Psychiatry Excellence Profile picture
Aug 16 12 tweets 2 min read Read on X
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 Image
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.

2/12🧵
Take this:

Textbook:

“How to manage akathisia”

Sounds simple.

But now look at a real-world MEQ slice:

“A 52-year-old male with schizophrenia on aripiprazole 10mg nocte for 1 year reports leg restlessness. It’s keeping him awake. Outline your approach.”

See the difference?

3/12🧵
If you jump straight to “akathisia”, you risk missing the bigger picture.

This could be:

● Restless legs syndrome
● Anxiety-related psychomotor agitation
● Poor sleep hygiene
● Partial dopamine agonist effect
● Or yes, akathisia

It’s not about finding the answer.

4/12🧵
It’s about understanding the phenomenology, the pattern, the context, the implications.

Only then does the management plan become meaningful.

This is what MEQs reward: diagnostic curiosity, clinical reasoning, and strategic thinking.

5/12🧵
And yet, we don’t train for it.

We train to pass the multiple-choice questions. To cite the protocol. To learn static facts.

But MEQs ask you to integrate.

To bring systems thinking into a 9-minute clinical problem.

6/12🧵
It’s like tennis.

Reading a textbook about footwork won’t help you when the ball’s flying at you.

A tennis player practises footwork thousands of times, under pressure, in motion.

Psychiatric reasoning needs the same training.

But we don’t get enough of it.

7/12🧵
That’s why MEQs feel like a punch in the gut.

And that’s also why they’re so valuable.

They prepare registrars for real-world chaos, where the patient isn’t a case vignette and the guideline doesn’t quite fit.

8/12🧵
So if you’re a supervisor, consultant, or trainee:

✅ Start practising this thinking daily.
✅ Don’t jump to labels.
✅ Train yourself to think in context.
✅ Use ward rounds, supervision, and case discussions to build the muscle.

9/12🧵
Because the MEQ doesn’t just test your memory.

It tests your clinical mind.

And that’s something worth training.

10/12🧵
We’ve put together a course to break this down, not with checklists, but by showing how psychiatrists think through diagnostic ambiguity.

Because real patients don’t come with multiple-choice options.

They come with complexity.

11/12🧵
To access this course and tailored MEQ marking feedback directly from Dr Sanil Rege, click the link below:



12/12🧵psychscene.co/3HyGwkP

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More from @psycheureka

Aug 13
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🧵Image
Initial Presentation

Molly presented in 1994.

Symptoms: 

● Disorientation

● Behavioural disinhibition

● Public agitation

Initial impression: primary psychotic disorder.

She had no prior mental health history.

2/14🧵
Autoimmune Features Identified

On assessment, clinicians noted:

🔍 Malar (butterfly) rash

🔍 Patchy alopecia

🔍 Positive anti-dsDNA antibodies

🔍 Low complement (C3)

Renal function remained normal.

These findings shifted diagnostic suspicion toward systemic autoimmunity.

But what could be the real diagnosis?

3/14🧵
Read 14 tweets
Aug 12
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.
Despite being GABA analogues, they do not act on GABA receptors. 

Instead, they influence synaptogenesis by inhibiting thrombospondin binding to α2δ-1—critical for excitatory synapse formation.
Read 12 tweets
Aug 9
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 🧵Image
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.

2/15 🧵
What QEEG does: records theta/alpha/beta rhythms and compares them to normative databases.

Deviations create a profile that may help plan treatment.

3/15 🧵
Read 15 tweets
Aug 4
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
The biggest diagnostic trap?

Most patients first present with depression, not mania.

Without a clear manic history, they’re often misclassified as having unipolar depression.
Read 14 tweets
Jul 31
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. 🧵👇Image
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.
What Does the Research Show?

🔹 Meta-analysis (McIntyre et al., 2016): Vortioxetine improved executive function, memory, and processing speed in MDD, beyond mood symptoms.

🔹 Bennabi et al. (2019): Cognitive benefits may be linked to 5-HT3 receptor antagonism, which modulates glutamate and GABA neurotransmission.

🔹 Post hoc analysis (Nierenberg et al., 2019): Vortioxetine significantly improved residual cognitive symptoms compared to placebo.

These effects appear distinct from traditional SSRIs.Image
Read 9 tweets
Jul 28
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 🧵Image
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.

2/14 🧵
fMRI studies reveal increased BNST connectivity to the posterior cingulate cortex, a hub of self-referential processing and interoception.

This suggests that the dissociative subtype of PTSD may involve neurocognitive rerouting of threat signals toward body-focused circuitry.

3/14 🧵
Read 14 tweets

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