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. 🧵👇
● 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.
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.
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.
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).
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. 🧵👇
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.