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Nov 4 10 tweets 2 min read Read on X
Chelsea, 20, says she’s “going mad with anxiety.”

Onset with VCE exams; now pervasive worry, decision paralysis, and no depressive features.

You suspect GAD. 

What would you do to confirm this? 👇 Image
Nature of Anxiety.
 
Worry is frequent, excessive, hard to switch off, and out of keeping with threat, often without a trigger.

It persists even when things are going well and becomes the problem, not the topic [Andrews et al., 2018].
DSM-5 anchors you can count.

Excessive worry more days than not for ≥6 months about multiple domains, difficult to control.

Plus ≥3 of restlessness, fatigue, poor concentration/mind blank, irritability, muscle tension, and sleep disturbance. Image
Diagnostic Interview

“Are you a worrier?”
“How long each day do worries occupy you?”
“What do you worry about?””

Probe tension headaches/neck tightness, sleep onset/maintenance, concentration, avoidance, and functional impact.
GAD-7 Self-Assessment

This diagnostic tool detects a patient’s latent anxiety.

These items are answered by frequency (not at all, most days, etc.)

[Spitzer et al., 2006] Image
Differentiate from OCD

OCD has circumscribed, unwanted intrusive thoughts with compulsions and harm/contamination themes; thoughts feel alien and are ritual-neutralised. 

GAD worries are internally congruent, everyday, predominantly verbal, and not ritual-driven.
Differentiate from MDD

MDD: primary low mood/anhedonia with past-oriented rumination (“Why did I…”) plus hopelessness. 

GAD: primary anxiety with future-oriented “what if…”, prominent muscle tension, and secondary low mood.
Medical Contributors to Rule Out

Substance-induced (intoxication, withdrawal, caffeine)

Medical Conditions (hyperthyroidism, seizures, hypoglycaemia)
Summary of Assessment Approach

Is it Anxiety?

Is the Anxiety Severe?

Is it an Anxiety Disorder?

Does it meet the criteria for GAD, PD, or SAD?

Use Clinical Practice Guidelines to plan treatment.

Consider other diagnoses and appropriate referral when necessary.
For an in-depth learning on diagnoses of anxiety and other mental disorders, visit The Academy

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More from @psycheureka

Nov 3
Females with ADHD constitute a silent minority, with a propensity towards underdiagnosis and undertreatment.

There is evidence to suggest that there is a significant discrepancy in the ratio of males to females diagnosed with ADHD. [Berry et al., 1985]

Let’s explore why ADHD manifests differently in females👇Image
ADHD is diagnosed far more often in males than females.

Early studies show teachers are more likely to refer boys for assessment, even when girls show identical symptoms.
(Young et al., 2020)
Girls often present with inattentive rather than disruptive symptoms.

They may appear dreamy, disorganised, or emotionally sensitive, not “hyperactive.”

These traits are less likely to trigger referral or concern.
Read 12 tweets
Nov 2
Lamotrigine prolongs the time between mood episodes and is particularly effective in preventing depressive relapses in bipolar I disorder.

Unlike lithium or antipsychotics, lamotrigine has no significant effect on acute mania but is a first-line option for bipolar depression (RANZCP Guidelines)​.

How does lamotrigine work? Let's explore its efficacy in bipolar disorder and important prescribing considerations. 🧵👇Image
Mechanism of Action

● Increases GABA release, supporting inhibitory neurotransmission​.

● Inhibits voltage-gated sodium (Na+) channels, reducing glutamate excitotoxicity​.

● Putative anti-kindling effects may help stabilise mood over time​.

The dual action on GABAergic and glutamatergic pathways may explain lamotrigine’s effectiveness in bipolar depression but lack of efficacy in mania.Image
Efficacy in Bipolar Disorder

1. Prolongs time to depressive relapse in bipolar I disorder (Goodwin et al., 2004)​.

2. Evidence from small trials suggests lamotrigine may be more effective than placebo in bipolar II depression, though data are limited (RANZCP Guidelines, 2020)

3. Combination therapy with lithium is more effective than either agent alone (LamLit Study)​.

Lamotrigine is not effective for acute mania but is an evidence-based long-term mood stabiliser for bipolar depression.Image
Read 8 tweets
Oct 28
A 53-year-old man with schizoaffective disorder on clozapine (700mg/day) had severe abdominal pain and vomiting to the ER.

Let’s walk through his case and explore why Clozapine induced Constipation (CIC) affects up to 60% of patients. 🧵👇 Image
Background:

Clozapine is highly effective for treatment-resistant psychosis, but its anticholinergic and antiserotonergic effects slow gut motility.

If untreated, CIC can progress to ileus, sepsis, or death.
History:

He’d been stable for a year on clozapine, olanzapine, lithium, iron, and multivitamins.

He’d complained of constipation once before but received no ongoing management.
Read 14 tweets
Oct 22
Lithium: still the most distinctive mood stabiliser we have.

70 years in practice with compelling evidence in mania, acute bipolar depression, and prophylaxis, yet its mechanisms remain multifaceted.

Here’s what makes Lithium so different and it’s mechanisms of action 🧵👇 Image
Lithium is a unique agent that has been used for over half a century for the treatment of bipolar affective disorder.

Lithium has compelling evidence in the treatment of mania, acute bipolar depression and prophylaxis in bipolar
affective disorder.

Despite its first discovery in 1949 and its subsequent use, the exact mechanisms of action in lithium are unclear.

Lithium’s Action On Neurotransmitters:
1/ Dopamine Pathways

Dopamine dysregulation in bipolar disorder involves elevated transmission during mania and decreased levels in depression. 

Lithium corrects this by modulating G proteins and dopamine-associated subunits.
Read 11 tweets
Oct 20
Studies suggest that up to 50% of adults with ADHD meet criteria for an anxiety disorder (Fu et al., 2025).

Anxiety is not simply “comorbid”; it is embedded in ADHD’s neurobiology and developmental trajectory.

Let’s explore how anxiety and ADHD intersect, and why recognising this link can improve diagnostic clarity, treatment planning, and patient outcomes. 👇🧵

Note: image is a conceptual illustration (uncertainty ↔ arousal ↔ anxiety), not a validated biomarker/model.Image
Across studies, anxiety co-occurs with adult ADHD in ~25–50% of cases; representative samples report ~47–56%.

Comorbidity tracks with earlier onset and greater impairment.
Shared mechanisms

Convergence across genetics (PRS links to anxiety/depression), neurobiology (monoaminergic & reward circuits), neurocognition (executive deficits), and neuroimaging (overlapping structural/functional changes).
Read 11 tweets
Oct 15
Borderline Personality Disorder (BPD) isn’t just “emotion dysregulation.”

It can be usefully conceptualised as a predictive-processing problem where salience, reward prediction errors (RPEs), and the endogenous opioid system (EOS) bias social learning.

Here’s how clinicians can help patients update predictions and reduce volatility. 🧵👇Image
Prediction errors = expectation vs outcome

Rapid, phasic dopamine/serotonin signalling in reward/salience networks encodes PEs, guiding attention, belief updating and affect regulation.
Salience network reactivity

In BPD, impaired habituation and sensitisation can bias attention toward negative social cues, making them feel overly salient.
Read 13 tweets

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