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Sep 2 12 tweets 2 min read Read on X
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 🧵Image
#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🧵
#2 Six Domains to Consider in ADHD Diagnosis & Management

● Cognition
● Reward learning
● Behavioural inhibition
● Fight-flight response
● Activity
● Behavioural activation

3/12🧵
#3 The Prefrontal Cortex & the Goldilocks Effect

Optimal prefrontal cortex functioning requires a balanced level of dopamine and noradrenaline.

Too much or too little can impair cognition and other domains.

4/12🧵
#4 High Comorbidity

ADHD often co-occurs with:

● Sleep disorders
● Trauma
● Autism spectrum disorders
● Bipolar disorder
● Depression

Comorbidity is the rule, not the exception, with up to 80% comorbidity.

5/12🧵
#5 Recognise the Complexity of ADHD – The Iceberg Model

ADHD is paradoxically a complex condition. Multiple factors can influence ADHD, including organic, psychological, social, dietary, and lifestyle aspects.

A comprehensive evaluation is essential for effective management.

6/12🧵
#6 The FRAME of ADHD Treatment

ADHD treatment should prioritise long-term outcomes and functionality.

A lifespan approach is key due to prefrontal and striatal circuit changes over the lifespan.

7/12🧵
#7 Not Just Stimulants

ADHD pharmacology requires a thorough evaluation of key functions and foreseeability.

Recognise the key role of non-stimulants in optimisation.

Consider non-pharmacological approaches alongside medication.

8/12🧵
#8 Understanding the Difference between Phasic vs Tonic Dopamine

Phasic dopamine = brief, high-intensity spikes

Tonic dopamine = steady and sustained

Proper balance is crucial for optimal ADHD treatment.

9/12🧵
#9 Avoid Sensitisation & Desensitisation Cycles

Long-term phasic dopamine activity can lead to sensitisation and desensitisation cycles.

This may cause a diminished sense of reward over time.

These cycles are associated with side effects, tolerance, and non-adherence.

10/12🧵
#10 Optimal Functioning & Mesolimbic Pathways

Successful ADHD management requires balanced modulation of mesolimbic pathways (arousal and stress) and tonic dopamine receptors in the dorsal striatum (goal-directed actions and habits).

11/12🧵
Want to put these principles into practice?

Refine your clinical skills and gain a deeper framework for assessment and management in ADHD by visiting our course, “Adult ADHD Clinical Training Program | 6-Course Series for Psychiatrists & GPs” on The Academy:



12/12🧵psychscene.co/4fHBxLf

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More from @psycheureka

Sep 3
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. 👇🧵Image
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.Image
The salience network

Dysregulation of the salience network drives hypervigilance.

When the anterior cingulate cortex (ACC) and insula over-detect threat, even benign stimuli trigger danger responses.

This hyperactivation not only fuels arousal but also diverts resources from other networks, reinforcing reactivity. 

(Yehuda et al., 2015)
Read 13 tweets
Aug 28
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. 👇🧵Image
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.
The Default Mode Network (DMN) & Aspects of the Ego

The DMN is active during daydreaming, rumination, and self-referential thoughts.

Increased activity: Linked to intrusive memories, depressive rumination, and trauma recall.

Task-related failure to suppress DMN: Seen in ADHD.

Dysconnectivity within the DMN: Observed in schizophrenia.

Many accounts link the DMN to self-referential/Ego functions; the SN is largely subcortical (amygdala/ventral striatum/brainstem reward).Image
Read 9 tweets
Aug 27
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. 👇🧵Image
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?
Sublingual Dexmedetomidine

Sublingual film, FDA-approved (2022).

● Rapid calming, non-invasive

● Sedation without respiratory depression

● May cause hypotension, bradycardia, somnolence

A practical option when patients resist injections.
Read 10 tweets
Aug 25
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.
The science of PMR

Patients activate the parasympathetic nervous system by intentionally tensing and releasing muscles, which is the body’s “rest and digest” mode.

Over time, this builds interoceptive awareness, helping patients recognise stress signals before they become overwhelmed.
Read 13 tweets
Aug 20
7 key differences in females with ADHD

Females present with a specific neurobehavioural profile that may contribute to an underdiagnosis and subsequent under-treatment.

Here’s what clinicians need to assess and look out for
🧵👇 Image
1/ Under-recognised, different profile.

Girls/women with ADHD often present with internalising symptoms (low mood, anxiety, emotional lability), so they’re mislabelled with mood/personality disorders and referred late.

💡 Psych Scene Tip:

If chronic anxiety/low mood rides alongside lifelong disorganisation, time-blindness, and procrastination across settings (since <12), screen for ADHD before defaulting to mood/BPD labels.
2/ Masking + compensation delay diagnosis.

Compliance, resilience, perfectionism, and high structure (supportive family/school) can temporarily “hide” impairment, until demands rise. 

Expect later recognition at transitions (primary→secondary school, university, new job, parenthood). 
Read 10 tweets
Aug 19
Which antidepressants work most effectively, and which barely beat placebo?

The largest meta-analysis (Cipriani et al., 2018) compared 21 antidepressants in 116,477 patients, revealing striking differences in efficacy and tolerability.

Here’s how this data can transform your prescribing practice 🧵👇Image
Most ‘Effective’ Antidepressants (Head-to-Head)

In the largest network meta-analysis to date, the following antidepressants consistently outperformed others in head-to-head comparisons for efficacy (odds ratio range: 1.19–1.96):

● Agomelatine
● Amitriptyline
● Escitalopram
● Mirtazapine
● Paroxetine

These consistently outperformed others.

Note: Just because a drug ranks high in efficacy doesn’t mean it’s the best choice for every patient.Image
The Numbers Behind Antidepressant’s Efficacy

Odds ratios (OR) provide a clearer picture.

● Amitriptyline: OR = 2.13 (113% higher odds vs. placebo)
● Reboxetine: OR = 1.37 (37% higher odds)

All drugs beat the placebo, but not equally.

Higher OR = greater efficacy. Image
Read 10 tweets

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