Is there an antipsychotic that acts like an antidepressant at one dose and an antipsychotic at another?

Amisulpride is unusual in psychiatry for this dose-dependent dual action.

At low doses, it can relieve depression and negative symptoms; at higher doses, it treats psychosis (Scatton et al., 1997).

Here’s how its mechanism, pharmacokinetics, and clinical applications can help you tailor care more precisely. 👇🧵 Amisulpride’s Mechanism of Action 

1. Low doses (<400 mg/day) → Blocks presynaptic D2/D3 autoreceptors → Increases dopamine release → Improves negative symptoms and depression.

2. High doses (400–1200 mg/day) → Blocks postsynaptic D2/D3 receptors → Reduces positive symptoms in schizophrenia (Scatton et al., 1997).

Why do some patients sleep 8–10 hours yet still wake exhausted?

Because fatigue is not only about sleep duration, it reflects disrupted brain networks that leave the mind feeling foggy, unrefreshed, or in a state of hyperarousal.

Here’s how to reframe fatigue clinically and apply four structured steps to support patients more effectively. Fatigue is more than tiredness

Patients describe:

● “My brain feels foggy.”

● “My body feels heavy.”

● “I’m wired but tired.”

Fatigue is not laziness. It’s a neuropsychiatric symptom that reflects disrupted energy regulation across cognitive, emotional, and physical domains.

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Up to 60–80% of patients with mood or anxiety disorders experience sexual dysfunction, often worsened by antidepressants (Taylor et al., 2021).

Yet most suffer in silence. They may feel embarrassed, fear being dismissed, or avoid raising it, so the problem remains hidden.

Here’s how you can uncover, validate, and manage this under-discussed side effect..

1/12 🧵 Sexual dysfunction is not “just a side effect.”

● It affects intimacy and relationships.

● It undermines treatment adherence.

● It worsens depression outcomes.

Patients may feel: “I got help for my mood, but lost a part of myself.”

Asking about it can be the first step toward restoring trust.

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Why do some patients remain 'trapped' in flashbacks, hypervigilance, and emotional dysregulation after trauma?

The answer lies in the breakdown of three large-scale brain networks: the salience network, the default mode network (DMN), and the central executive network (CEN).

Here’s how understanding these networks can help you interpret symptoms more precisely and tailor interventions for your patients. 👇🧵 The integrated model

The Integrated Model of PTSD highlights the interplay of three core networks:

● Salience network → prioritises threat-related stimuli.

● DMN → integrates autobiographical memory and self-reflection.

● CEN → enables cognitive control and flexible decision-making.

PTSD emerges when these networks fail to recalibrate after trauma.

ADHD has an ~80% chance of a comorbidity.

It is often missed or misdiagnosed, leading to delayed care or inappropriate treatment.

ADHD is not a checklist, it is a longitudinal diagnosis requiring developmental history, functional impact, and contextual formulation.

Here are 10 essential points to guide diagnosis and management. 🧠👇

1/11 🧵 #1 ADHD is a Heterogeneous Condition

An individualised approach is critical; there is no one-size-fits-all solution.

Focus on specific domains, not just the label.

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Did Freud anticipate the brain’s 'hidden' networks?

His model of the Id, Ego, and Superego was theoretical, but modern neuroscience points to striking parallels.

While Freud wasn’t describing brain networks, clinicians use his framework heuristically, with the Default Mode, Salience, and Executive Control Networks offering a useful analogy.

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

Brain function relies on three key networks:

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

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

3️⃣ Executive 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.

Do patients with schizophrenia or bipolar disorder always have to be heavily sedated when agitated?

A new study (Mashaw, 2025) highlights that agitation isn’t just disruptive. It signals distress, resistance to care, and safety risks.

Here are emerging treatments that can calm without over-sedation, helping you manage agitation more safely and effectively in daily practice. 👇🧵 Agitation is one of the most urgent psychiatric emergencies.

Traditional medications often calm quickly but bring significant risks:

● Extrapyramidal symptoms (EPS)

● Respiratory depression

● Falls, fractures, cognitive impairment, and over-sedation

Clinicians need safer pathways that preserve engagement.

So what are the new treatments that can reduce these risks?

What if your patient’s biggest struggle isn’t the thought, but the tension in their body?

Progressive Muscle Relaxation (PMR) helps interrupt that cycle, reducing arousal and reinforcing regulation.

Here’s how PMR can support patients with chronic anxiety and tension, and how clinicians can integrate it in practice. 👇🧵 When dysregulation hits, the body often reacts before the mind.

Tension builds → signals threat.

Release → signals safety.

PMR retrains patients to notice tension early, release it, and send calming cues through their nervous system.

7 key differences in females with ADHD

Females present with a specific neurobehavioural profile that may contribute to an underdiagnosis and subsequent under-treatment.

Here’s what clinicians need to assess and look out for
🧵👇 1/ Under-recognised, different profile.

Girls/women with ADHD often present with internalising symptoms (low mood, anxiety, emotional lability), so they’re mislabelled with mood/personality disorders and referred late.

💡 Psych Scene Tip:

If chronic anxiety/low mood rides alongside lifelong disorganisation, time-blindness, and procrastination across settings (since <12), screen for ADHD before defaulting to mood/BPD labels.

Which antidepressants work most effectively, and which barely beat placebo?

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

Here’s how this data can transform your prescribing practice 🧵👇 Most ‘Effective’ Antidepressants (Head-to-Head)

In the largest network meta-analysis to date, the following antidepressants consistently outperformed others in head-to-head comparisons for efficacy (odds ratio range: 1.19–1.96):

● Agomelatine
● Amitriptyline
● Escitalopram
● Mirtazapine
● Paroxetine

These consistently outperformed others.

Note: Just because a drug ranks high in efficacy doesn’t mean it’s the best choice for every patient.

Why is the MEQ (Modified Essay Question) one of the hardest exams in psychiatry?

Because it doesn’t just test what you know, it tests how you think.

And here’s the problem: most psychiatric training doesn’t actually teach us to think. 🧵

1/12 We’re taught to memorise.

To conform.

To defer to authority and quote the guidelines.

But real-world psychiatry? That’s messy. Uncertain. Full of grey zones.

The MEQ throws you right into that world.

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Molly, age 14, was found wandering in Cork city, confused, agitated, and rifling through bins.

She has no psychiatric history and was sectioned under suspicion of acute psychosis. But a butterfly-shaped rash redirected her diagnosis.

Let’s walk through this case and explore what it teaches clinicians about diagnosing neuropsychiatric disease.

1/14🧵 Initial Presentation

Molly presented in 1994.

Symptoms: 

● Disorientation

● Behavioural disinhibition

● Public agitation

Initial impression: primary psychotic disorder.

She had no prior mental health history.

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Pregabalin and gabapentin are widely prescribed for neuropathic pain and seizures

Yet, their rising misuse potential and risks of dependency are raising alarms among clinicians

Are we underestimating the dangers?

Here’s an evidence-based guide to their mechanisms, clinical uses, and how to balance the benefits and risks 👇🧵 Mechanism of Action

Gabapentinoids bind the α2δ subunit of voltage-gated calcium channels, reducing excitatory neurotransmitter release (glutamate, noradrenaline, substance P).

Pregabalin is 6x more potent in binding than gabapentin.

76% of ADHD patients achieved >50% symptom reduction when neurofeedback protocols were tailored to individual EEG profiles, 

Using QEEG, researchers matched each patient to a protocol based on their brainwave patterns — producing significant improvements in inattention and hyperactivity.

Here’s what you need to know about EEG subtypes in ADHD, and how they can guide treatment when standard approaches fail.

1/15 🧵 QEEG can reveal brain-activity heterogeneity in ADHD that checklists miss.

Important: major guidelines don’t recommend QEEG to diagnose ADHD. Think of it as a potential stratification aid when progress stalls.

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Why is bipolar disorder often diagnosed years after symptom onset?

A meta-analysis of 9,415 patients found the average delay to accurate diagnosis and treatment is 5.8 years (Dagani et al., 2016).

Let’s examine why this happens and how clinicians can diagnose it earlier. 👇🧵 This delay has consequences.

Nearly 6 years of:

– Unstable mood episodes

– Functional and interpersonal decline

– Missed opportunities for psychoeducation

– Risk of antidepressant-induced destabilisation

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.

The bed nucleus of the stria terminalis (BNST) plays a critical role in dissociative PTSD, modulating bodily awareness, not just fear.

In patients with the dissociative subtype, BNST connectivity reorganises toward interoceptive hubs like the insula and posterior cingulate cortex.

Let’s examine how these circuit-level adaptations may inform clinical approaches to diagnosing and treating dissociative symptomatology.

1/14 🧵 Unlike phasic fear responses governed by the amygdala, the BNST modulates sustained anxiety and defensive responses to uncertain threat.

This shift is crucial in dissociative PTSD, where patients often show passive, immobilised, or disconnected defensive postures.

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Adult ADHD remains vastly underdiagnosed, despite clear impacts on function, well-being, and comorbidity burden.

Yet most clinicians still miss it. Why?

Here are the steps clinicians can follow to better diagnose and manage Adult ADHD.

1/14 🧵 ADHD is the most common neurodevelopmental condition in children.
In Australia:

● Youth prevalence: 6–10%
● Adult prevalence: 2–6%

But adult presentations often go unrecognised, especially without obvious hyperactivity.

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What treatment strategies align best with the neurobiology of Internet Gaming Disorder (IGD)?

A 2016 six-week RCT in treatment-seeking young adult males suggests bupropion may be more effective than escitalopram for IGD, particularly for impulsivity and attention deficits, though findings are limited to a controlled cohort.

Let’s examine the neurobiological implications and clinical relevance for managing reward dysregulation and executive dysfunction.

1/13🧵 The trial asked a targeted clinical question:

Can pharmacotherapy improve core IGD symptoms, especially in those with attentional and impulse control challenges?

119 young males with IGD were randomised to:

● Bupropion SR (150–300 mg/day, n=44)

● Escitalopram (10–20 mg/day, n=42)

● Observation (n=33)

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Maltreated children are nearly 10x more likely to exhibit symptoms of three or more neurodevelopmental conditions.

Yet trauma is often prioritised in assessments, while underlying neurodevelopmental traits remain undetected.

Find out how Adverse Childhood Experiences (ACEs) and neurodevelopmental conditions intersect, compounding risk via stress responsivity and diagnostic oversight.

1/14 🧵 ACEs are associated with poor health outcomes in a dose-response manner.

The more adversity in early childhood, the higher the risk of adverse physical and mental health in adulthood.

But not all individuals exposed to adversity experience poor outcomes, suggesting more complex, interactive mechanisms.

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Can sleep loss induce brain changes that resemble psychiatric dysregulation?

Sleep deprivation resulted in a 60% amplification of amygdala reactivity, coupled with a loss of top-down regulation by the medial prefrontal cortex.

Let’s explore why sleep loss undermines emotional regulation, impairs decision-making, and complicates clinical presentations across psychiatry.

1/14 🧵 Sleep deprivation impairs the prefrontal cortex.

This reduces activation and degrades working memory, cognitive control, and attention, hallmarks of psychiatric and neurological dysfunction.

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