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Feb 2 10 tweets 3 min read Read on X
1 in 3 COVID-19 survivors may develop a neuropsychiatric or neurological condition within 6 months.

From anosmia to strokes, the virus can leave lasting effects on the brain.

Research shows over 33% of post-COVID patients develop conditions like anxiety, depression, or cognitive dysfunction (Taquet et al., 2021).

Here’s how SARS-CoV-2 impacts the Central Nervous System (CNS), its neuropsychiatric sequelae, and the key considerations for clinicians 👇🧵Image
How does SARS-CoV-2 'invade' the CNS (central nervous system)?

Olfactory route: The virus binds ACE2 (angiotensin-converting enzyme 2) receptors, travels via the olfactory bulb and enters the brain.

Bloodstream: Disrupted BBB (blood-brain barrier) allows infected monocytes and cytokines to enter.

Viral RNA in cerebrospinal fluid supports CNS involvement (Moriguchi et al., 2020).Image
Anosmia And Dysgeusia

Anosmia (loss of smell) and dysgeusia (loss of taste) occur as SARS-CoV-2 targets ACE2 receptors in the olfactory epithelium, impairing neural pathways.

Research shows anosmia often precedes respiratory symptoms (Spinato et al., 2020).

💡 Psych Scene Tip: Persistent anosmia >6 weeks may indicate neuroinflammation—monitor recovery timelines closely.Image
Pathophysiology Of CNS Involvement

SARS-CoV-2 affects the CNS via:

Direct infection: Viral invasion damages neurons.

Hypoxia: Oxygen deprivation triggers neuronal injury.

Cytokine storm: Pro-inflammatory cytokines disrupt the BBB.

Hypercoagulability: Microthrombi increase stroke risk.Image
Neuropsychiatric Symptoms In COVID-19 Patients

Hospitalised patients often present with delirium, agitation, or encephalopathy. Long-COVID symptoms include brain fog, anxiety, and PTSD (post-traumatic stress disorder).

69% of ICU survivors had agitation, and 33% developed dysexecutive syndrome (Helms et al., 2020).

💡 Psych Scene Tip: Use tools like the FAB (Frontal Assessment Battery) to evaluate dysexecutive symptoms post-ICU.
The Long Tail of COVID-19

Long-COVID includes:

• Chronic fatigue.
• Cognitive deficits resembling encephalopathy.
• Sleep disturbances and PTSD.

32% of long-COVID patients report persistent neurocognitive symptoms (Evans et al., 2021).
COVID-19 increases stroke risk

Hypercoagulability in COVID-19 causes:

Ischaemic strokes (microthrombi).
Haemorrhages (endothelial damage).

Elevated D-dimer correlates with thrombotic complications (Mao et al., 2020).

💡 Psych Scene Tip: Assess post-COVID patients for subtle neurovascular signs like aphasia or hemiparesis.
Psychiatric Manifestations In ICU Survivors

ICU stays often result in long-term psychiatric effects like PTSD, depression, or anxiety.

25–50% of ICU survivors experience lasting psychiatric symptoms (Sukantarat et al., 2007).

💡 Psych Scene Tip: For ICU survivors with PTSD, consider trauma-focused CBT (cognitive behavioural therapy) and short-term psychotropics.
The Psychiatrist’s Role In Covid-19 Care

When addressing neuropsychiatric complications like PTSD, depression, and cognitive dysfunction. Multidisciplinary collaboration is key.

Research shows early intervention reduces pandemic-related mental health fallout (Huremović et al., 2019).Image
Brain fog, fatigue, PTSD, and cognitive impairment are common post-COVID.

Improve your expertise in assessing and managing these conditions.

Join our Chronic Fatigue Syndrome (ME/CFS) & Long COVID Masterclass to learn:

✅ Neuropsychiatric sequelae of SARS-CoV-2
✅ Cognitive impairment & fatigue management
✅ Practical treatment strategies for Long COVID

Click the link below to get access:

psychscene.co/3Q3gpDn

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More from @psycheureka

Feb 2
A 22-year-old woman was misdiagnosed with schizophrenia after presenting with paranoia and agitation. 

Days later, seizures and hypoventilation revealed the true diagnosis: anti-NMDAR encephalitis.

75% of cases first present with psychiatric symptoms like psychosis or agitation, often leading patients to psychiatry before neurological signs appear (Espinola-Nadurille et al, 2022).

Learn more about its pathogenesis, illness progression and prognosis 👇🧵Image
What is Anti-NMDAR Encephalitis?

Anti-NMDAR (N-methyl-D-aspartate receptor) encephalitis is an autoimmune condition where antibodies target NMDA receptors (GluN1 subunit).

This disrupts synaptic signalling, leading to:

1️⃣ Psychiatric symptoms: Psychosis, paranoia, agitation

2️⃣ Neurological symptoms: Seizures, dyskinesias, autonomic instabilityImage
Pathogenesis Of Anti-NMDAR

Antibodies bind NMDA receptors, causing internalisation and dysfunction. 

This leads to:

• Psychosis: Dopaminergic disinhibition in the mesolimbic pathway
• Neurological impairment: Disrupted synaptic plasticity

The overlap between psychiatric and neurological symptoms is key to recognising this condition.Image
Read 11 tweets
Feb 1
Phenomenology in psychiatry is like ECG interpretation in cardiology—it’s about recognising patterns before a crisis unfolds.

Here’s a structured breakdown of thought pathology and why it’s clinically critical 👇 Image
Thoughts are shaped by salience—our mind’s ability to prioritise stimuli.

As salience intensifies, thoughts become more:

✅ Rigid
✅ Distressing
✅ Uncontrollable

Understanding this hierarchy is key to early intervention. 🧵
1️⃣ Normal Worry: Adaptive Thought Processing

✔️ A transient concern in response to stress
✔️ Flexible salience—relief occurs when shifting focus
✔️ No distress or impairment in daily life

Example: “I need to prepare for my presentation tomorrow.”

✅ Non-pathological
Read 10 tweets
Jan 30
Paliperidone Long-Acting Injectable (LAIs) may reduce schizophrenia relapse rates by up to 89% compared to oral antipsychotics.

Monthly (Sustenna), 3-monthly (Trinza), and 6-monthly (Hafyera) options offer tailored approaches for adherence and stabilisation. Studies, like the Route 6 trial, suggest that Hafyera and Trinza may sustain remission for over 12 months in most patients.

Learn about its dosing, pharmacokinetics, and missed-dose protocols for improved clinical outcomes👇🧵Image
How Paliperidone LAIs Work

Paliperidone, the active metabolite of risperidone, works through:

D2 receptor antagonism: May improve positive symptoms.

5-HT2A antagonism: May enhance mood and reduce EPS.

α1 & α2 effects: May stabilise mood and reduce anxiety.

Long-acting injections (LAI) formulations bypass first-pass metabolism, ensuring stable plasma levels.Image
Pharmacokinetics Of Paliperidone LAI

Why it matters: Tmax and half-life influence onset, duration, and dosing.

Sustenna (PP1M): Tmax ~13 days; half-life 25-49 days.

Trinza (PP3M): Tmax ~30-33 days; half-life up to 139 days (gluteal).

Hafyera (PP6M): Half-life ~159 days, detectable for >18 months post-injection.

Steady plasma levels may reduce peaks and troughs, improving symptom stability.Image
Read 10 tweets
Jan 30
How does alcohol rewire the brain to drive dependence and compulsivity?

Recent research shows that alcohol disrupts the brain’s reward and inhibitory systems, fueling compulsive behaviours and dependence. 

Let’s explore the neurobiology behind Alcohol Use Disorder (AUD). 👇🧵 Image
Image
Alcohol’s Shortcut to Pleasure

Here’s what happens: 

1️⃣ Alcohol triggers endorphin release, activating mu-opioid receptors.

2️⃣ This suppresses GABA release, removing the brakes on dopamine neurons in the ventral tegmental area (VTA).

3️⃣ Dopamine surges in the nucleus accumbens, reinforcing alcohol’s effects.
Why the Brain Demands More

Over time, dopamine sensitivity declines. 

The brain needs more alcohol to achieve the same reward, fueling compulsive use. 

This cycle underpins the neurobiology of AUD and its profound grip on behaviour.
Read 6 tweets
Jan 29
Women with PCOS are nearly 3x more likely to develop depression than those without it.

This multifaceted disorder impacts mental health, sleep, and metabolism, which demands a multidisciplinary approach.

Let’s explore the pathophysiology, psychiatric comorbidities, and treatment strategies every clinician should know. 👇🧵Image
PCOS Diagnostic Criteria 

The modified Rotterdam criteria require 2 out of 3 features:

• Biochemical or clinical hyperandrogenism
• Oligo/anovulation
• Polycystic ovarian morphology on ultrasound

Ethnicity and context matter when interpreting androgen levels. But what drives these systemic effects?
Pathophysiology of PCOS

PCOS disrupts the hypothalamus-pituitary-gonadal (HPG) axis, resulting in:

• ↑ LH: FSH ratio
• Impaired follicle maturation (cystic appearance on ultrasound)
• Excess androgens from theca cells
• ↓ Oestradiol from disrupted aromatase activity

These disruptions explain many of PCOS's downstream effects on health.Image
Read 10 tweets
Jan 27
ADHD affects 5.9% of children worldwide, with symptoms persisting into adulthood in up to 65% of cases (Faraone et al., 2021).

Untreated ADHD increases the risks of injuries, comorbidities, and even premature death.

Here’s how ADHD evolves across the lifespan—and what it means for psychiatric care. 🧵👇Image
ADHD doesn’t “end” in childhood—it transforms:

Childhood: Hyperactivity dominates, with academic challenges.

Adolescence: Emotional dysregulation and inattention emerge as hyperactivity subsides.

Adulthood: Inattention persists, affecting work and relationships.

Persistence rates vary: 34%–65%, depending on diagnostic criteria (Faraone et al., 2006).

💡 Psych Scene Tip: Regularly re-evaluate symptoms during transitions (e.g., school to work) to tailor care.
Genetics and ADHD

ADHD is one of the most heritable psychiatric disorders, with genetics contributing ~76% (Faraone et al., 2005).

Key insights:

Polygenic Basis: Genes like DAT1, DRD4, and SNAP-25 affect dopamine signalling (Gizer et al., 2009).

Gene-Environment Interactions: Prenatal stress, smoking, and low birth weight heighten risks (Thapar et al., 2013).

GWAS: Identified loci show small but significant effects on ADHD susceptibility.
Read 10 tweets

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