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neurodev model Flashcards

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1
Q

Q: Define a neurodevelopmental model of psychiatric disorder.

A

A:
* Abnormal brain development occurs early in life
* Neural circuits form atypically
* Symptoms emerge later when those circuits mature or are stressed
* Key phrase for exam: “Abnormal developmental trajectory of neural circuits.”

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2
Q

Q: What does “”abnormal developmental trajectory”” mean?

A

A:
* Brain development is dynamic and staged.
* If early deviation occurs: Later maturation stages amplify the abnormality.
* Symptoms emerge when:
* Cognitive demands increase
* Circuits fail under stress

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3
Q

Q: What are the 6 stages of normal brain development?

A

A:
* 1️⃣ Neurogenesis
* 2️⃣ Neuronal migration
* 3️⃣ Differentiation
* 4️⃣ Synaptogenesis
* 5️⃣ Synaptic pruning
* 6️⃣ Myelination
* Memory chain: Make → Move → Specialise → Connect → Refine → Insulate

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4
Q

Q: Neurogenesis — what, where, when?

A

A:
* Definition: Production of neurons from neural progenitor cells.
* Occurs:
* Mainly 2nd trimester
* Ventricular zone
* Adult neurogenesis:
* Limited to hippocampus
* Disruption → reduced neuronal numbers.

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5
Q

Q: Neuronal Migration — mechanism & relevance

A

A:
* Neurons move from ventricular zone to cortex.
* Mechanism:
* Radial glial scaffolding
* Timing:
* Prenatal
* If abnormal:
* Cortical disorganisation
* Subtle microstructural abnormalities
* Linked to schizophrenia vulnerability.

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6
Q

Q: Synaptogenesis — key features

A

A:
* Mass formation of synapses.
* Peaks:
* Infancy
* Early childhood
* Brain initially overproduces synapses.
* This creates temporary hyperconnectivity.

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7
Q

Q: Synaptic Pruning — mechanism & importance

A

A:
* Removal of weaker synapses.
* Mechanism:
* Microglia
* Complement proteins (C4)
* Occurs:
* Childhood
* Major wave in adolescence
* Especially prefrontal cortex
* Too much pruning → reduced connectivity (schizophrenia theory)
* Too little pruning → excess connectivity (autism theory)

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8
Q

Q: Myelination — timeline & psychiatric relevance

A

A:
* Myelin insulates axons → increases conduction speed.
* Timeline:
* Begins prenatally
* Continues to mid-20s
* Prefrontal cortex last to mature.
* Explains:
* Adolescent impulsivity
* Late psychosis onset

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9
Q

Q: What is a critical period?

A

A:
* A developmental window when brain circuits are especially sensitive to environmental input.
* Insults during these windows have lasting effects.

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10
Q

Q: Prenatal vulnerability — what can go wrong?

A

A:
* Processes active:
* Neurogenesis
* Migration
* Risks:
* Maternal infection
* Hypoxia
* Malnutrition
* Stress
* Outcome: Subtle structural abnormalities.

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11
Q

Q: Why is adolescence a second major vulnerability window?

A

A:
* Adolescence involves:
* Massive synaptic pruning
* Dopamine system reorganisation
* Prefrontal cortex maturation
* Increased stress reactivity
* Latent abnormalities become clinically visible.
* Peak onset:
* Schizophrenia
* Bipolar disorder
* Depression

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12
Q

Q: What does G × E mean?

A

A:
* The effect of environment depends on genotype.
* Genetic vulnerability + environmental exposure → amplified risk.
* Not additive — interactive.

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13
Q

Q: What is epigenetics?

A

A:
* Change in gene expression without altering DNA sequence.
* Mechanisms:
* DNA methylation
* Histone modification
* Early stress alters stress-response genes.

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14
Q

Q: What is heritability (exam trap)?

A

A:
* Proportion of population variance due to genetics.
* NOT:
* Individual destiny
* Percentage genetic cause
* Schizophrenia heritability ≈ 70–80%.

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15
Q

Q: What is the two-hit model?

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A:
* First hit: Early developmental abnormality.
* Second hit: Later stressor (e.g. cannabis, trauma).
* Symptoms emerge when compensatory capacity fails.

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16
Q

Q: What is the multiple-hit model?

A

A:
* Accumulation of risk across life:
* Polygenic risk
* Prenatal insult
* Childhood adversity
* Adolescent stress
* Substance exposure
* Illness results from cumulative burden.

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17
Q

Q: What are microglia?

A

A:
* Resident immune cells of the brain.
* Functions:
* Remove debris
* Remove synapses during pruning
* Overactive microglia → excessive pruning.

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18
Q

Q: What is the complement C4 hypothesis?

A

A:
* C4 gene overexpression → increased synapse tagging.
* Microglia remove more synapses.
* Result: Reduced cortical connectivity in schizophrenia.

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19
Q

Q: What are parvalbumin interneurons?

A

A:
* Fast-spiking GABA inhibitory neurons.
* Located in:
* Prefrontal cortex
* Hippocampus
* Function:
* Synchronise pyramidal neurons
* Generate gamma oscillations
* Support working memory
* Reduced function in schizophrenia.

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20
Q

Q: What happens to dopamine in adolescence?

A

A:
* Dopamine receptor density peaks
* Mesolimbic pathway becomes highly reactive
* Mesocortical pathway still maturing
* Creates vulnerability window.

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21
Q

Q: Mesolimbic vs Mesocortical dysfunction?

A

A:
* Mesolimbic hyperactivity → positive symptoms
* Mesocortical hypoactivity → negative & cognitive symptoms

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22
Q

Q: What is abnormal salience?

A

A:
* Dysregulated dopamine assigns importance to neutral stimuli.
* Leads to delusions.

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23
Q

Q: What is the HPA axis?

A

A:
* Hypothalamic–pituitary–adrenal stress system.
* Produces cortisol.

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24
Q

Q: How does stress increase psychosis risk?

A

A:
* Cortisol sensitises mesolimbic dopamine.
* Repeated stress → dopamine hyperreactivity.

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25
**Q: Why is schizophrenia neurodevelopmental?**
**A:** * **Obstetric risk** * Early **structural abnormalities** * Excessive **pruning** * **Dopamine** maturation * Late adolescent onset
26
**Q: Autism — developmental abnormality?**
**A:** * Early **brain overgrowth** * Abnormal **connectivity** * Early onset
27
**Q: ADHD — developmental abnormality?**
**A:** * Delayed **cortical maturation** * **Fronto-striatal** dysfunction
28
**Q: Neurodevelopmental vs Neurodegenerative**
**A:** * **Neurodevelopmental**: Abnormal early wiring. * **Neurodegenerative**: Progressive neuronal loss. * **Schizophrenia** = primarily developmental.
29
**Q: Why is schizophrenia considered neurodevelopmental?**
**A:** * Early brain abnormalities occur before symptoms * Structural changes present before chronic illness * Risk increased by **prenatal** & **perinatal** insults * Symptoms emerge during adolescent brain maturation 🔥 Prototype neurodevelopmental disorder.
30
**Q: What early risk factors support this model?**
**A:** * Prenatal: * Maternal **infection** (influenza, toxoplasma) * Maternal **malnutrition** * Maternal **stress** * Perinatal: * **Hypoxia** * **Low birth weight** * **Obstetric complications** * Childhood: * **Motor delay** * **Social withdrawal** * These suggest early abnormal brain development.
31
**Q: What brain findings support a developmental origin?**
**A:** * Enlarged **ventricles** * Reduced **hippocampal volume** * Reduced **prefrontal cortex** thickness * Cortical **grey matter** reduction * Important: These are seen **early**, not only after chronic illness.
32
**Q: What is the pruning hypothesis in schizophrenia?**
**A:** * Adolescence = major **synaptic pruning**. * If pruning is excessive: * → Loss of cortical connectivity * → Hypofrontality * → Cognitive deficits & negative symptoms * Linked to: Complement **C4** gene activity.
33
**Q: Why does schizophrenia usually begin in late adolescence?**
**A:** * **Prefrontal cortex** matures last * **Dopamine** system reorganises * Social stress increases * **Cannabis** exposure common * Latent vulnerability becomes clinically visible.
34
**Q: Why is autism clearly neurodevelopmental?**
**A:** * Symptoms begin early in childhood * Strong **genetic** contribution * Brain differences present very early * Abnormal **synapse** formation suspected
35
**Q: What brain development abnormalities occur in autism?**
**A:** * Early brain overgrowth (first 2 years) * Increased **head circumference** in infancy * Altered connectivity * Reduced **long-range connectivity** * Increased **local connectivity** * This suggests abnormal synaptogenesis & pruning.
36
**Q: What is the connectivity theory of autism?**
**A:** * Too much **local connectivity** * Too little **long-range connectivity** * Results in: * Detail-focused cognition * Social integration difficulty * Restricted behaviours
37
**Q: Why is ADHD neurodevelopmental?**
**A:** * Symptoms begin in childhood * Delayed **cortical maturation** * Strong **genetic** contribution * **Fronto-striatal** circuit dysfunction
38
**Q: What brain findings are seen in ADHD?**
**A:** * Reduced **prefrontal cortex** volume * Reduced **caudate nucleus** volume * Delayed cortical thickness peak * **Dopamine** dysregulation
39
**Q: What developmental delay is seen?**
**A:** * Cortical maturation delayed by ~2–3 years. * Particularly: **Prefrontal cortex**. * Explains: * **Impulsivity** * **Inattention** * Poor inhibition
40
**Q: Is bipolar disorder neurodevelopmental?**
**A:** * Not classically like autism or ADHD. * BUT: * Early emotional dysregulation seen * Structural abnormalities predate episodes * Strong genetic risk * **Limbic–prefrontal** imbalance
41
**Q: What circuits are implicated?**
**A:** * **Amygdala** hyperactivity * Prefrontal regulatory dysfunction * Abnormal emotional regulation networks * May reflect abnormal maturation of emotion circuits.
42
**Q: How can depression be neurodevelopmental?**
**A:** * Early stress alters: * **HPA axis** development * **Amygdala** reactivity * **Prefrontal** regulation * Stress response genes (epigenetics) * Creates long-term vulnerability.
43
**Q: What brain findings support this?**
**A:** * Reduced **hippocampal volume** * **Amygdala** hyperactivity * **Prefrontal** hypoactivity * Often linked to early adversity.
44
**Q: How does neurodevelopment relate to personality disorder?**
**A:** * Early trauma → altered development of: * **Amygdala** * **Prefrontal cortex** * **Attachment** circuits * Emotional regulation systems * Results in chronic dysregulation.
45
**Q: What biological changes are seen?**
**A:** * **Amygdala** hyperactivity * Reduced **prefrontal** inhibition * **HPA axis** dysregulation * Developmentally shaped by trauma.
46
**Q: ULTRA-COMPARISON TABLE — Disorder vs Onset vs Key Developmental Issue (Part 1)**
**A:** * Disorder: **Schizophrenia** * Onset: Late adolescence * Key Developmental Issue: Excessive pruning + dopamine
47
**Q: ULTRA-COMPARISON TABLE — Disorder vs Onset vs Key Developmental Issue (Part 2)**
**A:** * Disorder: **Autism** * Onset: Early childhood * Key Developmental Issue: Abnormal synaptogenesis/connectivity
48
**Q: ULTRA-COMPARISON TABLE — Disorder vs Onset vs Key Developmental Issue (Part 3)**
**A:** * Disorder: **ADHD** * Onset: Childhood * Key Developmental Issue: Delayed cortical maturation
49
**Q: ULTRA-COMPARISON TABLE — Disorder vs Onset vs Key Developmental Issue (Part 4)**
**A:** * Disorder: **Bipolar** * Onset: Adolescence * Key Developmental Issue: Limbic–prefrontal imbalance
50
**Q: ULTRA-COMPARISON TABLE — Disorder vs Onset vs Key Developmental Issue (Part 5)**
**A:** * Disorder: **Depression** * Onset: Adolescence * Key Developmental Issue: Stress system dysregulation
51
**Q: ULTRA-COMPARISON TABLE — Disorder vs Onset vs Key Developmental Issue (Part 6)**
**A:** * Disorder: **BPD** * Onset: Adolescence * Key Developmental Issue: Trauma-altered emotion circuits
52
**Q: What are microglia?**
**A:** * **Microglia** = immune cells of the **central nervous system**. * They: * Survey the brain * Remove debris * Remove synapses during development * They are essential for **normal pruning**.
53
**Q: How do microglia remove synapses?**
**A:** * They use the **complement system**. * Complement proteins (e.g., **C4**) tag synapses for removal. * Microglia then phagocytose (eat) them.
54
**Q: Why is microglia-mediated pruning important in schizophrenia?**
**A:** * In schizophrenia: * Increased **C4** gene expression identified * Suggests excessive synaptic tagging * Leads to excessive pruning * Result: Reduced cortical connectivity → cognitive deficits → negative symptoms * This is a modern biological mechanism supporting the pruning hypothesis.
55
**Q: What are interneurons?**
**A:** * Interneurons = inhibitory neurons that regulate cortical circuits. * Important subtype: **Parvalbumin-positive interneurons**. * They: * Synchronise cortical firing * Generate gamma oscillations * Support working memory
56
**Q: What happens to interneuron function in schizophrenia?**
**A:** * Reduced interneuron function → * Poor synchronisation * Cognitive dysfunction * Impaired executive function * This supports the idea of abnormal circuit maturation.
57
**Q: Dopamine system development — what happens during adolescence?**
**A:** * During adolescence: * Dopamine receptor density peaks * Mesolimbic pathway matures * Mesocortical pathway matures
58
**Q: How does developmental dopamine dysregulation link to psychosis?**
**A:** * If regulation is abnormal: * → Increased salience attribution * → Psychosis * Developmental dopamine dysregulation explains late onset.
59
**Q: Network-level abnormalities — what is the key modern idea?**
**A:** * Modern psychiatry moves beyond “chemical imbalance.” * Disorders reflect abnormal development of networks.
60
**Q: Fronto-striatal circuits — what are they involved in, and which disorder are they abnormal in?**
**A:** * Involved in: * Attention * Impulse control * Abnormal in ADHD.
61
**Q: Limbic–prefrontal circuits — what are they involved in, and which disorders are they abnormal in?**
**A:** * Involved in: * Emotion regulation * Abnormal in: * Bipolar disorder * Depression * Personality disorder
62
**Q: Cortico-cortical connectivity — what is it involved in, and which disorder is it abnormal in?**
**A:** * Involved in: * Thought integration * Abnormal in schizophrenia.
63
**Q: Default Mode Network (DMN) — what is it active during, and where is it abnormal?**
**A:** * Active during: * Self-referential thinking * Internal mental activity * Abnormal DMN connectivity seen in: * Schizophrenia * Depression
64
**Q: Salience Network — what does it do, and what happens if it is dysregulated?**
**A:** * Detects important stimuli. * If dysregulated: * Neutral events feel significant. * This may explain delusions. * Developmental miswiring → abnormal salience attribution.
65
**Q: What longitudinal developmental evidence supports schizophrenia as neurodevelopmental?**
**A:** * Children who later develop schizophrenia often show: * Subtle motor abnormalities * Social withdrawal * Cognitive delay * Years before psychosis. * This supports early developmental deviation.
66
**Q: Multiple-hit model (modern view) — what is it?**
**A:** * Modern understanding: * Not just 2 hits. * But accumulation: * Polygenic risk * Prenatal insult * Childhood adversity * Adolescent stress * Substance use * Risk accumulates across development.
67
**Q: What completes 3.8.2 (core layers list)?**
**A:** * ✔ Conceptual model * ✔ Developmental biology * ✔ G × E * ✔ Two-hit * ✔ Cellular mechanisms * ✔ Circuit models * ✔ Network models * ✔ Disorder applications * ✔ Evidence base
68
**Q: Next syllabus item after 3.8.2 is what?**
**A:** * 🧠 **3.8.3 Neurobiology of Attachment**
69
**Q: Would you like to move forward into 3.8.3 Neurobiology of Attachment now?**
**A:** * Would you like to move forward into that now? * We can continue seamlessly.
70
**Q: What is dopamine?**
**A:** * **Dopamine** is a neurotransmitter involved in: * **Reward** * **Motivation** * **Salience detection** * **Movement** * **Executive function**
71
**Q: Mesolimbic pathway — origin, projection, function, clinical link**
**A:** * Origin: Ventral tegmental area (**VTA**) * Projects to: **Nucleus accumbens** & **limbic system** * Function: * **Reward** * **Salience** * **Emotional significance** * Overactivity → **Positive psychotic symptoms**
72
**Q: Mesocortical pathway — origin, projection, function, clinical link**
**A:** * Origin: **VTA** * Projects to: **Prefrontal cortex** * Function: * **Executive function** * **Working memory** * **Planning** * Underactivity → **Negative** & **cognitive symptoms**
73
**Q: What happens to dopamine in adolescence?**
**A:** * **Adolescence** is a major dopamine reorganisation period. * During adolescence: * 1️⃣ Dopamine receptor density increases (peaks) * 2️⃣ Dopamine release becomes more reactive * 3️⃣ Mesocortical projections continue maturing * 4️⃣ Reward sensitivity increases * This creates: * Increased risk-taking * Increased novelty-seeking * Increased emotional reactivity * This is normal.
74
**Q: Why is adolescence a dopamine vulnerability window?**
**A:** * Because dopamine systems are still stabilising. * At the same time: * Synaptic pruning is occurring * Prefrontal cortex is maturing * Stress responsivity increases * So: * If early vulnerability exists (genetic or prenatal insult), * Adolescent dopamine changes may unmask it.
75
**Q: What goes wrong in schizophrenia during adolescence (dopamine developmental model)?**
**A:** * Developmental model proposes: * Early brain abnormality * → Subtle cortical inefficiency * During adolescence: * Dopamine system becomes hyperresponsive * Mesolimbic activity increases * Prefrontal control is weak * Result: * 🔴 Mesolimbic hyperdopaminergia → positive symptoms * 🔵 Mesocortical hypodopaminergia → negative & cognitive symptoms * This matches clinical picture.
76
**Q: Abnormal salience model — what is it and what does it cause?**
**A:** * Dopamine assigns “importance” to stimuli. * If dysregulated: * Neutral stimuli feel significant. * This leads to: * Delusions * Paranoia * Misinterpretation of events * This is called: * 👉 Abnormal salience attribution. * Developmental dopamine dysregulation explains why this appears in late adolescence.
77
**Q: How does cannabis link to dopamine development and psychosis risk?**
**A:** * **Cannabis** affects dopamine signalling. * In adolescence: * Dopamine system is highly plastic * Cannabis increases psychosis risk * Especially in genetically vulnerable individuals. * This is classic G × E example.
78
**Q: High-yield integration sentence — dopamine and schizophrenia**
**A:** * “Adolescent maturation of mesolimbic and mesocortical dopamine pathways may unmask earlier neurodevelopmental abnormalities, contributing to the typical late adolescent onset of schizophrenia.”
79
**Q: 5 things to remember — dopamine development in adolescence**
**A:** * 1️⃣ Dopamine reorganises in adolescence * 2️⃣ Receptor density peaks during this time * 3️⃣ Mesolimbic pathway → positive symptoms * 4️⃣ Mesocortical pathway → cognitive/negative symptoms * 5️⃣ Dopamine dysregulation explains late onset
80
**Q: What is the HPA axis?**
**A:** * HPA = **Hypothalamic–Pituitary–Adrenal axis** * It is the body’s main **stress-response system**. * Pathway: * 1️⃣ Hypothalamus releases **CRH** * 2️⃣ Pituitary releases **ACTH** * 3️⃣ Adrenal gland releases **cortisol** * **Cortisol** = main stress hormone.
81
**Q: What does cortisol do in the brain?**
**A:** * Cortisol affects: * **Amygdala** (emotion) * **Hippocampus** (memory) * **Prefrontal cortex** (control) * Dopamine neurons (salience & reward) * Short-term stress = adaptive. * Chronic stress = dysregulation.
82
**Q: How does the HPA axis develop (developmental sensitivity)?**
**A:** * The stress system develops across: * Prenatal period * Early childhood * Adolescence * It is highly sensitive to early adversity. * Examples: * Childhood trauma * Neglect * Institutionalisation * These can permanently alter cortisol regulation. * This happens via: * 👉 Epigenetic modification of glucocorticoid receptor genes.
83
**Q: What happens if the HPA axis is dysregulated?**
**A:** * Chronic stress exposure can lead to: * Elevated baseline cortisol * Blunted stress response * Increased amygdala reactivity * Reduced hippocampal volume * These changes increase vulnerability to: * Depression * Psychosis * PTSD * Personality disorder
84
**Q: How does stress interact with dopamine?**
**A:** * Cortisol directly influences dopamine neurons. * Stress: * Increases dopamine release in mesolimbic pathway * Sensitises dopamine system * In vulnerable individuals: * Repeated stress → dopamine hyperreactivity * → Increased risk of psychosis * This links: * Early trauma + adolescent stress * to late psychosis onset.
85
**Q: Why is HPA–dopamine interaction developmental?**
**A:** * Because: * If early life stress alters: * HPA axis set point * Dopamine regulation * Then during adolescence: * When dopamine system matures * The dysregulation becomes clinically significant. * This is another example of: * 👉 Latent vulnerability revealed during developmental transition.
86
**Q: Clinical integration — stress model in schizophrenia**
**A:** * In schizophrenia: * Childhood adversity ↑ risk * Urbanicity ↑ chronic stress * Migration ↑ stress burden * Stress sensitises dopamine system. * This supports neurodevelopmental + stress model.
87
**Q: High-yield summary sentence — HPA axis, epigenetics, dopamine, psychosis**
**A:** * “Early life stress may epigenetically alter HPA axis regulation, sensitising mesolimbic dopamine pathways and increasing vulnerability to psychosis during adolescence.”
88
**Q: 5 things to remember — HPA axis development & dopamine interaction**
**A:** * 1️⃣ HPA axis = stress regulation system * 2️⃣ Early stress alters cortisol regulation * 3️⃣ Cortisol influences dopamine neurons * 4️⃣ Stress sensitises mesolimbic dopamine * 5️⃣ Links trauma to psychosis risk
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