1
Q
Q: What is learning neurobiologically?
A
A:
Learning is:
> A lasting change in behaviour caused by experience, mediated by synaptic plasticity.
It means:
- Synapses strengthen or weaken
- Circuits reorganise
- Networks update predictions
Psychological therapy = structured learning.
2
Q
Q: What is neuroplasticity?
A
A:
Neuroplasticity is:
> The brain’s ability to change structure and function in response to experience.
It includes:
- LTP/LTD
- Dendritic remodeling
- Spine density changes
- Neurogenesis
- Myelination
- Network reorganisation
3
Q
“Q: Why is therapy a neuroplastic process?”
A
A:
Because therapy:
- Introduces new experiences
- Creates corrective emotional learning
- Updates threat/reward predictions
- Modifies maladaptive circuits
📌 Exam phrase:
> “Psychological therapies induce experience-dependent plasticity.”
4
Q
> “Q: Which brain systems are commonly modified by therapy?”
A
A:
- Prefrontal cortex (regulation)
- Amygdala (threat)
- Hippocampus (context)
- ACC (conflict monitoring)
- Striatum (habit/reward)
5
Q
“Q: What is the fundamental principle?”
A
A:
Maladaptive symptoms = maladaptive learning.
Therapy = corrective relearning.
6
Q
Q: What is the basic cellular mechanism of learning?
A
A:
Learning occurs through:
> Changes in synaptic strength between neurones.
That means:
- Some connections become stronger
- Some become weaker
This reshapes circuits.
7
Q
Q: What is LTP?
A
A:
LTP (Long-Term Potentiation) is:
> A long-lasting increase in synaptic strength following repeated stimulation.
It is the main cellular model of learning.
8
Q
Q: What receptor is central to LTP?
A
A:
🔥 VERY HIGH YIELD 🔥
NMDA receptor
Why?
Because NMDA receptors:
- Detect coincident firing
- Allow calcium influx
- Trigger intracellular cascades
- Increase AMPA receptor insertion
This strengthens the synapse.
9
Q
Q: What is the famous Hebbian principle?
A
A:
> “Neurones that fire together wire together.”
Repeated co-activation strengthens connections.
Therapy uses this principle.
10
Q
Q: What is LTD?
A
A:
LTD (Long-Term Depression) is:
> A long-lasting decrease in synaptic strength.
It weakens maladaptive circuits.
11
Q
Q: Why is LTD important in therapy?
A
A:
Because therapy doesn’t just build new circuits.
It also:
- Weakens fear associations
- Reduces maladaptive predictions
- Dampens compulsive habits
LTD = unlearning.
12
Q
Q: Beyond LTP/LTD, what structural changes occur?
A
A:
Learning can cause:
- Increased dendritic branching
- Increased spine density
- Synapse formation
- Network reorganisation
Repeated therapeutic exposure strengthens regulatory pathways.
13
Q
Q: In anxiety disorders, which circuits are strengthened maladaptively?
A
A:
- Amygdala threat circuits
- Fear conditioning pathways
14
Q
“Q: What does therapy aim to strengthen instead?”
A
A:
* Prefrontal cortex → amygdala inhibitory pathways
* Hippocampal contextual regulation
* Cognitive control networks
So therapy shifts the balance:
From:
> Limbic dominance
To:
> Prefrontal regulation
15
Q
> “Q: What computational process underlies learning?”
A
A:
> Learning involves:
> Prediction error correction.
The brain constantly asks:
- “Was that outcome expected?”
- “Was I wrong?”
When prediction error occurs:
- Dopamine signals update learning
- Synapses change accordingly
Therapy creates new prediction errors.
16
Q
Q: Example in CBT for panic disorder?
A
A:
Patient predicts:
> “If my heart races, I will die.”
Exposure produces:
- Heart races
- No death
Prediction error:
> Update threat belief
Synaptic change follows.
17
Q
Q: What is extinction learning?
A
A:
Extinction learning is:
> Learning that a previously feared stimulus is no longer dangerous.
Important:
❌ It does NOT erase the original fear memory.
✅ It creates a new inhibitory memory.
📌 Exam phrase:
> “Extinction represents new learning rather than unlearning.”
18
Q
> “Q: What is fear conditioning?”
A
A:
> Fear conditioning =
Neutral stimulus + threat → fear response.
Example:
Dog bite → dog now predicts danger.
This involves:
- Amygdala activation
- Strengthened threat associations
- Noradrenergic enhancement
19
Q
“Q: Where is the fear memory stored?”
A
A:
Primarily in:
- Amygdala (basolateral complex)
The amygdala encodes threat associations.
20
Q
Q: What occurs during extinction?
A
A:
Repeated exposure to feared stimulus without danger.
Example:
Dog seen repeatedly → no bite → no harm.
Prediction error occurs:
> Expected threat ≠ actual outcome.
New inhibitory memory forms.
21
Q
Q: Which brain regions mediate extinction?
A
A:
🔥 VERY HIGH YIELD 🔥
- Ventromedial prefrontal cortex (vmPFC)
- Hippocampus
- Amygdala
Roles:
- Amygdala → stores original fear
- vmPFC → inhibits amygdala
- Hippocampus → encodes context
22
Q
“**Q: If extinction occurs
A
why can fear return?**”
23
Q
Q: How does exposure therapy work neurobiologically?
A
A:
Exposure:
- Repeatedly activates fear circuit
- Creates prediction error
- Strengthens vmPFC inhibitory control
- Weakens behavioural avoidance
Repeated sessions enhance:
- Prefrontal regulation
- Fear extinction memory
24
Q
“Q: Why must exposure be repeated?”
A
A:
Because:
- LTP strengthens inhibitory pathways
- Consolidation requires repetition
- Context generalisation improves over time
Single exposure is not enough.
25
**Q: What is impaired in PTSD?**
**A:**
* Reduced vmPFC activation
* Impaired fear extinction
* Hyperactive amygdala
* Impaired hippocampal contextual processing
Result:
> Fear responses persist even in safe contexts.
26
> "**Q: Why is hippocampus important in extinction?**"
**A:**
> Hippocampus encodes:
* Context of safety
Without contextual processing:
* Fear generalises inappropriately
27
"**Q: What receptor is important in extinction learning?**"
**A:**
🔥 NMDA receptor again 🔥
Because extinction is:
* New learning
* Requires LTP in inhibitory circuits
This is why:
* NMDA modulators (e.g. D-cycloserine) have been studied to enhance exposure therapy.
28
"**Q: What computational process drives extinction?**"
**A:**
Prediction error:
Expected threat – Actual outcome = 0 threat.
This mismatch updates beliefs.
Dopamine signals prediction error.
29
**Q: What is memory reconsolidation?**
**A:**
Memory reconsolidation is:
> The process by which a retrieved memory becomes temporarily unstable and can be modified before being stored again.
Important:
* When a memory is recalled → it becomes **labile (unstable)**
* During this window → it can be updated
* Then it is stored again (reconsolidated)
📌 Exam phrase:
> “Memory retrieval opens a reconsolidation window.”
30
> "**Q: What is the key difference between extinction and reconsolidation?**"
**A:**
> Extinction:
* Creates a new inhibitory memory
* Original fear memory remains intact
Reconsolidation:
* Directly modifies the original memory trace
🔥 Very high-yield distinction 🔥
31
**Q: What happens when a memory is reactivated?**
**A:**
When a memory is recalled:
* Synapses encoding that memory destabilise
* Protein synthesis is required to restabilise it
* NMDA receptors are involved
* Intracellular signalling cascades activate
If new information is introduced during this window:
→ The memory can be altered.
32
**Q: What molecular process is required for reconsolidation?**
**A:**
Protein synthesis.
Blocking protein synthesis:
* Prevents reconsolidation
* Weakens the memory
(This is mostly shown in animal studies.)
33
**Q: How long is the reconsolidation window?**
**A:**
It is:
* Time-limited (hours)
* After retrieval
* During which the memory is malleable
This window is crucial for therapeutic updating.
34
**Q: How might therapy use reconsolidation principles?**
**A:**
Therapy may:
1️⃣ Activate distressing memory
2️⃣ Introduce new corrective emotional information
3️⃣ Allow updating before memory restabilises
Example:
Trauma memory:
> “I am powerless.”
Therapeutic processing:
> “I survived. I am safe now.”
The emotional meaning shifts.
35
**Q: Why is reconsolidation relevant in PTSD?**
**A:**
In PTSD:
* Trauma memories are strongly encoded
* Amygdala activation is high
* Hippocampal contextualisation is impaired
Therapy attempts to:
* Reactivate trauma memory safely
* Introduce safety signals
* Update meaning
36
"**Q: Which regions are involved in reconsolidation?**"
**A:**
* Amygdala (emotional memory)
* Hippocampus (contextual memory)
* Prefrontal cortex (cognitive updating)
NMDA receptors play a central role again.
37
**Q: What drives reconsolidation updating?**
**A:**
Prediction error again.
If during recall:
Expected emotional outcome ≠ actual safe outcome
The brain updates the memory.
Without prediction error:
* Memory remains unchanged.
38
"**Q: Which therapies may involve reconsolidation processes?**"
**A:**
* Trauma-focused CBT
* EMDR
* Prolonged exposure
* Some psychodynamic approaches
All involve:
* Memory activation
* Emotional processing
* Updating meaning
39
"**Q: What is CBT neurobiologically?**"
**A:**
CBT works by:
> Strengthening prefrontal control over limbic emotional systems and updating maladaptive predictions.
It modifies:
* Threat appraisals
* Cognitive biases
* Emotional responses
Through **experience-dependent plasticity**.
40
**Q: What does “cognitive restructuring” mean in brain terms?**
**A:**
It means:
* Activating maladaptive belief networks
* Introducing new interpretations
* Generating prediction error
* Strengthening alternative circuits
Example:
Old belief:
> “If someone criticises me, I am worthless.”
CBT introduces:
> “Criticism does not define my worth.”
Repeated activation + updating → synaptic change.
41
**Q: Which prefrontal regions are strengthened in CBT?**
**A:**
* **Dorsolateral PFC (dlPFC)** → cognitive control
* **Ventromedial PFC (vmPFC)** → emotion regulation
* **Anterior cingulate cortex (ACC)** → conflict monitoring
42
"**Q: Which limbic regions are downregulated?**"
**A:**
* Amygdala (threat detection)
* Insula (interoceptive anxiety signals)
Result:
> Better top-down control over emotional responses.
43
> "**Q: What is the maladaptive pattern in depression?**"
**A:**
* Hyperactive default mode network (rumination)
* Reduced PFC control
* Altered reward circuitry
* Negative cognitive bias
44
"**Q: What does CBT do in depression?**"
**A:**
CBT:
* Reduces rumination network activation
* Enhances dlPFC activity
* Improves connectivity between PFC and limbic regions
* Modifies negative bias
This reflects:
> Network-level plasticity.
45
> "**Q: What is the maladaptive anxiety pattern?**"
**A:**
* Hyperactive amygdala
* Increased insula activation
* Reduced PFC inhibition
* Threat overestimation
46
"**Q: What does CBT do in anxiety?**"
**A:**
CBT:
* Strengthens PFC inhibitory control
* Reduces amygdala reactivity
* Improves cognitive reappraisal ability
* Updates catastrophic predictions
Repeated cognitive reappraisal = synaptic strengthening.
47
**Q: What is cognitive reappraisal?**
**A:**
Reappraisal = changing the meaning of an emotional stimulus.
Neurobiologically:
* dlPFC activates
* vmPFC engages
* Amygdala activation decreases
This is measurable on fMRI.
48
**Q: How does behavioural activation work neurobiologically?**
**A:**
Behavioural activation:
* Increases dopaminergic reward signalling
* Re-engages ventral striatum
* Counteracts anhedonia
Repeated rewarding activity strengthens reward circuits.
49
**Q: Does CBT change neurotransmitter systems?**
**A:**
Indirectly, yes.
By altering experience and plasticity, CBT can:
* Reduce cortisol levels
* Improve serotonin function
* Enhance dopamine signalling via behaviour
But CBT works primarily through **network reorganisation**, not receptor blockade.
50
**Q: How does CBT differ neurobiologically from antidepressants?**
**A:**
Antidepressants:
* Directly modify neurotransmitter levels
* Enhance neurogenesis
CBT:
* Changes neural firing patterns
* Strengthens regulatory networks
* Induces experience-driven plasticity
Both may converge on:
* Increased hippocampal plasticity
* Improved PFC regulation
51
Sanity check: Processed 31 original Q&As (BIT 1–5) and produced 43 cards. Repetition removed: none (no exact duplicate points within the provided material).
52
**Q: What is CBT neurobiologically?**
**A:**
CBT works by:
> Strengthening prefrontal control over limbic emotional systems and updating maladaptive predictions.
It modifies:
* Threat appraisals
* Cognitive biases
* Emotional responses
Through **experience-dependent plasticity**.
53
**Q: What does “cognitive restructuring” mean in brain terms?**
**A:**
It means:
* Activating maladaptive belief networks
* Introducing new interpretations
* Generating prediction error
* Strengthening alternative circuits
Example:
Old belief:
> “If someone criticises me, I am worthless.”
CBT introduces:
> “Criticism does not define my worth.”
Repeated activation + updating → synaptic change.
54
**Q: Which prefrontal regions are strengthened in CBT?**
**A:**
* **Dorsolateral PFC (dlPFC)** → cognitive control
* **Ventromedial PFC (vmPFC)** → emotion regulation
* **Anterior cingulate cortex (ACC)** → conflict monitoring
55
"**Q: Which limbic regions are downregulated?**"
**A:**
* Amygdala (threat detection)
* Insula (interoceptive anxiety signals)
Result:
> Better top-down control over emotional responses.
56
> "**Q: What is the maladaptive pattern in depression?**"
**A:**
* Hyperactive default mode network (rumination)
* Reduced PFC control
* Altered reward circuitry
* Negative cognitive bias
57
"**Q: What does CBT do in depression?**"
**A:**
CBT:
* Reduces rumination network activation
* Enhances dlPFC activity
* Improves connectivity between PFC and limbic regions
* Modifies negative bias
This reflects:
> Network-level plasticity.
58
> "**Q: What is the maladaptive anxiety pattern?**"
**A:**
* Hyperactive amygdala
* Increased insula activation
* Reduced PFC inhibition
* Threat overestimation
59
"**Q: What does CBT do in anxiety?**"
**A:**
CBT:
* Strengthens PFC inhibitory control
* Reduces amygdala reactivity
* Improves cognitive reappraisal ability
* Updates catastrophic predictions
Repeated cognitive reappraisal = synaptic strengthening.
60
**Q: What is cognitive reappraisal?**
**A:**
Reappraisal = changing the meaning of an emotional stimulus.
Neurobiologically:
* dlPFC activates
* vmPFC engages
* Amygdala activation decreases
This is measurable on fMRI.
61
**Q: How does behavioural activation work neurobiologically?**
**A:**
Behavioural activation:
* Increases dopaminergic reward signalling
* Re-engages ventral striatum
* Counteracts anhedonia
Repeated rewarding activity strengthens reward circuits.
62
**Q: Does CBT change neurotransmitter systems?**
**A:**
Indirectly, yes.
By altering experience and plasticity, CBT can:
* Reduce cortisol levels
* Improve serotonin function
* Enhance dopamine signalling via behaviour
But CBT works primarily through **network reorganisation**, not receptor blockade.
63
**Q: How does CBT differ neurobiologically from antidepressants?**
**A:**
Antidepressants:
* Directly modify neurotransmitter levels
* Enhance neurogenesis
CBT:
* Changes neural firing patterns
* Strengthens regulatory networks
* Induces experience-driven plasticity
Both may converge on:
* Increased hippocampal plasticity
* Improved PFC regulation
64
"**Q: What is the core neurobiology of OCD?**"
**A:**
OCD involves dysfunction in the:
> **Cortico–Striato–Thalamo–Cortical (CSTC) loop**
This loop controls:
* Habit formation
* Action selection
* Error monitoring
* Compulsive behaviour
65
"**Q: What structures form the CSTC circuit?**"
**A:**
🔥 MUST KNOW 🔥
* Orbitofrontal cortex (OFC)
* Anterior cingulate cortex (ACC)
* Striatum (especially caudate)
* Thalamus
Loop pattern:
Cortex → Striatum → Thalamus → Cortex
66
**Q: What does this circuit normally do?**
**A:**
It:
* Filters intrusive thoughts
* Stops repetitive behaviours
* Regulates habit execution
* Signals when actions are complete
67
"**Q: What happens in OCD?**"
**A:**
In OCD:
* OFC becomes hyperactive
* ACC signals excessive “error”
* Striatum fails to inhibit loops
* Thalamus sends excessive signals back to cortex
Result:
> Persistent intrusive thoughts + compulsive behaviours.
68
> "**Q: What is the difference between habit and goal-directed systems?**"
**A:**
> Goal-directed system:
* Flexible
* Based on outcome value
* Involves prefrontal cortex
Habit system:
* Automatic
* Stimulus–response driven
* Involves dorsal striatum
69
"**Q: What happens in OCD?**"
**A:**
OCD shows:
* Overactive habit system
* Reduced goal-directed control
Compulsions become automatic habits.
70
**Q: What is ERP?**
**A:**
Exposure & Response Prevention:
* Exposure to feared stimulus
* Prevention of compulsive response
Example:
Touch contamination → do NOT wash hands.
71
**Q: What happens neurobiologically during ERP?**
**A:**
ERP:
* Activates fear circuit
* Prevents habitual response
* Creates prediction error
* Strengthens inhibitory circuits
Over time:
* vmPFC inhibits amygdala
* Prefrontal control over striatum improves
* Habit loop weakens
72
"**Q: What is the prediction error during ERP?**"
**A:**
Prediction:
> “If I don’t perform compulsion, something terrible will happen.”
Actual outcome:
> Nothing happens.
Mismatch → updating.
Repeated mismatches weaken compulsive belief.
73
**Q: What role does dopamine play in OCD habits?**
**A:**
Dopamine:
* Reinforces habitual loops
* Strengthens stimulus–response associations
Repeated compulsion:
* Temporarily reduces anxiety
* Reinforces habit loop
ERP breaks this reinforcement cycle.
74
**Q: What brain changes occur after successful ERP?**
**A:**
Studies show:
* Reduced OFC hyperactivity
* Reduced caudate overactivity
* Improved PFC–striatal connectivity
* Reduced amygdala activation
This reflects:
> Circuit rebalancing.
75
> "**Q: How is OCD different from simple phobia neurobiologically?**"
**A:**
> Phobia:
* Primarily amygdala-based fear circuit
OCD:
* CSTC loop dysfunction
* Habit system overdrive
Both use exposure, but OCD adds:
> Habit inhibition component.
76
> "**Q: What is psychodynamic therapy neurobiologically?**"
**A:**
> Psychodynamic therapy works by:
> Bringing implicit emotional patterns into conscious awareness and reorganising self-referential and relational brain networks.
It modifies:
* Emotional memory
* Attachment representations
* Self-schema
* Interpersonal predictions
77
"**Q: Which large-scale brain network is central here?**"
**A:**
🔥 VERY HIGH YIELD 🔥
**Default Mode Network (DMN)**
The DMN is involved in:
* Self-reflection
* Autobiographical memory
* Internal narrative
* Mentalising
Main regions:
* Medial prefrontal cortex (mPFC)
* Posterior cingulate cortex (PCC)
* Precuneus
* Hippocampus
78
"**Q: What happens to the DMN in depression?**"
**A:**
* Hyperactivation
* Excessive self-focus
* Rumination
* Negative self-referential processing
Psychodynamic therapy aims to:
* Modify maladaptive self-narratives
* Reduce rigid negative self-schema
79
"**Q: How does psychodynamic therapy affect attachment systems?**"
**A:**
It may modify:
* Amygdala (threat sensitivity)
* vmPFC (emotion regulation)
* ACC (social pain processing)
* Insula (interoception)
Through corrective relational experiences.
The therapeutic relationship acts as:
> A new attachment learning environment.
80
> "**Q: What is mentalising?**"
**A:**
> Mentalising =
> Understanding one’s own and others’ mental states.
Brain regions involved:
* Medial PFC
* Temporoparietal junction (TPJ)
* Superior temporal sulcus
Psychodynamic and mentalisation-based therapies:
* Strengthen these networks
* Improve emotion regulation via understanding
81
"**Q: How does emotional processing therapy affect the amygdala?**"
**A:**
Repeated safe exploration of emotions:
* Reduces amygdala hyperreactivity
* Improves PFC regulation
* Enhances extinction & reconsolidation processes
It overlaps with:
* Extinction mechanisms
* Memory updating
82
"**Q: What changes in self-schema involve neuroplasticity?**"
**A:**
Rigid self-beliefs are:
* Represented in medial prefrontal networks
* Reinforced through repetition
Therapy:
* Introduces new self-experiences
* Creates prediction error
* Updates self-representations
This reflects:
> Network-level restructuring.
83
> "**Q: How does psychodynamic therapy differ neurobiologically from CBT?**"
**A:**
> CBT:
* Strong dlPFC engagement
* Explicit cognitive restructuring
* Direct regulation of limbic activity
Psychodynamic therapy:
* More DMN engagement
* Self-referential processing
* Emotional memory updating
* Attachment circuit modification
Both:
* Increase PFC–limbic integration
* Promote plasticity
84
"**Q: How does relational therapy influence trauma circuits?**"
**A:**
Through:
* Safe emotional activation
* Memory reconsolidation
* Improved contextualisation
* Reduced threat generalisation
This modifies:
* Amygdala activity
* Hippocampal contextual memory
* Prefrontal integration
85
"**Q: Do psychotherapy and medication act on completely different systems?**"
**A:**
❌ No.
They act through **different entry points**, but often converge on:
> Enhancing neuroplasticity and restoring limbic–prefrontal balance.
86
> "**Q: What is the primary immediate action of SSRIs?**"
**A:**
> SSRIs:
* Block serotonin reuptake
* Increase synaptic serotonin
But that is **not** the full story.
87
**Q: What are the longer-term neuroplastic effects of antidepressants?**
**A:**
Over weeks, antidepressants:
* Increase BDNF (Brain-Derived Neurotrophic Factor)
* Enhance hippocampal neurogenesis
* Increase dendritic complexity
* Improve PFC–limbic connectivity
📌 Exam phrase:
> “Antidepressants enhance neuroplasticity.”
88
> "**Q: What is BDNF?**"
**A:**
> BDNF = Brain-Derived Neurotrophic Factor.
It:
* Promotes neurone survival
* Supports synapse formation
* Enhances LTP
* Facilitates plasticity
Reduced BDNF is associated with:
* Depression
* Chronic stress
89
"**Q: Why might combining medication and therapy be synergistic?**"
**A:**
Because:
Medication:
* Increases plasticity capacity
* Makes the brain more “changeable”
Therapy:
* Provides structured learning experiences
* Directs plasticity toward adaptive circuits
Together:
> Medication opens the plasticity window.
> Therapy shapes the new wiring.
90
> "**Q: What happens in depression before treatment?**"
**A:**
* Reduced hippocampal volume (functional)
* Hyperactive amygdala
* Reduced PFC regulation
* Reduced BDNF
91
"**Q: What does combined treatment do?**"
**A:**
Combined CBT + SSRI:
* Reduces amygdala hyperactivity
* Increases PFC engagement
* Improves network connectivity
* Enhances neurogenesis
This suggests additive plasticity effects.
92
**Q: Why might SSRIs enhance exposure therapy?**
**A:**
SSRIs:
* Reduce baseline anxiety
* Reduce amygdala reactivity
* Increase plasticity
This may:
* Facilitate extinction learning
* Strengthen inhibitory circuits
But too much anxiolysis may reduce prediction error — nuance matters.
93
**Q: Why have NMDA modulators been studied in therapy?**
**A:**
Because:
* NMDA receptors are central to LTP
* Extinction learning requires NMDA activation
Enhancing NMDA function may:
* Improve exposure outcomes
This shows:
> Therapy relies on plasticity mechanisms.
94
> "**Q: How do dopaminergic systems influence therapy?**"
**A:**
> Dopamine:
* Signals prediction error
* Reinforces learning
* Strengthens new behavioural patterns
Medications affecting dopamine may:
* Modify learning sensitivity
* Influence habit restructuring
95
"**Q: What is the convergence model?**"
**A:**
Different treatments:
* Pharmacological
* Psychological
* Neuromodulatory
May converge on:
* Restoring PFC–limbic balance
* Enhancing neuroplasticity
* Normalising network dynamics
96
"**Q: What is a biomarker in psychiatry?**"
**A:**
A biomarker is:
> A measurable biological indicator associated with a disease state or treatment response.
In therapy, biomarkers show:
* Neural change
* Plasticity
* Circuit normalisation
97
"**Q: What changes are seen in anxiety after CBT?**"
**A:**
Common findings:
* ↓ Amygdala activation
* ↑ Prefrontal cortex activation
* ↑ vmPFC–amygdala connectivity
This reflects:
> Improved top-down regulation.
98
> "**Q: What changes are seen in depression after CBT?**"
**A:**
* ↓ Default Mode Network hyperactivity
* ↑ dlPFC activation
* Normalisation of amygdala response
* Improved connectivity in cognitive control networks
This reflects:
> Reduced rumination + improved regulation.
99
> "**Q: What changes are seen in OCD after ERP?**"
**A:**
* ↓ OFC hyperactivity
* ↓ Caudate overactivation
* Improved CSTC connectivity
This reflects:
> Reduced habit-loop overdrive.
100
> "**Q: Can therapy change brain structure?**"
**A:**
> Yes — over time.
Some studies show:
* Increased hippocampal volume after depression treatment
* Increased cortical thickness in regulatory areas
* Changes in white matter integrity
These reflect:
> Structural plasticity.
101
> "**Q: Does therapy change neurotransmitter levels?**"
**A:**
> Indirectly, yes.
Psychotherapy can:
* Reduce cortisol levels
* Increase BDNF levels
* Normalise stress biomarkers
However, therapy works primarily through:
> Network-level changes.
102
> "**Q: What EEG changes may occur with therapy?**"
**A:**
> Possible changes:
* Reduced hyperarousal patterns
* Improved frontal alpha asymmetry in depression
* Normalised error-related negativity in OCD
These reflect:
> Improved regulatory control.
103
> "**Q: How does therapy affect cortisol?**"
**A:**
> Successful therapy can:
* Reduce baseline cortisol
* Improve diurnal cortisol rhythm
* Enhance stress recovery speed
This shows:
> Improved HPA regulation.
104
> "**Q: What is one of the most consistent biomarker changes?**"
**A:**
> Improved connectivity between:
* PFC and amygdala
* Cognitive control networks
* Limbic and cortical regions
Therapy = increased integration.
105
**Q: Can baseline brain activity predict therapy response?**
**A:**
Some findings suggest:
* Higher baseline PFC activation predicts better CBT response
* Lower amygdala hyperreactivity predicts better extinction learning
* Higher cognitive control capacity predicts better restructuring outcomes
But no single biomarker is definitive.
106
**Q: What biological markers indicate increased plasticity?**
**A:**
* Increased BDNF
* Improved neurogenesis
* Enhanced LTP markers
* Increased network flexibility
* Reduced stress markers
107
Sanity check: Processed 55 original Q&As (BIT 5–9 as provided) and produced 55 cards. Repetition removed: none (no exact duplicate statements within the provided material).
108
**Q: What is the one-sentence master summary for 3.8.4.2 Neurobiological Effects of Learning & Psychological Therapies?**
**A:**
If you remember one sentence:
> Psychological therapies induce experience-dependent neuroplasticity by modifying synaptic strength, network connectivity, and limbic–prefrontal balance through mechanisms including LTP/LTD, extinction learning, reconsolidation, and prediction-error driven updating.
If you understand that, you are exam-safe ✅
109
**Q: What are examiners really testing in 3.8.4.2?**
**A:**
They are testing whether you understand:
1️⃣ Therapy = learning
2️⃣ Learning = synaptic plasticity
3️⃣ Extinction ≠ erasure
4️⃣ Reconsolidation modifies memory
5️⃣ PFC regulates limbic systems
6️⃣ OCD involves CSTC loops
7️⃣ Medication enhances plasticity
8️⃣ Network connectivity changes after therapy
They are **not** testing therapy technique details.
110
**Q: What are the core circuit patterns to memorise for anxiety disorders (before vs after CBT/exposure)?**
**A:**
## 🔹 Anxiety Disorders
Before therapy:
* ↑ Amygdala
* ↓ vmPFC inhibition
* Impaired extinction
After CBT/exposure:
* ↓ Amygdala
* ↑ vmPFC activation
* Improved connectivity
111
"**Q: What are the core circuit patterns to memorise for depression (before vs after CBT)?**"
**A:**
## 🔹 Depression
Before therapy:
* ↑ Default Mode Network (rumination)
* ↓ dlPFC control
* Altered reward circuitry
After CBT:
* ↓ DMN hyperactivity
* ↑ dlPFC activation
* Improved network integration
112
"**Q: What are the core circuit patterns to memorise for OCD (before vs after ERP)?**"
**A:**
## 🔹 OCD
Before ERP:
* Hyperactive OFC
* Overactive caudate
* CSTC loop dysfunction
After ERP:
* Reduced OFC hyperactivity
* Improved PFC–striatal regulation
113
"**Q: If you see: “NMDA receptor involvement” — what should you think?**"
**A:**
Think:
* LTP
* Extinction
* Reconsolidation
* Synaptic plasticity
114
"**Q: If you see: “New inhibitory memory” — what should you think?**"
**A:**
Think:
* Extinction learning
* vmPFC regulation
115
"**Q: If you see: “Memory becomes labile after recall” — what should you think?**"
**A:**
Think:
* Reconsolidation
116
"**Q: If you see: “Cognitive reappraisal” — what should you think?**"
**A:**
Think:
* dlPFC activation
* Amygdala downregulation
117
"**Q: If you see: “Habit loop dysfunction” — what should you think?**"
**A:**
Think:
* CSTC circuit
* OCD
* ERP
118
"**Q: If you see: “BDNF increase” — what should you think?**"
**A:**
Think:
* Antidepressants
* Plasticity enhancement
* Combined treatment effects
119
"**Q: What is the EXTINCTION vs RECONSOLIDATION SBA trap (very common)?**"
**A:**
Extinction:
* Creates new inhibitory memory
* Original fear remains
Reconsolidation:
* Modifies original memory trace
* Requires protein synthesis
Never confuse these.
120
**Q: How do CBT and psychodynamic therapy compare neurobiologically?**
**A:**
CBT:
* dlPFC strengthening
* Explicit restructuring
* Top-down regulation
Psychodynamic therapy:
* DMN modulation
* Self-representation updating
* Attachment circuit reorganisation
Both:
* Increase PFC–limbic integration
* Use prediction error
* Induce plasticity
121
"**Q: How do therapy vs medication integrate neurobiologically (exam integration)?**"
**A:**
Medication:
* Enhances plasticity (BDNF, neurogenesis)
* Reduces limbic hyperactivity
Therapy:
* Directs plasticity
* Builds adaptive networks
Combined:
* Synergistic effect
Exam phrase:
> “Pharmacotherapy enhances plasticity; psychotherapy guides adaptive rewiring.”
122
> "**Q: What biomarkers should you recognise for therapy response & plasticity?**"
**A:**
* Reduced amygdala activation post-CBT
* Improved PFC–amygdala connectivity
* Reduced OFC hyperactivity in OCD
* Increased hippocampal volume post-treatment
* Reduced cortisol
123
"**Q: What is the ultra-high-yield conceptual framework for 3.8.4.2?**"
**A:**
Symptoms = maladaptive learning.
Therapy = corrective learning.
Corrective learning requires:
* Prediction error
* NMDA activation
* Synaptic plasticity
* Network reorganisation
124
"**Q: What are the classic exam traps (incorrect vs correct understanding) in 3.8.4.2?**"
**A:**
❌ Therapy works purely psychologically
❌ Extinction erases fear memory
❌ CBT only changes thoughts, not brain
❌ Medication and therapy act independently
❌ OCD is purely anxiety-based
Correct understanding:
✔️ Therapy changes neural circuits
✔️ Extinction = inhibition
✔️ Reconsolidation = modification
✔️ OCD = CSTC dysfunction
✔️ Medication enhances plasticity
125
**Q: What is the master map (final integration) for learning → symptom reduction?**
**A:**
Learning →
Synaptic plasticity →
Network reorganisation →
Improved limbic–prefrontal balance →
Symptom reduction
126
**Q: What is the final memory hook for 3.8.4.2?**
**A:**
Stress rewires the brain accidentally.
Therapy rewires the brain deliberately.
Medication makes the brain more rewritable.
127
**Q: After completing 3.8.4.2, what can you now do?**
**A:**
You can now:
* Explain therapy at cellular level
* Explain extinction vs reconsolidation
* Describe CBT neurobiology
* Describe OCD circuits
* Explain medication synergy
* Recognise exam buzzwords instantly
128
Sanity check: Processed 19 original Q&As (BIT 10 synthesis prompts) and produced 19 cards. Repetition removed: none (no exact duplicate statements within the provided material).
Cranial nerves
flashcards
Decks in class (64)
# Cards
-
CN3 OCCULOMOTOR55
-
CN4 TROCHLEAR51
-
Trigemnial nerve154
-
FACIAL NERVE75
-
VESTIBULOCOCHLEAR NERVE94
-
GLASSOPHARYNGEAL50
-
VAGAS78
-
ACCESSORY59
-
Hypoglossal84
-
Midbrain65
-
PONS80
-
Medulla151
-
Cerebellum100
-
Dexcending pyrMIDl trCT17
-
Cerebellar tract95
-
Cerebellar cells44
-
Efferent Cerebellar tract59
-
Cerebellar lesions92
-
Spinal chord anatomy132
-
Cerbrovascular circ151
-
CNS Cells236
-
Cerebral neocortex cells249
-
Bloodbrain barrier29
-
CSF system55
-
Action potential and synapse115
-
white matter tracts71
-
Cerbral cortex layers225
-
Synapses47
-
plasticity etc83
-
meurogenesis and migration0
-
Cortisol + CCK35
-
Ghrehlin/Leptin103
-
Endocannabinoids31
-
Endokephalin/Endorphins73
-
Orexin49
-
3.3.6 Links between neurotransmitter systems and findings from genetic association studies in psychiatry.178
-
high yeild31
-
neural circuit - appetite175
-
neural circuit - thirst72
-
neural circuit - aggression153
-
neural circuit - pain111
-
learning100
-
Habit and compulsions148
-
Motivation, reward and pelasure147
-
emotional regulation109
-
perception135
-
executive function + empathy/tom211
-
DMN and Salience118
-
Basic concepts: chromosomes, cell division, gene structure, transcription and translation,19
-
structure of the human genome, patterns of inheritance.29
-
Neurodevelopmental models40
-
neurodev model88
-
neurobiology of attatchment102
-
neurodev model88
-
stress182
-
CBT128
-
attatchment53
-
Learning and therapy41
-
neurobio learning39
-
LEARNING THERAPY40
-
LEARNING41
-
Brain injury86
-
Alzheimer's58
-
Vascular0
