ADHD is often discussed in terms of inattention, impulsivity, and hyperactivity...

But one domain is consistently under-recognised in assessment and treatment:

Sleep.

Here’s how sleep and ADHD are connected and the 5 clinically effective sleep strategies every clinician should know 👇🧵 Sleep disturbances are the rule, not the exception, in ADHD.

82.6% of individuals with ADHD report lifetime sleep problems.

And this extends far beyond delayed sleep onset.

Common presentations include:

• delayed sleep–wake phase
• restless legs / PLMD
• sleep-disordered breathing
• parasomnias (e.g., night terrors)

These often predate the ADHD diagnosis.

Autism isn’t “just genetic”. 

The gut–brain–immune axis can shape how symptoms show up—especially when GI problems are in the mix. 

Here’s what clinicians needs to know about the Gut Microbiome and Autism Spectrum Disorder (ASD) 👇🧵 ASD is highly heritable, but early life nudges—delivery mode, feeding, antibiotics, maternal metabolic health—can shift the microbiome and immune tone. 

Think genes × environment, not either/or.

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.

1/13 🧵 Familiar instability can become the norm.

Patients with BPD often report early environments marked by unpredictability, abandonment, or emotional neglect (consistent with the biosocial model and attachment research).

Over time, the individual may learn that instability is expected in close relationships.

2/13 🧵

Why do some individuals recover from trauma while others develop PTSD?

A useful lens is how three large-scale brain networks interact:

• The Salience Network (SN)

• The Default Mode Network (DMN)

• The Central Executive/Frontoparietal Network (CEN/FPN)

Understanding their dysregulation helps guide PTSD treatment. Here’s how 👇🧵 The Integrated Model of PTSD highlights these networks:

• Salience Network: Detects and prioritises salient/interoceptive and potential threat cues.

• Default Mode Network (DMN): Supports autobiographical memory and self-referential processing.

• Central Executive Network (CEN/FPN): Enables cognitive control, working memory and decision-making.

PTSD is associated with disrupted interactions among these systems after trauma.

A 19-year-old presents with daily “fits.”

Sudden leg collapse, violent shaking, awareness intact; episodes can run for hours. 

She senses the start and finish, but can’t change the course.

Let’s break down her case and see how multidisciplinary learning in medicine is vital 🧵👇 Neurologist review:

• 3 years of daily whole-body shaking episodes up to 7 hours.

• Fully lucid and able to converse; typically sits or lies down when they start.

• Home videos show irregular, intermittent, asynchronous jerks of arms/legs.

• Impression at the time: consistent with psychogenic non-epileptic seizures (PNES).

ADHD isn’t “just behavioural”...

Converging neuroimaging data show consistent structural and functional brain differences across development.

Here are 7 anatomical brain changes in ADHD and what clinicians need to know about each👇🧵 #1: Global Brain Volume Reduction

The most consistent finding in ADHD is an overall reduction in total brain size with specific changes in the caudate nucleus, prefrontal cortex white matter, corpus callosum and cerebellar vermis. [Tripp and Wickens, 2009]

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? 👇 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].

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👇 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)

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. 🧵👇 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.

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. 🧵👇 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.

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 🧵👇 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:

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.

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.

Why does ADHD frequently co-occur with sleep dysfunction and sometimes mimic other sleep disorders?

Sleep dysfunction isn’t just a secondary issue in ADHD.

It often reflects deeper interactions with emotion, arousal, and circadian regulation.

Here’s what you need to know about REM-atonia and how its disruption contributes to complex sleep issues in ADHD with comorbidities. 👇🧵 REM atonia: What happens in healthy REM sleep?

Normal REM sleep includes:

• Subcoeruleus (SLD) activation

• GABA/glycine release

• Motor inhibition

This suppresses movement during dreams, essential for sleep quality and neurological regulation.

ADHD isn’t just an “attention” problem.

It’s impaired prefrontal regulation across distributed circuits (PFC–striatal–cerebellar–salience networks) that shape attention, inhibition, and emotion.

Here’s how these circuits interact and what clinicians need to know about the neurobiology behind ADHD 🧵👇 The prefrontal cortex (PFC) directs top-down attention, choosing what’s relevant, suppressing distraction, and maintaining goal-oriented focus.

When this system falters, stimulus-driven (“bottom-up”) networks dominate, explaining distractibility and inconsistent attention in ADHD.

75% of anti-NMDA receptor encephalitis cases first present to psychiatrists, not neurologists.

Could a manic or psychotic episode be an immune-mediated brain ‘attack’?

Here’s what psychiatrists need to know about identifying and managing neuroinflammation.

1/10🧵 Atypical First-Episode Mania

A 21-year-old woman presents with:

• Pressured speech

• Disinhibition

• Decreased need for sleep

No prior psychiatric, substance, or trauma history.

Viral prodrome + non-response to antipsychotics.

2/10🧵

A 17-year-old student was brought to the clinic with a one-week history of unusual behaviour and beliefs.

He was convinced his laptop and phone were controlling his actions, and refused to use them.

Let’s walk through his case and explore what it teaches us about internet use, emerging psychosis, and psychiatry in the digital age.

1/15🧵 Initial Presentation

He believed unknown groups were tracking him through electronic devices.

As a result, he became reluctant to leave the house.

Mood was perplexed; insight partial.

2/15🧵

Why do many people with BPD feel constant discomfort in their own body?

French psychoanalyst Didier Anzieu used the “skin ego” as a metaphor—a psychological “container” that helps hold the self together.

In BPD, that container can feel fragile, porous, or easily disrupted.

Here’s how early experiences can shape self-boundaries and affect regulation and why recognising these patterns can improve care.

1/12🧵 Many people with BPD describe distress as a bodily experience: crawling skin, burning face, the urge to escape their body.

These may reflect disrupted self-boundaries and affect containment not just a dermatological problem.

2/12🧵

Cariprazine is a third-generation antipsychotic with D3-preferring D3/D2 partial agonism and 5-HT1A partial agonism. (Kiss et al., 2019)

Its unique receptor profile is associated with improved motivation, mood, and cognitive functioning.

Here’s what clinicians need to know about its mechanism, pharmacokinetics, and clinical application. 🧵👇 Mechanism of Action Overview

Cariprazine’s receptor activity includes:

• Partial agonism at D3 and D2 receptors
• Partial agonism at 5-HT1A receptors
• Antagonism at 5-HT2A receptors

D3 receptor engagement is linked to negative-symptom improvement; cognitive benefits remain postulated.

Why do two patients respond so differently to the same antidepressant?

Psychotropic efficacy isn’t just about dose or diagnosis. It’s also about how the drug is metabolised.

Here’s what you need to know about CYP450 metabolism in psychiatry, and how it can improve treatment outcomes and reduce adverse effects. 👇🧵 The CYP450 enzyme system metabolises many psychotropics.

Each patient inherits a metabolism “speed” for key enzymes:

 • Poor → slower clearance = ↑ side effects
 • Ultrarapid → faster clearance = ↓ efficacy

Same drug, same dose, different outcomes.

Are we reliably identifying comorbid Autism and ADHD in clinical assessments?

ADHD occurs in 30–80% of people with ASD, while ASD occurs in 20–50% of people with ADHD (Lau-Zhu, 2019; Young et al., 2020). Yet the pair is still missed too often.

Here’s what every clinician needs to know about their overlap, and what to do when it shows up in your practice. 🧵👇 Historically, these conditions were seen as mutually exclusive.

ASD was listed as an exclusion for ADHD until DSM-5 revised this in 2013 (APA, 2013).

Now, dual diagnosis is not only permitted, it’s essential.