The Academy by Psych Scene

The Academy by Psych Scene is a transformative platform tailored for psychiatry professionals who seek to excel in their field. Our meticulously curated content, crafted by psychiatry experts and elite learning designers, focuses on enhancing your practical knowledge and clinical expertise at an exceptional value.

Our dynamic courses will give you cutting-edge skills and insights to keep you at the forefront of the rapidly evolving psychiatry landscape. Each course also contributes towards your Psychiatry CME and CPD points, supporting your continuous professional development.

Our mission is to empower health professionals with advanced psychiatric knowledge, fostering transformative change in mental health care.

🎓 100+ hours of cutting-edge, interactive courses
🎓 Video interviews with experts
🎓 Free PDF downloads
🎓 Collaborations platform - ask and share
🎓 Advanced AI for efficient learning
🎓 Earn Psychiatry CME credits / CPD points
🎓 FREE CPD portfolio tracker


The Academy by Psych Scene

ADHD diagnosis is often reduced to symptom checklists, yet real-world, clinical cases are rarely that simple.

Led by Dr Sanil Rege, our live ADHD Masterclass provides clinicians with a clear, clinically usable framework grounded in neurobiology and real, evidence-based cases, designed to help strengthen ADHD diagnostic accuracy and improve treatment precision.

In this course, you’ll learn how to:

Apply systems-based and developmental frameworks to ADHD presentations

Understand dopamine/noradrenaline network dynamics, arousal regulation, and network switching

Identify ADHD using a structured, multi-modal diagnostic framework (history, collateral, tools)

Distinguish comorbidity and drivers of partial/non-response using a staged diagnostic hierarchy

Integrate behavioural/lifestyle interventions alongside ADHD pharmacotherapy

Accreditation:

âś… 7.5 CPD hours (EA 6, RP 1.5)

âś… Self-accreditable with RANZCP

âś… RACGP & ACRRM accredited

âś… Recognised within GPMHSC FPS CPD frameworks

Start learning today. Link in the comment section.

18 hours ago | [YT] | 4

The Academy by Psych Scene

Can Brain Insulin Resistance (BIR) Drive Alzheimer's Disease (AD)?

Most see metabolic disorders, such as BIR, and Alzheimer's as comorbid but distinct conditions.

However, clinical data suggest that BIR acts as a contributor to neurodegenerative processes seen in AD by disrupting central glucose metabolism and synaptic plasticity.

Here’s a neurobiological breakdown of the BIR-AD link.

To learn more about the nuanced neurobiological link between Brain Insulin Resistance (BIR) and Alzheimer's Disease (AD), click the link in the comments below and check out the full article on Psych Scene Hub.

4 days ago | [YT] | 6

The Academy by Psych Scene

Why Does Standard Exposure Therapy Sometimes Underperform in Dissociative PTSD?

Standard PTSD interventions often focus on reducing hyperarousal. However, dissociative symptoms can occur in approximately 15–30% of patients with PTSD, and neuroimaging studies have described distinct patterns of emotion modulation in this subgroup (Lanius et al., 2006).

For these patients, clinicians should assess dissociation before initiating exposure-based treatment, as dissociation has been linked to poorer treatment outcomes and can be associated with symptom worsening when not recognised and managed appropriately.

Here’s a breakdown of how the dissociative phenotype can interfere with exposure-based approaches:🧵👇

To learn more about the intricacies of the dissociative PTSD phenotype and dive deeper into the neurobiological spectrum of trauma, click the link in the comments below and check out the full article on Psych Scene Hub.

4 days ago | [YT] | 6

The Academy by Psych Scene

Can chronically elevated insulin levels contribute to brain insulin resistance (BIR)?

Chronic hyperinsulinaemia and BIR are often treated as separate metabolic phenomena.

However, evidence suggests elevated insulin levels are associated with impaired insulin transport across the blood–brain barrier, contributing to reduced central insulin signalling.

This peripheral–central mismatch is increasingly observed in metabolic and neurodegenerative disorders.

Here’s how this relationship unfolds 👇🧵

To learn more about the nuanced neurobiological link between chronically elevated insulin levels and Brain Insulin Resistance, click the link in the comments below and check out the full article on Psych Scene Hub.

1 week ago | [YT] | 7

The Academy by Psych Scene

Why is Postpartum Psychosis (PPP) Often Misdiagnosed as Postnatal Depression (PND)?

At face value, it’s not surprising how most see PPP and PND as similar points on a spectrum of postnatal mood distress.

However, clinical data suggest that while both manifest affective symptoms, PPP is driven by a hyper-dopaminergic state as compared to PND's typically non-psychotic, slower-onset depressive pathology.

Here’s a neurobiological breakdown of this nuanced distinction between PPP and PND.

To learn more about the nuanced distinction between Postpartum Psychosis (PPP) and Postnatal Depression (PND), click the link below and check out the full article on Psych Scene Hub:

psychscene.co/45PFfih

1 week ago | [YT] | 7

The Academy by Psych Scene

Why Is Psychotherapy Often Limited During Active Addiction?

Psychotherapy is essential in addiction care, but during active substance use or acute withdrawal, the brain may be in a state where higher-order cognitive engagement is biologically constrained.

Addiction is not simply a disorder of 'insight'.

It is a disorder of neurocircuitry.

Here’s the neuroscience behind why treatment sequencing matters: 🧵👇

To learn more about the nuances that delineates psychotherapy and addiction, click the link in the comments below and check out the full article on the Psych Scene Hub.

2 weeks ago | [YT] | 7

The Academy by Psych Scene

Can Smoking Compromise Antipsychotic Efficacy in Schizophrenia?

The interaction between smoking and schizophrenia is complex and multifaceted, with patients consistently showing higher rates of tobacco smoking and heavy nicotine dependence.

One important consideration is the influence smoking has on the CYP450 system.

🧵👇

To learn more about how smoking-induced CYP1A2 induction compromises antipsychotic efficacy in Schizophrenia, click the link below and check out the full article on Psych Scene Hub:

psychscenehub.com/psychinsights/smoking-and-schizo…

2 weeks ago (edited) | [YT] | 7

The Academy by Psych Scene

Why Do Standard Pharmacotherapy Sometimes "Backfire" in Autism Spectrum Disorder (ASD)?

Clinical studies suggest that for some drugs (notably ADHD medications), response may be less robust and adverse effects more common in ASD.

This likely reflects differences in neurodevelopmental wiring and network-level responsivity, rather than a uniform medication response profile.

While stimulants are first-line for ADHD—a condition comorbid in up to 80% of ASD cases—these agents can trigger "iatrogenic agitation" in the ASD population.

Here's a breakdown on why pharmacotherapy can backfire in ASD: 🧵👇

psychscene.co/3Yyv4e0

1 month ago | [YT] | 4

The Academy by Psych Scene

Frequent use of high-potency (high-THC) cannabis is associated with a substantially increased risk of psychotic disorder, particularly in people with underlying vulnerability.

Modern cannabis products often contain higher THC and relatively less CBD, a shift that may increase psychiatric and cognitive harms with early or heavy use: 🧵👇

The brain’s endocannabinoid system primarily involves two receptors:

• CB1 receptors → Abundant in the brain and CNS; involved in memory, reward, emotional processing, and pain modulation.

• CB2 receptors → Predominantly expressed in immune cells and peripheral tissues, with limited but inducible CNS expression, particularly in neuroinflammatory states.

THC is a partial CB1 agonist, disrupting dopamine, GABA, and glutamate signalling, pathways implicated in psychosis and cognitive impairment.

Cannabis & Psychosis

THC can induce acute psychotic-like experiences (e.g. paranoia, perceptual disturbances), even in people without prior psychosis.

Frequent use of high-potency cannabis (“skunk”) is associated with higher risk of schizophrenia-spectrum disorders, especially in those with genetic or clinical vulnerability.

In people who later develop psychosis, cannabis use is associated with an earlier age of onset, typically by several years, though estimates vary across studies.

Gene–environment interactions (e.g. AKT1, COMT) may increase sensitivity to THC, but findings are not yet clinically actionable.

Cognition & memory

THC acutely impairs attention and short-term memory, partly via CB1-rich hippocampal circuits.

Heavy or long-term use is associated with deficits in executive function, processing speed, and decision-making, with partial recovery after abstinence in some users.

Adolescents are particularly vulnerable, as cannabis exposure may interfere with ongoing neurodevelopment.

Cannabis withdrawal commonly includes sleep disturbance, irritability, anxiety, and craving, reflecting neuroadaptation rather than simple “THC accumulation”.

Depression, anxiety & motivation

Many people use cannabis to self-manage anxiety or low mood. However, observational studies link frequent or early use with higher rates of depression and anxiety, though causality is uncertain.

“Amotivational syndrome” remains debated and overlaps with depression, intoxication, and social confounders.

THC vs CBD

• THC: psychoactive; CB1 partial agonist; associated with euphoria, anxiety, transient psychotic symptoms, and memory impairment.

• CBD: non-intoxicating; modulates multiple systems. Shows preliminary antipsychotic signals, but evidence is limited and inconsistent.

The THC:CBD ratio matters.

Higher CBD content may attenuate some THC-related adverse effects, but this is not a reliable way to prevent psychosis and should not be presented as protective or therapeutic.

Sativa vs indica?

These labels have poor scientific validity.

Clinical effects depend on THC dose, THC:CBD ratio, route of administration, terpene profile, and individual vulnerability, not strain names.

Cannabis & Schizophrenia

Cannabis use is common in schizophrenia (often ~25–40%, varying by setting).

While some patients report short-term relief of affective symptoms, cannabis use is consistently associated with symptom exacerbation, higher relapse rates, and poorer long-term outcomes.

Clinical Takeaways for Psychiatrists

Screen for: age of first use, frequency, potency (THC content), route, and personal/family history of psychosis.

Counsel: early and heavy use increases psychosis risk; patients with psychotic disorders should avoid high-THC products. CBD is not an evidence-based treatment for psychosis.

Want to learn more about the link between cannabis and schizophrenia?

Deepen your knowledge of cannabis-induced psychosis and schizophrenia management with our article, The Psychopharmacology of Cannabis & its Impact on Mental Health by Dr Sanil Rege & Prof David Castle.

Deepen your knowledge of cannabis-induced psychosis and schizophrenia management with our article, The Psychopharmacology of Cannabis & its Impact on Mental Health by Dr Sanil Rege & Prof David Castle. Click the link below.

psychscene.co/3YWXqyG

1 month ago (edited) | [YT] | 6

The Academy by Psych Scene

How Do Brain Functions Differ in Patients With ASD?

Autism Spectrum Disorder involves complex neurobiological shifts across distinct functional domains.

While once viewed as a simple behavioural “deficit,” studies revealed a pattern of atypical connectivity and structural organisation that alters how the brain processes social and sensory data.

Meaning, the ASD brain follows a unique computational logic rather than a "broken" one.

Here’s a breakdown of the neurobiological substrate of ASD.

To understand the full scope of ASD neurobiology and its distinct clinical phenotypes, check out the full course on The Academy using the link below:

psychscene.co/4q0wnOJ

1 month ago | [YT] | 6