry, 2004).

📊 In Australia, physician suicide rates are similarly high when adjusted for population.

📊 Unlike the general population, female and male physicians die at similar rates—a unique pattern in suicide epidemiology.

A systematic review found that high-THC cannabis use is associated with a 2-3x increased risk of psychosis, especially in genetically vulnerable individuals (Di Forti et al., 2019).

Modern cannabis strains contain higher THC (Δ9-tetrahydrocannabinol) and lower CBD (Cannabidiol), potentially increasing the risk of psychiatric disorders and cognitive impairment.

Let’s break down how cannabis affects THC, CBD, psychosis, and cognitive function. 🧵👇 CB1 & CB2 Receptors

The brain has a cannabinoid system with two key receptors:

• CB1 receptors → Located in the brain & CNS, involved in mood, memory, reward, and pain regulation.
• CB2 receptors → Found in immune cells & peripheral tissues, linked to inflammation & immunity.

THC binds to CB1 receptors, altering dopamine, GABA, and glutamate transmission—key pathways involved in psychosis and cognition.

What if the key to therapeutic change lies in how the brain updates predictions after unexpected outcomes?

Neuroscience shows that RPEs don’t just shape learning. They regulate emotional adaptation.

Disrupting maladaptive RPE patterns could be central to effective psychotherapy. (Iglesias et al., 2013)

Let’s explore how Reward Prediction Errors (RPEs) shape psychodynamic therapy and behavioural change 👇🧵 What are Reward Prediction Errors (RPEs)?

RPEs occur when there's a mismatch between expected and actual outcomes. 

This "surprise signal" prompts the brain to adjust predictions, reinforcing or reshaping behaviour.

Study: Schultz (2016) describes dopamine neurons as “teaching signals” that adjust behaviour based on reward prediction errors.

Did Freud predict the brain’s ‘hidden’ architecture?

His model of the mind—Id, Ego, and Superego—was purely theoretical, but modern neuroscience suggests these structures have neurobiological correlates.

Studies show that the Default Mode Network (DMN), Salience Network (SN), and Executive Control Network (ECN) mirror Freud’s divisions of the psyche (Menon, 2011).

Let’s break down how these brain networks shape behaviour, trauma, and psychiatric disorders. 🧵👇 The Triple Network Model

Brain function relies on three key networks:

1️⃣Default Mode Network (DMN) – Self-reflection, memory, mind-wandering

2️⃣Salience Network (SN) – Detects & prioritises important stimuli

3️⃣Executive Control Network (ECN) – Goal-directed thinking, cognitive control

The Salience Network acts as a switch between internal thought (DMN) and external task focus (ECN).

🧠Dysfunction in this system is linked to schizophrenia, depression, and PTSD.

Could frontal lobe dysfunction be the missing key in treatment-resistant psychiatric disorders?

Frontal lobe atrophy is linked to executive dysfunction, apathy, and impaired emotional regulation—often misdiagnosed as primary psychiatric conditions (Felger & Miller, 2012).

Let’s examine its clinical relevance, diagnostic approach, and implications for treatment 👇🧵 The Case of Phineas Gage – A Life Altered by Frontal Injury

Phineas Gage survived an iron rod piercing his left frontal lobe but exhibited drastic personality changes:

• From responsible & organised → to impulsive, socially inappropriate
• Lost his job due to poor judgment & disinhibition

His case underscores how frontal damage can mimic psychiatric illness—something we still see in clinical practice today (Chow, 2000).

In moderate-to-severe Alzheimer’s disease, memantine improved cognitive and behavioural outcomes by up to 20% compared to placebo (Kishi et al., 2017).

Memantine might also reduce PTSD symptoms, chronic pain, and emotional dysregulation in BPD.

Here’s what clinicians need to know about its mechanism, clinical applications, and emerging benefits. 👇🧵 Why Does Memantine Matter?

Memantine targets glutamate dysfunction, a process linked to neurodegeneration and excitotoxicity.

By blocking excessive activity at N-methyl-D-aspartate (NMDA) receptors, memantine:

• Protects neurons from damage in Alzheimer’s disease.

• May reduce symptoms of PTSD, chronic pain, and Border Personality Disorder (BPD).

Prescribing psychotropic medications? Some combinations significantly increase the risk of life-threatening arrhythmias like Torsades de Pointes (TdP).

For patients with psychiatric disorders and medical comorbidities, this risk must not be overlooked. 

Learn more about QTc prolongation risks and clinical management below. 👇🧵 1️⃣ Understanding QTc Prolongation & TdP Risk

A QTc interval >500 msec markedly increases the risk of TdP. The risk escalates when multiple QT-prolonging medications are combined.

High-risk psychotropics include:

Antipsychotics: Haloperidol, Chlorpromazine, Ziprasidone

Antidepressants: Citalopram, Escitalopram, Amitriptyline

Mood stabilisers: Lithium

Non-psychotropic contributors:

- Fluoroquinolones (e.g., Ciprofloxacin)
- Macrolide antibiotics (e.g., Clarithromycin)
- Antiarrhythmics (e.g., Amiodarone)

Generalised Anxiety Disorder (GAD) is, on average, only diagnosed 10 years after onset.

It affects 6% of people in their lifetime, with a functional impairment comparable to Major Depressive Disorder (Andrews et al., 2018).

Let’s look at how to identify GAD, avoid missed diagnoses, and implement evidence-based treatments for better patient outcomes. 👇🧵 Recognising Key Symptoms of Generalised Anxiety Disorder (GAD)

• Persistent, excessive worry for ≥6 months.
• Difficulty controlling the worry.
• Symptoms: restlessness, fatigue, irritability, poor concentration, muscle tension, or sleep disturbance.

Ask: Is the patient’s worry pervasive, disproportionate, and impairing quality of life?

A 22-year-old woman was misdiagnosed with schizophrenia after presenting with paranoia and agitation. 

Days later, seizures and hypoventilation revealed the true diagnosis: anti-NMDAR encephalitis.

75% of cases first present with psychiatric symptoms like psychosis or agitation, often leading patients to psychiatry before neurological signs appear (Espinola-Nadurille et al, 2022).

Learn more about its pathogenesis, illness progression and prognosis 👇🧵 What is Anti-NMDAR Encephalitis?

Anti-NMDAR (N-methyl-D-aspartate receptor) encephalitis is an autoimmune condition where antibodies target NMDA receptors (GluN1 subunit).

This disrupts synaptic signalling, leading to:

1️⃣ Psychiatric symptoms: Psychosis, paranoia, agitation

2️⃣ Neurological symptoms: Seizures, dyskinesias, autonomic instability

1 in 3 COVID-19 survivors may develop a neuropsychiatric or neurological condition within 6 months.

From anosmia to strokes, the virus can leave lasting effects on the brain.

Research shows over 33% of post-COVID patients develop conditions like anxiety, depression, or cognitive dysfunction (Taquet et al., 2021).

Here’s how SARS-CoV-2 impacts the Central Nervous System (CNS), its neuropsychiatric sequelae, and the key considerations for clinicians 👇🧵 How does SARS-CoV-2 'invade' the CNS (central nervous system)?

Olfactory route: The virus binds ACE2 (angiotensin-converting enzyme 2) receptors, travels via the olfactory bulb and enters the brain.

Bloodstream: Disrupted BBB (blood-brain barrier) allows infected monocytes and cytokines to enter.

Viral RNA in cerebrospinal fluid supports CNS involvement (Moriguchi et al., 2020).

Phenomenology in psychiatry is like ECG interpretation in cardiology—it’s about recognising patterns before a crisis unfolds.

Here’s a structured breakdown of thought pathology and why it’s clinically critical 👇 Thoughts are shaped by salience—our mind’s ability to prioritise stimuli.

As salience intensifies, thoughts become more:

✅ Rigid
✅ Distressing
✅ Uncontrollable

Understanding this hierarchy is key to early intervention. 🧵