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.

Is dissociation in PTSD just a symptom, or the brain’s survival strategy?

Around 15–30% of patients with PTSD experience dissociative symptoms such as depersonalisation or derealisation.

Let’s discover why recognising dissociation is critical for tailoring therapy and improving outcomes. 👇🧵 Two PTSD phenotypes:

1️⃣ Emotional undermodulation → hyperarousal, re-experiencing.

2️⃣ Emotional overmodulation → numbing, detachment, dissociation.

Understanding these helps match interventions: 

- grounding for hyperarousal
- stabilisation before trauma processing in dissociation.

A woman was admitted with acute psychosis, marked by fixed somatic delusions.

She was convinced that parasites were crawling under her skin.

With no prior psychiatric history, her condition deteriorated rapidly as new syndromes emerged.

Let’s walk through her case and examine what it teaches us about the interface between neurology and psychiatry. 

1/16🧵 Initial presentation

The first phase was psychosis, dominated by delusions of infestation.

Her affect was disturbed, but she remained oriented and responsive.

There was no background of schizophrenia, bipolar disorder, or substance misuse.

2/16🧵

Sleep isn’t just “off.”

The locus coeruleus (LC), the brain’s noradrenaline hub, stays active in a patterned way, shaping when we sleep deeply, dream, or wake too easily. (Osorio-Forero 2022)

Here’s why it matters clinically.

1/11🧵 Classic view: LC goes quiet at night.

Revised view: it’s state-dependent.

• NREM: activity is low but rhythmic.
• REM: LC neurons are almost completely silent.

2/11🧵

Up to 90% of patients with ADHD experience at least one comorbidity, from anxiety to substance use disorders (Kessler et al., 2006).

These overlaps complicate diagnosis and treatment, making it essential for clinicians to recognise and address them effectively.

Here are 10 key ADHD comorbidities and evidence-based strategies to navigate them. 👇🧵 1. Behavioural Disorders & ADHD

Oppositional Defiant Disorder (ODD) overlaps with ADHD (irritability, reactivity) but includes defiance and vindictiveness.

→ Mild: Start with stimulants (e.g., methylphenidate).
→ Moderate-severe: Add CBT or parental training. 
→ Severe: Consider risperidone.

Conduct Disorder (CD) involves persistent aggression or deceit, risking antisocial outcomes.

→ Combine stimulants with therapy. 
→ Severe: Use SSRIs or antipsychotics like risperidone.

Why do two patients with the same trauma history follow such different paths, one recovers, while the other remains ‘stuck’?

Research shows PTSD is not a single disorder but a heterogeneous condition with distinct phenotypes and mechanisms.

Here are 10 clinician insights that explain these differences and can guide better outcomes in practice. 👇🧵 #1 PTSD is heterogeneous

Not all PTSD looks the same.

Fear, dysphoria, and distress contribute differently to each patient’s presentation.

Recognising this heterogeneity is the first step to tailoring treatment.

How many patients treated for depression are actually struggling with undiagnosed Obstructive Sleep Apnea (OSA)?

Up to 20% of the general population has OSA, and studies show a strong bidirectional link with major depressive disorder (MDD).

Here’s how OSA and depression overlap, and what clinicians can do to detect and treat it earlier. 👇🧵 Shared symptoms

OSA and depression often look alike:

● Fatigue, daytime sleepiness

● Poor concentration

● Irritability, psychomotor slowing

● Weight changes

This overlap blurs diagnosis and may delay appropriate treatment.

Is there an antipsychotic that acts like an antidepressant at one dose and an antipsychotic at another?

Amisulpride is unusual in psychiatry for this dose-dependent dual action.

At low doses, it can relieve depression and negative symptoms; at higher doses, it treats psychosis (Scatton et al., 1997).

Here’s how its mechanism, pharmacokinetics, and clinical applications can help you tailor care more precisely. 👇🧵 Amisulpride’s Mechanism of Action 

1. Low doses (<400 mg/day) → Blocks presynaptic D2/D3 autoreceptors → Increases dopamine release → Improves negative symptoms and depression.

2. High doses (400–1200 mg/day) → Blocks postsynaptic D2/D3 receptors → Reduces positive symptoms in schizophrenia (Scatton et al., 1997).

Why do some patients sleep 8–10 hours yet still wake exhausted?

Because fatigue is not only about sleep duration, it reflects disrupted brain networks that leave the mind feeling foggy, unrefreshed, or in a state of hyperarousal.

Here’s how to reframe fatigue clinically and apply four structured steps to support patients more effectively. Fatigue is more than tiredness

Patients describe:

● “My brain feels foggy.”

● “My body feels heavy.”

● “I’m wired but tired.”

Fatigue is not laziness. It’s a neuropsychiatric symptom that reflects disrupted energy regulation across cognitive, emotional, and physical domains.

2/12 🧵

Up to 60–80% of patients with mood or anxiety disorders experience sexual dysfunction, often worsened by antidepressants (Taylor et al., 2021).

Yet most suffer in silence. They may feel embarrassed, fear being dismissed, or avoid raising it, so the problem remains hidden.

Here’s how you can uncover, validate, and manage this under-discussed side effect..

1/12 🧵 Sexual dysfunction is not “just a side effect.”

● It affects intimacy and relationships.

● It undermines treatment adherence.

● It worsens depression outcomes.

Patients may feel: “I got help for my mood, but lost a part of myself.”

Asking about it can be the first step toward restoring trust.

2/12 🧵

Why do some patients remain 'trapped' in flashbacks, hypervigilance, and emotional dysregulation after trauma?

The answer lies in the breakdown of three large-scale brain networks: the salience network, the default mode network (DMN), and the central executive network (CEN).

Here’s how understanding these networks can help you interpret symptoms more precisely and tailor interventions for your patients. 👇🧵 The integrated model

The Integrated Model of PTSD highlights the interplay of three core networks:

● Salience network → prioritises threat-related stimuli.

● DMN → integrates autobiographical memory and self-reflection.

● CEN → enables cognitive control and flexible decision-making.

PTSD emerges when these networks fail to recalibrate after trauma.

ADHD has an ~80% chance of a comorbidity.

It is often missed or misdiagnosed, leading to delayed care or inappropriate treatment.

ADHD is not a checklist, it is a longitudinal diagnosis requiring developmental history, functional impact, and contextual formulation.

Here are 10 essential points to guide diagnosis and management. 🧠👇

1/11 🧵 #1 ADHD is a Heterogeneous Condition

An individualised approach is critical; there is no one-size-fits-all solution.

Focus on specific domains, not just the label.

2/11🧵

Did Freud anticipate the brain’s 'hidden' networks?

His model of the Id, Ego, and Superego was theoretical, but modern neuroscience points to striking parallels.

While Freud wasn’t describing brain networks, clinicians use his framework heuristically, with the Default Mode, Salience, and Executive Control Networks offering a useful analogy.

Here’s how these brain networks shape behaviour, trauma, and psychiatric disorders. 👇🧵 The Triple Network Model

Brain function relies on three key networks:

1️⃣ Default Mode Network (DMN) – Self-reflection, memory, mind-wandering

2️⃣ Salience Network (SN) – Detects & prioritises important stimuli

3️⃣ Executive Control Network (ECN) – Goal-directed thinking, cognitive control

The Salience Network acts as a switch between internal thought (DMN) and external task focus (ECN).

🧠 Dysfunction in this system is linked to schizophrenia, depression, and PTSD.

Do patients with schizophrenia or bipolar disorder always have to be heavily sedated when agitated?

A new study (Mashaw, 2025) highlights that agitation isn’t just disruptive. It signals distress, resistance to care, and safety risks.

Here are emerging treatments that can calm without over-sedation, helping you manage agitation more safely and effectively in daily practice. 👇🧵 Agitation is one of the most urgent psychiatric emergencies.

Traditional medications often calm quickly but bring significant risks:

● Extrapyramidal symptoms (EPS)

● Respiratory depression

● Falls, fractures, cognitive impairment, and over-sedation

Clinicians need safer pathways that preserve engagement.

So what are the new treatments that can reduce these risks?

What if your patient’s biggest struggle isn’t the thought, but the tension in their body?

Progressive Muscle Relaxation (PMR) helps interrupt that cycle, reducing arousal and reinforcing regulation.

Here’s how PMR can support patients with chronic anxiety and tension, and how clinicians can integrate it in practice. 👇🧵 When dysregulation hits, the body often reacts before the mind.

Tension builds → signals threat.

Release → signals safety.

PMR retrains patients to notice tension early, release it, and send calming cues through their nervous system.