Psychiatry Excellence Profile picture
Aug 20 10 tweets 2 min read Read on X
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). 
3/ Emotional dysregulation (ED) ≠ BPD by default

ED can be more common/severe in females with ADHD and overlaps with BPD; ED severity alone doesn’t distinguish the two.

💡 Psych Scene Tip: Take a developmental history and look for ADHD traits across settings.  
4/ Hyperactivity–impulsivity (H/I) looks different.

On average, girls show lower H/I severity than boys, with more subtle restlessness and impulsivity, which is one reason they’re missed. Meta-analyses and newer reviews converge on this signal. 

💡 Psych Scene Tip:

Screen for quiet hyperactivity: ask about leg-jiggling, hair-twirling, rapid speech, interrupting when excited, snap decisions, and “finding reasons to move” during long sits.
5/ Inattention: the giveaway.

Think “easily overwhelmed,” disorganised, task initiation problems, mental planning difficulties. 

Item-level evidence highlights attentional symptoms as especially informative for detecting ADHD in females.
6/ Hormones matter (across the lifespan).

Symptoms commonly fluctuate with the menstrual cycle and can change during pregnancy and perimenopause. 

💡Psych Scene Tip: ask patients to track symptoms vs. cycle; consider timing meds/adjuncts accordingly.
7/ Comorbidities to actively screen for.

• Eating disorders: ADHD is linked to a higher risk across AN/BN/BED; effect sizes are clinically meaningful (bi-directional association). 

• Substance use: Elevated alcohol/cannabis risk; some data suggest females with ADHD (without other comorbidity) may have a higher risk than males. Ask early. 
Clinician takeaway (save this):

Under-recognised internalising profiles + compensation → later diagnosis. Look for inattention/EF burden, subtle H/I, track hormones, and screen EDs/SUDs.
From screening to nuanced management of female ADHD presentations, the Adult ADHD Clinical Training Program delivers case-based tools across diagnosis, pharmacotherapy, perinatal care, and ASD, click the link below to learn more:

psychscene.co/4fHBxLf

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More from @psycheureka

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
Aug 16
Why is the MEQ (Modified Essay Question) one of the hardest exams in psychiatry?

Because it doesn’t just test what you know, it tests how you think.

And here’s the problem: most psychiatric training doesn’t actually teach us to think. 🧵

1/12 Image
We’re taught to memorise.

To conform.

To defer to authority and quote the guidelines.

But real-world psychiatry? That’s messy. Uncertain. Full of grey zones.

The MEQ throws you right into that world.

2/12🧵
Take this:

Textbook:

“How to manage akathisia”

Sounds simple.

But now look at a real-world MEQ slice:

“A 52-year-old male with schizophrenia on aripiprazole 10mg nocte for 1 year reports leg restlessness. It’s keeping him awake. Outline your approach.”

See the difference?

3/12🧵
Read 12 tweets
Aug 13
Molly, age 14, was found wandering in Cork city, confused, agitated, and rifling through bins.

She has no psychiatric history and was sectioned under suspicion of acute psychosis. But a butterfly-shaped rash redirected her diagnosis.

Let’s walk through this case and explore what it teaches clinicians about diagnosing neuropsychiatric disease.

1/14🧵Image
Initial Presentation

Molly presented in 1994.

Symptoms: 

● Disorientation

● Behavioural disinhibition

● Public agitation

Initial impression: primary psychotic disorder.

She had no prior mental health history.

2/14🧵
Autoimmune Features Identified

On assessment, clinicians noted:

🔍 Malar (butterfly) rash

🔍 Patchy alopecia

🔍 Positive anti-dsDNA antibodies

🔍 Low complement (C3)

Renal function remained normal.

These findings shifted diagnostic suspicion toward systemic autoimmunity.

But what could be the real diagnosis?

3/14🧵
Read 14 tweets
Aug 12
Pregabalin and gabapentin are widely prescribed for neuropathic pain and seizures

Yet, their rising misuse potential and risks of dependency are raising alarms among clinicians

Are we underestimating the dangers?

Here’s an evidence-based guide to their mechanisms, clinical uses, and how to balance the benefits and risks 👇🧵
Mechanism of Action

Gabapentinoids bind the α2δ subunit of voltage-gated calcium channels, reducing excitatory neurotransmitter release (glutamate, noradrenaline, substance P).

Pregabalin is 6x more potent in binding than gabapentin.
Despite being GABA analogues, they do not act on GABA receptors. 

Instead, they influence synaptogenesis by inhibiting thrombospondin binding to α2δ-1—critical for excitatory synapse formation.
Read 12 tweets
Aug 9
76% of ADHD patients achieved >50% symptom reduction when neurofeedback protocols were tailored to individual EEG profiles, 

Using QEEG, researchers matched each patient to a protocol based on their brainwave patterns — producing significant improvements in inattention and hyperactivity.

Here’s what you need to know about EEG subtypes in ADHD, and how they can guide treatment when standard approaches fail.

1/15 🧵Image
QEEG can reveal brain-activity heterogeneity in ADHD that checklists miss.

Important: major guidelines don’t recommend QEEG to diagnose ADHD. Think of it as a potential stratification aid when progress stalls.

2/15 🧵
What QEEG does: records theta/alpha/beta rhythms and compares them to normative databases.

Deviations create a profile that may help plan treatment.

3/15 🧵
Read 15 tweets
Aug 4
Why is bipolar disorder often diagnosed years after symptom onset?

A meta-analysis of 9,415 patients found the average delay to accurate diagnosis and treatment is 5.8 years (Dagani et al., 2016).

Let’s examine why this happens and how clinicians can diagnose it earlier. 👇🧵
This delay has consequences.

Nearly 6 years of:

– Unstable mood episodes

– Functional and interpersonal decline

– Missed opportunities for psychoeducation

– Risk of antidepressant-induced destabilisation
The biggest diagnostic trap?

Most patients first present with depression, not mania.

Without a clear manic history, they’re often misclassified as having unipolar depression.
Read 14 tweets

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