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.

2/15 🧵

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.

2/14 🧵

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.

2/14 🧵

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.

2/14 🧵

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.

2/14🧵

Up to 68% of perimenopausal women report clinically significant depressive symptoms, yet most are never formally diagnosed.

Their symptoms are somatised, cyclical, and hormonally modulated, often falling outside DSM-5 criteria and undetected by conventional tools like the PHQ-9 (Brown et al., 2009; Timur & Sahin, 2010).

Here’s how to recognise, differentiate, and manage this frequently overlooked depressive syndrome.

1/14 🧵 The diagnostic profile diverges from classic MDD.

Perimenopausal depression is associated with:

– Paranoid ideation

– Irritability or hostility

– Cognitive slowing

– Somatic complaints (e.g. joint pain, headaches)

– Decreased libido and sleep disturbance

These features complicate recognition through standard affective disorder criteria (Kulkarni et al., 2018).

2/14 🧵

Why do some patients respond poorly to antipsychotics despite adherence and diagnosis?

Emerging research points to muscarinic receptor dysfunction. M1 and M4 receptors are densely localised in memory circuits, especially the hippocampus, amygdala, and neocortex, where they modulate synaptic plasticity and cognitive processes.

Could a missing cholinergic signal explain what dopamine alone cannot?

1/13 🧵 Some have proposed a muscarinic receptor-deficit subtype of schizophrenia (MRDS), characterised by reduced cortical and hippocampal CHRM1 and CHRM4 expression.

While not yet a clinical diagnosis, the anatomical groundwork for this concept is supported by receptor mapping studies.

2/13 🧵

During fasting, the brain shifts to β-hydroxybutyrate (BHB) metabolism.

BHB is not just a fuel source; it upregulates brain-derived neurotrophic factor (BDNF), activates autophagy, and supports synaptic maintenance.

These changes may reduce neuroinflammation and support mood and cognitive stability.

1/15 🧵 Once glycogen stores are depleted, the brain shifts from glucose to ketones like β-hydroxybutyrate (BHB).

BHB is not just a fuel; it’s a signalling molecule that activates pathways associated with neuronal growth and resilience.

2/15 🧵

A 2010 study found that 25% of obese individuals with serious mental illness met criteria for Night Eating Syndrome (NES), a rate significantly higher than in the general population.

This has significant implications for psychiatric care, yet remains under-recognised.

1/12 🧵 This study (Lundgren et al., 2010) examined 68 overweight or obese, treatment-seeking adults with serious mental illness (SMI), including schizophrenia, bipolar disorder, schizoaffective disorder, or major depression.

The goal is to determine the prevalence of Night Eating Syndrome (NES) and Binge Eating Disorder (BED).

2/12 🧵

How does pregnancy reshape the brain?

One study found structural changes are so distinct that it could predict pregnancy with 95.6% accuracy, just by looking at brain scans.

Here’s why it matters for understanding peripartum mood disorders, attachment, and psychiatric vulnerability.

1/14 🧵 Hormones trigger brain-wide shifts.

Estrogen and progesterone surge rapidly in early pregnancy.

This isn’t just systemic but neuroplastic.

These hormonal cascades remodel the maternal brain to prepare for caregiving, bonding, and attunement.

2/14 🧵

Experienced psychiatrists don’t merely assign diagnoses.

They construct dynamic formulations.

Diagnosis begins the process.
Formulation guides the intervention.

Here’s how hypothesis-driven thinking reshapes psychiatric practice.

1/12 🧵 Too often, we diagnose forward:

Symptom → Label → Treatment

But when treatment fails, is the drug at fault—or was the label flawed?

Diagnosis must be more than categorisation.

It’s about understanding why symptoms exist.

2/12 🧵

Why do some patients feel unsafe in stable relationships?

In Borderline Personality Disorder (BPD), what looks like ‘attention-seeking’ is often an automated survival pattern, deeply encoded through implicit memory and prediction mechanisms.
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1/13 🧵 Familiar instability becomes the norm.

Patients with BPD often experience early environments marked by unpredictability, abandonment, or emotional neglect.

Over time, the brain learns: instability = safety.

Stability feels foreign, not soothing.

2/13 🧵

Antidepressant withdrawal is not rare.

Up to 56% of patients experience withdrawal symptoms when stopping antidepressants. Nearly half of those describe them as severe (Davies & Read, 2019).

Yet antidepressant withdrawal is often under-recognised in clinical practice, despite clear evidence of neuroadaptive changes, serotonergic dysregulation, and symptom trajectories distinct from relapse.

1/13 🧵 Withdrawal ≠ Relapse.

Discontinuation symptoms may mimic the return of illness, but the mechanisms are distinct:

● Synaptic serotonin drops

● Downregulated receptors remain hypoactive

● Dysregulation of downstream GABA/dopamine systems

2/13 🧵

Up to 40% reduction in depression risk has been observed with adherence to anti-inflammatory diets like the Mediterranean diet, according to the PREDIMED study.

Emerging research links dietary patterns to neuroinflammation, neurotransmitter synthesis, and gut–brain signalling.

Here’s what clinicians need to know about nutritional strategies in psychiatric care, from gut microbiota to therapeutic nutrients. 🧵👇 The Gut–Brain Axis and Mental Health

The GI tract hosts 100 trillion microbes influence mood, cognition, and stress regulation.

Disruptions (e.g., from a Western diet) are associated with depression and anxiety.

Some strains produce neurotransmitters (e.g., serotonin precursors).

Which patients with schizophrenia are at the highest risk of suicide?

In a 3-year pan-European study of 8,871 outpatients, the suicide attempt rate was 4.3%, with key predictors including prior attempts, depressive symptoms, prolactin-related side effects, male gender, and prior hospitalisation.

1/12 🧵 Lifetime suicide attempts increased future risk nearly fivefold (OR: 5.2), and suicide attempts in the 6 months prior raised risk 3.7× compared to none.

This finding reinforces the need for detailed longitudinal histories.

2/12 🧵