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Light enters the eye through which two structures?
The cornea and the pupil (cornea = transparent outer coating, principal means of focus; pupil = hole in the iris through which light passes).
Rods vs cones — function?
Rods: vision at low light levels, very sensitive to darkness, coarse spatial structure, ~120 million. Cones: vision in bright light, colour vision, fine detail, ~6 million.
Are rods/cones unique to vertebrates?
No — that's a distractor. Cones = colour vision; rods = vision in dim light.
What is the blind spot and why don't we notice it?
The point on the retina where the optic nerve exits no photoreceptors there. We don't notice it because it falls in peripheral vision and the brain "fills in" the gap.
What is the cortical magnification factor, and what's a key example of it?
The area of cortex thats dedicated more cortical area to processing central vision than peripheral vision. e.g. the fovea gets a disproportionately large amount of brain space for detailed light
Dorsal vs ventral visual pathway (Milner & Goodale)?
Dorsal = action (vision for action); Ventral = perception (vision for perception).
What is a double dissociation?
When two patients show complementary/opposite performance deficits — each impaired on the task the other can do — showing the two functions rely on independent mechanisms.
Case of DF (visual form agnosia) — what can and can't she do?
Damage to ventral pathway (perception). Can't visually recognise objects/shapes (e.g. can't describe a screwdriver by sight but can by touch) BUT can perform accurate visually-guided actions (posting a card through an oriented slot).
How are modules defined in cognitive science (Fodor) vs physiologically?
Physiological modules = defined by location/what they process. Fodor's cognitive modules are functionally, not physiologically, defined — i.e., modules can be hypothetical/theoretical.
What features does Fodor say modules tend to have, and which one does Coltheart say is most critical?
Domain specific, innately specified, informationally encapsulated, fast, hardwired, autonomous (modules don't need all of these). Coltheart argues domain specificity (only responding to a particular class of stimuli) is the defining feature.
Endogenous vs exogenous covert attention — sources and effects?
Endogenous = from within (you choose where to focus); exogenous = from without (something in the environment grabs your focus automatically). With covert attention you react faster and notice detail better there — even without moving your eyes.
Why does head movement matter in Patient "AI" (Gilchrist, Brown & Findlay, 1997)?
AI cannot make eye movements, so she uses head movements to direct her fovea to areas of interest in the visual field — i.e., to sample the visual field with the area of retina with the highest photoreceptor density.
What did Findlay & Gilchrist (2003) conclude about covert attention during fixation?
Covert attention shifts are slow and linked to eye molvement planning meaning they dont typically occur during a single fixation.
What implication does the prevalence effect have for screening tasks (e.g. baggage, medical screening)?
Screeners get worse at spotting rare targets because they rarely see them. So training them using practice runs where the target is present much more often than in real life helps keep their detection skills sharp
What did Rayner et al. (2001) conclude about teaching reading?
Mastering the alphabetic principle (phonics) is essential and more effective than approaches that don't teach it directly, though whole-language activities can usefully supplement phonics.
How do speed readers compare to normal readers (Just, Carpenter & Masson, 1982)?
Speed readers read ~3x faster and get equally good general comprehension, but — because they use fewer fixations/less visual information — they perform worse than normal readers on detailed questions about content they didn't fixate.
Which papillae type has NO taste buds?
Filiform papillae (cone-shaped) — all other types (fungiform, foliate, circumvallate) contain taste buds.
Where can salty taste receptors be found?
In fungiform, foliate, or circumvallate papillae (not filiform, which has no taste buds).
What are orthonasal vs retronasal olfaction, and what happens when you pinch your nose?
Orthonasal = smelling via the nose (sniffing). Retronasal = odorant molecules from the mouth/pharynx reaching the olfactory mucosa (contributes to flavour while eating). Pinching your nose blocks BOTH orthonasal and retronasal olfaction, and therefore affects flavour — but does not affect basic taste discrimination (you can still tell salty from sweet).
Which mechanoreceptors are close to the surface vs deep, and how does that relate to receptive field size?
Merkel & Meissner are close to the surface (smaller receptive fields). Ruffini & Pacinian are deeper in the skin (larger receptive fields).
We sense light touch thanks to which receptor type?
Rapidly-adapting receptors close to the surface of the skin (Meissner corpuscles).
Which receptors matter most for holding an object without letting it slip?
Rapidly adapting receptors, both deep and close to the surface (Meissner + Pacinian working together for grip control and detecting slip).
What determines loudness vs pitch?
Amplitude (pressure difference between peaks/troughs) determines loudness. Frequency (Hz) determines pitch.
Why do the ossicles matter (why do we need them)?
They amplify vibrations: (1) prevent attenuation when sound passes from air to the liquid medium of the inner ear, (2) concentrate force on a small surface (stapes footplate), (3) act as a lever — all increasing pressure at the stapes.
In the cochlea, where do high frequency sounds cause the most vibration?
More accentuated at the base of the tectorial/basilar membrane (basal region); low frequencies are processed more at the apex.
Patients JG and ES (Clarke et al., 2002) — what and where?
ES: can't localize sounds but can recognize them. JG: can localize sounds but can't recognize them. Double dissociation between sound identification ("what") and sound localisation ("where") pathways.
Broca's vs Wernicke's aphasia?
Broca's area damage: impaired speech production/fluency, but comprehension is largely intact. Wernicke's area damage: fluent speech but poor comprehension.
Older adults and signal-to-noise ratio for speech — what does this mean practically?
Older adults need a higher signal-to-noise ratio to understand speech — meaning they have more difficulty understanding speech specifically when background noise is present (not simply in silence, and not specifically about loudness alone).
McCaul & Haugtevdt (1982) — attention and pain (cold water task)?
Distraction (attending to slides) vs. attending to pain sensations: distraction group took longer to feel pain (76s vs 20s) and tolerated pain longer (99s vs 69s) than the sensation-focused group.
Placebo vs nocebo effect — definitions?
Placebo effect = beneficial response to a treatment with no active ingredient. Nocebo effect = negative side effect from a treatment with no active ingredient.
What factors increase the placebo effect
Branded (vs generic) pills; certain colours (red/yellow/orange = stimulant association, blue/green = tranquilising); a doctor (vs machine) administering it; medication that produces side effects (vs none); higher expectancy of relief (Price et al., 1999).
Kaptchuk et al. (2014) — "open-label" placebo finding?
The placebo effect still occurred even when patients with migraines were explicitly told the treatment was a placebo.
Bingel et al. (2011) — expectation and pain ratings (all 4 conditions actually received painkiller except baseline)?
Positive expectation (told receiving painkiller) → lowest pain (39). No expectation (told still receiving saline) → moderate (55). Negative expectation (told painkiller stopped) → high pain (64), similar to baseline/no treatment (66) — even though the same painkiller was being given in all 3 non-baseline conditions.
A study compares no-treatment, sugar-pill (told it's a painkiller), and real painkiller (told it's a painkiller); pain tolerance rises step-wise across the three groups. What can we conclude?
The beneficial effect of the real painkiller reflects a combination of the placebo effect (sugar pill > no treatment) and the pharmacological effect of the active ingredient (painkiller > sugar pill) — not one or the other alone.
In an experiment where males take longer than females to report first feeling pain from holding a weight, what does that tell us — threshold or tolerance?
It reflects pain threshold (time until pain is first reported), not tolerance (which would be time until they can no longer bear it/give up) — so males have a higher pain threshold than females in this design.
Glaucoma — what does it damage and what part of vision is lost first?
Build-up of intraocular pressure (aqueous fluid not draining properly) damages the optic nerve; affects peripheral vision first, producing "tunnel vision" — central vision is relatively preserved until later stages.
Given a glaucoma patient looking straight ahead, what happens to an object directly in front (central) vs 45° to the side (peripheral)?
They can still see the central object (Object A) but have trouble seeing the peripheral object (Object B) — because glaucoma affects peripheral vision first.
Age-related macular degeneration (AMD) — what part of vision is affected?
Central vision loss (scotoma) due to deterioration of the macula; peripheral vision is usually unaffected. People often adopt a "preferred retinal locus" to use peripheral vision instead.
Name the 4 hypotheses for the link between age-related sensory and cognitive decline.
(1) Common cause — a shared third factor (e.g. cardiovascular changes) drives both. (2) Cognitive load on perception — poor cognition affects perceptual task performance. (3) Information degradation — poor perceptual input consumes extra cognitive resources, leaving fewer for the task itself. (4) Sensory deprivation — sensory loss leads to social isolation/reduced stimulation → cognitive decline over time.
Dr Musa's research shows metabolic processes explain both reduced acuity and memory decline with age. Which hypothesis does this support?
Common cause hypothesis (a general/third factor — here, metabolic processes — underlies decline in both perception and cognition).
Dementia with Lewy Bodies — key features and hallucination type?
Alpha-synuclein protein deposits in neurons; cognitive decline, movement problems, hallucinations (up to 80% of patients) — hallucinations are usually complex (people/animals), often unpleasant, linked to lewy body density in amygdala/parahippocampus.
Parkinson's Disease Dementia — key link?
50–80% of Parkinson's patients eventually develop dementia; PD dementia (like DLB) is associated with Lewy bodies; ~40% of PD patients report a hallucination (visual and auditory) within a 3-month period; PD itself involves tremor, slow movement, muscle stiffness.
Charles-Bonnet syndrome — what is it and what theory explains it?
Visual hallucinations (often distressing, can be simple patterns or complex scenes/people) resulting from sight loss (not associated with cognitive impairment). Explained by the sensory deprivation theory: loss of visual input changes excitability of the visual association cortex.
Phantom limb syndrome — congenital vs acquired amputation?
Virtually absent in congenital amputees (born without the limb) but occurs in the majority of people who lose a limb later — showing there's a critical period in sensory system development (Melzack et al., 1997: only 20% born without limbs vs 50% amputated early in life experienced phantom sensations).
Congenital vs acquired nystagmus — key perceptual difference?
Acquired nystagmus often causes oscillopsia (the world appears to move); congenital nystagmus typically does NOT — the person has a stable perception of the world despite the involuntary eye movements, because their visual system developed while adapting to the eye movement pattern from birth.
Two patients have involuntary eye movements; Patient O has a stable world, Patient T's world seems to constantly move. Most likely explanation?
Patient O has congenital nystagmus (adapted since birth, stable perception); Patient T has acquired nystagmus (develops later, causes oscillopsia).
Congenital vs acquired cataracts — outcome after removal?
Congenital cataracts, if not removed quickly (ideally before ~12 weeks of age), can cause permanent visual impairment (amblyopia) even after removal, because the developing visual system was deprived of clear input during a critical period. Adult (acquired) cataracts usually have very good visual outcomes after surgery.
What is the axon's main function?
To send information to other neurons via action potentials (active conduction).
What is the resting membrane potential, and which side is more negative?
Around -70mV, with the inside of the neuron more negative relative to the outside.
During hyperpolarisation, which direction does the membrane potential move first?
More negative (undershooting below resting potential), before returning to the resting membrane potential.
Grey matter vs white matter — what are they made of?
Grey matter = mainly neuronal cell bodies (e.g. cerebral cortex, subcortex). White matter = mainly myelinated axons and support (glial) cells — axons and support cells are most abundant here.
What structures make up the limbic system, and their functions?
Amygdala (fear response), cingulate gyrus (emotion & cognition), hippocampus (learning & memory), mammillary bodies (memory consolidation) — olfactory bulb is also connected to it.
What does the diencephalon regulate?
Thalamus: major subcortical sensory relay to the cortex. Hypothalamus: homeostasis (temperature, hunger, thirst, endocrine function). Together: sensory relay and homeostasis.
What does the thalamus specifically do?
Relays sensory information (of all modalities, e.g. auditory) to the cortex.
Effects of unilateral vs bilateral cerebellar lesions?
Unilateral: poor coordination on the ipsilateral (same) side of the body. Bilateral: wide staggering gait, slurred speech, nystagmus.
What did Hubel & Wiesel find recording from cat visual cortex?
Visual cortex cells are selectively tuned to orientation, size, motion direction, and speed of a stimulus.
What does EEG measure, and is it invasive?
Dendritic currents/electrical signals from populations of neurons, via scalp electrodes; non-invasive.
EEG's strengths and weaknesses (resolution)?
Good temporal resolution; poor/limited spatial resolution.
Two methods for measuring electrical potentials in the brain?
Single unit recording and EEG.
Key advantages of MRI over CT?
Differentiates white/grey matter, no radiation, much better spatial resolution, can be adapted for fMRI.
What is the BOLD signal in fMRI based on?
The paramagnetic properties of deoxyhaemoglobin, which introduce distortions in the local magnetic field — more deoxyhaemoglobin (after oxygen use) = more distortion = inferred greater neural activity.
fMRI resolution trade-off?
High spatial resolution (up to ~1mm) but poor temporal resolution (several seconds) — the HRF is slow (~15–20 sec), so fMRI can't capture very rapid (millisecond) cognitive processes.
What does PET measure, and what's the signal chain?
Metabolic characteristics of tissue. A radioactive isotope is injected → travels to active brain areas via blood → breaks down/emits positrons → produces gamma rays → used to construct an image; greater blood flow/metabolism = more gamma ray signal.
Two ways to measure cerebral blood flow?
fMRI and PET.
Classical vs strong single dissociation?
Classical: patient performs normally on task B but is impaired on task A. Strong: patient is impaired on both tasks, but significantly more so on one.
Broca's area — location and function?
Left frontal lobe; controls motor aspects of speech production. Damage → impaired speech production, but comprehension of spoken/written language is preserved.
What is TMS (transcranial magnetic stimulation) based on, and what does it produce?
Magnetic induction: electric current in a coil generates a magnetic field, which induces a secondary electric current in the brain, causing interference in neuronal activity ("virtual lesion") at the stimulation site.
Depolarisation vs hyperpolarisation in the context of TMS?
Depolarisation (more positive inside) → neuron more likely to fire → TMS induces activity. Hyperpolarisation (more negative inside) → neuron less likely to fire → TMS blocks/inhibits activity.
Key difference between TMS and fMRI?
TMS can be used for group studies and offers causal (not just correlational) evidence by directly interfering with neural activity, but TMS is limited to targeting neurons near the cortical surface (can't reach subcortical structures), and it has better temporal precision than fMRI, though fMRI has better spatial resolution overall.