1
Q
What is perception? (exam-safe definition)
A
• Perception is the process by which sensory input is transformed, organised, and interpreted
• Creates a meaningful experience of the world
• Perception ≠ sensation
2
Q
What is the difference between sensation and perception?
A
• Sensation = detection of physical stimuli at receptors
• Perception = interpretation of sensory data using cortex, memory, and meaning
• Psychiatry focuses mainly on perception
3
Q
Why is perception considered an active process?
A
• The brain does not passively record reality
• It actively constructs experience
• Combines bottom-up sensory data with top-down expectations
4
Q
What are the two main components that shape perception?
A
• Bottom-up input (sensory data)
• Top-down processing (expectations, beliefs, memory)
5
Q
What is bottom-up processing in perception?
A
• Data-driven
• Sensory receptors → cortex
• Builds perception from raw input
• Example: lines → shapes → objects
6
Q
What is top-down processing in perception?
A
• Concept-driven
• Uses memory, beliefs, and context
• Fills in gaps in sensory data
• Example: hearing your name in noise
7
Q
Why is top-down processing important in psychopathology?
A
• Excess top-down influence can dominate perception
• Leads to illusions, hallucinations, delusions
• Common in psychosis
8
Q
What is the general neural pathway for perception?
A
• Sensory receptor
• Thalamus (relay station)
• Primary sensory cortex
• Secondary and association cortices
9
Q
Which sensory system bypasses the thalamus initially? (exam favourite)
A
• Olfaction
• Smell projects directly to cortex before thalamic relay
10
Q
Why is visual perception the most tested modality in exams?
A
• Highly mapped cortical pathways
• Clear structure–function links
• Strong relevance to psychosis and neglect
11
Q
What is the basic visual pathway?
A
• Retina → Lateral Geniculate Nucleus (LGN)
• LGN → Primary visual cortex (V1)
12
Q
What happens to visual information after V1?
A
• Splits into two processing streams
• Ventral stream and dorsal stream
13
Q
What is the ventral visual stream (“WHAT” pathway)?
A
• Occipital → temporal cortex
• Object recognition
• Faces, colour, form
• Damage → visual agnosia
14
Q
What is the dorsal visual stream (“WHERE/HOW” pathway)?
A
• Occipital → parietal cortex
• Spatial location and movement
• Action guidance
• Damage → visuospatial neglect
15
Q
What are Gestalt principles of perception?
A
• Innate organisational rules
• Figure–ground separation
• Proximity
• Similarity
• Continuity
• Closure
16
Q
Why are Gestalt principles important in psychiatry?
A
• They organise perception automatically
• Disturbance leads to fragmented perception
• Seen in psychosis
17
Q
What is the predictive processing model of perception?
A
• Brain acts as a prediction machine
• Constantly predicts sensory input
• Updates beliefs using prediction errors
18
Q
What is a prediction error?
A
• Difference between expected input and actual sensory input
• Used to update internal models of the world
19
Q
Why is perception described as a ‘best guess’?
A
• Perception reflects the brain’s most likely interpretation
• Not an objective copy of reality
• Influenced by expectations and beliefs
20
Q
What is the role of glutamate in perception?
A
• Main excitatory neurotransmitter
• Drives cortical sensory processing
• NMDA receptors integrate perception
21
Q
What is the role of GABA in perception?
A
• Provides inhibitory control
• Filters sensory noise
• Sharpens perceptual signals
• Reduced GABA → sensory overload
22
Q
What is the role of dopamine in perception?
A
• Modulates salience
• Assigns importance to stimuli
• Excess dopamine → irrelevant stimuli feel meaningful
23
Q
What is an illusion? (exam-safe definition)
A
• Misinterpretation of a real external stimulus
• External stimulus is present
• Common in anxiety, fatigue, delirium
24
Q
Why are illusions not psychosis by themselves?
A
• Occur in normal individuals
• Require an external stimulus
• Insight often preserved
25
**What is a hallucination? (exam-safe definition)**
• **Perception without an external stimulus**
• Experienced as real
• Occurs in any sensory modality
26
**Which hallucination modality is most common in psychosis?**
• **Auditory hallucinations**
27
**What is the core neurobiology of hallucinations?**
• Overactive sensory cortices
• Excess top-down influence
• Failure to suppress internal signals
28
**What causes auditory hallucinations specifically?**
• Hyperactivity in auditory cortex
• Failure to recognise **inner speech** as self-generated
29
**How are delusions linked to perception?**
• Delusions arise from **abnormal perceptual experiences**
• Aberrant salience assigned to perceptions
• Beliefs form around false percepts
30
**What are the core perceptual abnormalities in schizophrenia?**
• Hallucinations
• Abnormal salience
• Fragmented perception
31
**What is the pathophysiology of perceptual disturbance in schizophrenia?**
• Dopamine dysregulation
• **NMDA receptor hypofunction**
• Excess top-down predictions
• Weak error correction
32
**What is the key perceptual result in schizophrenia?**
• Brain trusts **expectations more than reality**
33
**How is perception altered in depression?**
• Negative perceptual bias
• Reduced sensitivity to positive stimuli
34
**How is perception altered in mania?**
• Heightened sensory intensity
• Increased salience attribution
35
**What perceptual disturbances occur in delirium?**
• Illusions
• Visual hallucinations
• Fluctuating attention
• Impaired sensory integration
36
**How is perception affected in PTSD?**
• Heightened threat perception
• Sensory re-experiencing
• Poor context discrimination
37
**Why do antipsychotics reduce hallucinations and delusions?**
• **D2 receptor blockade**
• Reduces aberrant salience
• Restores balance between prediction and input
38
**What is the biggest exam trap regarding perception?**
• Confusing perception with sensation
• Assuming hallucinations are imagination
39
**What is the key exam distinction between illusions and hallucinations?**
• **Illusions** = stimulus present
• **Hallucinations** = no external stimulus
40
**What is the key exam phrase for psychosis and perception?**
• **Psychosis is a disorder of salience attribution**
41
**Give the one-sentence exam summary of perception.**
• **Perception is an active, predictive process integrating sensory input and expectations; psychiatric disorders arise when prediction errors and salience are misweighted**
42
**What is perception? (exam-safe definition)**
• **Perception** is the process by which the brain **receives, organises, and interprets sensory information**
• Creates a **meaningful experience of the world**
• It is **active interpretation**, not passive recording
43
**What is the general sensory pathway for most senses?**
• **Sensory receptor**
• **Thalamus** (relay and gating station)
• **Primary sensory cortex**
• **Secondary and association cortices**
44
**What is the role of the sensory receptor?**
• Detects **physical energy** (light, sound, pressure, chemicals)
• Converts it into **neural signals** (transduction)
• Answers: **“Is there a stimulus?”**
45
**Why is the thalamus important in perception?**
• Acts as a **relay station**
• **Filters and modulates** sensory input
• Directs information to the correct cortical area
• Exam phrase: **Thalamus gates sensory input to cortex**
46
**What happens in the primary sensory cortex?**
• Processes **basic stimulus features**
• Is **modality-specific**
• Examples:
– **V1** → vision
– **S1** → somatosensation
– **A1** → audition
47
**What is the role of secondary and association cortices?**
• **Integrate features**
• Combine multiple sensory inputs
• Attach **meaning and recognition**
• This is where perception becomes **interpretation**
48
**What is the key exam exception to the general sensory pathway?**
• **Olfaction bypasses the thalamus initially**
• Pathway: olfactory receptor → olfactory bulb → cortex
• Very common **exam favourite**
49
**Why is visual perception heavily tested in psychiatry exams?**
• Neuroanatomy is well mapped
• Explains **hallucinations, agnosias, neglect**
• Demonstrates how perception is **constructed**
50
**What is the basic visual pathway from eye to cortex?**
• **Retina**
• **Lateral Geniculate Nucleus (LGN)** in thalamus
• **Primary visual cortex (V1)**
• Preserves **retinotopic organisation**
51
**What does the retina do beyond light detection?**
• Performs **early visual processing**
• Detects **contrast, edges, motion**
• Sends processed signals onward
• The eye is effectively **part of the brain**
52
**What is the lateral geniculate nucleus (LGN)?**
• A **thalamic nucleus**
• Relays visual information
• Maintains spatial organisation
• Modulates signals based on **attention**
53
**What is processed in primary visual cortex (V1)?**
• **Orientation**
• **Edges**
• **Contrast**
• **Basic motion**
• Answers: **“What visual features are present?”**
54
**What happens to visual information after V1?**
• Processing **splits into two streams**
• **Ventral stream**
• **Dorsal stream**
• Known as the **dual stream model**
55
**What is the ventral visual stream?**
• The **WHAT pathway**
• Runs from **occipital → temporal cortex**
56
**What does the ventral (WHAT) stream process?**
• **Object identity**
• **Faces**
• **Colour**
• **Form**
• Answers: **“What am I looking at?”**
57
**What happens if the ventral stream is damaged?**
• Causes **visual agnosia**
• Vision intact but objects not recognised
• Patient: **“I can see it but don’t know what it is”**
58
**What is the dorsal visual stream?**
• The **WHERE / HOW pathway**
• Runs from **occipital → parietal cortex**
59
**What does the dorsal stream process?**
• **Spatial location**
• **Movement**
• **Visual guidance of action**
• Answers: **“Where is it?”** and **“How do I interact with it?”**
60
**What happens if the dorsal stream is damaged?**
• **Visuospatial neglect**
• Impaired spatial awareness
• Difficulty guiding movement
• Common with **right parietal lesions**
61
**What is the one-line exam memory hook for visual streams?**
• **Ventral = WHAT (temporal)**
• **Dorsal = WHERE/HOW (parietal)**
62
**What is perceptual organisation?**
• How the brain **groups sensory elements**
• Constructs **coherent objects**
• Imposes structure on raw input
63
**What are Gestalt principles?**
• **Innate organisational rules**
• Show perception is **rule-based**
• Not a simple reflection of data
64
**What is figure–ground separation?**
• Ability to distinguish **object (figure)** from **background (ground)**
• Failure leads to perceptual confusion
65
**What is the Gestalt principle of proximity?**
• Elements **close together** are perceived as belonging together
66
**What is the Gestalt principle of similarity?**
• Elements that look **similar** are grouped together
67
**What is the Gestalt principle of continuity?**
• Preference for **smooth, continuous forms**
• Avoids abrupt changes
68
**What is the Gestalt principle of closure?**
• Brain **fills in missing information**
• Perceives complete objects even when parts are absent
69
**Why are Gestalt principles important in psychiatry?**
• Their disruption causes **fragmented perception**
• Leads to abnormal meaning-making
• Seen in **psychosis**
70
**How does disturbed perceptual organisation relate to psychosis?**
• Sensory input feels disorganised
• Brain imposes **delusional explanations**
• Hallucinations and misinterpretations emerge
71
**What are the most common exam traps in perception pathways?**
• ❌ Perception = sensation
• ❌ Thalamus is passive
• ❌ All senses go through thalamus
• ❌ Vision is a single pathway
72
**What are the correct exam principles for perception pathways?**
• Perception is **constructed**
• Thalamus **modulates**, not just relays
• **Olfaction bypasses thalamus initially**
• Vision uses **dual streams**
73
**Give the one-sentence exam summary of neural pathways of perception.**
• **Perception arises from hierarchical sensory processing with thalamic gating, cortical specialisation, dual visual streams, and Gestalt organisation—disruption of which underlies perceptual abnormalities in psychiatric illness**
74
**How is perception normally generated in the brain (physiology)?**
Normal perception arises from interaction between **bottom-up sensory input** (receptors → cortex) and **top-down predictions** (memory, expectations, beliefs). The brain constructs perception by **weighing both sources**.
75
**Why does the brain use predictions at all?**
Sensory input is **noisy**, **incomplete**, and **delayed**. Predictions allow the brain to **fill gaps**, **respond quickly**, and **reduce uncertainty**. This is normally **adaptive**, not pathological.
76
**What keeps perception accurate in healthy brains?**
Accuracy is maintained by **sensory precision**, **prediction error signalling**, and **error correction via learning**. When predictions are wrong, the brain **updates them**.
77
**What is a prediction error?**
A prediction error is the **difference between what the brain expects and what the senses report**. It signals: *“My model of the world is wrong.”*
78
**Which neurotransmitter systems encode prediction errors?**
Primarily **dopamine** (salience and learning signals) and **glutamate via NMDA receptors** (updating synaptic weights).
79
**What happens when prediction errors are encoded correctly?**
The brain **updates beliefs**, **refines predictions**, and **improves future perception**. Reality gradually **wins over expectation**.
80
**What is the fundamental pathophysiological error in hallucinations?**
The brain **mistakes internally generated neural activity for external sensory input**.
81
**Which three interacting failures cause hallucinations?**
1) **Sensory cortex hyperexcitability** 2) **Excess top-down predictions** 3) **Failure of self-monitoring/suppression**. These occur **together**, not in isolation.
82
**What does “overactive sensory cortex” mean physiologically?**
It means **increased baseline firing**, **spontaneous neural activity**, and **reduced inhibitory control (↓ GABA)**, so cortex fires **without external input**.
83
**Why does overactive cortical activity feel real to the patient?**
Because **perception equals cortical activation**. The brain has **no direct access to the outside world** and therefore trusts cortical signals as reality.
84
**What role does glutamate play in hallucinations?**
Excess or dysregulated **glutamate** increases cortical excitation, **amplifies internally generated signals**, and promotes **perceptual flooding**.
85
**What is self-monitoring in neurophysiology?**
Self-monitoring is the brain’s ability to **recognise actions and thoughts as self-generated** and **suppress their sensory consequences**.
86
**What is a corollary discharge / efference copy?**
A predictive signal sent from **action or thought-generating areas to sensory cortex** that says: *“This signal is coming from me — ignore it.”*
87
**What happens to corollary discharge in hallucinations?**
It is **weak or absent**, so internally generated signals are **not cancelled**, sensory cortex responds fully, and experiences feel **external**.
88
**Why are auditory hallucinations especially common?**
Because **inner speech** uses language production areas, activates auditory cortex, and normally requires **strong self-monitoring**.
89
**What goes wrong with inner speech in auditory hallucinations?**
Inner speech is generated normally but **not recognised as self-generated**, so it is perceived as an **external voice**.
90
**Which cortical areas are abnormally active in auditory hallucinations?**
The **superior temporal gyrus (auditory cortex)** and language perception areas activate **as if hearing real speech**.
91
**What are top-down predictions biologically?**
Signals from **prefrontal cortex**, **memory networks**, and **belief systems** that shape what sensory cortex expects to perceive.
92
**How do excessive predictions cause hallucinations?**
When predictions are **too strong**, **too precise**, and **insufficiently corrected**, they **override absent sensory input**.
93
**What does “precision weighting” mean in hallucinations?**
It determines whether the brain trusts **sensory input or predictions** more. In hallucinations, **predictions are overweighted** and **sensory evidence underweighted**.
94
**Why do delusions follow hallucinations or odd perceptions?**
Because the brain experiences something abnormal, **assigns importance**, and **tries to explain it**. Beliefs form as **explanatory models**.
95
**What is aberrant salience biologically?**
**Inappropriate dopamine firing** that assigns importance **without valid cause**, so neutral stimuli feel **urgent and meaningful**.
96
**How does dopamine distortion affect learning?**
Dopamine signals prediction errors and learning importance. When dysregulated, **errors are signalled at the wrong times** and beliefs **update incorrectly**.
97
**Why do delusions become fixed?**
Because abnormal salience is **repeated**, **NMDA-dependent belief updating is impaired**, and **contradictory evidence is discounted**.
98
**What are the four core biological abnormalities in schizophrenia-related perception?**
1) **Dopamine dysregulation** 2) **NMDA receptor hypofunction** 3) **Excess top-down predictions** 4) **Weak sensory error correction**.
99
**How does NMDA receptor hypofunction contribute to psychosis?**
It causes **poor integration of sensory inputs**, **weak learning from prediction error**, and **fragmented perception**.
100
**Why does the brain trust expectations more than reality in schizophrenia?**
Because predictions are **precise and loud**, sensory signals are **noisy and weak**, and **error correction fails**.
101
**What is the key pathological signal targeted by antipsychotics?**
**Dopamine-mediated aberrant salience**.
102
**How does D2 receptor blockade change perception?**
It **reduces inappropriate importance signals**, **dampens prediction errors**, and **weakens reinforcement of false beliefs**.
103
**Why do hallucinations often improve before delusions?**
Hallucinations depend on **current salience**, whereas delusions are **learned belief structures** that take longer to unlearn.
104
**Give the exam-perfect one-sentence summary.**
**Hallucinations arise when overactive sensory cortices, excessive top-down predictions, and failed self-monitoring cause internally generated signals to be perceived as external, while delusions emerge through dopamine-driven aberrant salience and faulty prediction-error learning that stabilises false beliefs.**
105
**How is perception normally generated in the brain (physiology)?**
Normal perception arises from interaction between **bottom-up sensory input** (receptors → cortex) and **top-down predictions** (memory, expectations, beliefs). The brain constructs perception by **weighing both sources**.
106
**Why does the brain use predictions at all?**
Sensory input is **noisy**, **incomplete**, and **delayed**. Predictions allow the brain to **fill gaps**, **respond quickly**, and **reduce uncertainty**. This is normally **adaptive**, not pathological.
107
**What keeps perception accurate in healthy brains?**
Accuracy is maintained by **sensory precision**, **prediction error signalling**, and **error correction via learning**. When predictions are wrong, the brain **updates them**.
108
**What is a prediction error?**
A prediction error is the **difference between what the brain expects and what the senses report**. It signals: *“My model of the world is wrong.”*
109
**Which neurotransmitter systems encode prediction errors?**
Primarily **dopamine** (salience and learning signals) and **glutamate via NMDA receptors** (updating synaptic weights).
110
**What happens when prediction errors are encoded correctly?**
The brain **updates beliefs**, **refines predictions**, and **improves future perception**. Reality gradually **wins over expectation**.
111
**What is the fundamental pathophysiological error in hallucinations?**
The brain **mistakes internally generated neural activity for external sensory input**.
112
**Which three interacting failures cause hallucinations?**
1) **Sensory cortex hyperexcitability** 2) **Excess top-down predictions** 3) **Failure of self-monitoring/suppression**. These occur **together**, not in isolation.
113
**What does “overactive sensory cortex” mean physiologically?**
It means **increased baseline firing**, **spontaneous neural activity**, and **reduced inhibitory control (↓ GABA)**, so cortex fires **without external input**.
114
**Why does overactive cortical activity feel real to the patient?**
Because **perception equals cortical activation**. The brain has **no direct access to the outside world** and therefore trusts cortical signals as reality.
115
**What role does glutamate play in hallucinations?**
Excess or dysregulated **glutamate** increases cortical excitation, **amplifies internally generated signals**, and promotes **perceptual flooding**.
116
**What is self-monitoring in neurophysiology?**
Self-monitoring is the brain’s ability to **recognise actions and thoughts as self-generated** and **suppress their sensory consequences**.
117
**What is a corollary discharge / efference copy?**
A predictive signal sent from **action or thought-generating areas to sensory cortex** that says: *“This signal is coming from me — ignore it.”*
118
**What happens to corollary discharge in hallucinations?**
It is **weak or absent**, so internally generated signals are **not cancelled**, sensory cortex responds fully, and experiences feel **external**.
119
**Why are auditory hallucinations especially common?**
Because **inner speech** uses language production areas, activates auditory cortex, and normally requires **strong self-monitoring**.
120
**What goes wrong with inner speech in auditory hallucinations?**
Inner speech is generated normally but **not recognised as self-generated**, so it is perceived as an **external voice**.
121
**Which cortical areas are abnormally active in auditory hallucinations?**
The **superior temporal gyrus (auditory cortex)** and language perception areas activate **as if hearing real speech**.
122
**What are top-down predictions biologically?**
Signals from **prefrontal cortex**, **memory networks**, and **belief systems** that shape what sensory cortex expects to perceive.
123
**How do excessive predictions cause hallucinations?**
When predictions are **too strong**, **too precise**, and **insufficiently corrected**, they **override absent sensory input**.
124
**What does “precision weighting” mean in hallucinations?**
It determines whether the brain trusts **sensory input or predictions** more. In hallucinations, **predictions are overweighted** and **sensory evidence underweighted**.
125
**Why do delusions follow hallucinations or odd perceptions?**
Because the brain experiences something abnormal, **assigns importance**, and **tries to explain it**. Beliefs form as **explanatory models**.
126
**What is aberrant salience biologically?**
**Inappropriate dopamine firing** that assigns importance **without valid cause**, so neutral stimuli feel **urgent and meaningful**.
127
**How does dopamine distortion affect learning?**
Dopamine signals prediction errors and learning importance. When dysregulated, **errors are signalled at the wrong times** and beliefs **update incorrectly**.
128
**Why do delusions become fixed?**
Because abnormal salience is **repeated**, **NMDA-dependent belief updating is impaired**, and **contradictory evidence is discounted**.
129
**What are the four core biological abnormalities in schizophrenia-related perception?**
1) **Dopamine dysregulation** 2) **NMDA receptor hypofunction** 3) **Excess top-down predictions** 4) **Weak sensory error correction**.
130
**How does NMDA receptor hypofunction contribute to psychosis?**
It causes **poor integration of sensory inputs**, **weak learning from prediction error**, and **fragmented perception**.
131
**Why does the brain trust expectations more than reality in schizophrenia?**
Because predictions are **precise and loud**, sensory signals are **noisy and weak**, and **error correction fails**.
132
**What is the key pathological signal targeted by antipsychotics?**
**Dopamine-mediated aberrant salience**.
133
**How does D2 receptor blockade change perception?**
It **reduces inappropriate importance signals**, **dampens prediction errors**, and **weakens reinforcement of false beliefs**.
134
**Why do hallucinations often improve before delusions?**
Hallucinations depend on **current salience**, whereas delusions are **learned belief structures** that take longer to unlearn.
135
**Give the exam-perfect one-sentence summary.**
**Hallucinations arise when overactive sensory cortices, excessive top-down predictions, and failed self-monitoring cause internally generated signals to be perceived as external, while delusions emerge through dopamine-driven aberrant salience and faulty prediction-error learning that stabilises false beliefs.**
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
